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Textbook of Peripheral Vascular Interventions
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Textbook of Peripheral Vascular Interventions Second Edition Edited by
Richard R Heuser
MD FACC FACP FESC
Director of Cardiology, St. Luke's Medical Center; Clinical Professor of Medicine, University of Arizona College of Medicine Phoenix, AZ USA and
Michel Henry MD Interventional Cardiologist Cabinet de Cardiologie Nancy France and Global Research Institute, Apollo Clinic Hyderabad India
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© 2008 Informa UK Ltd First edition published in the United Kingdom in 2004 Second edition published in the United Kingdom in 2008 by Informa Healthcare, Telephone House, 69-77 Paul Street, London EC2A 4LQ. Informa Healthcare is a trading division of Informa UK Ltd. Registered Office: 37/41 Mortimer Street, London W1T 3JH. Registered in England and Wales number 1072954. Tel: +44 (0)20 7017 5000 Fax: +44 (0)20 7017 6699 Website: www.informahealthcare.com All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted, in any form or by any means, electronic, mechanical, photocopying, recording, or otherwise, without the prior permission of the publisher or in accordance with the provisions of the Copyright, Designs and Patents Act 1988 or under the terms of any licence permitting limited copying issued by the Copyright Licensing Agency, 90 Tottenham Court Road, London W1P 0LP. Although every effort has been made to ensure that all owners of copyright material have been acknowledged in this publication, we would be glad to acknowledge in subsequent reprints or editions any omissions brought to our attention. Although every effort has been made to ensure that drug doses and other information are presented accurately in this publication, the ultimate responsibility rests with the prescribing physician. Neither the publishers nor the authors can be held responsible for errors or for any consequences arising from the use of information contained herein. For detailed prescribing information or instructions on the use of any product or procedure discussed herein, please consult the prescribing information or instructional material issued by the manufacturer. A CIP record for this book is available from the British Library. Library of Congress Cataloging-in-Publication Data Data available on application ISBN-10: 1 84184 643 0 ISBN-13: 978 1 84184 643 9 Distributed in North and South America by Taylor & Francis 6000 Broken Sound Parkway, NW, (Suite 300) Boca Raton, FL 33487, USA Within Continental USA Tel: 1 (800) 272 7737; Fax: 1 (800) 374 3401 Outside Continental USA Tel: (561) 994 0555; Fax: (561) 361 6018 Email:
[email protected] Book orders in the rest of the world Paul Abrahams Tel: +44 207 017 4036 Email:
[email protected] Composition by Cepha Imaging Pvt. Ltd., Bangalore, India. Printed and bound in India by Replika Press Pvt. Ltd.
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I would like to dedicate the textbook to my wife, Shari; my daughter, Alexandra; and the research staff at the Phoenix Heart Center and the staff at the Phoenix Heart Center, all of whom have made this possible. RRH I would like to dedicate the textbook to my wife, Annick; my daughters, Brigitte and Dr Isabelle Henry; my grand-children, Eva, Nicolas and Romain; my sister and brother-in-law, Mr and Mrs Jacques Vallet and Hervé. I would also like to thank Mrs Michele Hugel, my assistant, for our fruitful collaboration, and Mr Noureddine Frid for his technical collaboration, as well as Dr Antonios Polydorou, for his valuable support, skills and assistance. MH
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Contents List of Contributors
xiii
Preface
xix
Color plates SECTION I: INTRODUCTION
1
1.
Epidemiology and pathophysiology of peripheral arterial disease (PAD) GI Pandele and C Dima-Cozma
3
2.
The endovascular suite and equipment K Dougherty and Z Krajcer
7
SECTION II: TECHNIQUES
13
3.
Arterial access for endovascular interventions: vascular access JS Jenkins
15
4.
Arterial access for endovascular interventions: radial and brachial arterial access PW McMullan Jr and JS Jenkins
21
5.
Arterial access for endovascular interventions: transradial approach I Henry, M Henry, and M Hugel
26
6.
Arterial access for endovascular interventions: popliteal access to peripheral procedures M Henry, I Henry, and M Hugel
29
7.
Introducer sheaths, catheters, guiding catheters, and guidewires K Dougherty and Z Krajcer
34
8.
Percutaneous transluminal angioplasty T Collins and PW McMullan Jr
39
9.
Cutting balloon angioplasty S Tyagi
45
10.
SilverHawk® atherectomy device RS Gammon and JR Nelson
50
11.
Percutaneous peripheral atherectomy using the Rotablator I Henry, M Henry, and M Hugel
59
12.
A new rotational thrombectomy and atherectomy catheter: the Rotarex system I Henry, M Henry, and M Hugel
69
13.
Orbital atherectomy system: a novel means of peripheral vascular rotational atherectomy DT Cragen and RR Heuser
79
14.
Subintimal angioplasty G Markose and A Bolia
83
15.
Recanalization devices for chronic total occlusions (including optical coherent reflectometry) G Baweja and RR Heuser
92
16.
Catheter-directed intra-arterial thrombolytic therapy NN Khanna and RR Kasliwal
99
17.
Thromboaspiration and thrombectomy in peripheral vessels NN Khanna
111
18.
The future of thrombolysis T McNamara
118
vii
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19.
Endovascular treatment for acute and chronic lower extremity deep vein thrombosis PE Thorpe and FJ Osse
119
20.
Stents RR Heuser, KL Waters, CW Hatler, and LM Kelly
132
21.
Role of covered stents in peripheral arterial diseases M Henry, I Henry, and M Hugel
140
22.
Embolic protection devices M Henry, I Henry, A Polydorou, and M Hugel
156
23.
Vascular closure devices ZG Turi
168
24.
Other techniques of percutaneous intervention: retrieval devices, embolization therapy, and angiogenesis JA Silva and JS Jenkins
179
SECTION III: NEUROVASCULAR
185
25.
Epidemiology and pathophysiology of neurovascular disease C Klonaris, A Papapetrou, and A Katsargyris
187
26.
Neuroradiological anatomy MH Wholey and WS Wu
192
27.
Doppler ultrasound and carotid angioplasty: carotid ultrasonography and transcranial Doppler S Kownator and F Luizy
199
28.
The value of transcranial Doppler ultrasonography before, during, and after surgery for carotid occlusive disease NM Bornstein and AY Gur
207
29.
Carotid plaque characterization using ultrasound AN Nicolaides, M Griffin, S Kakkos, G Geroulakos, E Kyriacou, and N Georgiou
211
30.
Cerebral perfusion imaging W-J Jiang
229
31.
Stent-assisted angioplasty for symptomatic atherosclerotic intracranial stenosis W-J Jiang
238
32.
Intracranial stenting for cerebrovascular pathology EI Levy, AS Boulos, BR Bendok, SH Kim, AI Qureshi, LR Guterman, and LN Hopkins
247
33.
The stroke unit P Lylyk and JF Vila
255
34.
Interventional treatment of acute ischemic stroke: past, present, and future CS Eddleman, ZA Hage, DL Surdell, EI Levy, RM Samuelson, YA Mikhaeil, and BR Bendok
288
35.
Carotid angioplasty and stenting under protection: techniques, indications, results, and limitations M Henry, A Polydorou, I Henry, Ad Polydorou, and M Hugel
300
36.
Complications of internal carotid artery stenting and their management DL Surdell, ZA Hage, CS Eddleman, S Das, E Duckworth, MK Eskandari, IA Awad, HH Batjer, and BR Bendok
336
37.
Which patients should be referred for surgical endarterectomy and not have carotid stenting FJ Criado and C Gallagher
345
38.
Common carotid artery: PTA stenting J Franke, G Robertson, and H Sievert
348
39.
Percutaneous transluminal angioplasty of the subclavian arteries M Henry, I Henry, A Polydorou, Ad Polydorou, and M Hugel
353
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ix
40.
Percutaneous transluminal angioplasty and stenting of extracranial vertebral artery stenosis V Polydorou, I Henry, A Polydorou, M Henry, Ad Polydorou, J Stephanides, M Hugel, and S Anagnostopoulou
371
41.
Elective endovascular revascularization of the intracranial cerebral arteries HC Schumacher, PM Meyers, B Bateman, and RT Higashida
382
SECTION IV: UPPER EXTREMITY ARTERIAL DISEASES
399
42.
Upper extremity arterial diseases J Laredo and BB Lee
401
43.
Compression syndromes of the superior thoracic aperture JE Molina
408
SECTION V: THORACIC AORTA
415
44.
Thoracic aorta: epidemiology and pathophysiology EB Diethrich
417
45.
Radiology and anatomy of the thoracic aorta AR Owen, GH Roditi, and AW Reid
422
46.
Thoracic aorta: thoracic aortic aneurysms EB Diethrich
432
47.
Thoracic aortic dissection J May, GH White, and JP Harris
439
SECTION VI: ABDOMINAL AORTA
447
48.
Abdominal aortic aneurysm treatment by endoluminal exclusion: a historical perspective JC Parodi, CJ Schönholz, and RR Heuser
449
49.
Role of Doppler ultrasound in the assessment of peripheral vascular disease K Irshad, M Ali, AW Reid, A Sinha, and DB Reid
456
50.
Abdominal aortic dissections OC Morcos, JC Pereda, and ML Marin
461
51.
Endovascular treatment of abdominal aortic occlusive disease C Klonaris and A Katsargyris
467
SECTION VII: THORACOABDOMINAL ANEURYSMS AND DISSECTIONS
473
52.
475
Thoracoabdominal aneurysms and dissections: current indications and management JF Dowdall, Q Lu, and RK Greenberg
SECTION VIII: ATHEROSCLEROTIC RENAL ARTERY STENOSIS
485
53.
Atherosclerotic renal artery stenosis: epidemiology and pathophysiology KI Paraskevas, DP Mikhailidis, and G Hamilton
487
54.
Radiological assessment of the renal arteries A Al-Kutoubi
494
55.
Endovascular treatment of a renal artery stenosis: techniques, indications, and results M Henry, I Henry, A Polydorou, Ad Polydorou, and M Hugel
502
56.
Renal angioplasty and stenting under protection devices M Henry, I Henry, A Polydorou, Ad Polydorou, and M Hugel
525
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57.
Renal artery stenosis: when to refer to surgery? C Klonaris, A Katsargyris, and A Giannopoulos
539
58.
Non-atherosclerotic renovascular disease JM Garasic and K Rosenfield
544
SECTION IX: CELIAC AND MESENTERIC ARTERIES
551
59.
Etiology, natural history, and pathophysiology of mesenteric ischemia JA Silva
553
60.
Assessment of mesenteric ischemia JA Silva
557
61.
Conventional angiography, CTA, and MRA of the mesenteric arteries Y-W Chi and JA Silva
562
62.
Duplex ultrasound of the mesenteric arteries Y-W Chi and JA Silva
570
63.
Endovascular therapy for mesenteric ischemia JA Silva
574
64.
Mesenteric ischemia: surgical revascularization and indications for surgery JA Silva and DE Allie
581
SECTION X: LOWER EXTREMITY
587
65.
Epidemiology and pathophysiology of peripheral arterial disease of the lower extremities C Klonaris, A Papapetrou, and A Giannopoulos
589
66.
Lower extremity arterial disease assessment KF Murphy, K Irshad, A Sinha, and DB Reid
593
67.
Lower extremity: other techniques ML Brennan and L Cho
601
68.
Iliac occlusive diseases DT Cragen and RR Heuser
606
69.
Procedures for the hypogastric artery J Cynamon and P Prabhaker
614
70.
Femoropopliteal disease E Calabrese and F Camerano
625
71.
When to refer to surgery for femoropopliteal disease N Morrissey
630
72.
Infrapopliteal arterial diseases: angioplasty and stenting E Calabrese
633
73.
Critical limb ischemia DE Allie, CJ Hebert, EV Mitran, CM Walker, and RR Patlola
639
74.
Acute limb ischemia DE Allie, CJ Hebert, EV Mitran, CM Walker, and RR Patlola
648
75.
Endovascular treatment for infrainguinal failing graft A de Carvalho Lobato and DF Colli Jr
656
76.
Thromboangiitis obliterans (Buerger’s disease) A Pokrovsky and AV Chupin
661
77.
Percutaneous endovascular treatment of peripheral aneurysms M Henry, I Henry, and M Hugel
670
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SECTION XI: OTHER LOCALIZATIONS
681
78.
Embolization in peripheral territory CJ Schönholz, E Mendaro, and K Ehrens
683
79.
Uterine artery embolization for fibroids J Pisco and M Duarte
692
80.
Hemodialysis access intervention E Calabrese and B Yasin
699
81.
Endovascular surgery in treatment of some congenital heart defects BG Alekyan, VP Podzolkov, VA Garibyan, MG Pursanov, KE Kardenas, and E Yu Danilov
703
82.
Endovascular treatment of some congenital diseases: hemangiomas and vascular malformations BB Lee, J Laredo, DH Deaton, and RF Neville
712
SECTION XII: UNUSUAL VASCULAR DISEASES OF THE EXTREMITIES 83.
Endovascular management of Budd-Chiari syndrome – suprahepatic inferior vena cava occlusive disease BB Lee, J Laredo, DH Deaton, and RF Neville
723 725
84.
Unusual vascular conditions of the extremities DH Deaton, RF Neville, J Laredo, and BB Lee
732
85.
Interventions in inflammatory arterial disease S Rajagopal and L Gopalakrishnan
736
86.
Vascular involvement in Behçet’s disease TW Kwon
743
SECTION XIII: MULTIVASCULAR DISEASE 87.
Potential of endovascular surgery in the treatment of patients with ischemic heart disease associated with other arterial pools’ pathology LB Bockeria, BG Alekyan, Yu I Buziashvili, EZ Golukhova, TG Niritina NP Mironov, AV Ter-Akopyan, NV Zakarian, and AV Staferov
749 751
SECTION XIV: TREATMENTS FOR RESTENOSIS
761
88.
Pathophysiology of restenosis E Kedhi, J-F Tanguay, and L Bilodeau
763
89.
Interventional therapy: new approaches E Kedhi and L Bilodeau
770
90.
Update on peripheral vascular brachytherapy R Waksman
776
91.
Gene-based and angiogenesis therapy in cardiovascular diseases R Baffour, S Fuchs, and R Kornowski
782
SECTION XV: PTA/STENTING COMPLICATIONS
789
92.
Complications of peripheral interventions DT Cragen and RR Heuser
791
93.
Contrast-induced nephropathy G Marenzi and AL Bartorelli
799
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SECTION XVI: PHARMACOLOGICAL TREATMENTS AND RISK FACTOR MANAGEMENT
809
94.
Pharmacological treatment in peripheral arterial disease GI Pandele and C Dima-Cozma
811
95.
Risk factors in peripheral arterial disease GI Pandele and C Dima-Cozma
822
SECTION XVII: VENOUS DISEASE
827
96.
The anatomy, epidemiology, and pathophysiology of venous disease JI Greenberg, N Angle, and J Bergan
829
97.
Diagnostic evaluation of venous disease B Abai and N Labropoulos
835
98.
Contrast imaging studies of the lower extremity GE Pineda and D Mukherjee
841
99.
Interventional therapy for pulmonary embolism S Faintuch, FB Collares, and GM Martinez Salazar
849
100.
Superior and inferior vena cava thrombosis J Pisco and M Duarte
858
101.
Varicose veins CK Shortell and J Bergan
864
102.
Endovenous laser therapy for varicose veins NN Khanna
870
103.
Vena caval filters NN Khanna
873
104.
Foam treatment of varicose veins JI Greenberg, N Angle, and J Bergan
879
Index
889
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Contributors B Abai
Department of Surgery, Robert Wood Johnson Medical School, Cooper University Hospital, Camden, NJ, USA.
MD
BG Alekyan M Ali
MD PhD
Department of Radiology, King Edward Medical University, Lahore, Pakistan.
MD
A Al-Kutoubi DE Allie
Interventional Cardiology and Angiology Department, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
Department of Diagnostic Radiology, The American University of Beirut Medical Center, Beirut, Lebanon.
MD FRCR DMRD
Cardiovascular Institute of the South, Medical Center of Southwest Louisiana, Lafayette, LA, USA.
MD
S Anagnostopoulou
MD PhD
Anatomy Department, University of Athens, Greece.
N Angle
MD FACS
IA Awad
BS MSC MD DABNS FACS FICS
R Baffour
B Bateman HH Batjer G Baweja
J Bergan
Interventional Cardiology, Centro Cardiologico Monzino, IRCCS, Institute of Cardiology of the University of Milan, Milan, Italy.
College of Physicians and Surgeons, Columbia University Medical Center, New York, NY, USA.
MD FACS
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
Sarver Heart Center, University of Arizona, Tucson, AZ, USA.
MD
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
MD
Department of Surgery, San Diego School of Medicine, University of California, La Jolla, CA, USA.
MD
L Bilodeau
Montreal Heart Institute, Montreal, Quebec, Canada.
MD
LB Bockeria A Bolia
MD
MD
BR Bendok
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
The Cardiovascular Research Institute, Washington Hospital Center, Washington, DC, USA.
PhD
AL Bartorelli
Section of Vascular Surgery, San Diego School of Medicine, University of California, La Jolla, CA, USA.
MD PhD
Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
MBChB DMRD FRCR
Department of Radiology, Leicester Royal Infirmary, Leicester, UK.
NM Bornstein
MD
AS Boulos
Section of Endovascular Surgery, The Neuroscience Institute; Division of Neurosurgery, Albany Medical Center, Albany, NY, USA.
MD
ML Brennan
Stroke Unit, Department of Neurology, Tel Aviv Sourasky Medical Center, Tel Aviv, Israel.
Department of Cell Biology, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH, USA.
PhD
Clinical and Diagnostic Department, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
Yu I Buziashvili
MD PhD
E Calabrese
National Center for Limb Salvage Clinical Institute “Città di Pavia,” Pavia, Italy.
MD
F Camerano National Center for Limb Salvage, Clinical Institute “Città di Pavia,” Pavia, Italy. Y-W Chi L Cho
DO RVT RPVI FSVMA
Vascular Lab Cardiology, Heart and Vascular Institute, Metairie, LA, USA.
Women’s Cardiovascular Center, The Cleveland Clinic Foundation, Cleveland, OH, USA.
MD FACC
AV Chupin, AV Vishnevsky Institute of Surgery, Moscow, Russia. FB Collares DF Colli Jr TJ Collins
MD MD
Vascular and Interventional Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
Angiography Unit, Hospital Samaritano-SP, São Paulo, Brazil.
MD FACC
DT Cragen
MD
Department of Cardiovascular Diseases, Ochsner Medical Center, New Orleans, LA, USA.
Department of Cardiology, St. Luke's Hospital and Medical Center, Phoenix, AZ, USA.
Frank J Criado
MD FACS FSVM
J Cynamon
Division of Vascular Interventional Radiology, Montefiore Medical Center, Bronx, NY, USA.
MD
Vascular Surgery and Endovascular Intervention, Union Memorial Hospital-MedStar Health, Baltimore, MD, USA.
Department of Psychology and Center for Neuroscience, University of Wisconsin-Madison, Madison, WI, USA.
E Yu Danilov
PhD
S Das
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
MD PhD
A de Carvalho Lobato DH Deaton
MD FACS
EB Diethrich
MD
PhD
Vascular & Endovascular Surgery Institute, Beneficência Portuguesa de São Paulo Hospital, São Paulo, Brazil.
Division of Vascular Surgery, Georgetown University School of Medicine, Washington, DC, USA.
Department of Cardiovascular Surgery, Arizona Heart Institute and Hospital, Phoenix, AZ, USA.
xiii
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Contributors
C Dima-Cozma Department of Internal Medicine, 6th Medical Clinic, Iasi University of Medicine and Pharmacie, “Gr. T. Popa,” Iasi, Romania. K Dougherty JF Dowdall M Duarte
CRTT SICP
Peripheral Vascular Interventional Research, St. Luke’s Episcopal Hospital and the Texas Heart Institute, Houston, TX, USA.
Cleveland Clinic Foundation, Cleveland, OH, USA.
MD
Hospital Pulido Valente, Lisbon, Portugal.
MD
E Duckworth
MD
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
CS Eddleman
MD PhD
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University Chicago, IL, USA.
K Ehrens Phoenix Heart Center, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA. M K Eskandari
MD
S Faintuch
Department of Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA.
J Franke S Fuchs
MD
Cardiovascular Center Frankfurt, Seckbacher Landstrasse, Frankfurt, Germany.
MD MD
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
The Cardiovascular Research Institute, Washington Hospital Center, Washington, DC, USA.
C Gallagher
MD
Union Memorial Hospital-MedStar Health, Baltimore, MD, USA.
RS Gammon
MD
Austin Heart Physician’s Association, Austin, TX, USA.
JM Garasic
Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA.
MD
VA Garibyan N Georgiou
MD
RN
Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
Vascular Screening and Diagnostic Centre, Nicosia, Cyprus.
G Geroulakos FRCS DIC PhD Department of Cardiology, Charing Cross and Ealing Hospital; Imperial College of Science Technology and Medicine; Royal Society of Medicine, London, UK. A Giannopoulos EZ Golukhova
MD
MD PhD
L Gopalakrishnan Chennai, India. JI Greenberg
AY Gur
MD
LR Guterman NY, USA.
Non-Invasive Arrhythmology Department, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia. Department of Cardiology, Institute for Cardiac Treatment and Research, Southern Railway Headquarters Hospital, Perambur, Department of Surgery, San Diego School of Medicine, University of California, La Jolla, CA, USA.
Department of Endovascular Research, Cleveland Clinic Foundation, Cleveland, OH, USA.
MSc PhD
MD PhD
ZA Hage
MD
MD FRCS
RK Greenberg M. Griffin
Department of Surgery, Athens University Medical School, Athens, Greece.
The Vascular Noninvasive Screening and Diagnostic Centre, London, UK.
Department of Neurology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel.
PhD MD
Department of Neurosurgery, Toshiba Stroke Research Center, University at Buffalo State, University of New York, Buffalo,
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University Chicago, IL, USA.
MD
G Hamilton MD FRCS Academic Department of Surgery, Royal Free Hospital and Royal Free University College Medical School, University College London, London, UK. JP Harris, Department of Surgery, University of Sydney, Sydney, New South Wales, Australia. CW Hatler CJ Hebert I Henry
PhD RN
RT-R RCIS
Cabinet de Cardiologie, Nancy, France; Global Research Institute, Apollo Clinic, Hyderabad, India.
MD
RR Heuser
Cardiovascular Institute of the South, Medical Center of Southwest Louisiana, Lafayette, LA, USA
Polyclinique Bois Bernard, Bois Bernard, France.
MD
M Henry
Phoenix Heart Center, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA.
MD FACC FACP FESC
RT Higashida
MD
Department of Cardiology, St. Luke's Medical Center; University of Arizona College of Medicine, Phoenix, AZ, USA.
Department of Radiology, University of California, San Francisco Medical Center, San Francisco, CA, USA.
LN Hopkins
MD
M Hugel
RN
Cabinet de Cardiologie, Nancy, France.
K Irshad
FRCS
JS Jenkins
Department of Neurosurgery, Toshiba Stroke Research Center, University at Buffalo, Buffalo, NY, USA.
King Edward Medical University, Lahore, Pakistan.
MD FACC FSCAL
Ochsner Heart & Vascular Institute, New Orleans, LA, USA.
W-J Jiang MD PhD Department of Neuroradiology and Interventional Neuroradiology, Beijing Tiantan Hospital, Capital Medical University (CPU), Beijing, People’s Republic of China. S Kakkos
MD PhD DIC
KE Kardenas
MD PhD
Division of Vascular Surgery, Imperial College, London, UK. Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
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Contributors
xv
RR Kasliwal Indraprastha Apollo Hospitals, New Delhi, India. A Katsargyris E Kedhi
Medisch Centrum Rijnmond Zuid (MCRZ) - Hospital Rotterdam, Rotterdam, The Netherlands.
MD
LM Kelly
1st Department of Surgery, Vascular Division, Athens University Medical School, Athens, Greece.
MD
Phoenix Heart Center, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA.
RN MBA
NN Khanna
MBBS MD DM FICC FEISI
Department of Cardiology, Indraprastha Apollo Hospitals, New Delhi, India.
SH Kim MD Department of Neurosurgery, Toshiba Stroke Research Center, School of Medicine and Biomedical Sciences, University at Buffalo, State University of New York, Buffalo, NY, USA. C Klonaris
R Kornowski S Kownator Z Krajcer
Athens University Medical School, Athens, Greece.
MD
Baylor College of Medicine, University of Texas Health Science Center, Houston, TX, USA.
Department of Computer Science and Engineering, Frederick University Cyprus, Palouriotisa, Nicosia, Cyprus.
PhD
N Labropoulos
MD PhD
EI Levy
MD
MD
BSc (Med) PhD DIC RVT
MD PhD RVT
BB Lee
Q Lu
Department of Surgery, University of Ulsan College of Medicine and Asan Medical Center, Songpa-gu, Seoul, South Korea.
MD PhD
E Kyriacou
J Laredo
Cabinet de cardiologie, Thionville, France.
MD
MD
TW Kwon
Cardiac Catheterization Unit, Department of Cardiology, Rabin Medical Center, Petah Tikva, Israel.
MD
Department of Surgery, Stony Brook University Medical Center, Stony Brook, NY, USA.
Division of Vascular Surgery, Georgetown University Hospital, Washington, DC, USA.
Division of Vascular Surgery, Georgetown University School of Medicine, Washington, DC, USA.
Department of Neurosurgery, Toshiba Stroke Research Center, University at Buffalo, Millard Fillmore Gates Circle Hospital, NY, USA.
Cleveland Clinic Health Systems Foundation, Cleveland, OH, USA.
F Luizy
MD
Cabinet de cardiologie, Thionville, France.
P Lylyk
MD
Clinica Medica Belgrano and FLENI, Buenos Aires, Argentina.
G Marenzi ML Marin
MD
Department of Surgery, Mount Sinai School of Medicine, New York, NY, USA.
MD
G Markose
Coronary Care Unit, Centro Cardiologico Monzino, IRCCS, Institute of Cardiology of the University of Milan, Milan, Italy.
BSc (HONS.) MBBS MRCP (UK) FRCR
Department of Radiology, Leicester Royal Infirmary, Infirmary Square, Leicester, UK.
GM Martinez Salazar MD Vascular and Interventional Radiology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA. J May
MD MS FRACS FACS
Department of Surgery, University of Sydney, New South Wales, Australia.
PW McMullan Jr
MD
T McNamara
Section of Interventional Radiology, University of California School of Medicine, Los Angeles, CA, USA.
MD
Department of Interventional Cardiology, Ochsner Medical Center, New Orleans, LA, USA.
E Mendaro MD Department of Vascular Interventional Radiology, Phoenix Heart Center, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA. PM Meyers MD Neuroendovascular Services, Department of Radiology and Neurosurgery, Columbia and Cornell University Medical Centers, New York, NY, USA. YA Mikhaeil
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
MD
DP Mikhailidis BSc MSc MD FACB FFPM FRCP FRCPath Department of Clinical Biochemistry (Vascular Disease Prevention Clinic), Royal Free Hospital and Royal Free University College Medical School, University College London, London, UK. NP Mironov
Volynskaya Hospital, Moscow, Russia.
MD
EV Mitran
MD PhD
JE Molina
MD
OC Morcos
Division of Vascular Surgery, University of Illinois at Chicago, Chicago, IL, USA.
MD FACS
D Mukherjee KF Murphy
Cardiothoracic Surgery, Minneapolis, MN, USA.
MD
N Morrissey
Cardiovascular Institute of the South, Medical Center of Southwest Louisiana, Lafayette, LA, USA.
MD
MRCS
JR Nelson
BS
RF Neville
MD
Division of Vascular Surgery, New York-Presbyterian Hospital, Weill Medical College, Cornell University, New York, NY, USA.
Division of Cardiovascular Medicine, Gill Heart Institute, University of Kentucky, Lexington, KY, USA. Vascular & Endovascular Institute, Wishaw Hospital, Scotland.
Austin Heart Physician’s Association, Austin, TX, USA. Division of Vascular Surgery, Georgetown University School of Medicine, Washington, DC, USA.
AN Nicolaides MS FRCS FRCSE PhD (HON.) Imperial College, London; University of Cyprus, Vascular Screening and Diagnostic Centre, Nicosia, Cyprus.
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Contributors
TG Niritina
MD PhD
FJ Osse
Endovascular Surgery, Sanmaritano Hospital, São Paulo, Brazil.
MD
AR Owen
Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
BSc MRCP FRCR
GI Pandele
MD PhD
A Papapetrou
Department of Radiology, Glasgow Royal Infirmary, Glasgow, UK.
Department of Internal Medicine, 6th Medical Clinic, Iasi University of Medicine and Pharmacie, “Gr. T. Popa,“ Iasi, Romania. Department of Vascular Surgery, Athens University School of Medicine, Athens, Greece.
MD FEBVS
KI Paraskevas MD FASA Department of Clinical Biochemistry (Vascular Disease Prevention Clinic) and Academic Department of Surgery, Royal Free Hospital and Royal Free University College Medical School, University College London, London, UK. JC Parodi
Department of Vascular Surgery, Phoenix Heart Center, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA.
MD
RR Patlola JC Pereda
Cardiovascular Institute of the South, Medical Center of Southwest Louisiana, Lafayette, LA, USA.
MD
South Miami Hospital, Miami, FL, USA.
MD
GE Pineda
MD
J Pisco
New University of Lisbon, Lisbon, Portugal.
MD
Division of Cardiovascular Medicine, Gill Heart Institute, University of Kentucky, Lexington, KY, USA.
VP Podzolkov A Pokrovsky
MD PhD
Congenital Heart Disease Surgery Department, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
AV Vishnevsky Institute of Surgery, Moscow, Russia.
MD
A Polydorou General Hospital “Agios Panteleimon,” Nikaea, Piraeus, Greece. Ad Polydorou
MD
General Hospital “Agios Panteleimon,” Nikaea, Piraeus, Greece.
V Polydorou
MD
General Hospital Nikaea Piraeus “Agios Panteleimon,” Greece.
P Prabhaker
MD
Division of Vascular Interventional Radiology, Montefiore Medical Center, Bronx, NY, USA.
MG Pursanov AI Qureshi
MD PhD
Department of Interventional Cardiology, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
Department of Neurology and Neurosciences, University of Medicine and Dentistry of New Jersey, Newark, NJ, USA.
MD
S Rajagopal MD Department of Cardiology, Institute for Cardiac Treatment and Research, Southern Railway Headquarters Hospital, Perambur, Chennai, India. AW Reid DB Reid
MD FRCR FRCP
Vascular & Endovascular Institute, Wishaw Hospital, Scotland.
MD FRCS
G Robertson GH Roditi
MD
Emory University Heart and Vascular Center, Atlanta, GA, USA.
FRCP FRCR
K Rosenfield
MD
Glasgow Royal Infirmary, Glasgow, Scotland.
Department of Radiology, Glasgow Royal Infirmary, Glasgow, UK.
Division of Vascular Medicine and Intervention, Massachusetts General Hospital, Boston, MA, USA.
RM Samuelson MD Department of Neurosurgery, Toshiba Stroke Research Center, University at Buffalo, Millard Fillmore Gates Circle Hospital, Buffalo, NY, USA. CJ Schönholz CK Shortell
MD
MD
Department of Radiology, Phoenix Heart Center, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA.
Division of Vascular Surgery, Duke University Medical Center, Durham, NC, USA.
HC Schumacher MD Doris and Stanley Tanenbaum Stroke Center, Neurological Institute, Interventional Neuroradiology, New York Presbyterian Hospital, Columbia University Medical Center, NY, USA. H Sievert MD FSCAI FESC FACC Cardiovascular Center Frankfurt, Sankt Katharinen, Frankfurt, Germany; Cath Lab for Peripheral Vascular Interventions and Structural Heart Defects, Washington Hospital Center and Cardiovascular Research Institute, Washington, DC, USA. JA Silva
MD FACC FACAI
A Sinha
FRCS
Tchefuncte Cardiovascular Associates and TCA Research, Covington, LA, USA.
Vacular & Endovascular Institute, Wishaw Hospital, Scotland.
AV Staferov MD PhD Department of Interventional Cardiology and Angiology, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia. J Stephanides DL Surdell
MD
MD
J-F Tanguay
Department of Neurological Surgery, Feinberg School of Medicine, Northwestern University, Chicago, IL, USA.
MD
Montreal Heart Institute, Montreal, Quebec, Canada.
AV Ter-Akopyan PE Thorpe ZG Turi
Department of Surgery, Veterans Hospital, Athens, Greece.
MD PhD
MA MD FSIR
MD
Hospital Volynskaya, Moscow, Russia.
Endovascular Surgery & Interventional Radiology, Arizona Heart Hospital, Phoenix, AZ, USA.
Robert Wood Johnson Medical School, Camden, NJ, USA.
S Tyagi MD DM FAMS Department of Cardiology, G.B. Pant Hospital & Maulana Azad Medical College, New Delhi, India. R Waksman
MD
Cardiovascular Research Institute, Washington Hospital Center, Washington, DC, USA.
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MD
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Cardiovascular Institute of the South, Medical Center of Southwest Louisiana, Lafayette, LA, USA.
KL Waters
FNP-C
Phoenix Heart Center, St. Joseph’s Hospital and Medical Center, Phoenix, AZ, USA.
GH White
MBBS FRACS
Department of Surgery, University of Sydney, Sydney, New South Wales, Australia.
MH Wholey MD MBA Central Cardiovascular Institute of San Antonio, University of Texas Health Science Center, San Antonio, TX, USA. WS Wu
MD
Central Cardiovascular Institute of San Antonio, University of Texas Health Science Center, San Antonio, TX, USA.
B Yasin
MD
National Center for Limb Salvage, Clinical Institute “Città di Pavia,“ Pavia, Italy.
NV Zakarian MD PhD Department of Interventional Cardiology and Angiology, Bakoulev Scientific Center for Cardiovascular Surgery, Moscow, Russia.
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Preface This textbook, the second edition of our original Textbook of Peripheral Vascular Intervention, is a collaborative effort with Dr. Henry, myself, and Alan Burgess from Informa Healthcare Publishing. We have incorporated contributions from world opinion leaders in the areas of technical developments of endovascular devices and new treatment strategies. Our goal is to make the second edition the most definitive textbook available. As the nature of medical care becomes more preventive, rather than crisis-driven, the diagnosis of treatments for peripheral vascular disease becomes more relevant to everyday practice. Helping patients deal with lifestyle changes resulting from disease becomes more relevant as our population ages. Approximately two million patients in Europe and the United States suffer from critical limb ischemia. Nearly half of these sufferers will require major amputation within one year after the onset of limb ischemia. In addition, in the United States, prevalence of abdominal aortic aneurysm is quite significant. In 2002, 200 000 abdominal aortic aneurysms were diagnosed, adding to the estimated one and half million patients who currently experience this disease. In fact, 10% of men older than 80 years of age have had a significant abdominal aortic aneurysm. Furthermore, 20% of the patients who undergo coronary intervention have renal artery stenosis, with as many as 50% of those patients having critical stenosis. Embolic protection traditionally used for carotid intervention is now being applied in both femoral and renal applications.
We have also seen an explosion in our ability to screen patients with peripheral vascular disease; a potent predictor of comorbid cardiovascular disease. The Textbook of Peripheral Vascular Interventions, Second Edition will discuss therapies that can make a real difference in the lives of patients. Effective, less invasive approaches to therapies for critical limb ischemia, chronic total occlusions, as well as therapies for some subsets, will be discussed. It is clear that in the future patients will be demanding less invasive procedures. This book stands as a tribute to the pioneering work of Charles Dotter and Andreas Gruentzig. Their initial vision and successful demonstration of early techniques for peripheral intervention have guided the development of these endovascular interventions for the last 43 years. We hope that this textbook will serve as a practical source of information for students, physicians in training, radiologists, cardiologists, and vascular surgeons performing peripheral intervention, and that it will become a comprehensive introduction to endovascular techniques. Dr. Henry and I would like to acknowledge the hard work of Mrs Valérie Davot whose help in coordinating our contributing authors was invaluable. Richard R Heuser MD has donated all his royalties for this textbook to The American Heart Association and the Osler Fund at Johns Hopkins Hospital. Richard R Heuser MD
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SECTION I Introduction
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Epidemiology and pathophysiology of peripheral arterial disease (PAD) GI Pandele and C Dima-Cozma
Epidemiology Peripheral arterial occlusive disease (PAD) of atherosclerotic origin has an incidence and prevalence nearly equal to coronary artery disease.1 The reported prevalence of PAD depends greatly on the demographic factors of the population and on the method of diagnosis. The first step is to measure the ankle–brachial index resting and during exercise, which is normally greater than 0.90. PAD is still underdiagnosed because only 10–30% of all PAD patients have symptoms such as intermittent claudication.2,3 It affects almost 12 million people in the US and 20% of symptomatic patients with PAD have diabetes. PAD is also a risk factor for lower-extremity amputation and for systemic vascular disease in coronary, cerebral, and renal vessels.4 Incidence and prevalence The incidence of PAD in the Framingham Study5 was 3.5/1000 for women and 7.1/1000 for men. In a study of 2327 subjects conducted in the Netherlands6, the incidence for asymptomatic PAD was 7.8/1000 for women and 12.4/1000 for men. The PARTNERS program enrolled 6979 patients and characterized patients with polyvascular determinations. Of the total number of patients enrolled, 16% had PAD and cardiovascular disease, 13% had PAD but no cardiovascular disease, 24% had no PAD but had cardiovascular disease, and 47% had evidence of neither.7,8 Another survey of patients with diabetes9 who were more than 50 years of age showed a prevalence of PAD of 29%. Morbidity and mortality Patients with PAD have a higher risk of contracting coronary, renal, and cerebrovascular disease. In the ARIC study, subjects with PAD had twice the frequency of cardiovascular disease than those without PAD. The ankle–brachial index (ABI) is an independent predictor of mortality. The total mortality relative risk (RR) is 4.5 for all patients with an ABI smaller than 0.40. The total mortality is slightly increased in men.7
Pathophysiology The main cause of PAD is atherosclerosis, responsible for more than half of all deaths in Western industrialized countries. Atherosclerosis, a slowly progressing arterial disease with
an asymmetric and asynchronous evolution, is initiated in intima by the deposition of fibrous and lipid materials that gradually narrow the lumen and diminish the blood supply to various tissues such as the brain, heart, kidney, intestine, and limbs (in particular the lower limbs). The process of atherogenesis is, in order of site frequency, localized at the abdominal aorta, coronary arteries, popliteal, and cerebral arteries.2 Endothelial damage seems to be the primary event and is produced by high mechanical stress caused by hypertension. A direct effect of chlamydial infection may lead to plaque formation, as a consequence of increased lipid uptake in the vessel wall and the adhesion of monocytes and thrombocytes, under the influence of homocysteine.7 After monocytes penetrate into the intima, they transform into macrophages. The macrophage is able to release reactive O2 radicals, the superoxide anion that damages the endothelial cells and inactivates endothelium-formed nitric oxide (NO). The loss of NO action results in adhesion of platelets and monocytes to the endothelium, with proliferation and vasoconstrictive effects in the vascular musculature that favors spasm. The low-density lipoprotein cholesterol (LDL) particles that penetrate into the endothelium are modified by oxidation, and oxidized LDL aggresses the endothelium by enhancing expression of adhesion molecules, which allows the vessel musculature to proliferate. Unrecognized by Apo B 100 receptors, the oxidized LDL particles are gathered by scavenger receptors, which are numerous within macrophages. The macrophages phagocytize LDLs (oxidized lipoprotein particles) and become foam cells. At the same time, chemotactic factors, synthesized and released by monocytes and thrombocytes, determine the migration of smooth muscle cells from the media into the intima, where they are stimulated to proliferate under the influence of PDGF (platelet-derived growth factor) and other growth-promoting factors produced by damaged endothelium and from the muscle cells. They too are transformed into foam cells by the uptake of oxidized LDLs and can also form an extracellular matrix from collagen, elastin, and proteoglycans.11 By plaque deposition, the lumen of the arteries in cerebral, coronary, mesenteric, renal, and peripheral territories is progressively diminished and the consequences are painful ischemia, such as that found in coronary, mesenteric, and peripheral disease, or painless symptoms with critical ischemia in all vascular territories, resulting in cerebral infarction or stroke, mesenteric and renal infarction, and peripheral gangrene. Another consequence is the stiffening of the vessel wall, and bleeding into the plaques and the vessel wall, with 3
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the development of a thrombus which narrows and obstructs the lumen and is the source of emboli in cerebral, coronarian, renal, mesenteric, and peripheral arteries. In addition, the hemorrhage into the plaque-generating hematoma is able to narrow the arterial lumen.11 The atherosclerotic process gives way to the development of aneurysms by weakening the vessel wall. In 90–95% of cases, an aneurysm is caused by atherosclerosis with hypertension. In order of frequency, the location of aneurysms is abdominal and thoracic aorta, cerebral, and peripheral arteries. Besides atherosclerosis, other etiologies of aneurysms include: ● ●
●
congenital; cystic medial necrosis: Marfan’s, Ehlers-Danlos or GsellErdheim syndrome; infection: lues, mycosis in immune-deficient patients.
One of the complications of aneurysms is rupturing, accompanied by hemorrhagic shock if it occurs in a large vessel. Rupture of an intracranial artery will result in a cerebral hematoma and subarachnoid bleeding and a dissecting aneurysm near the heart can lead to acute pericardial tamponade or aortic regurgitation, if the aortic root is involved and thrombosis in the aneurysm occurs with emboli to distal vessels.12,13 Peripheral arterial disease of other etiology than atherosclerosis Acute occlusion of arteries may be the result of a thromboembolism, which usually originates in the heart: from the left atrium in mitral stenosis, atrial fibrillation, left atrial mixoma, the left ventricle in myocardial infarction, dilated cardiomyopathy, or from cardiac valves, which can occur in aortic stenosis, endocarditis, from prosthetic valves, or by paradoxical embolism in intracardiac shunts.14 Pathophysiological characteristics of PAD PAD is generally a bilateral disease and, in the presence of intermittent claudication, the lower extremity blood flow may be normal or slightly diminished in rest with an inability to increase it with exercise.15 In experimental models of ischemic limb, performed in animals by arterial ligation, the intact capacity to produce angiogenic factors is important for maintaining blood flow. The impaired angiogenic response in basic fibroblast growth factor (bFGF) or vascular endothelial growth factor (VEGF) will result in a severe reduction in blood flow, reproducing the clinical situation of patients with critical limb ischemia.16 The extent and intensity of ischemia is more important and sustainable in diabetes, hypercholesterolemia, and hyperhomocysteinemia. Most patients with diabetes demonstrate abnormalities of endothelial function. Hyperglycemia blocks the function of endothelial nitric oxide synthase (eNOS) and free fatty acids may have numerous deleterious effects on normal vascular homeostasis. Diabetes leads to a hypercoagulable state and abnormalities in platelet biology.17 In observational studies, elevated homocysteine levels are associated with PAD. Among other atherothrombotic biomarkers, the total cholesterol/ high density lipoprotein (HDL) cholesterol ratio and C-reactive protein (CRP) were the strongest independent predictors of development of PAD.18,19
Atherothrombosis, an insidious and long-term progressive phenomenon, begins as the result of action of biological, chemical, and mechanical factors that can change the vascular endothelium in different segments of arteries, beginning with the aorta and muscular arteries. Aggression of the endothelium leads to deposition and oxidation of LDL cholesterol, which triggers the subendothelial migration of blood monocytes, which are recognized as scavengers by oxidized LDL and transformed into foam cells. At the site of the injury, foam cells and T-lymphocytes accumulate into the intima and form the fatty streak. The progressive plaque growth is realized by migration of the smooth muscle cells from the media to the intima, where, in response to locally released growth factors, they proliferate. The plaque may be the place of rupture or erosion, followed by exposure of the lipid-rich content to the blood flow allowing platelet adhesion to the damaged endothelium. Platelet activation will determine structural and biochemical modification with the release of adenosine diphosphate, serotonin, thromboxane A2, fibrinogen, and thrombin. By aggregation of the activated platelets, the arterial thrombus will be initiated with partial or total occlusion, producing ischemia in arterial territories of coronary, cerebral, mesenteric, renal, or peripheral vessels. The severity of ischemia depends on the size of the thrombus and also of the possibility of supplying the ischemic territory by collateral circulation. Until now it has remained unclear whether all lesions containing lipids are necessarily precursors of clinically significant atherosclerotic plaques.20 Both age and atherosclerosis are able to determine intimal and total wall thickening besides the lumen diameter modification. Intimal thickening may represent the adaptive response of increased wall stress as has been observed in infants and intrauterine life and was demonstrated experimentally in coronary, carotid, superficial femoral arteries, and the abdominal aorta.21 The direct effect of intimal plaque deposition is the decrease in lumen diameter, which increases the blood flow velocity and wide shear stress, both of which induce dilatation of the lumen to restore the baseline shear stress levels. An increase in intimal plaque volume will determine the increase in outside artery diameter. Another process that maintains an adequate lumen calibrum of the artery is the medio-atrophy that allows the wall to bulge at the level of the atherosclerotic plaque. The selective distribution of plaques is dependent on wall shear stresses that act as a tangential force produced by the blood progression in the artery. The wall shear stress is directly proportional in magnitude to blood flow and blood viscosity and inversely proportional with r3, where r is the radius of the lumen. Acute experimental shear stress enhancement could cause endothelial fracture which starts the process of platelet activation, aggregation, and clot formation.22 The oscillation of shear stress is proportional to the heart rate, which is considered nowadays as an independent risk factor for atherosclerosis. Another important factor in the evolution of atherosclerotic plaque is turbulence of the flow. Turbulence is not an initiating factor of atherogenesis, but may play an important role in plaque disruption and atherothrombosis.23 Hypertension is recognized as an important risk factor for the increase in extent and severity of atherosclerosis. Isolated elevated blood pressure does not reduce atherosclerosis in
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Epidemiology and pathophysiology of peripheral arterial disease (PAD) experimental animal models, but associated with hyperlipemia, hypertension will induce and enhance plaque formation. Even in the presence of hypertension, plaque formation is reduced when cholesterol levels are decreased.24,25 Natural history of atherosclerosis Evolution of atherosclerosis is not always continuous and is characterized by artery stenosis and plaque complications like fracture and thrombosis. After the initiation of the process characterized by biochemical and cellular recruitment into the intima because of the altered endothelial function, smooth muscle cells migrate and proliferate into the subendothelial tissue induced by circulating mitogens. In the evolution of atherosclerosis it is not clear whether inhibiting the recruitment of activated cells will be able to control the evolution of clinical events. For very old people with no clinically manifest atherosclerotic disease in their life, angioscopy of different vascular territories and, finally, the autopsy may reveal advanced atherosclerotic plaques. A very important process operating in atherosclerosis is plaque regression, which may be determined by the resorption of lipids or the extracellular matrix or by cell death and migration. Recently, lipid-lowering diets and treatment with statins have been shown to increase plaque regression. The regression of atherosclerotic lesions has been demonstrated by angiography in the coronary and peripheral arteries.26 The vascular tree susceptibility to plaque formation At the level of the abdominal aorta, the infrarenal segments are particularly susceptible to the development of obstructive
5
atherosclerotic plaques, thrombosis, ulcerations, and aneurysms. The blood flow in the infrarenal aorta is conditioned by muscular activity in lower limbs. Reduced physical activity and sedentarism may result in the reduction of flow velocity in the abdominal aorta. Another factor contributing to atheromatous degeneration of the abdominal aorta is the tendency of the aorta to enlarge with age, and the poor development of intramural vasa vasorum in this segment.27 Superficial femoral artery The arteries of the lower limbs are the elective site of atherosclerotic plaque deposition, because of the differences in hydrostatic pressure and marked variations in flow, depending on the level of physical activity. As shown previously, cigarette smoking and diabetes mellitus are the main risk factors associated with atherosclerosis in femoropopliteal and tibial territories.28 Although the superficial femoral artery is most likely to be affected by multiple stenotic lesions, the profunda femoris tends to be spared. An explanation may be the increased susceptibility to plaque deposition in the superficial femoral artery at the site of stretching by the tendon of adductor magnus. The pathophysiology of intermittent claudication is also explained by metabolic changes present in ischemic skeletal muscle fiber (accumulation of metabolic intermediates, altered control of mitochondrial respiration, increased systemic oxidative stress, and accumulation of somatic mitochondrial DNA mutations) compatible with an “acquired metabolic myopathy” that manifests clinically as muscle weakness, functional impairment, and walking limitation.29
REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
11.
Gardner AW, Poehlman ET. Exercise rehabilitation programs for the treatment of claudication pain. A meta-analysis. JAMA 1995; 274: 975–80 Almahameed A. Peripheral arterial disease: recognition and medical management. Cleve Clin J Med 2006; 73 (7): 621–6 McDermott MM, Greenland P, Liu K, et al. Leg symptoms in peripheral arterial disease: associated clinical characteristics and functional impairment. JAMA 2001; 286: 1599–606 Criqui MH. Peripheral arterial disease: epidemiological aspects. Vasc Med 2001; 6 (Suppl. 1): 3–7 Kannel WB, McGee DL. Update on some epidemiologic features of intermittent claudication: The Framingham Study. J Am Geriatr Soc 1985; 33: 13–18 Stoffers HE, Rinkens PE, Kester AD. The prevalence of asymptomatic and unrecognized peripheral arterial occlusive disease. Int J Epidemiol 1996; 25: 282–290. Higgins JP, Higgins JA. Peripheral arterial disease (part I): diagnosis, epidemiology and risk factors. J Okla State Med Assoc 2002; 95 (12): 765–71 Hirsch AT, Hiatt WR, Criqui MH, McDermott MM. PARTNERS: a national survey of peripheral arterial disease symptoms and treatment intensity. J Am Coll Cardiol 2001; 37 (Suppl. A): 126–91 Fowkes FG, Housley E, Cawood EH. Edinburgh Artery Study: prevalence of asymptomatic and symptomatic peripheral arterial disease in the general population. Int J Epidemiol 1991; 20: 384–392 Aboyans V, Criqui MH, Denenberg JO, Knoke JD, Ridker PM, Fronek A. Risk factors for progression of peripheral arterial disease in large and small vessels. Circulation 2006; 113 (22): 2623–9 Ross R. The pathogenesis of atherosclerosis: a perspective for the 1990s. Nature 1993; 362: 801–9
12. 13. 14. 15. 16.
17. 18.
19.
20. 21.
Silbernag I, Lang A. Color Atlas of Pathophysiology. Stuttgart: Thieme, 2000: 236–41 Kinlough-Rathbone RL, Mustard JF. Atherosclerosis: current concepts. Am J Surg 1981; 141: 638 Meru AV, Mittra S, Thyagarajan B, Chugh A. Intermittent claudication: an overview. Atherosclerosis 2006; 187 (2): 221–37 Hiatt WR, Hoag S, Hamman RF. Effect of diagnostic criteria on the prevalence of peripheral arterial disease. The San Luis Valley Diabetes Study. Circulation 1995; 91: 1472–79 Rajagopalau S, Mohler ER, Raderman RI, et al. A phase II randomized double blind controlled study of adenoviral delivery of VEGF121 in patients with disabling intermittent claudication. Regional angiogenesis with vascular endothelial growth factor (VEGF) in peripheral arterial disease. Circulation 2003; 108: 1933–38 Steinberg HO, Baron AD. Vascular function, insulin resistance and fatty acids. Diabetologia 2002; 45: 623–34 Guallar E, Silbergeld EK, Navas-Acien A, et al. Confounding of the relation between homocysteine and peripheral arterial disease by lead, cadmium and renal function. Am J Epidemiol 2006; 163 (8): 700–8 Ridker PM, Stampfer MJ, Rifai N. Novel risk factors for systemic atherosclerosis. A comparison of C-reactive protein, fibrinogen, homocysteine, lipoprotein (a) and standard cholesterol screening as predictors of peripheral arterial disease. JAMA 2001; 285 (19): 2481–85 Geng YJ, Libby P. Progression of atheroma: a struggle between death and procreation. Arterioscler Thromb Vasc Biol 2002; 22: 1370–80 Zarins CK, Zatino MA, Giddens DP, et al. Shear stress regulation of artery lumen diameter in experimental atherogenesis. J Vasc Surg 1987; 5: 413
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26. 27. 28. 29.
McDermott MM, Guralnik JM, Greenland P, et al. Statin use and leg functioning in patients with and without lower-extremity peripheral arterial disease. Circulation 2003; 107: 757–61 Cozzi PI, Lyon RT, Davis HR, et al. Aortic wall metabolism in relation to susceptibility and resistance to experimental atherosclerosis. J Vasc Surg 1988; 7: 706 Gordon T, Kannel WB. Predisposition to atherosclerosis in the head, heart and legs: The Framingham Study. JAMA 1972; 221: 661–6 Brass EP, Hiatt WR. Acquired skeletal muscle metabolic myopathy in atherosclerotic peripheral arterial disease. Vasc Med 2000; 5: 55–9
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The endovascular suite and equipment K Dougherty and Z Krajcer
Introduction Endovascular interventions have enjoyed an explosive growth over the last decade. As the number of endovascular procedures being performed each year continues to rise, so does the demand for technologies to improve patient care. Designing the endovascular suite requires careful planning so that all necessary options are taken into consideration. First of all it is important to know who will be using the room. Will it be a vascular surgeon, cardiothoracic surgeon, interventional cardiologist, or interventional radiologist? Consequently, a multidisciplinary team should be created to determine the optimal environment for performing combined surgical and endovascular procedures. The endovascular suite should offer sterile conditions to allow the endovascular specialist a complete gamut of options to treat patients with complex vascular disease. Fully operative sterile conditions will allow immediate conversion from endovascular intervention to a conventional surgical procedure if unexpected complications should occur. The endovascular suite should be large enough to accommodate the equipment and staff needed for emergent surgical conversions, and endoscopic, robotic and hybrid (combined off-pump bypass and coronary angioplasty and stent implantation) surgical procedures.
Design of the procedure room In order to comfortably accommodate the core equipment needed for a state-of-the-art endovascular suite, the size of the suite should be at least 1000 square feet (Figure 2.1),1 with at least two-thirds of the space devoted to procedure area and 350 square feet to the control/observation area (Figure 2.2). The ceiling height should be at least 10 feet2 and the walls should be shielded with 1 mm of lead to provide radiation protection for personnel in surrounding work areas. Observation windows and doors should also be lead treated. The suite should be equipped with emergency power outlets located on the operating table and all four walls of the suite. The endovascular suite should have compressed air, oxygen, and extra suction outlets at both ends of the operating table. The operating table should be non-metallic or radiolucent to minimize radiation exposure and provide exceptional visualization. Communications capabilities should include in-room intercoms, video input and output links to high-bandwidth image routing network, and video/audio recording.
Most of the typical angiography suites and cardiac catheterization suites are primarily designed for catheterbased procedures and do not meet operating room requirements. To offer operating room sterility the endovascular suite should have laminar or negative airflow, and seamless floors, ceilings, and walls that can be washed. An electronic imaging workstation should also be available in the room so that digital computed tomography (CT), magnetic resonance (MR) and ultrasound images can be reviewed during the procedure (Figure 2.2). The suite should be equipped with limited inroom storage using stainless steel cabinets with glass doors. Procedure specific equipment should be stored on carts that can be easily moved in and out of the room (Figure 2.3). In addition, the suite should have certified operating-room shatterproof lighting that allows low, medium, and ultra-bright capabilities. Individual xenon headlamps are also necessary for hybrid procedures. Vascular instrumentation and instrument tables should be readily available in the room. There should also be adequate space for the anesthesiologists, anesthesia equipment, and circulators. The room should have controlled access and outside indicators to specify activation of the fluoroscopic equipment so that inadvertent radiation exposure is prevented.
Requirements for anesthesia The anesthesiologist is consulted for a variety of procedures that are performed in an endovascular suite. The spectrum of anesthesia needed in the endovascular suite ranges from local to general, depending on the needs of the patient and the endovascular team. The organization of the procedural area, therefore, is case-specific, and identifying the location of the high-pressure lines is important to determine where to place the anesthesia equipment. Use of compact anesthesia equipment specifically designed for remote or ambulatory applications allows anesthetic flexibility and improves the efficiency in smaller spaces. Additional portable lead glass shields should be available to protect the anesthesiologist during fluoroscopy and angiography (Figure 2.4).
Fluoroscopy equipment The key component and success of endovascular procedures are dependent on high-quality imaging equipment.1–3 Digital imaging has made large steps since its introduction in the 1980s. 7
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Figure 2.1 A large room is necessary when accommodating endovascular, hybrid, and robotic equipment, and the support staff needed to perform those procedures.
Digital flat-panel detector technology is a film-less environment that has the capability to store images easily in a picture archiving and communications system (PACS) and can be modified at any time.4 Flat-panel detectors not only increase image quality, but also significantly reduce the radiation dose to the patient, staff, and physician, due to improved detective quantum efficiency (DQE).5–7 Additional high-resolution dual LCD video monitors that provide display during live fluoroscopy is of great benefit (Figure 2.5). The video monitors should be able to move from side to side. In addition many systems are also equipped with an integrated optional ultrasound display to improve patient diagnosis and treatment. The operating table should be able to rotate from side to side, tilt for Trendelenburg and Fowlers positions and should be able to rotate on its center axis 180° to allow unobstructed access for antegrade, as well as retrograde, panning. They should be equipped with a table side-controlled system that permits selection of table height, gantry rotation, image magnification,
and storage. In addition, the table should be motor-driven to allow remote high-speed bolus-chase during digital peripheral studies, as well as digital stepping angiography. Digital subtraction angiography has many advantages, including lower contrast amount for diagnostic studies and the ability to perform post-image acquisition to magnify images and improve the image resolution. This digital feature is extremely valuable when using other contrast agents such as CO2 or gadolinium in patients who might be at increased risk for iodinated contrast angiography. CO2 and gadolinium provide lower resolution than iodinated (nephrotoxic) agents and are commonly used for patients with chronic renal insufficiency and for patients with severe allergy to iodinated agents. The fluoroscopy system can be either single or bi-plane. Almost all neuro-endovascular interventions require a biplane system (Figure 2.6); however, for other peripheral endovascular interventions a single plane system will suffice. The fluoroscopy equipment is either fixed or mobile. A fixed
Figure 2.2 A separate control room/observation area protected with lead shielding allows staff members to process and record procedural data without interrupting the intervention. An electronic imaging workstation should also be included so that CT scans, MRAs and ultrasound images can be reviewed during the procedure.
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The endovascular suite and equipment
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Figure 2.3 Procedure-specific equipment carts should be able to move easily in and out of the suite and be stored in a secured central storage.
Figure 2.4 Additional portable lead glass shields should be available to protect the anesthesiologist during long procedures that require general anesthesia.
(a)
(b)
Figure 2.5 (a) Multiple high-resolution screens provide AP and lateral image storage, as well as live fluoroscopy; and (b) additional high-resolution screens should be positioned around the endovascular suite for endoscopic and robotic procedures. (See Color plates.)
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Figure 2.6 The Axiom Artis dBA flat-panel imaging system (Axiom Artis BA, Siemens Medical Solutions, Erlangen, Germany) has a much larger field of view and 3D digital subtraction angiography.
flat-panel detector system uses less radiation and provides approximately 40% more coverage with a larger field of view than older image-intensifier systems. The dynamic range of a flat-panel detector system is 5–10 times greater than the conventional image-intensifier, which allows improved visualization of the vasculature. With improved visualization, contrast agent use can be reduced by approximately 30%.8 This is particularly important when imaging patients with existing renal dysfunction. Advancements in technologies have lead to the implementation of new angiographic applications that provide the interventionalist with information that was previously unavailable in the endovascular suite. Angiographic computed tomography (ACT) offers two-dimensional fluoroscopic images that appear in real time, and superimposes threedimensional reconstructions to provide CT-like 3D images (Dyna CT, Seimens Medical Solutions, Erlangen, Germany) (Figure 2.7a and b). Other system features include orbital and rotational C-arm movements as fast as 60° per second. This feature offers 3D imaging, collimator adjustments, extended dynamic range filtering, and injection triggering during rapid panning. An adjustable source to intensifier distance and
Figure 2.7
processing offers results in immediate image availability. Fixed systems also allow image-review functions to be directly accessible from handheld, in-room remote controls. This option can streamline procedures and minimize delays while archiving angiographic information. Post-processing, and digital image archiving are usually performed at the system console in the control/observation bay area (Figure 2.2). Variable frame rates can also be used to acquire angiographic images, from 0.5 to 30.0 frames per second. Coronary angiography requires 30 frames per second, while most peripheral procedures use 1–5 frames per second. Slower frame rates also reduce radiation exposure, but compromise image clarity.
Imaging techniques Proper positioning of the equipment and good radiographic imaging technique are crucial to the safety and success of endovascular procedures. Angiography using calibrated marker catheters and a graduated marker tape are useful safety measures when deploying stents and stent grafts. The flat-panel
(a) Digitally subtracted and; (b) 3D reconstructed angiography of a carotid pseudoaneurysm.
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The endovascular suite and equipment detector imaging system provides constant resolution over the entire field of view up to ten times greater than the standard 7- or 9-inch image intensifiers that are used in the cardiac catheterization laboratory.8 The square surface configuration of the flat panel eliminates the need for panning or multiple runs. During endovascular thoracic or abdominal aortic aneurysm repair, it is important that the entire field of endograft deployment can be seen on a single view. “Road-mapping” is an imaging technique that allows superimposition of a real-life fluoroscopy on a previously recorded angiographic image. These images are retained as a road map and used to facilitate the positioning of interventional devices. They are also helpful to compare anatomy before and after intervention, and to perform online measurement of the severity of stenosis. This technique is extremely beneficial when negotiating wires and catheters through tortuous vessels and reduces the contrast dose when there is concern of contrast-induced renal dysfunction. High-speed rotation is another useful imaging technique. This is especially helpful when evaluating the degree of stenosis and eccentricity of the vasculature like in the extra-cranial carotid arteries. It can also be used effectively to evaluate the thoracic and abdominal aorta, iliac, and femoral arteries. Like all digital images, however, the drawback of road-mapping and high-speed rotation is that any motion of the vascular structures decreases the quality of the image. Primary sources of movement include cardiac, diaphragmatic, ureteric, and intestinal. Pain is also a frequent cause of movement of the patients. Adequate sedation of patients and the use of lower-osmolality radiographic dyes can help reduce the motion artifact. Because the x-ray beam is shaped like a cone, radial elongation or distortion of the structures occurs at the edges of the field, known as parallax. This type of artifact is also exaggerated by movement and was a problem when using imaging equipment prior to the introduction of flat-panel technology. There is no distortion in the center of the field, but if the position changes from the road map, relative distances change dramatically increasing the parallax artifact. To avoid image artifacts caused by parallax, it is important for the patient and the table to remain stationary during the crucial part of the intervention. Therefore, for precise placement of stents or stent grafts, no movement should occur once the road map has been obtained and no measurements attempted in the outer 20% of the field of view. Parallax is not present when using flat-panel technology. Image storage and reproduction are other important features. Angiographic runs stored on digital memory can be played back for immediate review and can be stored in magnetic or optical discs. Post-processing allows the elimination of artifacts that degrade image quality. Motion artifacts can be eliminated by selecting a new digital mask frame just before the contrast arrives.
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greater need for significant lead shielding to ensure the safety of patients and health-care personnel. Mechanisms to reduce radiation exposure can be divided into those directed at reducing the output of the x-ray unit and those designed to limit the amount radiation in contact with the endovascular team. Staff members should be properly trained in radiation safety principles, equipment, potential complications, and trouble-shooting. Staff members should be able to demonstrate their understanding of the basic concepts of medical imaging and the use of newer imaging systems. The most important method to reduce scatter radiation is to minimize patient dose and the ultimate source of scatter to the operator.9–13 Staff members should monitor judicious use of fluoroscopy and terminate imaging runs as soon as relevant information has been obtained. Other key elements to reduce radiation exposure include collimation, pulsed fluoroscopy, imaging acquisition, frame rates, last image hold, and lower field of magnification. During long procedures the operator and staff members should stand as far back from the unit as possible to take advantage of the fact that radiation exposure decreases exponentially with increased distance from the source. Lead shielding requirements are dictated by stringent radiation safety regulations. Protective lead aprons, thyroid shields, leaded glass screens and leaded eye glasses with side shields are the most effective way to reduce radiation exposure. The suite itself must be lead-lined including the doors, glass, and walls9–13 and all personnel in the room should wear film badges that detect radiation exposure.
Endovascular equipment Supplying an endovascular suite with the necessary tools and equipment can be overwhelming and costly. This task is best solved with a collaborative effort between the endovascular suite, the interventional cardiology suite, and the interventional radiology suite. Much of the same equipment is used for all three specialties and trying to stock a suite with every piece of equipment possible is not practical. The most economical solution is for the departments to work together and have a reimbursement arrangement. However, the endovascular suite should be stocked with the basic necessities such as: ●
●
● ● ●
● ●
puncture needles and guidewires (soft-tip J-wire and peripheral torque wire); various sizes of sheaths (5-French for diagnostics and up to 22-French for stent-grafts); various preformed diagnostic and guiding catheters; non-ionic contrast and power injector (for aortograms); interventional guidewires (0.014–0.018 inches, 180–300 cm in length); balloons (3–40 mm in diameter and 20–60 mm in length); inflation device with gauge; stents and covered stents.
Radiation safety and training
●
With the advent of stents and endoluminal grafts and other endovascular procedures, the use of fluoroscopy is extensive. High-quality, fixed-imaging systems need high heat-capacity tubes to minimize the need for heat-cooling delays that often occur with long imaging times. Furthermore, there is an even
Over time, equipment needs for the endovascular suite will become apparent. Ordering supplies for a special case can be accomplished with careful preplanning on the interventionalist part and collaboration with industry, so that over-expenditure can be avoided.
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Conclusion Endovascular procedures have already changed the way arterial and venous diseases are managed with a greater emphasis on catheter-based interventions. It is likely these techniques will have an even greater influence because of the widespread acceptance of minimally invasive techniques and miniaturization of endovascular devices. Endovascular therapy is the fastest growing area of vascular medicine and requires the fundamental knowledge of modern catheter-based interventions and dedication on the part of practitioners.
Endovascular techniques require specialized skills and training in peripheral vascular diseases, diagnostic angiography, interventional techniques, and therapeutic alternatives. The challenge to the practitioner is intensified by the continual introduction of new products and methods. The establishment of a modern endovascular suite arranged in an ergonomically devised fashion is crucial to remaining on the forefront of developments and will undoubtedly enhance the ability of physicians to provide quality health care to vascular patients with arterial and venous disorders.
REFERENCES 1.
2. 3.
4. 5. 6.
Hodgson KJ, Mattos MA, Summer DS. Angiography in the operating room: Equipment, catheter skills, and safety issues. In: Yao JS, Pearce WH, eds. Techniques in Vascular and Endovascular Surgery. Connecticut: Appleton and Lange, 1998: 25–45 Queral LA. Operating room design for the future. In: Yao JS, Pearce WH, eds. Techniques in Vascular and Endovascular Surgery. Connecticut: Appleton and Lange, 1998: 1–5 Diethrich EB. Endovascular suite design: An integrated approach for optimal interventional performance. In: Criado FJ, ed. Endovascular Intervention: Basic Concepts and Techniques, Armonk. NY: Futura Publishing, 1999: 5–16 Kotter E, Langer M. Digital radiography with large-area flat-panel detector. Eur Radiol 2002; 12: 2562–70 Spahn M, Strotzer M, Völk M, et al. Digital radiography with a largearea, amorphous-silicon, flat-panel x-ray detector system. Invest Radiol 2000; 35: 260–6 Neitzel U, Böhm A, Maack I. Comparison of low contrast detail detectability with five different conventional and digital radiographic imaging systems. In: Krupinski EA, ed. Medical Imaging 2000: Image Perception and Performance. Proc SPIE 2000: 398: 216–23
7. Geijer H, Beckman KW, Andersson T, et al. Image quality vs radiation dose for flat-panel amorphous silicon detector: a phantom study. Eur Radiol 2001; 11: 1704–9 8. Tsapaki V, Kottou S, Kollaros N. Comparison of conventional and a flat-panel digital system in interventional cardiology procedures. Br J Radiol 2004; 77: 562–7 9. ACC/ACR/NEMA Ad Hoc Group. American College of Cardiology, American College of Radiology, and industry develop standards for digital transfer of angiographic images. J Am Coll Cardiol 1995; 25: 800 10. DICOM Media Interchange Standards for Cardiology: Initial interoperability demonstration by Jonathan L. Elion, Brown University 11. Implementation of the principle of as low as reasonable achievable (ALARA) for medical and dental personnel. NCRP Report No. 107. Bethesda, MD: National Council on Radiation Protection and Measurements, 1990 12. Lowe FC, Auster M, Beck TJ, et al. Monitoring radiation exposure to medical personnel during percutaneous nephrolithotomy. Urology 1986; 28: 221–6 13. Bush WH, Jones D, Brannen GE. Radiation dose to personnel during percutaneous renal calculus removal. Am J Radiol 1985; 145: 1261–4
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SECTION II Techniques
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Arterial access for endovascular interventions: vascular access JS Jenkins
Introduction Multiple methods of arterial access have been described since the first documented arterial cannulation in 1733 when Reverend Stephen Hales inserted a brass rod into the surgically exposed artery of a horse and measured pressure via a manometer.1 Since the most common procedural complications involve the initial access to the circulation, this important step deserves full study. The widely used technique of percutaneous retrograde common femoral artery access will not be described here, as it is well described in the literature.2 This chapter will describe the percutaneous techniques of antegrade femoral artery access, contralateral iliofemoral artery access, and popliteal artery access.
Antegrade femoral artery access Anatomy Although the common femoral artery (CFA) is considered by many angiographers to be the safest site for arterial puncture, there is little published data relating the CFA and its bifurcation to the landmarks used to guide arterial puncture. Lechner et al. showed the inguinal skin crease to be distal to the bifurcation of the CFA in 75% of limbs but did not consider other landmarks.3 A thorough understanding of the relationship of the CFA to anatomical landmarks is necessary to ensure safe antegrade CFA puncture. Dotter and Judkins first described the technique of antegrade CFA puncture in 1964.4 The regional anatomy relevant to percutaneous femoral artery puncture is demonstrated in Figure 3.1. The femoral artery and vein are shown coursing underneath the inguinal ligament, which is a band of dense fibrous tissue connecting the anterior superior iliac spine to the pubic tubercle. The inguinal skin crease, which can be highly variable in location, is shown as a dotted line.3 The most important landmark shown in this illustration is the femoral head. In a morphological study of computed tomographic (CT) scans in 50 patients, there was not a single case in which a puncture would have passed cranial to the inguinal ligament or caudal to the femoral artery bifurcation if the common femoral artery were entered at the level of the center of the femoral head.5 Caudal to the femoral head, the CFA is encased in the femoral sheath and bifurcates to the superficial femoral artery medially and the profunda femoral artery laterally. With these anatomical observations in mind, entry of the needle into the CFA at the
center of the femoral head is desirable where osseous support is optimal. Indications and contraindications Endovascular treatment of patients with femoral–popliteal atherosclerotic disease is becoming increasingly more common. Antegrade CFA puncture may be useful or desirable for diagnostic angiography, angioplasty, thrombolytic therapy, or use of atherectomy devices. Anatomical considerations where antegrade CFA puncture may be desirable include an acutely angled common iliac bifurcation and aortoiliac grafts where a contralateral femoral approach may be impossible. Contraindications to antegrade CFA puncture include extreme obesity and atherosclerotic disease involving the CFA. Equipment Equipment necessary to perform antegrade CFA puncture includes a percutaneous needle, a steerable guidewire, and an arterial sheath. A steerable guidewire is desirable to negotiate the CFA bifurcation. A 6-French arterial sheath is the initial size chosen until successful entry is obtained. The sheath size is upgraded if necessary to accommodate larger devices once a treatment plan is formulated. After the arterial sheath is placed in an antegrade fashion, a wire, catheter, or obturator is maintained at all times within the sheath lumen to prevent sheath kinking. Braided sheaths, coiled metal sheaths, or kink resistant sheaths are also useful for antegrade punctures to prevent sheath kinking. Procedure Anatomical landmarks are initially identified by palpation of the anterior superior iliac spine and the pubic tubercle to locate the inguinal ligament, and the femoral head position is confirmed fluoroscopically. Depending on the amount of the subcutaneous fat, a skin incision should be made 1–2 cm cranial to the level of the center of the femoral head. The needle is directed through an oblique downward course while palpating the CFA over the center of the femoral head. Once the CFA has been entered, a steerable guidewire is then advanced under fluoroscopic guidance to select the desired branch. The bifurcation of the CFA is best separated fluoroscopically by a 20° lateral view. Once the sheath has been placed, its lumen is always occupied with a wire or catheter to prevent sheath kinking. 15
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Textbook of peripheral vascular interventions Anterior superior Iliac spine Inguinal skin crease Femoral head
Profunda femoral artery
Inguinal ligament Common femoral artery
Superficial femoral artery
Figure 3.1 The most important landmark is the femoral head. Puncture of the femoral artery at this level almost assures entry caudal to the inguinal ligament and cranial to the femoral artery bifurcation.
Complications Complications of antegrade CFA puncture are most commonly related to either too high or too low arterial entry. When the puncture is too high, a retroperitoneal hemorrhage may occur.6–8 The presence of loose connective tissue in the retroperitoneum can cause large hematomas. The lack of osseous support and the presence of the tense inguinal ligament at the arterial puncture site render manual compression inadequate. Low punctures are complicated by formation of arteriovenous fistulas, false aneurysms and hematomas as well as inadvertent entry into the deep femoral artery or superficial femoral artery, which precludes treatment of ostial disease of either of these vessels.6,7 These complications are avoided by proper identification of bony landmarks and entry into the CFA caudal to the inguinal ligament where the artery can be compressed against the common femoral head. Summary The consistent relationship of the CFA to the femoral head cited in the literature make it the landmark of choice in obtaining antegrade femoral artery access. Reluctance to perform such high skin incision for fear of entering the abdominal cavity has to be avoided to prevent complications of too low a needle entry. Antegrade femoral artery access is a safe technique for performing femoropopliteal angioplasty when reliable landmarks are used.
whether peripheral intervention is a success or failure.6–10 Retrograde common femoral artery access remains by far the most commonly used site and the easiest arterial access method. Peripheral interventionalists should be well familiarized with the contralateral iliofemoral approach as it may be the access of choice for many lesions and a successful technique where other approaches fail. Anatomy Anatomical considerations of the femoral artery and its relationship to the common femoral head have been discussed previously in detail (Figure 3.1). The needle puncture is made in a retrograde fashion through a skin incision 1–2 cm below the midline of the femoral head. The standard retrograde common femoral artery access technique is used and a sheath is placed in the common femoral artery.8 Evaluation of the anatomy of the aortic bifurcation and common iliac arteries is important when considering a crossover technique. The two most common reasons for failure are an acutely angled aortic bifurcation or diffusely diseased and calcified common iliac arteries (Figure 3.2). Initial evaluation begins with an abdominal aortogram performed by placing a pigtail catheter in the terminal aorta. Once suitable anatomy is identified, a flexible guidewire placed in the terminal aorta is directed to the contralateral iliac by means of a 5- or 6-French diagnostic internal mammary artery or Judkins right 4 catheter (Figure 3.3). Once a guidewire is
< 90°
Contralateral iliofemoral artery access Introduction The acquisition and maintenance of vessel access from arterial puncture until sheath removal plays a major role in determining
Figure 3.2 Failure to advance this catheter is caused by the acutely angled aortic bifurcation. Heavily calcified aortic bifurcations also present difficulty in crossing with catheters.
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Guide
Guidewire
6-French IMA diagnostic catheter
Sheath Guidewire
Figure 3.3 A 6-French internal mammary artery (IMA) or Judkins right 4 catheter will direct the guidewire to the contralateral iliac artery.
secured into the contralateral external iliac or common femoral artery, a guiding catheter or long sheath can be advanced to the contralateral side. Indications and contraindications One approach to perform angioplasty of the superficial femoral and profunda femoral artery is via an ipsilateral antegrade common femoral artery puncture.11,12 A contralateral approach is desirable when antegrade access my be difficult to obtain as in obese patients with large panniculus or if lesions are located within the common femoral artery or involve the ostium of the superficial femoral or profunda femoral artery. The proximity of these lesions to the arterial puncture site preclude their treatment if an antegrade ipsilateral approached is used (Figure 3.4). Bifurcation anatomy of the common femoral artery into the superficial femoral and profunda femoral arteries may also render an ipsilateral approach technically impossible and require either a contralateral or popliteal approach.13,14 A contralateral approach also allows treatment of bilateral disease with a single arterial puncture. Other anatomical considerations where a contralateral approach may be desirable include angioplasty of internal iliacs or renal transplant artery stenosis (Figure 3.5). Contraindications to the contralateral approach are generally related to the anatomy of the terminal aortic bifurcation and the anatomy of the lesions to be treated. Acute bends at the bifurcation of the terminal aorta make it difficult to manipulate catheters around the iliac bifurcation and maintain enough pushability in tortuous arteries to cross heavily calcified or obstructive lesions. There is a tendency for guidewires and even guide catheters to prolapse or buckle into the aorta at the bifurcation if the angle is too acute. Aortobifemoral grafts can be negotiated unless the bifurcation angle is too acute. If bulky devices such as peripheral atherocaths or nonsegmented Palmaz stents longer than 30 mm are to be used then
Figure 3.4 The proximity of these lesions to the common femoral artery puncture site precludes antegrade femoral artery access.
a contralateral approach is contraindicated.15 The currently manufactured flexible, premounted balloon expandable stents and self-expanding stents negotiate the aortoiliac bifurcation angle with ease. Equipment and procedure Equipment used to gain contralateral iliofemoral access includes a percutaneous needle, guidewire and arterial sheath to obtain standard retrograde CFA access. Once arterial access is obtained, a guidewire is advanced into the abdominal aorta and a catheter is chosen to access the contralateral common iliac artery. Diagnostic catheters useful in crossing the aortic bifurcations include 5- or 6-French diagnostic Judkins right 4, internal mammary artery, pigtail, and Simmons catheters (Figure 3.3). These catheters placed at the level of the aortic bifurcation will direct a wire into the
Crossover guide Guidewire
Sheath
Figure 3.5 Internal iliac stenoses are best treated from a contralateral approach. An ipsilateral approach necessitates negotiating an acute angle, which is rarely successful.
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contralateral common iliac artery. After positioning a catheter in this manner, either a steerable floppy guidewire such as a 0.035-inch Wholey or an angled Glidewire with its superior lubricity is advanced far into the contralateral femoral artery. The catheter is then advanced over the guidewire into the iliac artery. There are a number of guiding systems that may be used for contralateral iliofemoral angioplasty. They all add the ability to inject contrast during lesion dilations and provide more back-up support when crossing stubborn lesions. Guide catheters which may be used, include a Mullins transseptal sheath, a 40-cm-long Arrow Flex sheath (Arrow International, Inc., Reading PA 19605, USA), a 55-cm-long multipurpose coronary or renal guiding catheter, or a kinkresistant crossover guide currently available from a number of manufactures. Any long sheath chosen should be a braided one as non-braided sheaths have a tendency to kink. The guide is advanced over the aortic bifurcation using the stiff wire. If the guide is a long sheath it is inserted with a dilator. If a guiding catheter is used then a diagnostic multipurpose catheter approximately one French size smaller is inserted through the lumen to extend approximately 1 cm distal to the end of the guide and is secured in place with a Tuohey–Borst Y connector. This minimizes the chance of dissection of the terminal aorta during advancement of the guide contralaterally. Once a guiding system is in place, selective injection of contrast allows visualization of the target lesion. The angioplasty catheter and wire can be positioned under direct visualization with contrast, thus avoiding the need for multiple catheter exchanges over the terminal aortic bifurcation. Complications Complications of contralateral iliofemoral access are most commonly related to the retrograde common femoral artery puncture. They include pseudoaneurysms, arteriovenous fistulas, thromboembolism, infection, retroperitoneal hematomas, and bleeding complications.16–18 The most common bleeding complication is hematoma formation at the arterial access site.19–23 If care is not taken to protect large-bore guides when advancing them over the iliac bifurcation, terminal aortic and common iliac dissections may occur. This complication can be best avoided by protecting the tip of the guide with a diagnostic catheter placed within its lumen to provide a smooth transition from the guidewire to the guiding catheter (Figure 3.6). Crossover sheaths with dilators that create a smooth transition minimize this complication. Summary Historically the ipsilateral approach has been used for superficial femoral artery angioplasty but is limited when treating common femoral artery and proximal superficial artery lesions.12,13,15 With the development of peripheral guiding catheter systems, the contralateral approach extends our ability to perform percutaneous transluminal angioplasty of bilateral disease with a single arterial puncture and treatment of proximal superficial femoral, proximal profunda, and
Guide Guide
6-French catheter
Guidewire (a)
(b)
Figure 3.6 (a) Without protection, the large-bore guide can cause complications; (b) a 6-French diagnostic catheter through the guide lumen will protect against these complications.
common femoral artery lesions, which would be impossible with an ipsilateral approach. Many devices can be used and most stents implanted through this access if the anatomy of the terminal aortic bifurcation is not excessively acute and allows passage of a guiding system. Bulky devices such as the directional atherectomy catheter and long rigid stents are difficult if not impossible to deliver using a contralateral approach. This technique can be performed safely as described and broadens the indications for endovascular treatment of peripheral vascular disease in the lower extremities.
Percutaneous popliteal access Introduction Endovascular treatment of atherosclerotic peripheral vascular disease is most commonly approached via the common femoral artery. Lesion location and anatomy in some scenarios dictate the use of an alternative approach from the brachial artery or popliteal artery which may be successful when standard approaches fail. This section will describe the popliteal anatomy, the technique of popliteal access and its indications. Anatomy It is critical to understand the anatomy of the popliteal fossa when performing percutaneous popliteal artery access to prevent the creation of an arteriovenous fistula. Anatomy textbooks describe the popliteal artery as being anterior and medial to the popliteal vein.24 This anatomical relationship between the artery and vein predisposes percutaneous posterior access to puncture of the popliteal vein (see Figure 3.7). The popliteal artery, vein, and sciatic nerve are encased in a common sheath, which courses upwards along the diagonal of the popliteal fossa as shown. These structures usually remain superficial in location well above the level of the joint space. The semitendinous muscle is seen anterior to the artery.
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Sciatic nerve
Popliteal artery Popliteal vein Tibial nerve Common peroneal nerve
Figure 3.7 The popliteal artery courses medial to the popliteal vein and overlaps 60% of the time at a level of 6.5 cm above the joint space.
Anatomic variations were described by Jean Paul Trigaux et al. by the use of cadaveric specimens, CT scans and plain radiographs of the knee in 67 patients.25 Five levels were studied on a CT scan ranging from the joint space to 6.5 cm cranially. In 92% of all levels studied on CT, the artery was anterior to the vein and in 87% of the levels, more than 25% of the artery overlapped the vein. However, when the most cranial level was considered (6.5 cm cranial to the joint space), overlap occurred in only 60% and the artery was medial to the vein in 25% resulting in the most desirable location for arterial puncture. The plain radiographs of the knee demonstrated the popliteal skin crease to be above the femorotibial joint space in 97% of the cases. This study would indicate the most reliable bony landmark to be the femorotibial joint space and the most favorable puncture site to be 6.5 cm cranial to this space with the puncture needle directed from a medial to lateral course. Puncture of the popliteal artery at this level will also avoid arterial entry below an anomalous high popliteal bifurcation, which occurs in 4.7% of cases.26 Indications and contraindications The popliteal approach is utilized for lesions that have failed the antegrade approach, flush occlusions of the superficial femoral artery or superficial femoral arteries that end in
19
large collaterals which have a tendency to divert angioplasty wires into them. An antegrade approach to superficial femoral artery occlusions generally fails due to the inability to maintain an angioplasty wire within the true lumen of the vessel. Ostial superficial femoral artery and common femoral artery lesions may also be approached via the popliteal access in patients with acute-angled terminal aortic bifurcations. Obese patients with large panniculus and acute-angled terminal aortic bifurcations can be approached with the popliteal access to treat superficial femoral artery disease. Strict contraindications to popliteal artery puncture include aneurysms of the popliteal artery and pathology of the popliteal fossa such as Baker’s cyst. Procedure The patient is first placed in a supine position and retrograde ipsilateral common femoral artery sheath or a contralateral retrograde access is placed for direct visualization of the popliteal artery with contrast medium. This access is secured in place and connected to a high-frequency pressure monitoring line for contrast injections. Visualization of the site to be treated may be afforded with this access. The patient is then turned and placed in a prone position on the angiography table and the popliteal fossa is prepared and draped. The femorotibial joint is the most reliable landmark determined fluoroscopically. An area 3–4 cm above this space is then infiltrated with local anesthetic and a skin incision is made medial to the popliteal artery. Contrast is then injected into the previously placed common femoral artery access for direct fluoroscopic visualization of the popliteal artery during puncture. The puncture needle is directed obliquely from medial to lateral so that the artery is entered 6–7 cm above the level of joint space. A 0.035-inch floppy guidewire is then advanced into the popliteal artery over which a 6-French arterial sheath is placed. In addition to direct contrast visualization, ultrasound guidance can be employed to gain retrograde popliteal artery access. This technique avoids ipsilateral or contralateral CFA access. Complications As with any arterial puncture, hematomas occur at rates of 2–4% when popliteal artery access is used.15,27,28 The anatomical relationship of the popliteal artery to popliteal vein increases the risk of arteriovenous fistula due to transvenous arterial puncture. The risk can be minimized with attention to the anatomical considerations previously discussed and higher punctures directed from medial to lateral. Summary Popliteal access is a useful technique which allows endovascular treatment of peripheral arterial disease not approachable by other techniques. Still, it is probably the least-used access by the peripheral interventionalist. With close attention to the anatomical considerations and technique, it is a safe and reliable approach to many lesions using percutaneous methods.
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REFERENCES 1. 2. 3.
4. 5. 6.
7. 8. 9. 10. 11. 12.
13.
Hales S, Hales S. Statical essays, 3rd edition with amendments. London: Printed for W. Innys and R. Manby, T. Woodward and J. Peele; 1738 Seldinger SI. Catheter replacement of the needle in percutaneous arteriography; a new technique. Acta Radiol 1953; 39(5): 368–76 Lechner G, Jantsch H, Waneck R, et al. The relationship between the common femoral artery, the inguinal crease, and the inguinal ligament: a guide to accurate angiographic puncture. Cardiovasc Intervent Radiol 1988; 11(3): 165–9 Dotter CT, Judkins MP. Transluminal treatment of arteriosclerotic obstruction. Description of a new technic and a preliminary report of its application. Circulation 1964; 30: 654–70 Spijkerboer AM, Scholten FG, Mali WP, et al. Antegrade puncture of the femoral artery: morphologic study. Radiology 1990; 176(1): 57–60 Altin RS, Flicker S, Naidech HJ. Pseudoaneurysm and arteriovenous fistula after femoral artery catheterization: association with low femoral punctures. AJR Am J Roentgenol 1989; 152(3): 629–31 Rapoport S, Sniderman KW, Morse SS, et al. Pseudoaneurysm: a complication of faulty technique in femoral arterial puncture. Radiology 1985; 154(2): 529–30 Greenfield AJ. Femoral, popliteal, and tibial arteries: percutaneous transluminal angioplasty. AJR Am J Roentgenol 1980; 135(5): 927–35 Grossman M. How to miss the profunda femoris. Radiology 1974; 111(2): 482 Keller FS. Percutaneous angioplasty of the femoral, popliteal and tibial arteries. In: Jang GD, ed. Angioplasty. New York: McGrawHill, 1986: 61–82 Bachman DM, Casarella WJ, Sos TA. Percutaneous iliofemoral angioplasty via the contralateral femoral artery. Radiology 1979; 130(3): 617–21 Schwarten DE. Aortic, iliac and peripheral artery angioplasty. In: Castaäneda-Zuäniga WR, Tadavarthy SM, eds. Golden’s Diagnostic Radiology. Baltimore: Williams & Wilkins, 1988: 268–97 Kaufman SL. Angioplasty from the contralateral approach: use of a guiding catheter and coaxial angioplasty balloons. Radiology 1990; 177(2): 577–8
14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27.
28.
White CJ, Nguyen M, Ramee SR. Use of a guiding catheter for contralateral femoral artery angioplasty. Cathet Cardiovasc Diagn 1990; 21(1): 15–7 Henry M, Armor M. Stenting of femoral and popliteal arteries. In: Sigward U, ed. Endoluminal Stenting. London: WB Saunders, 1996: 476–86 Cleveland KO, Gelfand MS. Invasive staphylococcal infections complicating percutaneous transluminal coronary angioplasty: three cases and review. Clin Infect Dis 1995; 21(1): 93–6 Ricci MA, Trevisani GT, Pilcher DB. Vascular complications of cardiac catheterization. Am J Surg 1994; 167(4): 375–8 Trerotola SO, Kuhlman JE, Fishman EK. Bleeding complications of femoral catheterization: CT evaluation. Radiology 1990; 174(1): 37–40 Fraedrich G, Beck A, Bonzel T, et al. Acute surgical intervention for complications of percutaneous transluminal angioplasty. Eur J Vasc Surg 1987; 1(3): 197–203 Garti I, Salinger H. Complications in brachial countercurrent arteriography and in retrograde femoral arteriography. Isr J Med Sci. 1969; 5(6): 1192–7 Lang EK. A survey of the complications of percutaneous retrograde arteriography: Seldinger technic. Radiology 1963; 81: 257–63 Redman HC, Reuter SR. Percutaneous transarterial angiography: complications and their avoidance. Angiology 1970; 21(9): 575–9 Sigstedt B, Lunderquist A. Complications of angiographic examinations. AJR Am J Roentgenol 1978; 130(3): 455–60 Paturet G. Traité d’anatomie humaine. Paris: Masson, 1951 Trigaux JP, Van Beers B, De Wispelaere JF. Anatomic relationship between the popliteal artery and vein: a guide to accurate angiographic puncture. AJR Am J Roentgenol 1991; 157(6): 1259–62 Kim D, Orron DE, Skillman JJ. Surgical significance of popliteal arterial variants. A unified angiographic classification. Ann Surg 1989; 210(6): 776–81 Tonnesen KH, Sager P, Karle A, et al. Percutaneous transluminal angioplasty of the superficial femoral artery by retrograde catheterization via the popliteal artery. Cardiovasc Intervent Radiol 1988; 11(3): 127–31 Zaitoun R, Iyer SS, Lewin RF, et al. Percutaneous popliteal approach for angioplasty of superficial femoral artery occlusions. Cathet Cardiovasc Diagn 1990; 21(3): 154–8
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Arterial access for endovascular interventions: radial and brachial arterial access PW McMullan Jr and JS Jenkins
Introduction Transradial arterial access is a valuable skill for the coronary or peripheral interventionist. In the early days of endovascular intervention, sheath and catheter sizes precluded the use of the radial artery.1 However, since 1989 when Campeau first described the technique of successful transradial coronary angiography with 6-French catheters,2 equipment has become progressively more miniaturized and streamlined. Annually, transradial cases account for less than 10% of coronary procedures in the US,3 but this number is expected to rise with increasing operator familiarity and growing patient expectations for procedural comfort and rapid ambulation.
The routine use of heparin during sheath dwell time significantly reduces the probability of occlusion,15 and operator experience correlates directly with procedural success and reduced complication rates.16,17 In one prospective series of 300 radial cases, nine complications occurred in the first 100 patients and only two in the last 100.18 There is evidence that repeated access does not affect procedural success or complication rates.19 Also, the risk of radial artery occlusion is only slightly increased in repeat cases demonstrated by a 117 patient series with 2.6% occlusion in repeated access versus 0% in initial access.12 Obese patients20 and those requiring anticoagulation derive a particular safely benefit from the radial approach.21
Advantages of transradial access
Procedural success
Unlike the common femoral and brachial arteries, the radial artery is not an end vessel; the radial and ulnar arteries come together to form the deep and superficial palmar arches. Therefore, if the arch anatomy is intact, occlusion of one or the other does not compromise the vascular supply of the hand.4 No major nerves or veins lie in the immediate vicinity of the radial artery where it passes just proximal to the styloid process, therefore arteriovenous malformation or nerve damage is infrequent (Figure 4.1).5 Furthermore, a randomized study of transradial versus transfemoral cardiac catheterization demonstrated that patients strongly preferred the radial approach and that it improved measures of bodily pain, back pain, and walking ability both on the day of and over the week following the procedure. Hospital cost and length of stay were also significantly reduced.6
Procedural success via the transradial approach has been clearly demonstrated in coronary angiography and intervention. In a landmark study in 1997 by Kiemeneij and colleagues, 900 patients were randomized to transradial, transbrachial, and transfemoral coronary angioplasty with 6F guiding catheters.9 Successful coronary cannulation was achieved in 279 (93.0%), 287 (95.7%) and 299 (99.7%) patients, respectively (p < 0.001). Inability to access the artery caused most failures. Major entry site complications were encountered in seven patients (2.3%) in the transbrachial group, six patients (2.0%) in the transfemoral group and no patients in the transradial group (p = 0.035). Angioplasty success was achieved in 91.7, 90.7 and 90.7% (p = NS), indicating that the main obstacle to successful intervention was initial access to the radial artery. In more recent years, reported rates of radial access failure range from 1 to 5%.22 In the last decade, numerous studies have validated the concept of the radial approach for elective and emergent coronary intervention9,14,23,24 including primary angioplasty for acute myocardial infarction,11,13,25,26 routine successful access of coronary artery bypass grafts,27 and rotational atherectomy.28 There are also numerous reports of successful peripheral and cerebral angiography29 and endovascular intervention via this approach, including stent placement in the vertebral arteries,30 carotid arteries,31,32 renal arteries,33–35 and the common iliac arteries.36,37 Neuroendovascular interventionists who routinely use lytic therapy along with potent platelet
Safety Safety of radial access has been well established by numerous investigators. Entry site complications and radial artery occlusion occur at a low rate. A meta-analysis of 1,472 radial procedures reported an access site complication rate of only 0.3%.7 The incidence of radial artery occlusion in a series of 563 patients following coronary angioplasty via 6-French radial sheaths was 5.3% at discharge and dropped to 2.8% at followup.8 Other large series report occlusion rates of 0–5%.3,6,9–14
21
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Ulnar artery
Radial artery
Needle entry
2 cm
1 cm
Ulnar nerve Median nerve
Radial styloid process
Deep palmar arch Superficial palmar arch
Figure 4.1
Anatomy of the palmar arch and bony landmarks.
inhibitors are able promptly to remove the radial sheath without reversal of anticoagulation or concerns about major bleeding complications.38
Anatomy and Allen’s testing Approach to the patient’s vascular supply should by begin with palpating for an adequate radial pulse and ensuring that there are no orthopedic deformities that would render the patient unable to extend the wrist or straighten the arm. One should measure blood pressure in both upper extremities to screen for significant narrowing in the proximal arterial supply. Evaluation for adequate collateral supply from the ulnar artery has traditionally been performed by the modified Allen’s test39 (termed “modified” because the original test described in 1929 by Edgar V. Allen demonstrated arterial occlusion, not collateral flow).40 It is accomplished by compressing simultaneously the radial and ulnar arteries while the patient squeezes a fist to express blood from the hand. The hand is then reopened and held in a relaxed position without hyperextension of the fingers while the ulnar artery is released and the radial artery remains compressed.41 A blush indicates adequate blood return, the exact normal timing of which varies from 5 to 10 seconds according to various sources. Reported results from the Allen’s test vary widely. In a study of 1,000 consecutive patients, test responses were divided into categories by the number of seconds to maximal blush. Fortynine percent filled in less than 5 seconds, 24% filled in 5–10 seconds, and 27% filled in greater than 10 seconds;
leading the investigators to conclude that over one-quarter of screened patients would be unsuitable candidates for radial access.42 Another method described by Barbeau and colleagues involves the use of pulse oximetry and plethysmography.43 Barbeau studied both wrists of 1,010 patients who underwent evaluation with the modified Allen’s test followed by placement of a pulse oximeter on the thumb. After release of the clenched fist with continued ulnar compression, plethysmography was recorded for up to 2 minutes. Waveforms were recorded as normal, damped or absent. Results showed that the traditional modified Allen’s test was normal in 93.7% of patients with a mean time to maximal blushing of 4.7 seconds. Plethysmography found 98.5% of patients to have at least a damped wave form at the end of a 2-minute period on one hand or the other, indicating some degree of collateral circulation. Therefore, only 6.3% by standard modified Allen’s testing and 1.5% by plethysmographic testing would be ineligible for radial artery access in one wrist or the other. As it turns out, cadaveric studies indicate that a complete superficial palmar arch is present in 85–96%44,45 and a complete deep palmar arch in 90%46 of the general population, and most hands typically have at least one major vessel connecting the radial and ulnar arteries. This has led some highvolume operators to abandon entirely the use of the Allen’s test prior to radial cannulation,47,48 citing large numbers of unscreened patients who have undergone transradial coronary intervention with no resultant hand or forearm ischemia.49 Nevertheless, the authors recommend vigilant confirmation and documentation of adequate collateral circulation prior to radial artery instrumentation.
Right versus left Choice of access in the right versus the left wrist depends on operator proficiency, patient needs and goals of the case. Access from the right wrist with the arm adducted permits use of a standard lab configuration and does not require the operator to reach across the patient. However, when coronary cannulation is the goal, the acutely angulated path through the right subclavian and innominate arteries down to the aortic root frequently requires special catheters. The Kimny catheter (brand name derived from the catheter’s inventor, Dr. Ferdinand Kiemeneij) is a double-curve catheter designed to fit the left main coronary from the right radial approach. Standard Judkins and other catheters can often be used as well. A good rule of thumb is to choose a catheter one half-size smaller than the equivalent catheter from the standard femoral approach. For example, if the catheter of choice from the femoral approach is a Judkins left 4.0, use a Judkins left 3.5 instead. Benefits of access in the left wrist are ease of approach to the left internal mammary artery and normal functionality of standard catheters for coronary work from that side. There is also evidence that catheter manipulation time is greater from the right than from the left, translating to longer fluoroscopy and total procedure times.50
Procedural technique and equipment The technique of radial artery puncture should be carried out by or under the supervision of an experienced operator.
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Arterial access for endovascular interventions: radial and brachial arterial access Most authors recommend positioning the patient in the supine position on the catheterization table with the access arm abducted at a 45–70° angle and the wrist hyperextended.3,9,24 Prior to sterile prep, one can maintain wrist extension and immobility during access by placing a strip of silk tape across the palm and around the supporting arm-board. The ideal site of puncture is 1–2 cm proximal to the radial styloid process over the pulse’s point of maximal impulse in a direction consistent with the course of the more proximal radial artery. The operator’s index finger should palpate for the pulse and then withdraw to the edge of the artery so that the fingertip abuts the edge of the pulsation. Apply lidocaine sparingly and superficially to avoid eliciting arterial spasm or causing distortion of the anatomy. With a 21-gauge, 4-cm micropuncture needle at a 30–45° angle and the bevel facing up, entry is made without a prior skin nick. Pulsatile flow may not be evident as quickly as in femoral entry, due to the smaller bore needle. Filling the needle with saline allows the operator to see flow immediately upon entry into the artery. The operator should then advance a 0.018-inch floppy-tipped wire with great care to avoid dissection. If smooth wire passage is not immediate, the needle should be withdrawn slightly with one hand while the other hand makes gentle serial attempts at wire advancement. This method allows withdrawal of the needle from the back wall of the vessel without losing access entirely. If initial access attempts are unsuccessful, radial artery spasm may ensue, which makes the pulse weak or absent and the artery much more difficult to cannulate. Adequate sedation lessens the propensity for spasm, and one study demonstrated spasm resolution with subcutaneous injection of 400 µg of nitroglycerin over the radial artery.51 With the wire in place, the operator should advance the plastic tip of the sheath dilator into the vessel until the sheath tip comes within 1–2 mm of the skin. At this point, the operator makes a 1–2 mm longitudinal incision in the skin over the plastic dilator, which facilitates passage of the sheath. Keeping the sheath wet with moist gauze and using a corkscrew insertion motion will ease passage into the artery. A minimum of 2,000 units of heparin should then be administered. Dilution in 10 cm3 of saline lessens discomfort in the hand. Most operators also use a vasodilatory cocktail to flush the sheath throughout the procedure. This mixture contains nitroglycerin and verapamil; some operators also add heparin, lidocaine, or bicarbonate.4 Others advocate the use of hydrophilic sheaths in lengths up to 25 cm to maximize ease of insertion and extraction, which also minimizes the potential for spasm.52 Once access is established, one may adduct the arm and proceed with the catheterization in a standard laboratory setup in which the operator stands along the right side of the patient. The other option is to keep the arm in an abducted position and use a separate table to support the injection manifold. The latter method requires movement of monitors to the head of the patient, and limited upper body shielding increases significantly the operator’s radiation dose compared with the femoral approach.53
Sheath removal Radial artery sheath removal should be performed immediately following the procedure to minimize the risk of thrombosis
23
and occlusion. One should take care to remove the sheath slowly and to be alert to complaints of forearm pain from the patient. This can indicate spasm around the sheath, and there are rare reports of traumatic endarterectomy with sheath removal.3,54,55 Manual compression over the radius with application of a dressing is an adequate method for obtaining hemostasis. There are also several available wrist-strap compression devices that are time-saving and particularly useful when anticoagulation is a factor. Some of these include a thrombin-impregnated pad that overlies the puncture site and promotes surface coagulation. In the immediate period following sheath removal, careful watch for hematoma formation is crucial. Although a rare complication, since a radial artery hematoma has little soft tissue space in which to expand, compartment syndrome requiring fasciotomy can develop if left unattended.14,56
Brachial artery access In addition to percutaneous transradial access, three other methods of upper extremity arterial access remain. These are the percutaneous axillary approach, the percutaneous brachial approach, and the brachial cutdown approach. The axillary approach is used with extreme rarity and will not be covered in this context. The Sones brachial arteriotomy57 requires surgical expertise and has been supplanted largely by the percutaneous method of entry, initially described in 1981 in conjunction with left heart catheterization.58 Indications and success Indications for the brachial approach include peripheral arterial disease precluding femoral access and inadequate collateral hand circulation excluding the radial approach. Occasionally, brachial is preferable to radial access due to inadequate equipment length for work in the lower extremities or needs for sheath diameters 7 French and higher to accommodate larger catheters and equipment. As previously stated, when transbrachial and transfemoral routes were compared in randomized fashion for coronary intervention, coronary cannulation was achieved in 95.7% of the brachial group and in 99.7% of the femoral group.9 Procedural success rates in the modern era for coronary and peripheral angiography and intervention are reported in the range 84–99%, technical failure being more likely in operators who use the technique infrequently.59–62 Complications The most serious complication of percutaneous brachial artery access is thrombotic occlusion of the artery with resultant compromise of the entire vascular supply of the forearm and hand. This event mandates immediate surgical or percutaneous thrombectomy and repair to avoid permanent nerve injury or limb loss.63 Reported rates of brachial artery occlusion from series published over the mid-1980s to the late-1990s vary from 1 to 6%,64 and more recent series employing 4- and 5-French sheaths and catheters report rates below 1%.61,64 The likelihood of thrombosis is greater in
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females (1.24 vs. 0.28% in males in a series of 1,326 procedures by a single experienced operator), probably due to smaller vessel caliber,64 and Duplex ultrasound has demonstrated efficacy in preprocedural screening for unusually small brachial arteries.65 When thrombosis is promptly diagnosed, treatment is generally effective and leaves the patient without long-term sequelae.66 Other complications include arterial dissection, pseudoaneurysm formation, and hematoma. Hematoma enlargement in the antecubital fossa must be diligently monitored due to the potential for median nerve compression, which can lead to long-term disability,67 and large hematomas may rarely require surgical exploration. Randomized data indicate that brachial access site complication rates for experienced operators are roughly equivalent to transfemoral rates,9 but operators who use brachial access only occasionally (ten or fewer cases per year) are more prone to major and minor complications of the technique. Technique Percutaneous entry of the brachial artery is performed with the patient’s upper extremity in the abducted, supinated position with the support of an arm-board. The medial and lateral humeral epicondyles serve as the bony landmarks of the antecubital fossa. Palpation for the brachial pulse should be performed 1 cm proximal to the antecubital skin fold, just medial to the biceps tendon (Figure 4.2). Following sterile skin preparation, draping, and infiltration of the skin with lidocaine, an 18- or 21-gauge needle is inserted at a 30–45° angle to the skin in a direction consistent with the path of the brachial artery. An arterial sheath is then inserted over a wire. Following the
Brachial artery Lateral humeral epicondyte Biceps tendon
Medial Humeral epicondyte 1 cm
Radial artery
Figure 4.2
Needle entry
Ulnar artery
Anatomy of the antecubital fossa.
procedure, sheath removal should be immediate with manual compression applied to the area for a minimum of 15 minutes. Some authors also advocate the use of a moderate-tightness tourniquet for an additional hour59 or transparent pneumatic compression which is released slowly over time.68
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68.
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Gellman H, Botte MJ, Shankwiler J et al. Arterial patterns of the deep and superficial palmar arches. Clin Orthop Relat Res. Feb 2001; 383: 41–6 Ikeda A, Ugawa A, Kazihara Y et al. Arterial patterns in the hand based on a three-dimensional analysis of 220 cadaver hands. J Hand Surg [Am]. Jul 1988; 13(4): 501–9 Ruengsakulrach P, Eizenberg N, Fahrer C et al. Surgical implications of variations in hand collateral circulation: anatomy revisited. J Thorac Cardiovasc Surg. Oct 2001; 122(4): 682–86 Gilchrist IC. Is the Allen’s test accurate for patients considered for transradial coronary angiography? J Am Coll Cardiol. Sep 19 2006; 48(6): 1287; author reply 1288 Hildick-Smith D. Use of the Allen’s test and transradial catheterization. J Am Coll Cardiol. Sep 19 2006; 48(6): 1287; author reply 1288 Ghuran A DG, de Belder A, Holmberg S, Hildick-Smith D. Transradial coronary intervention without pre-screening for a dual palmar blood supply (abstr). Heart. 2005; 91(Supplement): A5-i122 Kawashima O, Endoh N, Terashima M et al. Effectiveness of right or left radial approach for coronary angiography. Catheter Cardiovasc Interv. Mar 2004; 61(3): 333–37 Pancholy SB, Coppola J, Patel T. Subcutaneous administration of nitroglycerin to facilitate radial artery cannulation. Catheter Cardiovasc Interv. Sep 2006; 68(3): 389–91 Kiemeneij F, Fraser D, Slagboom T et al. Hydrophilic coating aids radial sheath withdrawal and reduces patient discomfort following transradial coronary intervention: a randomized double-blind comparison of coated and uncoated sheaths. Catheter Cardiovasc Interv. Jun 2003; 59(2): 161–64 Lange HW, von Boetticher H. Randomized comparison of operator radiation exposure during coronary angiography and intervention by radial or femoral approach. Catheter Cardiovasc Interv. Jan 2006; 67(1): 12–16 Dieter RS, Akef A, Wolff M. Eversion endarterectomy complicating radial artery access for left heart catheterization. Catheter Cardiovasc Interv. Apr 2003; 58(4): 478–80 Abu-Ful A, Benharroch D, Henkin Y. Extraction of the radial artery during transradial coronary angiography: an unusual complication. J Invasive Cardiol. Jun 2003; 15(6): 351–52 Lin YJ, Chu CC, Tsai CW. Acute compartment syndrome after transradial coronary angioplasty. Int J Cardiol. Nov 2004; 97(2): 311 Sones FM, Jr., Shirey EK. Cine coronary arteriography. Mod Concepts Cardiovasc Dis. Jul 1962; 31: 735–38 Fergusson DJ, Kamada RO. Percutaneous entry of the brachial artery for left heart catheterization using a sheath. Cathet Cardiovasc Diagn. 1981; 7(1): 111–14 Hildick-Smith DJ, Khan ZI, Shapiro LM et al. Occasional-operator percutaneous brachial coronary angiography: first, do no arm. Catheter Cardiovasc Interv. Oct 2002; 57(2): 161–165; discussion 166 Nolan J, Batin P, Welsh C et al. Feasibility and applicability of coronary stent implantation with the direct brachial approach: results of a single-center study. Am Heart J. Nov 1997; 134(5 Pt 1): 939–44 Basche S, Eger C, Aschenbach R. Transbrachial angiography: an effective and safe approach. Vasa. Nov 2004; 33(4): 231–34 Kaukanen ET, Manninen HI, Matsi PJ et al. Brachial artery access for percutaneous renal artery interventions. Cardiovasc Intervent Radiol. Sep-Oct 1997; 20(5): 353–58 Mills JL, Wiedeman JE, Robison JG et al. Minimizing mortality and morbidity from iatrogenic arterial injuries: the need for early recognition and prompt repair. J Vasc Surg. Jul 1986; 4(1): 22–27 Armstrong PJ, Han DC, Baxter JA et al. Complication rates of percutaneous brachial artery access in peripheral vascular angiography. Ann Vasc Surg. Jan 2003; 17(1): 107–10 Rath J, Ganschow US, Kelm M et al. [Duplex ultrasound risk stratification of percutaneous puncture of the brachial artery for diagnostic and interventional coronary angiography]. Z Kardiol. Apr 1998; 87(4): 249–57 Khoury M, Batra S, Berg R et al. Influence of arterial access sites and interventional procedures on vascular complications after cardiac catheterizations. Am J Surg. Sep 1992; 164(3): 205–09 Kennedy AM, Grocott M, Schwartz MS et al. Median nerve injury: an underrecognised complication of brachial artery cardiac catheterisation? J Neurol Neurosurg Psychiatry. Oct 1997; 63(4): 542–46 Cardenas JA, Yellayi S, Schatz RA et al. A new method for brachial artery hemostasis following percutaneous coronary angiography. J Invasive Cardiol. Nov-Dec 1994; 6(9): 285–88
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Arterial access for endovascular interventions: transradial approach I Henry, M Henry, and M Hugel
Femoral access is the most often-used approach way for peripheral arterial procedures. However, the management of sheath removal and the prevention of vascular access complications still remain a practical day-to-day problem, including personnel involved to compress, cost of the mechanical compression device or percutaneous closure device, and nursing time and in-hospital stay time, particularly after interventional procedures which require an aggressive anticoagulation therapy. Furthermore, the femoral approach is sometimes impossible for anatomical reasons; for example, iliac stenosis or occlusion, tortuosities, or aneurysm. The transradial approach was first described for coronary procedures and is currently largely used with a very low rate of vascular complication,1,2 allowing an early discharge of the patient. The approach should be well known and should be used more frequently for some good indications.
Technique Patient selection The major inclusion criteria are a good pulsating right or left radial artery, associated with a good cubital artery pulse and the absence of digital ischemia by Allen’s test. This test is considered as normal if, after compression of both ulnar and radial arteries, hand color returns to normal within 10 seconds after releasing the ulnar artery. Exclusion criteria are the following: ● ● ●
● ● ●
absence of radial or ulnar pulse; digital ischemia by Allen’s test (15% of patients); lesions, which can necessitate techniques requiring large guiding catheters. A 7-French guiding catheter is possible in 70% of the patients, an 8-French in 60%; upper extremity vascular disease; Burger’s disease; severe Raynaud’s.
Which radial artery? A right transradial approach is easier to perform for a righthanded operator. The left radial approach may be used with equal success. The choice of the radial artery should also depend on the location of the angioplasty. For example, the 26
right radial artery is preferred to treat a left carotid lesion and the left for the right carotid artery. Patient position The patient’s arm may be extended a few inches from the body for the puncture, but the arm may rest along the body. The patient’s hand may be hyperextended in a supine position, or in a relaxed supine position without hyperextension. Artery puncture Depending on the procedure a neuroleptanalgesia may be performed in addition to local anesthesia with a superficial injection of 1–2 ml 2% lidocaine followed by a light massage. The puncture of the radial artery may be done with an 18–22 gauge bare needle (needle diameter selected in relation to the guidewire) at a 30–45° angle approximately 1 cm from the styloid process. Puncture with a venous catheter is possible and allows injections of antispastic medications before sheath insertion. Several kits (Arrow kit, Cordis kit) are now on the market and can facilitate the technique. Failure of radial artery puncture is rare (6% for Wiper et al.).5 Insertion of sheath The operator may use a long (23 cm), standard (13 cm), or short (7 cm) sheath. A long sheath may serve to mechanically prevent spasm and facilitate movement of a guiding catheter, although it is harder to withdraw. Following puncture using a bare needle, a straight Teflon 0.025-inch wire, 1.50 m in length is used to catheterize the ascending aorta and permits identification of antebrachial or brachial loops. The extremity of the wire is slightly bent manually in order to facilitate insertion in the artery and crossing of tortuous segments. The needle is then withdrawn and the introducer advanced into the artery over the wire (a cut in the skin may be made cautiously). Following puncture with a venous catheter or a kit, the guide is inserted through the small catheter already in place. This wire may be short as it is only used to insert the introducer. Inadequate guiding catheter support with transcranial approach is rare (0.5% for Wiper et al.5 A recent study with 1125 patients undergoing transradial PCI demonstrated similar figures.7
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Arterial access for endovascular interventions: transradial approach Medication cocktail Medication is administered for prevention of spasm and radial thrombosis. We combine fast-acting nitrates (isosorbide dinitrate, molsidomine) and prolonged action verapamil (3–5 mg) injected simultaneously in the radial artery through the side lumen of the introducer. Subsequently, 5000 IU heparin are injected to prevent radial thrombosis, but higher doses can be given to have an actual clotting time (ACT) > 250 seconds for some angioplasty-like carotid angioplasty stenting. Catheterization of the aorta and other arteries This procedure is performed by the combined action of the guidewire and angiographic or angioplasty catheter. In the presence of severe loops (antibrachial, brachial) or tortuous subclavian arteries, hydrophilic wires may be used. Any catheters, guiding catheters, or guidewires can be used in this approach, allowing the catheterization of not only coronary arteries but also renal, mesenteric, vertebral, carotid, and subclavian arteries. Catheterization of the iliac and femoropopliteal arteries is limited by the length of the devices. Introducer sheath removal and hemostasis The arterial sheath is removed immediately after the withdrawal of the guiding catheter at the end of the procedure. The artery is manually compressed only for the time necessary to place a tourniquet set over the puncture site. Local compression is held in place for 30–45 minutes and then pressure is gradually released until hemostasis is obtained. A compressive bandage is applied for 6 hours. The patient may be allowed to stand up for 1 hour after the end of the procedure and the radial pulse is checked by clinical examination. Different devices are currently available on the market to compress the arterial puncture site such as the Radistop radial compression system, Terumo TR Band. Assisted compression devices have also been proposed as topical hemostasis pads and patches.
Advantages There are several advantages of the transradial approach. The sheaths are removed immediately after the procedure and no personnel are needed to compress the radial artery. The patient is able to ambulate 2 hours after the procedure and, if after an observation period of 6 hours no access site-related complications occur, an early discharge in carefully selected patients is possible. Peripheral procedures on an outpatient basis can now be performed, which reduces cost and patient discomfort.
Complications Vascular access complications (hematomas, bleeding, pseudoaneurysms) are reduced compared with femoral access and may occur in 1–2% of the cases, mainly forearm or arm hematomas. Asymptomatic radial artery occlusion has been reported in 6–10%, although 40% appear to spontaneously recanalize after 1 month.10,11 Consistent variables that influence the frequency of these occlusions include artery size at baseline, sheath-to-artery size ratio, duration of sheath placement, prior procedures, and the presence of diabetes mellitus.11–13 A palpable radial artery can be re-punctured and the transradial approach repeated with no increased technical challenge.6 Some concerns about the radial approach must be reported: ●
●
Indications for radial approach Femoral artery access may be difficult in obese patients, patients with extensive post-operative scarring, and in cases of severe peripheral disease; and is impossible in the case of aortic or iliac occlusion, or relatively contraindicated (coagulopathy). For these patients the radial approach may be useful to catheterize supra-aortic, mesenteric, renal, or iliac arteries.8 Angiography and interventional procedures may be performed in this way and most of the stents can be implanted through 6–8-French introducers. This method should be more often used to treat supraaortic and renal arteries, not only when the femoral approach is contraindicated but also in some specific indications like carotid angioplasty stenting in the case of bovine arch or type-3 aortic arch. The transradial approach is safe when used in fully anticoagulated patients with a low risk for subsequent bleeding complications.9
27
The possibility of neurological embolic complications. Some aortic plaques may be detached by catheters or guidewires and can emboli to the brain. The risk is higher in elderly patients with atheromatous aortic arch and/or ulcerated plaques. This radial approach therefore has to be discussed in such patients when the femoral approach is feasible. We always try to perform our peripheral angioplasty by the femoral route to avoid these neurological complications and we reserve the radial or brachial approach for specific indications. The effects of catheterization-induced changes on future clinical uses of the vessel are not nearly as trivial. The radial artery can be used as an additional arterial conduit for aorto-coronary bypass surgery and as the preferred initial artery used in the creation of an arteriovenous fistula for hemodialysis access. Some reports exist in the literature suggesting that prior instrumentation of a radial artery destined for service as a bypass graft may result in a significantly higher likelihood of graft closure,14,15 and although less well studied, pre-existing radial intimal hyperplasia is closely associated with failure of radiocephalic arteriovenous fistulas in hemodialysis patients.16, 17
Conclusion Radial access is a new approach for peripheral procedures and indications should widen as a result of the new generation of
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miniaturized equipment, fewer access site complications, and the development of the procedures on an outpatient basis. However, some concerns may be kept in mind, particularly in multivascular elderly patients where there is a risk of brain embolism (which could be avoided by the use of the femoral approach) and the possibility of a higher graft closure rate after cardiac surgery. So it is perhaps better to reserve the radial approach for patients at low-risk for endothelial
dysfunction and intimal hyperplasia and for those with a low likelihood of requiring future surgical use of the radial artery.17 Also in patients with renal insufficiency the femoral approach could be preferred to preserve the radial artery in the event of a subsequent need for a hemodialysis shunt. Nevertheless, this technique should be known by all interventionists involved not only in coronary procedures but also in peripheral procedures.
REFERENCES 1. 2.
3. 4. 5. 6. 7. 8. 9.
Campaud L. Percutaneous radial artery approach for coronary angiography. Cathet Cardiovasc Diagn 1989; 16: 3–7 Kiemeneij F, Laarman GH, Oderkerken D et al. A randomized comparison of percutaneous transluminal coronary angioplasty by the radial, brachial and femoral approaches. The Access Study. J Am Coll Cardiol 1997; 29: 1269–75 Mann T, Cubeddu G, Bowen J et al. Stenting in acute coronary syndrome. A comparison of radial versus femoral access sites. J Am Coll Cardiol 1998; 32: 572–6 Slagboom T, Kiemeneij F, Laarman GJ et al. Outpatient coronary angioplasty: feasible and safe. Catheter Cardiovasc Interv 2005; 64: 421–7 Wiper A, Kumar S, Mac Donald J et al. Day case transradial coronary angioplasty: a four year single center experience. Cath and Cardiovasc Interventions 2006; 68: 549–53 Eccleshall SC, Banks M, Carroll R et al. Implementation of a diagnostic and interventional transradial programme: resource and organisational implications. Heart 2003; 89: 561–2 Valsecchi O, Musumeci G, Vassileva A et al. Safety and feasibility of transradial coronary angioplasty in elderly patients. Ital Heart J 2004; 5: 926–31 Galli M, Tarantino F, Mameli S et al. Transradial approach for renal percutaneous transluminal angioplasty and stenting: a feasibility pilot study. J Invasive Cardiol 2002; 14: 386–90 Hildick-Smith DJ, Walsh JT, Lowe MD et al. Coronary angiography in the fully anticoagulated patient: the transradial route is successful and safe. Catheter Cardiovasc Interv 2003; 58: 8–10
10. 11.
12. 13.
14. 15. 16.
17.
Marco J, Fajadet J, Cassagneau B et al. Transradial coronary stenting: a passing fad or widespread use in the future. J Invasive Cardiol 1996; 8(suppl E): 16E–21E Stella PR, Kiemeneij F, Laarman GH et al. Incidence and outcome of radial artery occlusion following transradial artery coronary angioplasty. Cathet Cardiovasc Diagn 1997; 40: 156–8 Nagai S, Abe S, Sato T et al. Ultrasonic assessment of vascular complications in coronary angiography and angioplasty after transradial approach. Am J Cardiol 1999; 83: 180–6 Saito S, Ikei H, Hosokawa G et al. Influence of the ratio between radial artery inner diameter and sheath outer diameter on radial artery flow after transradial coronary intervention. Catheter Cardiovasc Interv 1999; 46: 173–8 Kamiya H, Ushijima T, Kanamori T et al. Use of the radial artery graft after transradial catheterization: is it suitable as a bypass conduit? Ann Thorac Surg 2003; 76: 1505–9 Deligonul U. Transradial cardiac catheterization and the use of the radial artery as bypass graft. J Invasive Cardiol 2001; 13: 576–7 Kim YO, Song HC, Yoon SA et al. Preexisting intimal hyperplasia of radial artery is associated with early failure of radiocephalic arteriovenous fistula in haemodialysis patients. Am J Kidney Dis 2003; 41: 422–8 Barman N, Chiuj H, Ellis SG. Transradial catheterization: the Rood Less Travelled. J Invasive Cardiol 2004; 16: 639–40
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Arterial access for endovascular interventions: popliteal access to peripheral procedures M Henry, I Henry, and M Hugel
Introduction In endovascular treatment of peripheral arterial disease, the antegrade or retrograde femoral approach is the most often used access. Lesions at the femoral bifurcation prevent guidewires and introducers from being placed. This leads to the use of other approaches such as the brachial, radial, contralateral, or popliteal accesses. Described herein are the antegrade and retrograde popliteal approaches, as well as the present authors’ experiences, so defining the current technique and its indications.1–9
Techniques Retrograde percutaneous popliteal approach The popliteal artery, together with the sciatic nerve and the popliteal vein, goes upward along the diagonal of the popliteal triangle. The superficial location of the popliteal artery allows retrograde puncture, which is usually performed just above the joint. The patient is preferably in the ventral decubitus position but may alternatively be in the lateral decubitus position. The procedure is usually performed under local anesthesia and complemented by intravenous sedation. General anesthesia, which may still be performed, is rarely required. Before choosing the popliteal approach, one should check that the artery is free from any atheromatous lesion or significant stenosis. Angiography may be sufficient. However, echography provides more information regarding the state of the artery, particularly the presence of an aneurysm, which is a strict contraindication to puncture. Due to overlying lesions, the artery may not be pulsatile. It should then first be located, for which several techniques may be used: ●
●
Angiography: A 4- or 5-French catheter is placed in the abdominal aorta, generally through contralateral access. Contrast media is injected to visualize the course of the popliteal runoff. “Road mapping” renders the puncture easy. Doppler echocardiography (echo-Doppler): Angiography and/or echo-Doppler assists in locating the popliteal artery and the puncture site.
●
“Smart Needle”: A Doppler probe is connected to the needle. The sound of the Doppler helps in locating the popliteal artery.
Once the artery is punctured, an introducer, generally 6- or 7French, is placed in the artery. Larger introducers (8- or 9French) may be used in cases where larger devices are needed, such as burrs or covered endoprostheses, as long as the artery is at least 6 mm in diameter. Although contrast media injections are performed through a contralateral access, the femoral bifurcation and the origin of the deep femoral artery are usually well opacified. The introducer is withdrawn at the end of the procedure. Hemostasis is obtained with manual compression of the puncture site for 10–20 minutes, and then a bandage is applied for 24 hours. Arterial puncture-site-closure devices may also be used at this level.10 Antegrade percutaneous popliteal approach The popliteal artery may be accessed through an antegrade approach in the case of femoral artery obstruction, by using short introducers 6–8 cm in length. This allows access to lesions on the leg, which may be helpful for limb salvage. Applicable endovascular techniques Almost all angioplasty techniques may be performed through this approach, including balloon angioplasty, atherectomy, such as rotational atherectomy (Rotablator),11 or recanalization devices, such as the laser fiber. All stents that may be implanted in the femoral artery may be introduced through this access. This also allows placement of covered stents,13 as compared to the contralateral access, which is limited due to the rigidity of the introduction of some materials. Intravascular ultrasound examinations may also be performed through this access and all mechanical thrombectomy devices may be used, for example, Hydrolyser, AngioJet,14 Rotarex, etc. In situ fibrinolysis may be attempted for limb salvage.4–6 However, it should be performed carefully due to risks of compression hematomas at this level. Small-diameter introducers should be used with preference. 29
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Drugs (pharmacological milieu) The pharmacological environment for an angioplasty performed through the popliteal approach is the same as for any angioplasty performed from another approach. The day before the procedure, patients are given aspirin, ticlopidine, or clopidogrel if a stent is envisaged. During the procedure, a bolus injection of 5000 units of heparin is given intravenously after the introducer is placed. Following the procedure, they are given aspirin indefinitely and ticlopidine or clopidogrel if stents are implanted.
Indications to popliteal approach Retrograde femoral approach There are two major classes of indications. Popliteal approach as first choice There are three types of indications. 1. The femoral approach is contraindicated or may not be performed due to severe atheromatous lesions at the puncture site or due to heavy calcifications. An arterial echo-Doppler examination at the puncture site should be performed prior to the procedure to reveal lesions that were previously undetected, thus contraindicating the femoral approach. 2. The other contralateral or brachial approach may not be used or are contraindicated. The contralateral approach may be difficult due to tortuous, stenosed, very atheromatous arteries, or an aortobifemoral bypass at a very acute aortic angle. They may also prevent the introduction of some devices. Certain atherectomy devices may not be used or long covered stents may not be placed though contralateral access due to the rigidity of the materials that may not cross the bifurcation. In addition, risks through the brachial access are even higher (thrombosis at the puncture site, cerebral embolization risks, etc.).
(a)
(b)
3. The popliteal approach may be chosen as first choice due to the localization of the lesions: a. ostial lesions of the superficial femoral artery i. lesions in the proximal part of the artery ii. diffuse lesions (proximal and mid-third) b. lesions of the common femoral artery i. associated lesions (common femoral, proximal part of the superficial femoral artery) ii. stenosis of a superior anastomosis of a bypass graft c. total occlusion of the superficial femoral, which now often requires placement of long covered stents. Indeed, these lesions are often difficult to treat when the catheterization is done through puncture of the ipsilateral common femoral artery since the puncture site is not far enough away from the lesion. Popliteal approach as second choice After failure of the angioplasty procedure through an antegrade femoral access, particularly in the case of femoral desobstruction, it seemed logical to us that the popliteal approach should be proposed, thus increasing the chances of success of interventional techniques. The contralateral (or crossover) access did not seem to present more benefits in those cases. This approach may also be proposed after failure of the brachial or contralateral access chosen as first choice to treat proximal femoral lesions. Antegrade popliteal puncture In cases where femoral obstructions and leg lesions are combined, one may propose to treat the leg arteries using an antegrade popliteal puncture. We have used this limb salvage procedure but it requires skill and experience. The puncture site is localized through “road mapping.” It may therefore be the only therapeutic access if surgery more proximally (e.g. femoropopliteal bypass graft) may not be performed and if the patient suffers from critical ischemia.
(c)
Figure 6.1 (a) Partial thrombosis of the right SFA; (b) result of desobstruction with Kensey catheter; and (c) results of angioplasty using the popliteal approach.
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Arterial access for endovascular interventions: popliteal access to peripheral procedures Techniques used The techniques used are as follows:
Table 6.1 Location of lesions Location
Number
Superficial femoral Ostial lesions (2–4 cm) Diffuse lesions > 15 cm Thromboses < 4 cm 4–8 cm > 8 cm Aneurysm Post-surgery chronic dissection Common femoral Stenoses (2–4 cm) Thromboses (4–6 cm) Superior anastomosis stenosis of a bypass graft
133 7 27 97 5 12 80 1 1 17 10 7 3
Authors’ personal experience A total of 153 patients under this group’s care have benefited from transluminal angioplasty using the percutaneous retrograde popliteal approach. During the same period, 5230 peripheral angioplasties of the legs were performed by the group, so transluminal angioplasties represent 2.8% of our procedures. These patients comprised 124 males and 29 females, with a mean age of 63 years (range 39–86 years). Risk factors were: diabetes (n = 29), hypertension (n = 76), smoking (n = 120), dyslipidemia (n = 84). Of these patients, 117 were in stage II of Fontaine’s classification, 24 in stage III, and 12 in stage IV. Lesion locations were as given in Table 6.1. Sixty-seven percent of the lesions were heavily calcified. Distal arterial runoff Distal arterial runoff was as follows: Three patent vessels: Two patent vessels: One patent vessel:
70 46 13 16 8
patients patients patients patients patients
(stage (stage (stage (stage (stage
IIb) IIc) III) III) IV)
Seventy-five patients underwent angioplasty through the popliteal access as first choice and 78 as second choice after failure of recanalization, either antegrade through the ipsilateral femoral despite the use of hydrophilic guidewires, laser fibers or other recanalization devices, or through brachial or contralateral access sites. Technical success Success of the popliteal access was as follows: No puncture failure Immediate success: Success of first choice: Success of second choice:
31
138/153 (90%) 69/75 (92%) 69/78 (88%)
The ankle brachial index increased from 0.52 ± 0.15 before the procedure to 0.92 ± 0.13 after the procedure. Failures occurred in 15/153 (10%) of cases and were mostly observed in long calcified lesions.
Laser recanalization: Recanalization with Kensey catheter: Simpson atherectomy device: Rotablator: Stent placement:
24 4 1 16 87
patients patients patient patients patients
(Palmaz, n = 36; Strecker, n = 2; nitinol stents, n = 28; covered stents, n = 26.) Several stents were implanted in the same patient. Complications Two hematomas were reported at the puncture site; they did not lead to compression symptoms and did not require surgery. Nine acute thromboses in the superficial femoral artery appeared at the angioplasty site during the first day; five required a bypass, two were successfully treated with mechanical thrombectomy (Hydrolyser) and/or thromboaspiration, and two patients who refused surgery were treated with drugs. Six thromboses appeared during the first month following the procedure; three were treated successfully with fibrinolysis and a new angioplasty, and three required a bypass graft. Six arteriovenous fistulas without hemodynamic consequences were also reported.
Discussion The popliteal access is still not often used, although it is reliable thanks to a good localization technique (e.g. road mapping, echo-Doppler). Indeed, in a series of 50 angioplasties, Tonnesen et al.1 reported results equivalent to ours, with an immediate success rate of 100%. Some contraindications must be respected (e.g. respiratory insufficiency, obesity) which would prevent obtaining a satisfactory ventral decubitus position. Other cases were also encountered where this approach could not be used, such as an inability to hyperextend the knee. Anatomical characteristics may also prevent popliteal access such as a thin popliteal artery, or a femoral or femoropopliteal obstruction near the puncture site. However, even when these contraindications are taken into account, this still is very often a usable approach. As a first-choice treatment, this approach competes with the contralateral femoral and brachial accesses. However, those are not always usable for anatomic reasons and certain techniques may be difficult to use through these two access sites, whereas the popliteal access allows nearly all endovascular techniques. All endoprostheses currently available may be implanted through popliteal access, especially covered stents, which allow the creation of internal bypass through a percutaneous access. The stent may be implanted very precisely at the femoral ostium through the popliteal access, whereas this is not always easy through contralateral access. The popliteal approach may be used to treat aneurysms in the leg arteries2,3 or for in situ fibrinolysis for limb salvage.4–6 This approach has high technical success rates and 88% of the antegrade femoral access failures could be recovered. Complications of this access are rare as long as a preprocedure echo-Doppler is performed to check the patency of
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(a)
(b)
(c)
(d)
(e) Figure 6.2 (a) Tight stenosis at the origin of the right external iliac artery; (b) partial thrombosis of the origin of the right superficial femoral artery; (c) laser recanalization of the right superficial femoral artery; (d) result of angioplasty of the right superficial femoral artery; and (e) result of angioplasty and placement of a Palmaz stent at the level of the right external iliac artery stenosis.
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Arterial access for endovascular interventions: popliteal access to peripheral procedures the artery and that there is no aneurysm at this level. Risk of thrombosis at the puncture site is rare, never having been observed by this group. The hematomas observed were without any consequence and new arterial-puncture-site closure devices should decrease the risk. Tonnesen et al.1 reports two popliteal hematomas in 50 cases, neither of which required surgery. These hematomas caused edema and pain for 2–3 months. There remains an unsolved problem: the arteriovenous fistulas, which seem to be frequent. They are, however, without any obvious hemodynamic consequence. Long-term results of the procedure do not depend on the approach but on the technique itself and on the lesions treated. The place of the popliteal access as compared to the contralateral and brachial approach ways is still debatable. The other two access sites allow manual compression remote from the treatment site, which is not associated with a decrease in flow related to the compression, which can result in the complication of thrombosis. Since the contralateral approach permits the use of large introducers, it thus also allows for procedures such as the “kissing” technique in the femoral bifurcation, which is not usable through the popliteal access.
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The brachial access, although useful, is limited by the diameter of the introducers. With preference, this group uses the popliteal access to treat superficial femoral lesions, which may not be treated at first or second choice, by an upper access. The antegrade popliteal approach enables treatment of popliteal lesions or threatening leg lesions.
Conclusion The popliteal access seems reliable and efficient, enabling the operator to recover numerous failures of the antegrade femoral access. However, because of the lack of familiarity with this technique, it has not been widely used in the treatment of peripheral arterial diseases. Its complication rate is low, as long as one adheres to a strict technique and locates the artery precisely. Its indications should be compared with those of the other access sites (i.e. contralateral and brachial). The popliteal approach accommodates all of the endovascular techniques and, by broadening the indications for angioplasty, it improves the success rate of the procedures. This approach should be better known and more frequently used by interventionists.
REFERENCES 1.
2. 3. 4. 5.
6.
7.
Tonnesen KH, Sager P, Karle A et al. Percutaneous transluminal angioplasty of the superficial femoral artery by retrograde catheterization via the popliteal artery. Cardiovasc Intervent Radiol 1988; 11: 127–31 Edwards H, Martin E, Nowygrod R. Nonoperative management of a traumatic peroneal artery false aneurysm. J Trauma 1982; 22: 323–6 McIvor J, Treweeke PS. Case report: direct percutaneous embolization of a false aneurysm with steel coils. Clin Radiol 1988; 39: 205–7 Perler BA, Osterman FA. Immediate postoperative urokinase infusion: extending the limits of limb salvage surgery. J Cardiovasc Surg 1990; 31: 184–8 Schroeder J. Catheter lysis and percutaneous transluminal angioplasty below the knee via the popliteal artery in a patient with femoral artery obstruction: technical note. Cardiovasc Intervent Radiol 1989; 12: 344–5 Weisman ID, Standchfield WR, Herzog CA Jr et al. Left ventricular thromboembolic occlusion of the popliteal artery treated nonoperatively with local urokinase infusion. A case report. Angiology 1988; 39: 179–86 Zeitler E, Richter EJ, Roth FJ et al. Results of percutaneous angioplasty. Radiology 1983; 146: 57–60
8. 9.
10. 11. 12. 13. 14.
Henry M, Amicabile C, Amor M et al. Angioplastie artérielle périphérique. Intérêt de la voie poplitée. A propos de 30 cas. Arch Mal Cœur 1993; 88: 463–9 (abstract) Henry M, Amor M, Henry I et al. Percutaneous transluminal angioplasty of peripheral arteries with retrograde catheterization through the popliteal artery: series of 63 cases. Radiology 1994; 193: 192 (abstract) Henry M, Amor M, Allaoui M et al. A new access site management tool: the AngioSeal haemostatic puncture closure device. J Endovasc Surg 1995; 2: 289–96 Henry M, Amor M, Ethevenot G et al. Percutaneous peripheral atherectomy using the Rotablator. J Endovasc Surg 1995; 2: 51–66 Henry M, Amor M. Stenting of femoral and popliteal arteries. In: Sigwart U, ed. Endoluminal stenting. WB Saunders: London, 1996; 476–86 Henry M, Amor M, Cragg A et al. Clinical experience with a new stent-graft for treatment of occlusive and aneurysmal peripheral arterial disease. Radiology 1996; 201: 717–24 Henry M, Amor M, Porte JM et al. La thrombectomie par le catheter Hydrolyser. A propos de 50 cas. Arch Mal Cœur (in press)
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Introducer sheaths, catheters, guiding catheters, and guidewires K Dougherty and Z Krajcer
Introduction Increased experience with endovascular techniques has caused an explosion of new technology. The number of vascular pathologies where surgical repair is the only option is rapidly decreasing. The endovascular specialist has a considerable assortment of commercially available sheaths, guidewires, and catheters to choose from. Choosing the correct equipment, however, can only be learned through hands-on experience.
Introducer sheaths Hemostatic introducer sheaths are generally used for all endovascular procedures. They establish a secure path from the skin to the vascular lumen. In addition to providing a safe port of access to the vascular system, they allow catheter instrumentation without ongoing blood loss or damage to the vessel wall. Sheath size is dependent upon the type of procedure and the outer diameter of the catheters or equipment used during the intervention. Most of the diagnostic peripheral procedures can be performed with 4-French sheaths. Smaller sheaths are particularly useful when performing diagnostic or interventional procedures on an outpatient basis. Catheter-directed thrombolysis should be performed with 4-French or 5-French sheaths to avoid the risk of bleeding around the sheath. Sheaths are generally 10–11 cm in length. Longer (30–100 cm) sheaths are used for a variety of purposes. This includes straightening out the tortuous iliac vessels, improving torque control and facilitating guide catheter, stent, and stent graft advancement. The Super Arrow-Flex introducer sheath (Arrow International Inc., Reading, PA) is popular for peripheral intervention because of its flexibility, and the numerous sizes and lengths. It is available from 40-cm to 100-cm lengths and from 5-French to 10-French diameters. It can provide all of the features of a guide catheter, with the added advantages of a builtin hemostatic valve and side-port. It incorporates a highly radio-opaque coil-wire design that allows it to flex at any point, in any direction, without kinking. This is particularly important for treating contralateral iliac, femoropopliteal and tibioperoneal lesions. A hydrophilic coating added to the tip allows successful negotiation through the tortuous peripheral anatomy. Many introducer sheaths can be used in place of guiding catheters for selective catheterization and visceral/branch artery intervention. Cook Endovascular has a variety of 34
peripheral introducer sheath sizes, lengths, and configurations to accommodate radial, brachial, axillary, or femoral access. The Flexor Check-FloII (Cook Inc., Bloomington, IN) introducer systems are thin-walled, with large lumens (Figure 7.1). The Flexor is equipped with a Tuohy–Borst side-arm that allows contrast injections, prevents blood reflux, and permits unimpeded catheter and guidewire introduction. It is kinkresistant with a hydrophilic coating and easily accommodates contralateral access. The Flexor Balkin Up and Over Contralateral Sheath (Cook Inc., Bloomington, IN) is frequently used for contralateral iliofemoral approach. The Flexor Shuttle Select (Cook Inc., Bloomington, IN) has a stiff proximal shaft with an atraumatic tip (Figure 7.2a). The lubricious hydrophilic coating promotes easier introduction but maximum pushability and support during endoluminal maneuvers in the supra-aortic vessels. The selective feature allows the sheath to be paired with the compatible 6.5-French Slip-Cath for selective engagement of the carotid vessels and is available in a variety of shapes (Figure 7.2b). The Beacon radio-opaque tip offers optimal visualization of catheter tip manipulation. The Flexor Shuttle Select has a Tuohy–Borst hemostasis valve with manual adjusting seal to allow unimpeded catheter or device introduction. Cook Endovascular also makes the Extra Large (14– 24-French) introducers. The 22- and 24-French sheath with Flexor Keller–Timmerman valve has a hydrophilic coating and is used to introduce large devices like endovascular stent grafts for abdominal aortic aneurysm exclusion (Figure 7.3). These sheaths range from 25 to 50 cm in length are equipped with a special hemostasis valve or Check-Flo valve that prevents blood reflux and allows flushing around the larger devices while they are positioned inside the sheath (Figure 7.2). The Pinnacle Destination (Terumo Corp, Tokyo, Japan) was developed as a renal guide sheath. There are three tip shapes, two detachable valve types and two French sizes to allow for procedural specific requirements. Like the Flexor Shuttle Select, the Destination is coil-reinforced and kink-resistant.
Angiographic catheters Diagnostic angiography is always performed prior to the endovascular intervention since it determines the complexity of the procedure, the access site, and the equipment that may be needed to successfully complete the intervention.
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Figure 7.1 The Flexor Check-Flo II (Cook Inc., Bloomington, IN) introducer systems are thin walled with large lumens and are equipped with a side-arm and hemostasis valve that allows contrast injections.
Angiographic catheters are constructed of polyethylene, polyurethane, nylon, Teflon, or a combination of these materials. Catheters made of polyethylene have a low coefficient of friction, can be torqued and have a good preshaped memory. Polyurethane catheters are softer and pliable, but have a higher coefficient of friction. Nylon catheters are stiffer and tolerate high flow rates and are generally used for aortography. Teflon is the stiffest material and is mainly used for sheaths and dilators. Many catheters are wire braided for extra torqueability. Others are coated with a hydrophilic polymer to improve trackability. Catheters vary in length and diameter. Outer diameter is designated by French size (3 French = 1 mm). Angiographic catheters are available in multiple shapes and sizes and can be divided into two basic categories: selective and non-selective. Non-selective catheters are usually designed with multiple side-holes, like the “pigtail” or “Omniflush” (AngioDynamics Inc., Queensbury, NY) and are used for angiography of large vessels, such as the aorta or vena cava (Figure 7.4). These non-selective shapes provide high flow and dispersion of a contrast agent without injuring the vessel wall. Angiography of high-flow vessels requires contrast injection by a power injector to obtain adequate opacification. These catheters typically come in either 4- or 5-French sizes, but are available in a wider range of 3–8 French. The “pigtail” catheter is designed to protect the vessel walls from the whipping effect during power-injected boluses of contrast. Calibrated marker “pigtail” catheters are used to determine accurate sizing of vessel lumen prior to endoluminal abdominal aortic aneurysm repair. This is particularly important during endoluminal intervention. Radio-opaque marker bands delineate a 20 cm segment, at 1 cm intervals, for precise measuring accuracy. When injecting into the pulmonary artery, stiffer catheters and higher flow rates maybe necessary. In these instances a Grollman or Montefore catheter may be more effective and both can easily manipulate through the cardiac chambers and into the pulmonary artery. Selective angiography catheter types and shapes are infinitely variable and choice is based on type and location of the lesion being treated (Figure 7.5). The standard inner diameters of a selective or flush catheter are 0.035 inches and 0.038 inches. Standard guidewires can be used to advance the catheters through the vasculature. Selective catheters are
35
(a)
(b) Figure 7.2 (a) The Flexor Shuttle Select (Cook Inc., Bloomington IN) has a stiff proximal shaft with an atraumatic tip. The lubricious hydrophilic coating promotes easier introduction but maximum pushability and support during endoluminal maneuvers in the supra-aortic vessels; (b) 6.5-French Slip-Cath for selectively engagement of the carotid vessels and is available in a variety of shapes. The Beacon radio-opaque tip offers optimal visualization of catheter tip manipulation.
preshaped to allow direct branch vessel engagement, pressure measurements, and contrast angiography. Specific catheters are recommended for specific anatomical locations and are designed to facilitate selective manipulation into branch vessels. It is best to have a variety of catheter shapes available for challenging anatomical situations. Precise knowledge of the
Figure 7.3 The 22- and 24-French sheath with Flexor KellerTimmerman valve has a hydrophilic coating and is used to introduce large devices like endovascular stent grafts for abdominal aortic aneurysm exclusion.
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Figure 7.4 Angiographic catheters are available in multiple shapes and sizes and non-selective catheters generally come with multiple side-holes to accommodate injections of large amounts of contrast.
type of catheter is very important for angiography so that appropriate and accurate information can be obtained prior to the intervention. Each company provides detailed product information on the catheters and their use. Hydrophilic catheters are useful for a selective approach of the carotid arteries, and to study the intra-cranial branches. Shorter length catheters (50 cm) are used for visceral, renal, or contralateral iliac artery injections. Catheters with side-holes should be avoided. Selective catheters generally have a single hole, located at the tip, through which all injected contrast exits. Because of the single end-hole flow rates are much lower than non-selective catheters and therefore power injectors should not be used. Furthermore, high-flow power injection through an end-hole catheter carries a considerable risk of vessel injury due to the end-hole jet effect. While catheter size or outer diameter is measured in French, catheter inner lumen diameter is measured in inches. Common sizes range from 0.018 to 0.038 inches. This inner
diameter measurement denotes the acceptable guidewire size for the catheter. A mismatch in sizes can cause problems; such as either the guidewire not fitting inside the catheter or blood leakage around the guidewire. Diagnostic catheter size and length range from 4 to 6 French, and from 50 to 125 cm, respectively. Most of these catheters are braided, with a soft tip, without braiding. Different catheter materials have specific functional characteristics such as stiffness or rigidity and kink-free torque control. Some catheters have inner and outer hydrophilic coating to reduce friction for ease of passage and manipulation.
Guide catheters Like diagnostic catheters, guiding catheters come in a variety of lengths and shapes designed to facilitate their manipulation into branch vessels. However, they differ from diagnostic catheters by having a substantially larger luminal diameter (Figure 7.6). Guiding catheters are sized like diagnostic catheters with the outer diameter in French and the inner diameter in inches. But, to allow passage of the endovascular instruments, guide catheters must have a lumen diameter at least twice that of a typical diagnostic catheter. Guide catheters are similar to sheaths in that they provide protection to the vasculature when passing multiple devices into the same vessel. Important guiding catheter characteristics include the ability to provide stable coaxial alignment between the catheter tip and the ostium of the vessel and kink-free torque control.
C1
C2
C3
MIK
HK 1.0
CONTRA 2
SHK 0.8
SHK 1.0
RC1
RC2
RDC
DUCK
CHGB
CHGC
CHG2.5
TRAIN
VAN
WEIN
H1
H3
MANI
BARN
BERN
H1H
H3H
JB1
JB2
JB3
ST
CK
SIM1
SIM2
SIM3
SIM4
GEN
HN1
HN2
HN3
HN4
HN5
Figure 7.5 Selective angiography catheter types and shapes are infinitely variable and choice is based on type and location of the lesion being treated.
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ALI MP1 Burke H1 HY1
Figure 7.6 Guiding catheters come in a variety of lengths and shapes designed to facilitate their manipulation into branch vessels. However, they differ from diagnostic catheters by having a substantially larger luminal diameter.
A properly selected guide catheter should also provide back-up support for balloon catheter advancement and withdrawal, reliable pressure monitoring, and adequate contrast delivery during injections. In comparison to diagnostic catheters, guiding catheters have reinforced construction and a much stiffer shaft to provide back-up support for the advancement of guidewires, balloons, and stents. Peripheral guiding catheters are generally 6, 7, or 8 French and range from 65 to 100 cm in length with internal diameters ranging between 0.064 and 0.088 inches.
Guidewires Guidewires permit safe transluminal navigation of catheters and devices. Basic guidewire construction affects handling characteristics. Design variables include tip configuration, length, diameter, stiffness, antifriction coatings, and radioopaque markers. Mastering guidewires involves observation of guidewire behavior under fluoroscopy and understanding the interaction between the guidewire leading edge and the lesion. The fundamental attributes of a guidewire include the ability to transmit torque, minimize friction, tip flexibility, and steerability. Guidewires should only be advanced under fluoroscopic guidance and never advanced when resistance is met. This will eliminate the risk of subintimal wire passage, vessel dissection, and perforation. Guidewire diameters are measured in inches. The standard range is 0.014–0.038 inches. The diameter of the guidewire should match the required diameter of the catheter. This provides better support of the catheter during manipulation and decreases the amount of leakage around the wire. Guidewires are either straight, angled, or have a J-shaped tip and have varying lengths of flexibility at the tip ranging from 3 to 20 cm. The J-tipped wire is the most commonly used guidewire for initial passage into the vessel because of its lowrisk of subintimal dissection. The main components of the traditional guidewire are the central core, which provides body, steerability, and torque control, and a tightly wound outer spring coil (Figure 7.7) and contains a forming ribbon for tip shaping and a Teflon outer coating to decrease friction.
Figure 7.7 The main components of the traditional guidewire are the central core, which provides body, steerability, and torque control, and a tightly wound outer spring coil.
Hydrophilic guidewires were developed to satisfy a wide variety of procedural requirements. The Glidewire guidewires, (Terumo, Somerset, NJ) use a unique design of a nitinol inner core, which is only minimally elastic, a markedly tapered distal tip that has a polyurethane outer surface instead of a spring coil, and a hydrophilic polymer coating. The hydrophilic coating is chemically bonded to the polyurethane jacket to reduce friction and thrombogenicity. They range in size from 0.018 to 0.038 inches in diameter and come in regular (180 cm) and exchange lengths (260 cm). The Magic Torque guidewire (Boston Scientific Corp, Natick, MA) has enhanced radio-opacity with distal platinum markers to facilitate accurate vessel measuring and device placement. It also has a hydrophilic coating on the distal 10 cm and PTFE on the distal 11–50 cm to help reduce access friction. Magic Torque is available in 0.035-inch diameter and is either 150 cm or 260 cm in length. The length of the wire is determined by its intended use. Most regular length guidewires are 145–175 cm long. Exchange length guidewires are 260–450 cm long and allow catheters, balloons, and other device exchanges while the guidewire is maintained in the distal position. The length of the guidewire will generally depend on the distance of the lesion from the access site and on the length of the catheter or the device that is being used. For diagnostic angiography procedures it is usually not necessary to use guidewires that are longer than 180 cm. However, during the interventional procedure it is generally recommended to use exchange length (260 cm) guidewires. This length is necessary to have adequate length of the guidewire to be able to remove the device without losing the wire position across the lesion. It is occasionally necessary to use longer wires when brachial access is used for an intervention of femoral, popliteal, and tibioperoneal arteries. In this circumstance a 400 cm Nitrex (ev3, Plymouth, MN) or a 450-cm-long Geenan and Zebra (Boston Scientific, Natick, MA) guidewire is very useful. When attempting to traverse severely stenotic lesions or occlusions of vessels it is essential to select a guidewire that is flexible and can be easily steered, yet has sufficient body stiffness. There are several products that are commonly used for this purpose. A 0.035-inch Super Stiff angled Glidewire (Terumo, Somerset, NJ), because of good steerability and sufficient support is the wire of choice when crossing occluded vessels. The 0.018-inch angled Glidewire Goldtip wire (Terumo, Somerset, NJ) is another guidewire that has a hydrophilic coating and can be of a great advantage for crossing severely stenotic or occluded tibioperoneal arteries. For neuro applications, the Glidewire Goldtip wire is available with an 8-cm floppy tip in sizes that range from 0.011 to 0.018 inches. One of the disadvantages of wires with a hydrophilic coating is their propensity to cause perforations of the vessels when not used with caution. For this particular reason it is not advisable to use these wires for renal or visceral interventions.
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Shorter guidewires are suitable for the renal and visceral interventions like the 0.014-inch Hi-Torque Spartacore 14 (Guidant Corp., Santa Clara, CA) with a 3- and 5-cm floppy tip for support. Several guidewires offer even more support and stiffness of the body than the Super Stiff Glidewire. For endoluminal repair of an abdominal aortic aneurysm (AAA) it is essential to have a sufficient support to advance a large-profile stent graft device across the iliac arteries. In this type of procedure a 0.035-inch Super Stiff Amplatz (Boston Scientific, Natick, MA) guidewire, a Nitrex (ev3, Plymouth, MN) or an even stiffer 0.035-inch Lunderquist (Cook Inc., Bloomington, IN) guidewire should be used. The 0.035-inch Super Stiff Amplatz guidewires are available with different lengths of the flexible segments at their distal ends. Some of the products are available with 3-mm J, 1-cm, 6-cm and 10-cm flexible-tip segments. The purpose of the flexible segment of the wire is to conform itself to the vessel anatomy, and avoid vessel trauma and spasm. The choice of length of the flexible segment will depend on the location of the vessel and the amount of support that will be needed to advancement the device. For endovascular abdominal aortic aneurysm repair, the 6-cm or 10-cm flexible-tip length should be used to advance the large-bore stent graft into the aorta. The Bentsen (Cook Inc., Bloomington, IN) wire is a 0.035-inch guidewire with a very soft body that allows easy tracking in a tortuous vessel. This wire is frequently used for advancing the catheter in the renal and other visceral vessels when other wires are not able to achieve this goal. It is also routinely used for advancing the vascular coils through the catheter for coil embolization. Deflectable tip wires are also available such as the Reuter Tip Deflecting Wire (Cook Inc., Bloomington, IN), which is used to deflect catheter tips. The Reuter wire is available in either 0.025-, 0.035-, or 0.038-inch diameters and are 110 cm or 145 cm in length and is not intended to exit the tip of the catheter it is deflecting. The Venture (St. Jude Medical, Minnetonka, MN) is a wirecontrol catheter which deflects at the tip up to 90∞. The wire control catheter is compatible with all 0.014-inch wires and is
an over-the-wire design to enable wire exchanges. The outside diameter is 0.022 inches and has an inside diameter of 0.017 inches. The Venture provides backup support for crossing total occlusions and a deflectable tip more precise steering capabilities.
Infusion wires and catheters Other specialty guidewires include infusion wires like the ProStream (Micro Therapeutics Inc., San Clemente, CA), the Katzen and the Cragg (Meditech, Boston Scientific Corp., Natick, MA) (Figure 7.2) which have an outside diameter of either 0.035 or 0.038 inches and range from 145 to 180 cm in length. Multiple side-holes with various infusion port lengths from 3 to 15 cm and/or an open end-hole allow pharmacological agents to be delivered over a predetermined distance or to distal vessels. This configuration also permits coaxial use through 5-French infusion catheters (Meiwissen, Boston Scientific Corp, Natick, MA). A smaller 2.9-French MicroMewi (Micro Therapeutics Inc., San Clemente, CA) infusion catheter is inserted over a 0.018-inch guidewire and permits coaxial infusion. The Meiwissen catheter is a 5-French infusion catheter, 150 cm long, that has an infusion length of either 5 or 30 cm.
Microcatheters Microcatheters are used when the target vessel is smaller than the conventional catheter and can be placed through the standard angiographic catheter. These catheters are generally used for therapeutic purposes, such as embolizing bleeding vessels, vascular malformations, and small aneurysms. The Echelon (ev3, Plymouth, MN) is a 2.1-French, 150-cm, braided nitinol and PTFE guidewire-supported microcatheter that tapers to 1.7-French. Microcatheters have allowed treatment of a number of vascular pathologies that were previously untreatable or could only be treated with microsurgery.
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Percutaneous transluminal angioplasty T Collins and PW McMullan Jr
Introduction Angioplasty is the mechanical alteration of a narrowed or occluded vessel lumen. The word derives from the roots “angio” or vessel and “plasticos” or fit for molding. Nowadays it is used to describe a variety of percutaneous vascular interventions. Percutaneous transluminal angioplasty (PTA) is used to describe angioplasty of vessels other than the coronary arteries. Charles Dotter, a vascular radiologist, introduced transluminal angioplasty in 1964. By using progressively increasing sizes of catheter he was able to dilate stenosed leg arteries. Andreas Gruentzig performed the first balloon angioplasty of a human peripheral artery in 1974. PTA has been most commonly used to treat iliac and leg arteries with atherosclerotic disease. The progression of expertise and equipment has expanded the use of PTA to all vascular beds, both venous and arterial. In many situations stenting has become the treatment of choice for completing percutaneous procedures; however, there remain clinical situations where PTA alone is acceptable if not preferred. Mechanism of PTA The application of peripheral balloon angioplasty exerts a centrifugal force from within the vessel lumen. This force is delivered via a balloon that is inserted percutaneously and inflated adjacent to the treatment area. The outward radial force, called hoop stress, stretches or separates the components of the vessel wall. This radial force is a product of the pressure applied and the area against which it is applied. The Laplace law describes this force as: Hoop stress = pressure × diameter Indications In general, the indications for percutaneous transluminal angioplasty in non-coronary arteries are prevention and/or reversal of ischemia. This broad classification includes preservation of function, restoration of function, improvement of quality of life, and end-organ salvage. Technique PTA is performed in an angiographic laboratory under fluoroscopic and cine-angiographic visualization. Arterial or venous access is gained most commonly by the modified Seldinger approach followed by insertion of a valved sheath which
prevents back-bleeding and allows repeated atraumatic entry into the vessel lumen. Through the sheath, an appropriately sized and shaped catheter is introduced over a leading wire. Once the vessel of interest is cannulated, angiography is performed in multiple orthogonal projections to delineate the diseased or abnormal portion and determine the severity of stenosis. Views should include the entire vascular bed to identify collateral arteries and the run-off vessels. Angiography of peripheral arteries is done optimally by digital subtraction angiography, which allows masking of bony structures, and this technique may be performed in an automated, stepwise fashion to capture the entirety of the distal aorta and lower extremities with a single injection of contrast from a power injector. Iso-osmolar contrast is used in order to maximize patient comfort. When the stenosis in question is of dubious severity or particularly difficult to image, catheter “pullback” to determine the pressure gradient across the lesion, intravascular ultrasound, or the use of a flow wire may assist in assessment. Numerous wires may be used to cross the diseased arterial segment. In general, wires range from 0.014 to 0.035 inches in diameter. The choice of wires is dependant upon the anatomy, stenosis versus occlusion, and balloon catheter to be utilized. The operator should be familiar with the available inventory prior to the procedure and plan appropriately.
Vascular territories Iliac vessels Roughly one-third of obstructive atherosclerotic disease affecting the patient with claudication is aortoiliac disease.1 In patients under the age of 40 with PAD, disease in the aortoiliac segment is the most common site of atherosclerosis.2 Reasons for intervention in the iliac vessels include lifestyle-limiting claudication, limb-threatening ischemia, and maintaining vascular access for procedures such as intraaortic balloon pump placement or coronary angiography.3 The TransAtlantic Inter-Society Consensus on Management of Peripheral Arterial Disease working group published an initial series of guidelines in 20004 for the direct management of PAD which were updated in January 2007 based on more current data.5 These guidelines recommend treatment with surgical versus percutaneous means based on lesion extent and morphology. Focal lesions (types A and B) are classified as likely responsive to PTA, whereas more complex or completely 39
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Textbook of peripheral vascular interventions Recommendation 36 Treatment of aortoiliac lesions TASC A and D lesions: Endovascular therapy is the treatment of choice for type A lesions and surgery is the treatment of choice for type D lesions [C]. TASC B and C lesions: Endovascular treatment is the preferred treatment for type B lesions and surgery is the preferred treatment for good-risk patients with type C lesions. The patient's co-morbidities, fully informed patient preference and the local operator's long-term success rates must be considered when making treatment recommendations for type B and type C lesions [C].
Figure 8.1 Lesions.5
TASC Recommendations for Treatment of Aortoiliac
occlusive lesions (types C and D) are considered surgical (Figures 8.1 and 8.2) Access for work in the iliac vessels is most commonly gained in the ipsilateral common femoral artery with a retrograde approach. Occasionally anatomy will require a crossover approach from the contralateral common femoral artery, in which case a braided, non-kinking 55-cm sheath with an inner
Type A lesions • Unilateral or bilateral stenoses of CIA • Unilateral or bilateral single short (≤3 cm) stenosis of EIA
Type B lesions: • Short (≤3cm) stenosis of infrarenal aorta • Unilateral CIA occlusion • Single or multiple stenosis totaling 3–10 cm involving the EIA not extending into the CFA • Unilateral EIA occlusion not involving the origins of internal iliac or CFA
Type C lesions: • Bilateral CIA occlusions • Bilateral EIA stenoses 3–10 cm long not extending into the CFA • Unilateral EIA stenosis extending into the CFA • Unilateral EIA occlusion that involves the origins of internal iliac and/or CFA • Heavily calcified unilateral EIA occlusion with or without involvement of origins of internal iliac and/or CFA
Type D lesions • Infra-renal aortoiliac occlusion • Diffuse disease involving the aorta and both iliac arteries requiring treatment • Diffuse multiple stenoses involving the unilateral CIA, EIA, and CFA • Unilateral occlusions of both CIA and EIA • Bilateral occlusions of EIA IIiac stenoses in patients with AAA requiring treatment and not amenable to endograft placement or other lesions requiring open aortic or iliac surgery
Figure 8.2
TASC Classification of Aortoiliac Lesions.5
diameter of 6 French or greater is used. Standard 0.035-inch Jwires or 0.035-inch hydrophilic wires are used to cross lesions after which it is common to change wires via a diagnostic catheter for a stiffer support wire. Over this wire, monorail, or over-the-wire peripheral balloons can then be inserted. Lesion dilation in the iliac vessels is performed very cautiously due to the risk of rupture, which causes lifethreatening retroperitoneal bleeding. A common method for balloon sizing is to perform angiography with a reference object in the field, measure the adjacent normal vessel with reference to the object, and choose a balloon size slightly smaller than the reference vessel. Common sizes are 6–8 mm. Upon inflation, the operator must be alert to any back or flank pain the patient experiences, which is a sign of vessel stretch. Dilatations beyond this point risk vessel dissection or rupture. Indications that balloon angioplasty has failed and stenting is required include a resultant dissection or a residual hemodynamic gradient of greater than 10 mmHg. Primary stenting is usually performed for treatment of a total occlusion.6 Compiled results of balloon angioplasty analyzed in 1989 reported the following: in 2697 iliac PTA procedures, the technical success rate was 92% with 2- and 5-year primary patency rates of 81 and 75%.7 Another meta-analysis performed in
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Percutaneous transluminal angioplasty 1997 based on 1473 procedures including 80% stenoses and 20% occlusions yielded a 91% technical success rated with primary patency rates of 74, 66, 61, and 58% at 1, 2, 3, and 4 years, respectively.8 Due to stent results which are generally superior (10–15% higher at each interval), the recently published ACC/AHA Guidelines for the Management of PAD9 list provisional iliac stent placement as a class I recommendation (level of evidence: B) for a suboptimal or failed result from balloon dilatation (persistent translesional gradient, residual diameter stenosis greater than 50%, or flow-limiting dissection). Primary stent placement is also listed as a class-I recommendation for the common iliac artery (level of evidence: B) and the external iliac artery (level of evidence: C).
Type A lesions Type B lesions
Type C lesions
Type D lesions
Superficial femoral and popliteal arteries In patients with PAD and claudication, superficial femoral artery (SFA) and popliteal disease is present in over 50% of cases.1 These vessels are characterized by a long course and often have diffuse segments of disease. When the muscles and joints of the lower extremity move, external forces of compression, torsion, shortening, and elongation act on the arterial wall. These arteries consequentially have very high rates of restenosis and remain a challenging area of treatment for the endovascular specialist. TASC guidelines divide SFA and popliteal disease into four categories, A–D.5 TASC A lesions are considered amenable to percutaneous intervention, whereas surgery is recommended for TASC D lesions. Lesions in the intermediate realm are categorized as TASC B and C (Figures 8.3–8.5). The ideal treatment for these lesions remains a topic of ongoing debate, and therapy favoring PTA versus surgery varies widely based on local practice. As in most areas of endovascular therapy, improvement in technology is allowing for more aggressive percutaneous approaches to femoropopliteal disease, and indications will evolve as data builds to support PTA. Factors that predict a favorable outcome in percutaneous treatment of SFA lesions include the presence of intermittent claudication, location in the proximal portion of the vessel, shorter stenosis length, lack of complete occlusion, adequate distal runoff, large diameter of treated artery, and a balloon result without significant residual stenosis.10,11 Access to the SFA and popliteal territories is most often gained in the contralateral common femoral artery in retrograde fashion. Crossover to the target limb is accomplished with an IMA or similarly curved catheter which directs passage Recommendation 37 Treatment of femoral popliteal lesions TASC A and D lesions: Endovascular therapy is the treatment of choice for type A lesions and surgery is the treatment of choice for type D lesions [C]. TASC B and C lesions: Endovascular treatment is the preferred treatment for type B lesions and surgery is the preferred treatment for good-risk patients with type C lesions. The patient's co-morbidities, fully informed patient preference and the local operator's long-term success rates must be considered when making treatment recommendations for type B and type C lesions [C].
Figure 8.3 TASC Recommendations for Treatment of Femoral Popliteal Lesions.5
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Single stenosis ≤10 cm in length Single occlusion ≤5 cm in length Multiple lesions (stenoses or occlusions), each ≤5 cm Single stenosis or occlusion ≤15 cm not involving the infra geniculate popliteal artery Single or multiple lesions in the absence of continuous tibial vessels to improve inflow for a distal bypass Heavily calcified occlusion ≤5 cm in length Single popliteal stenosis Multiple stenoses or oclusions totalling >15 cm with or without heavy calcification Recurrent stenoses or occlusions that need treatment after two endovascular interventions Chronic total occlusions of CFA or SFA (>20 cm, involving the popliteal artery) Chronic total occlusion of popliteal artery and proximal trifurcation vessels
CFA – common femoral artery; SFA – superficial femoral artery.
Figure 8.4 TASC classification of femoral popliteal lesions.5 Used with permission.
of a wire over the aortic bifurcation and down the common iliac. Following necessary focal angiography with this catheter, a stiff exchange-length wire is then employed for removal of the catheter and sheath and placement of a braided, nonkinking crossover sheath down to the level of the common femoral artery. Contralateral access may be impossible in certain cases due to the presence of an aortobifemoral graft or iliac occlusion. When necessary, ipsilateral antegrade common femoral or retrograde ipsilateral popliteal access is considered. Following insertion of the crossover sheath, uncomplicated lesions may frequently be crossed with the same straight, floppy-tipped stiff wire which then serves as a platform for balloon insertion. More complex lesions or total occlusions often require a more methodical technique with an angled 0.035-inch hydrophilic wire for initial approach delivered with the support of a 4-French catheter which can be angulated (IMA, JR4, MP) or hydrophilic for difficult-to-cross lesions. On occasion, a straight hydrophilic wire or a smaller 0.014–0.018-inch wire may facilitate lesion crossing. There are also newer devices designed for total occlusions which allow re-entry into the distal true lumen after initial wire passage creates a parallel dissection plane. Once the lesion is crossed, the stiff support wire is advanced, the catheter removed, and the balloon catheter inserted. Since injection through the sheath becomes difficult or impossible with the indwelling balloon catheter, it is important to establish bony landmarks on cine-angiography which correlate with the level of the lesion. Balloons of 4–6 mm in diameter are most often used in the SFA and popliteal arteries, and inflation is performed until the stenosis “waist” yields to the balloon (Figure 8.6). Following PTA, significant residual stenosis at the lesion site and flow-limiting dissection are indications for stent placement. Results of balloon angioplasty in the femoropopliteal arteries including initial technical success and durability are largely determined by lesion morphology. Early PTA data from the mid-1980s demonstrated that short, easily dilatable lesions had a 5-year patency of 75%, but lesions greater than 3 cm in
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Type B lesions: • Multiple lesions (stenoses or occlusions), each ≤5cm • Single stenosis or occlusion ≤15cm not involving the infrageniculate popliteal artery • Single or multiple lesions in the absence of continuous tibial vessels to improve inflow for a distal bypass • Heavily calcified occlusion ≤5cm in length • Single popliteal stenosis
Type C lesions • Multiple stenoses or occlusions totaling > 15cm with or without heavy calcification • Recurrent stenoses or occlusions that need treatment after two endovascular interventions
Type D lesions • Chronic total occlusions of CFA or SFA (>20 cm, involving the popliteal artery) • Chronic total occlusion of popliteal artery and proximal trifurcation vessels
Figure 8.5
TASC Classification of Femoral Popliteal Lesions.
length had markedly lower 1-year patency rates.12 Other series showed that PTA without stenting in lesions greater than 10 cm has a high initial technical success rate of over 90%, and cumulative patency rates at 18 months have been reported as high as 69%.13 The STAR registry, which was published in 2001 reported 5-year follow-up on 219 limbs in 205 patients. Primary patency for femoropopliteal PTA was 87% at 1 year, 80% at 2 years, and 55% at 4–5 years. The condition which was most predictive of occlusion was poor infrapopliteal runoff, defined as a single vessel with 50–99% stenosis or occlusion.14 In the modern era, devices which allow the operator to cross back into the distal true lumen following guidewire dissection are increasing operator aggressiveness in long segments of total occlusion. This yields higher initial technical success rates, but such results are often suboptimal with balloon therapy alone. Primary stenting in the femoropopliteal territory remains an ACC/AHA class III recommendation, but
stent placement is required in conditions of a suboptimal or failed balloon result.9 Improving stent technology is allowing for lower profile delivery systems, self-expanding nitinol designs, and exceptional fracture-resistant recoil properties. These advancements promise to make percutaneous therapy applicable to a broader variety of lesion subsets which have traditionally required surgery.
Tibioperoneal arteries In contrast to femoropopliteal lesions, the indication for angioplasty in the tibioperoneal vascular bed is generally not symptom-limiting claudication but rather chronic critical limb ischemia or limb salvage.5 Only 1.4% per year of patients with intermittent claudication progress to the degree of severity that ischemia at rest is a problem. Those who do are more prone to be diabetics and smokers.2 The goal of angioplasty in these patients is the establishment of inline flow to the level
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Figure 8.7 Left peroneal artery (a) before and (b) after balloon angioplasty. Figure 8.6 Left superficial femoral artery (a) before and (b) after balloon angioplasty.
of the foot in order to alleviate rest pain or promote healing of ulcers. Even though this initial patency may not be long lasting, the window of improved flow frequently allows wound healing prior to restenosis or reocclusion. Many of the technical methods employed in below-theknee angioplasty have been adopted from work in the coronary vasculature, a field which has rapidly evolved to deal with atherosclerosis in similarly sized vessels. Operators frequently use coronary equipment including guiding catheters, 0.014 specialty coronary guidewires, and small-diameter monorail coronary balloons. Retrograde access from the contralateral common femoral artery is possible with utilization of a crossover sheath followed by a guiding catheter. At times, antegrade access is necessary in order to deliver equipment to the distal vasculature due to equipment length constraints. Recently, balloons 1.5–4.0 mm in diameter have been developed with lengths as great as 120 mm specifically for use in the tibial vessels. These allow operators to treat the long diffuse
Figure 8.8
lesions that are typical in the tibial territory with a minimal number of balloon inflations (Figure 8.7). Results of tibioperoneal PTA are encouraging. In a large series of 235 patients, technical success of PTA in the tibioperoneal arteries was reported as 95%. A series of 284 critically ischemic limbs were treated with a success rate of 92% in a total of 529 lesions. Clinical success defined as the relief of rest pain or improvement of flow to the lower extremity was documented in 95%. A 5-year follow-up revealed a need for bypass surgery in 8% and significant amputations in 9%, yielding a 91% salvage rate.15 Renal arteries Etiologies for renal artery stenosis include atherosclerosis, fibromuscular dysplasia, arteritis, and radiation-induced injury, all of which cause renal hypo-perfusion and can induce elevated renin levels with resultant hypertension. Atherosclerosis is the most prevalent of these causes and most commonly affects the ostium of the renal artery so that bulky aortic plaque, which is
Right renal artery with fibromuscular dysplasia (a) before and (b) after balloon angioplasty.
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frequently calcified, extends into renal artery plaque. This phenomenon, coupled with the dilation-resistant nature of these lesions, produce a restenosis rate for balloon angioplasty approaching 50% due to recoil.16,17 Randomized trial data support routine stent placement for ostial atherosclerotic stenoses and produce a 6-month angiographic restenosis rate for stents of only 14%.18 Balloon angioplasty alone may be utilized for the other aforementioned types of lesions and has been studied extensively in fibromuscular dysplasia.19 Access for renal artery intervention is most often gained through the femoral artery, although brachial and radial access is sometimes the approach of choice. From the femoral approach, a 50-cm 6-French guiding catheter (hockeystick, renal double curve, or IMA) can be safely advanced over a 4-French diagnostic catheter (IMA or JR4) in telescopic fashion once a supporting 0.014-inch angioplasty wire has been advanced through the 4-French catheter for support. The 4-French catheter is then removed while leaving the guiding catheter and wire in place over which a monorail balloon (sizes range from 3 to 7 mm) is then advanced. Alternatively, a “no touch” technique may be used to position the angioplasty wire and guide catheter. In this technique a J-tipped wire is inserted into a guide catheter which is then positioned adjacent to the renal ostium with the J-wire extending out of the end of the catheter. An angioplasty wire is then manipulated into the renal artery and the J-wire is removed while advancing
the guide to the ostial position. Angiography should allow visualization of the entire renal cortex to avoid missing an accessory renal artery prior to angioplasty and to ensure visualization of wire perforation or poor reflow following angioplasty. Fibromuscular dysplasia is typically responsive to balloon therapy since it produces a tearing of the fibrous band or curtain which impedes flow (Figure 8.8).19 Rates of restenosis following PTA have been reported as 7–27% over follow-up periods ranging from 6 months to 2 years.17,20–22 Likelihood of a favorable clinical response to PTA correlates with an age of less than 57, lack of concomitant disease in the carotid and coronary vessels, and presence of hypertension for less than 9 years.23
Conclusion PTA in peripheral vessels has evolved dramatically in the four decades since its inception and now offers thousands of patients annually relief from ischemia without the necessity of surgical intervention. While many procedures in the periphery now include the use of stents, there remains a significant role for balloon angioplasty alone. As advancing technology puts new tools in the hands of increasing numbers of well-trained operators, the future of the endovascular field holds great promise.
REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9.
10. 11.
Henry M, Rath PC, Klonaris C et al. Peripheral vascular diseases: an update on endovascular therapy. Indian Heart J. Nov-Dec 2005; 57(6): 747–66 Bittl JA, Hirsch AT. Concomitant peripheral arterial disease and coronary artery disease: therapeutic opportunities. Circulation. Jun 29 2004; 109(25): 3136–44 Ansel G. Primary stenting of the iliac artery. Endovascular Today. 2005; 5: 39–42 TransAtlantic Inter-Society Consensus (TASC) on Management of Peripheral Arterial Disease (PAD). Journal of Vascular Surgery. 2000; 31S: 1–296 Norgren L, Hiatt WR, Dormandy JA et al. Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC II). J Vasc Surg. Jan 2007; 45(1 Suppl): S5–S67 Bates MC, Aburahma AF. An update on endovascular therapy of the lower extremities. J Endovasc Ther. Dec 2004; 11 Suppl 2: II107–127. Becker GJ, Katzen BT, Dake MD. Noncoronary angioplasty. Radiology. Mar 1989; 170(3 Pt 2): 921–40 Bosch JL, Hunink MG. Meta-analysis of the results of percutaneous transluminal angioplasty and stent placement for aortoiliac occlusive disease. Radiology. Jul 1997; 204(1): 87–96 Hirsch AT, Haskal ZJ, Hertzer NR et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease) endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. J Am Coll Cardiol. Mar 21 2006; 47(6): 1239–1312 Johnston KW. Femoral and popliteal arteries: reanalysis of results of balloon angioplasty. Radiology. Jun 1992; 183(3): 767–71 Capek P, McLean GK, Berkowitz HD. Femoropopliteal angioplasty. Factors influencing long-term success. Circulation. Feb 1991; 83(2 Suppl): I70–80
12. 13.
14. 15.
16.
17. 18. 19. 20. 21.
22. 23.
Krepel VM, van Andel GJ, van Erp WF et al. Percutaneous transluminal angioplasty of the femoropopliteal artery: initial and longterm results. Radiology. Aug 1985; 156(2): 325–28 Murray JG, Apthorp LA, Wilkins RA. Long-segment (> or = 10 cm) femoropopliteal angioplasty: improved technical success and long-term patency. Radiology. Apr 1995; 195(1): 158–62 Clark TW, Groffsky JL, Soulen MC. Predictors of long-term patency after femoropopliteal angioplasty: results from the STAR registry. J Vasc Interv Radiol. Aug 2001; 12(8): 923–33 Dorros G, Jaff MR, Dorros AM et al. Tibioperoneal (outflow lesion) angioplasty can be used as primary treatment in 235 patients with critical limb ischemia: five-year follow-up. Circulation. Oct 23 2001; 104(17): 2057–62 Sos TA, Pickering TG, Sniderman K et al. Percutaneous transluminal renal angioplasty in renovascular hypertension due to atheroma or fibromuscular dysplasia. N Engl J Med. Aug 4 1983; 309(5): 274–79 Plouin PF, Darne B, Chatellier G et al. Restenosis after a first percutaneous transluminal renal angioplasty. Hypertension. Jan 1993; 21(1): 89–96 van de Ven PJ, Kaatee R, Beutler JJ et al. Arterial stenting and balloon angioplasty in ostial atherosclerotic renovascular disease: a randomised trial. Lancet. Jan 23 1999; 353(9149): 282– 86 Slovut DP, Olin JW. Fibromuscular dysplasia. N Engl J Med. Apr 29 2004; 350(18): 1862–71 Jensen G, Zachrisson BF, Delin K et al. Treatment of renovascular hypertension: one year results of renal angioplasty. Kidney Int. Dec 1995; 48(6): 1936–45 Klow NE, Paulsen D, Vatne K et al. Percutaneous transluminal renal artery angioplasty using the coaxial technique. Ten years of experience from 591 procedures in 419 patients. Acta Radiol. Nov 1998; 39(6): 594–603 Baumgartner I, Triller J, Mahler F. Patency of percutaneous transluminal renal angioplasty: a prospective sonographic study. Kidney Int. Mar 1997; 51(3): 798–803 de Fraissinette B, Garcier JM, Dieu V et al. Percutaneous transluminal angioplasty of dysplastic stenoses of the renal artery: results on 70 adults. Cardiovasc Intervent Radiol. Jan-Feb 2003; 26(1): 46–51
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Cutting balloon angioplasty S Tyagi
Introduction Balloon angioplasty is an established revacularization procedure for coronary and non-coronary vascular stenosis. However, conventional balloon dilatation results in application of force in a random manner to the components of the stenosis. This circumferential shear stress often causes irregular intimal tear, splits, and stretches. Vessel wall trauma can cause dissection, intimal proliferative response, and restenosis.1 Elastic recoil also limits response to balloon angioplasty. Some lesions either in native vessels or grafts may be difficult to dilate with conventional balloon angioplasty. This may be as a result of the simultaneous presence of atherosclerosis, fibrosis, and calcification. To overcome these limitations, Barath et al.2 designed a hybrid device, a cutting balloon (CB), that has tiny razor-sharp blades mounted on its surface. It is designed to minimize the vessel wall trauma that is traditionally associated with conventional balloon angioplasty. The concept of the CB is to cut first and dilate next, and the balloon pressure serves primarily to propagate the incisions.3 Use of the CB has been explored mainly in coronary arteries. Initial studies suggests its usefulness in treatment of concentric lesions, ostial lesions, small vessels, and long diffuse lesions.1,3,4 Long-term effectiveness of balloon angioplasty is limited by restenosis. Pathogenesis of restenosis is mainly intimal hyperplastic reaction in response to vessel injury. CB angioplasty reduces the force needed to dilate an obstructive lesion thereby minimizing barotrauma to the vessel.4 This was supposed to reduce restenosis. However, the proposed mechanism has not been found to be effective for prevention of restenosis in coronary arteries.5,6 Pathology of in-stent restenosis is different: it results from smooth muscle cell proliferation. CB offers a simple, safe, and effective option for treatment of in-stent restenosis in coronary arteries. Initial reports suggest that it may achieve a better result than conventional percutaneous transluminal coronary angioplasty (PTCA), by making the tissue more amenable to being pushed outward through the stent struts.1,7–10 Experience with CB angioplasty in peripheral arteries is presently limited. However its use is being explored in number of situations.
Device description and mechanism of cutting balloon angioplasty The CB (Boston Scientific, Natick, MA) features a noncompliant balloon with three or four Atherotomes (microsurgical blades) depending on balloon diameter, mounted
longitudinally on the outer surface. The Atherotomes are microtome-grade blades, approximately three to five times sharper than surgical scalpel blades. When the CB is inflated the Atherotomes are exposed (Figure 9.1). As inflation continues and the balloon expands, the blades concentrate the dilation force upon an extremely small area along the entire length of the Atherotome. The hoop strength of the vessel is overcome and a cut occurs along the line of the Atherotome. These incisions facilitate dilatation of the target lesion with less dilating force, thus minimizing trauma to the vessel. This should decrease the inflammatory response and in turn restenosis.11 Concentration of dilating force enables more resistant stenosis to be overcome. The device available for small vessels has a 2–4-mm-diameter balloon on a monorail or over-the-wire 139-cm shaft, for use on 0.014-inch guidewire through a 5- to 6-French sheath. Coronary CBs have a 6-, 10-, or 15-mm-long Atherotome while the peripheral CB has a 15-mm-long Atherotome and a 0.127-mm working height. The larger peripheral CB is available in 5–8-mm diameter for use on 0.018-inch guidewire as an over-the-wire system through a 7-French sheath. Each of these balloons has four Atherotomes of 1-cm length and 50-, 90-, or 135-cm working catheter length.
Technical aspects of cutting balloon angioplasty The CB has a special folding manufactured into the balloon to protect the three or four blades from being exposed; therefore only a negative prep should be used. No air or fluid should be introduced into the CB until the first inflation of the lesion. Dilation as well as deflation should be performed in a slow manner to allow extrusion and refolding of the blades. The metal blades on the CB make it stiffer and somewhat larger than the regular balloons. For successful advancement of the balloon across the lesion the guiding catheter should be coaxial and should provide a strong back-up. The guidewire should be stiff to allow the CB to be advanced smoothly to the stenotic area. Rigidity of the CB affects navigation across steep bifurcations in contralateral use. In a tortuous/angled vessel or in a diffuse, tight stenosis a shorter balloon would provide better trackability and crossability. A CB is selected with a diameter equal to the diameter of the adjacent normal segment of the artery. Balloon pressure should be increased gradually stepwise (1 atmosphere per second) up to 6 atmospheres to reach nominal size. If an indentation is still noted, pressure is gradually increased 45
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AtherotomeTM
Figure 9.1 Illustration of inflated cutting balloon with Atherotome (blades) and depiction of protection of blade by fold of balloon when deflated.
to 8 atmospheres. If further dilatation is needed, adjunctive balloon angioplasty with a standard angioplasty balloon of appropriate size can be performed. If the lesion is longer than the length of the CB, inflate the CB in the distal portion of the lesion first and move proximal with further inflations.
Clinical experience Aortoarteritis (Takayasu’s disease) Stenotic lesions in aortoarteritis often require high inflation pressure (> 10 atmospheres) for dilatation and residual
(a)
stenosis is not uncommon.12 This is because the stenosis is caused by dense transmural fibrosis. We evaluated the use of CB in dilating stenotic arterial lesions at various sites in this condition. In 22 patients, aged 7–45 years (mean 14.6 ± 7.5 years), 29 stenotic lesions (≥ 75%) were treated by CB. Twenty-one lesions were in the renal, two in the carotids, two in the subclavian, one in the axillary artery and three in the aorta. Of the 21 lesions in the renal artery, 17 were de novo and 4 had in-stent restenosis. For renal angioplasty, CB 4–5 mm in diameter with an Atherotome length of 10–15 mm was passed through an 8-French coaxial guiding catheter or a 7-French sheath over 0.014–0.018-inch diameter, extrasupport guidewire. Femoral approach was used in 15 patients and a high-brachial approach in 3 patients with severe caudal angulation of renal artery. The balloon could be negotiated through stenosis with ease in all patients. In patients with de novo lesions inflation of the balloon at 6–8 atmospheres could eliminate “waste” on the CB in 14 of 17 (82.3%) lesions. Adjunctive balloon angioplasty to further enlarge the lumen was performed in 17 lesions using a 5–6-mm conventional balloon. The stenosis decreased from 87.5 ± 7.8% (mean ± SD) to 28.2 ± 9.3% (mean ± SD) after CB and further reduced to 14.2 ± 4.9% (p < 0.001) after further dilatation/stent implantation (Figure 9.2). There was no complication. Failure to abolish “waste” in CB in three patients could be due to the inability of the 0.127-mm working height of the blade to reach the dense fibrosis in the media through markedly thickened intima, which is often the pathology.13 Follow-up angiographic restudy performed after 6–24 months in 14 lesions showed restenosis in two patients (14.3%). Both of these underwent redilation. CB was found to be especially effective in dilating four lesions with in-stent renal artery restenosis. Good dilatation with smooth lumen could be achieved at low pressure (5–6 atmospheres) in these patients (Figure 9.3). Follow-up angiogram after 6–12 months showed no evidence of restenosis in these four patients. Studies have shown that in-stent restenosis results from smooth muscle cell proliferation9
(b)
Figure 9.2 (a) Aortogram showing severe bilateral renal artery stenosis due to aortoarteritis in a young girl with severe hypertension and congestive heart failure; and (b) good dilatation of both renal arteries after CB angioplasty. Patient had marked improvement in hypertension and congestive heart failure after angioplasty.
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(a)
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(b)
Figure 9.3 (a) Severe in-stent restenosis (arrow) of the proximal segment of upper left renal artery in a young girl with aortoarteritis; and (b) good dilatation of the stenosed segment after 4 × 10 mm CB angioplasty with relief in hypertension.
which can be easily sliced by CB. Stenosis at other sites – aorta, carotid, subclavian, or axillary – could also be relieved effectively by CB angioplasty without any complication. Our experience, along with a few case reports in literature15,16 on CB angioplasty in aortoarteritis show that the procedure is safe and permits dilatation at lower pressure in a number of patients, with less dissection, reducing the need for stent implantation. However, some patients may still have residual “waste” on the balloon due to dense transmural fibrosis. Lower extremity arteries Angioplasty of long stenotic lesions or chronic total occlusions in the superficial femoral (SFA), popliteal, and tibial arteries may be suboptimal. Implantation of stent in this region has a high restenosis rate. Changes in arterial flexion with daily activity can result in fatigue and fracture of metallic stents in the femoropopliteal arterial system.16,17 Angioplasty with a
(a)
(b)
CB may cause less barotrauma and dissection reducing the need for stent implantation and therefore may be an attractive option for such patients. Ansal et al.18 reported initial technical success with the use of CB in 89% of 73 patients with popliteal or crural obstruction. At 1-year mean follow-up 89.5% of treated limbs were salvaged. They concluded that CB angioplasty is a safe and feasible option for the treatment of popliteal and infrapopliteal vessels.17 Our experience and a few other reports19 also show promising results with CB for treatment of atherosclerotic disease of SFA and crural arteries (Figure 9.4). However there are no randomized control trials comparing percutaneous transluminal angioplasty (PTA) with CB for peripheral arteries. Lower-limb vein bypass graft Recurrent stenotic lesions associated with vein bypass grafts are often fibrous and smooth. Unlike de novo atherosclerotic lesions,
(c)
Figure 9.4 (a) Severe stenosis (arrow) of femoral artery; (b) good dilatation of the stenosed segment after 4 × 10 mm CB angioplasty; and (c) further improvement in femoral artery lumen after adjunctive balloon angioplasty. There was no dissection and no need of stent implantation.
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they respond poorly to balloon angioplasty and may often result in a dissection requiring stent placement to avoid early recurrent thrombosis or open repair for residual stenosis. Recent reports have found CB angioplasty to be an acceptable option for focal infrainguinal vein graft stenosis.20,21 This technique reduces the requirement for bail-out stenting or conversion to open surgery in this situation. In-stent restenosis of peripheral arteries In-stent restenosis (ISR) occurs in up to 5% of cases of carotid angioplasty and stenting,22,23 and between 9–24% in patients undergoing renal angioplasty and stenting.24 ISR lesions tend to be more resistant than de novo lesions because of the presence of more smooth muscle and proliferative cells, and fewer macrophages, collagen, and tissue factor.25 There is a rationale for using CB in ISR as it has an ability to achieve acute luminal gain with minimum tissue injury. The longitudinal blades of the CB concentrate the dilation force, creating radially directed fissures and enabling more resistant stenosis to be overcome and thus achieving more acute luminal gain compared to conventional balloon angioplasty. Better lumen gain after dilation may be related to the extrusion of the fibrous residual neointimal plaque from the stent struts, which results in less tissue injury compared with other revascularization modalities. There are few case reports regarding the successful use of CB in ISR of renal26 and carotid arteries.27 Cutting balloon angioplasty for resistant venous stenosis of a hemodialysis fistula Venous stenosis in a hemodialysis shunt is often resistant to high-pressure balloon dilatation.28 This could be due to dense fibrous strands incorporated in the venous neointimal layer or caused by scar tissue developing from recurrent puncture trauma to the venous wall in hemodialysis shunts. Vorwerk et al.29 performed CB angioplasty in 19 stenosed hemodialysis fistulas and grafts. In seven patients, CB angioplasty was followed by conventional balloon angioplasty to achieve the desired diameter without residual stenosis. The balloon expanded completely in all patients and no balloon waste remained. The degree of stenosis decreased from 65 ± 15% (mean ± SD) to 14 ± 9% (mean ± SD). Primary patency rates were 94 ± 6% after 1 month, 86 ± 9% after 2 and 3 months, and 64 ± 15% after 6 and 9 months. No major complications occurred; there was only one case of dislodgement of a microtome from the CB, which occurred while retrieving the CB. CB increased the technical success of balloon dilatation of hemodialysis fistulas and grafts. Other studies30,31 have also reported good initial success and primary-assisted patency at 6 months. A recently published prospective, randomized trial reported more sobering results in that CB and standard balloon angioplasty had equivalent 6-month patency rate for stenotic or thrombosed hemodialysis grafts.32 Severe peripheral pulmonary stenosis Pulmonary artery stenosis presents a therapeutic challenge, given the variety in its presentation and severity, because surgical access to the lesions is difficult. It can present as an
isolated lesion, affecting one of the main branches of the pulmonary artery, or multiple lesions affecting smaller, peripheral branches. In peripheral pulmonary stenosis, if prolonged dilation does not lead to a morphologically and/or hemodynamically satisfying result, stent placement would be the next logical step. However, stent placement in a child or adolescent is undesirable, because growth of the pulmonary artery can leading to relative stenosis in the stented segment. Recent studies have shown usefulness of CBs in treatment of branch pulmonary artery stenosis and angioplasty-resistant pulmonary artery stenosis. Butera et al.33 successfully treated eleven peripheral pulmonary artery stenoses in four patients. The main vessel diameter increased by 81% (p < 0.001) and RV/LV pressure ratio decreased from 1.15 to 0.75 (p = 0.05). There was no intraprocedural or late complication. Results were stable on 18 months of follow-up. Bergersen et al.34 performed CB angioplasty of 79 vessels in 29 patients for relieving stenoses in small pulmonary arteries. Minimal luminal diameter increased from 1.5 ± 0.8 to 3 ± 1.1 mm (p < 0.001). On follow-up 79% of patients showed sustained improvement. These results suggest that CB angioplasty is a promising technique for the treatment of highly challenging pathologies such as small-vessel pulmonary artery stenosis and intra-stent restenosis. However, further studies with longer follow-up are needed to confirm these initial results. Recently CB has also been used in palliative treatment in tetralogy of Fallot.35 Pulmonary vein stenosis After radio-frequency ablation for atrial fibrillation, patients may develop pulmonary vein stenosis requiring stent angioplasty. Cook et al.36 compared CB angioplasty with standard angioplasty in 21 patients with pulmonary vein in-stent stenosis. Although initially both the techniques significantly improved the lesion diameter, on follow-up, restenosis was seen more often in angioplasty alone group (4/6 vessels) as compared to the CB group (2/15 vessels) showing superiority of CB angioplasty in this situation. In a recent report, Seale et al.37 found CB angioplasty to be safe in palliation of pulmonary vein stenoses. It gave good acute relief but often needed to be repeated. Complications of cutting balloon angioplasty Use of the CB requires caution to prevent complications because of its specific design. Rupture of the balloon, aneurysm formation, and (rarely) rupture of the artery after CBA has been reported in a few cases and is an area of concern.38,39 Rated burst pressure should not be exceeded as balloon rupture can lead to microtome dislodgement during balloon retrieval. Balloon rupture and entanglement with stent struts during dilatation for ISR has also been reported.
Conclusion CB angioplasty in peripheral arteries is safe, easy to use and has the potential to improve the efficacy of balloon angioplasty in resistant stenotic lesions. Previously, the maximum available
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Cutting balloon angioplasty diameter of 4-mm CB limited the use of this balloon to small arteries and veins. However with the availability of 5–8-mm CB, larger vessels can now be treated. It has proved useful in several clinical indications such as peripheral arterial stenosis in native arteries below the inguinal ligament, resistant stenosis of dialysis fistulas and grafts, and neointimal hyperplasia in the infrainguinal arterial bypass graft salvage. Efficacy has also been reported in fibrotic lesions of aortoarteritis and in-stent restenosis of carotid and renal arteries. The more-than-theoretical
49
advantage is that the CB can “focus” the force, overcome fibrous stenosis, create less wall injury, and could decrease the need for adjunctive stent placement in most cases.
Acknowledgments The author thanks Dr Girish MP and Dr Mohit D Gupta for their help in preparation of this manuscript.
REFERENCES 1. 2. 3. 4. 5.
6. 7. 8. 9.
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12.
13. 14. 15. 16. 17. 18. 19. 20.
Yamaguchi T, Nakamura M, Nishida T et al. Update on cutting balloon angioplasty. J Interven Cardiol 1998; 11 (Suppl.1): S114–9 Barath P, Fishbein MC, Vari S, Forrester JS. Cutting balloon: A novel approach to percutaneous angioplasty. Am J Cardiol 1991; 68: 1249–52 Cejna M. Cutting balloon: Review on principles and background of use in peripheral arteries. Cardiovasc Intervent Radiol 2005; 28: 400–8 Voigt B, Pfitzer P, Weismueller P et al. Cutting balloon angioplasty: An alternate way in the treatment of complex coronary lesions. J Am Coll Cardiol 2000; 35(Suppl A): 1062–78 Bittl JA, Chew DP, Topol EJ, Kong DF, Califf RM. Meta-analysis of randomized trials of percutaneous transluminal coronary angioplasty versus atherectomy, cutting balloon atherotomy, or laser angioplasty. J Am Coll Cardiol 2004; 43: 936–42 Mauri L, Bonan R, Weiner BH et al. Cutting balloon angioplasty for the prevention of restenosis: results of the cutting balloon global randomized trial. Am J Cardiol 2002; 90: 1079–83 Albiero R, Nishida T, Karvouni E et al. Cutting balloon angioplasty for in stent restenosis. Catheter Cardiovasc Interv 2000; 50: 452–9 Kurbaan AS, Foale RA, Sigwart U. Cutting balloon angioplasty for in-stent restenosis. Catheter Cardiovasc Interv 2000; 50: 480–8 Cin VG, Pekdemir H, Akkus MN et al. Cutting balloon angioplasty for the treatment of in-stent restenosis in diabetics: A matched comparison of 6 months’ outcome with conventional balloon angioplasty. Angiology 2006; 57(4): 445–52 Tsetis D, Morgan R, Belli AM. Cutting balloons for the treatment of vascular stenoses. Eur Radiol 2006; 16: 1675–83 Inoue T, Sakai Y, Hoshi K et al. Lower expression of neutrophil adhesion molecule indicates less vessel wall injury and might explain lower restenosis rate after cutting balloon angioplasty. Circulation 1998; 97: 2511–8 Tyagi S, Verma PK, Gambhir DS et al. Early and long term results of balloon angioplasty in aortoarteritis (Takayasu Disease): Comparison with atherosclerosis. Cardiovasc Intervent Radiol 1998; 21: 219–4 Hotchi M. Pathological studies on Takayasu arteritis. Heart Vessels 1992; Suppl 7: 11–7 Henry M, Rath PC, Lakshmi G, Henry I, Hugel M. Percutaneous transluminal angioplasty using a new peripheral cutting balloon for stenosis of arch vessels in aortoarteritis. Int Angiol 2004; 3: 403–9 Rath PC, Lakshmi G, Henry M. Percutaneous transluminal angioplasty using a cutting balloon for stenosis of the arch vessels in aortoarteritis. Indian Heart J 2004; 56: 54–7 Wensing PJ, Scholten FG, Buijs FC et al. Arterial tortuosity in femoralpopliteal region during knee flexion: a magnetic resonance angiographic study. J Anat 1995; 187: 133–9 Diaz JA, Villegas M, Tamashiro G et al. Flexions of the popliteal artery: dynamic angiography. J Invas Cardiol 2004; 16: 712 Ansel GM, Sample NS, Botti III Jr CF et al. Cutting balloon angioplasty of the popliteal and infrapopliteal vessels for symptomatic limb ischemia. Catheter Cardiovasc Interv 2004; 61: 1–4 Rabbi JF, Kiran RP, Gersten G, Dudrick SJ, Dardik A. Early results with infrainguinal cutting balloon angioplasty limits distal dissection. Ann Vasc Surg 2004; 18: 640–3 Kasirajan K, Schneider PA. Early outcome of “cutting” balloon angioplasty for infrainguinal vein graft stenosis. J Vasc Surg 2004; 39: 702–8
21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33.
34. 35. 36. 37. 38.
39.
Muller-Hulsbeck S, Order BM, Jahnke T. Interventions in infrainguinal bypass grafts. Cardiovasc Intervent Radiol 2006; 29: 17–28 Levy EI, Hanel RA, Lau T et al. Frequency and management of recurrent stenosis after carotid artery stent implantation. J Neurosurg 2005; 102: 29–37 Bendok BR, Roubin GS, Katzen BT et al. Cutting balloon to treat carotid in-stent stenosis: technical note. J Invasive Cardiol 2003; 15: 227–32. Van de Ven PJ, Kaatee R, Beutler JJ et al. Arterial stenting and balloon angioplasty in ostial atherosclerotic renovascular disease: a randomized trial. Lancet 1999; 353: 282–6 Kearney M, Pieczek A, Haley L et al. Histopathology of in-stent restenosis in patients with peripheral artery disease. Circulation 1997; 95: 1998–2002 Munneke GJ, Engelke C, Morgan RA, Belli AM. Cutting balloon angioplasty for resistant renal artery in-stent restenosis. J Vasc Interv Radiol 2002; 13(3): 327–31 Tamberalla MR, Yadav JS, Bajzer CT, Bhatt DL, Chebl AA. Cutting balloon angioplasty to treat carotid instent restenosis. J Invas Cardiol 2004; 16: 133–5 Trerotola SO, Kwak A, Clark TW et al. Prospective study of balloon inflation pressures and other technical aspects of hemodialysis access angioplasty. J Vasc Interv Radiol 2005; 16: 1613–8 Vorwerk D, Adam G, Muller-Leisse C, Guenther RW. Hemodialysis fistulas and grafts: Use of cutting balloon to dilate venous stenosis. Radiology 1996; 201: 864–7 Singer-Jordan J, Papura S. Cutting balloon angioplasty for primary treatment of hemodialysis fistula venous stenoses: preliminary results. J Vasc Interv Radiol 2005; 16: 25–9. Carrafiello G, Lagana D, Mangini M et al. Cutting balloon angioplasty for the treatment of hemodialysis vascular accesses: midterm results. Radiol Med 2006; 111: 724–32 Vesely TM, Siegel JB. Use of the peripheral cutting balloon to treat hemodialysis-related stenoses. J Vasc Interv Radiol 2005; 16: 1593–603 Butera G, Antonio LT, Massimo C, Mario C. Expanding indications for the treatment of pulmonary artery stenosis in children by using cutting balloon angioplasty. Catheter Cardiovasc Interv 2006; 67: 460–5 Bergersen L, Jenkins KJ, Gauvreau K, Lock JE. Follow-up results of Cutting Balloon angioplasty used to relieve stenoses in small pulmonary arteries. Cardiol Young 2005; 15: 605–10 Carlson KM, Neish SR, Justino H et al. Use of cutting balloon for palliative treatment in Tetralogy of Fallot. Catheter Cardiovasc Interv 2005; 64: 507–12 Cook AL, Prieto LR, Delaney JW, Rhodes JF. Usefulness of cutting balloon angioplasty for pulmonary vein in-stent stenosis. Am J Cardiol 2006; 98: 407–10 Seale AN, Daubeney PE, Magee AG, Rigby ML. Pulmonary vein stenosis: initial experience with cutting balloon angioplasty. Heart 2006; 92: 815–20 Oguzkurt L, Tercan F, Gulcan O, Turkoz R. Rupture of the renal artery after cutting balloon angioplasty in a young woman with fibromuscular dysplasia. Cardiovasc Intervent Radiol 2005; 28: 360–3 Murakami R, Tajima H, Kumita S. Cutting balloon-associated hemodialysis fistula rupture after failed standard balloon angioplasty. Kidney Int 2006; S70(5): 825
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SilverHawk® atherectomy device RS Gammon and JR Nelson
Introduction Successful treatment of infrainguinal peripheral arterial disease (PAD) has proven to be one of the greatest challenges in vascular intervention. Some of this is explained by the disease characteristics: diffuse involvement with long lesions and multi-level disease, propensity to calcification and total occlusions, and high resistance or low flow states. This is further compounded by the unique mechanical characteristics of the arteries, including extension, contraction, rotation, compression, and extreme flexion especially within the joint spaces. These mechanical challenges contribute to stent failure both in terms of restenosis and stent fracture. Disappointing results with angioplasty and stenting have led to the development of many alternative devices in search of more consistent and durable results. The most intuitive solution in the treatment of vascular disease is plaque removal, or atherectomy. The concept was introduced in the 1980s and many devices following that successfully removed plaque by one means or another.1–13 Unfortunately, most of these devices were relatively inefficient at addressing the large plaque burden present. Furthermore, they often induced vessel injury and embolization as they could not effectively collect the majority of plaque liberated from the vessel wall. Trials of coronary atherectomy have shown that suboptimal atherectomy does not significantly reduce restenosis compared to angioplasty, whereas more aggressive, or “optimal,” atherectomy does.14–21 The SilverHawk® system received Food and Drug Administration (FDA) approval in 2003 for the treatment of peripheral arteries, including Femoropopliteal and tibioperoneal vessels.22 It provides a unique approach to removing plaque from de novo or restenotic lesions of any length. Both calcified and non-calcified lesions are treatable with the device. Because the cutter is apposed to the plaque mechanically, the catheter excises large amounts of plaque without causing significant barotrauma to the arterial wall. The device can also remove eccentric plaque and create a more optimal environment for laminar flow. By excising plaque and avoiding stretch, the chance of dissection is minimized, and the signals that initiate intimal hyperplasia are postulated to be minimized. SilverHawk® atherectomy, or plaque excision, may also offer the opportunity to learn more about underlying atherosclerotic disease processes. Histological analyses can identify inflammatory cell infiltration, the presence of thrombus, calcification, or fibrosis, the degree of smooth muscle cell proliferation, and the lipid content of the plaque removed. Genomic and proteomic analyses of the excised tissue also provide further insight into 50
the pathophysiology of restenosis and identify predictive markers of restenosis and cardiovascular risk. The SilverHawk® device is a 0.014-inch-based monorail catheter designed for single-operator use (Figure 10.1). It consists of a motor drive unit that contains a battery pack and a thumb switch to activate the cutter. The working end consists of a hinged housing unit containing a carbide cutting blade. The blade is activated from the motor drive unit at a rate of 8,000 rpm, and the catheter is then advanced into an area of plaque. With each pass, the cutter is used to pack the tissue into the distal tip of the nosecone to maximize collection capacity. The length of each pass is limited to the length of the remaining empty portion of the collection chamber to avoid embolization of excess material after a pass through the lesion. The device can then be either removed or rotated to treat a different quadrant in the same lesion or other lesions. A single device can be used to treat multiple lesions and/or multiple vessels. A variety of cutter sizes exist (Table 10.1) which allows treatment of vessels ranging from 2.0 to 7.0 mm diameter. Different length collection chambers may allow more extensive tissue storage before needing to remove the device to empty plaque. Immediate gross assessment of lesion composition is possible while emptying the device (e.g. presence of thrombus) and may impact treatment decisions and dictate adjunctive therapy. The device can be used from either antegrade or contralateral approach, typically through a 6-French or 7-French sheath.
Clinical outcomes The TALON (Treating Peripherals with SilverHawk®: Outcomes Collection) Study23 was a prospective, multi-center, non-randomized, observational outcomes registry that enrolled consecutive patients undergoing plaque excision for lower extremity PAD. In addition to demographics, risk factors, and procedure characteristics, TALON collected acute, 6-, and 12-month outcome data. Tissue and blood samples were collected from consenting participants. The registry enrolled 728 patients with 906 limbs involved. A total of 1517 lesions were treated in 1001 procedures. Demographics were typical of peripheral series, with an average age of 70: 50% were diabetics, and 66% had a history of, or were currently, smoking. The majority or patients had claudication, but 275 (30.6%) had critical limb ischemia (CLI) as defined as a Rutherford–Becker24 score of 4 or 5. Lesion locations included iliac (68 or 4.5%), common femoral/profunda (102 or 6.7%), superficial femoral
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(b)
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(d) Figure 10.1 (a) SilverHawk® device; (b) SilverHawk® magnified to show cutting unit. The carbide coated disc spins at 8,000 rpm; (c) SilverHawk® devices shown with motor dive units; and (d) SilverHawk® under fluoroscopy within the common femoral artery.
(730 or 48.1%), popliteal (226 or 14.9%), tibioperoneal/ peroneal (183 or 12.1%), anterior or posterior tibial (198 or 13.1%), and dorsalis pedis/calcaneal (10 or 0.7%). Average lesion length for the series was 58 mm, with average superficial femoral artery (SFA) lesion length of 82 mm. Moderate or severe calcification was reported in 62.9% of lesions, and 28.6% of lesions were total occlusions. The majority of lesions (87.5%) were de novo, but 12.5% represented restenosis, including in-stent restenosis. This series represented a realworld, “all-comers” patient cohort with a large PAD burden. Procedural characteristics were recorded in this early experience with the device. Average SilverHawk® procedure time was 27.5 minutes. This is notable considering that 40.7% of procedures involved the treatment of more than one lesion, and the early generation devices available at that time were considerably less efficient than current devices. Adjunctive therapy was used in 26.5% of cases and was primarily balloon angioplasty, with stents deployed in only 6.1% of cases.
Twelve-month outcome data are available on 335 patients with 658 lesions. Patency was defined as freedom from target lesion revascularization (TLR). At 1 year, 79% of these lesions were free from revascularization. For patients with claudication, defined as a Rutherford–Becker score of less than 4, the patency rate was 85%. Remarkably, there was no significant difference between diabetics and non-diabetics, with patency rates of 82 and 78%, respectively. Zeller et al. published the earliest experience with the SilverHawk® device from Europe, reporting the 6-month patency rates of infrapopliteal atherectomy as determined by duplex ultrasound.25 Balloon predilation was frequently used to allow passage of first-generation cutters. Adjunctive balloon angioplasty was performed in 29% of cases. The mean ankle–brachial index for the group improved from 0.46 to 0.80 before discharge and remained improved during follow-up. The restenosis rate, defined as 70% or greater stenosis by duplex ultrasonography, was 14% at 3 months and 22% at 6 months.
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SilverHawk® devices available for use
SilverHawk® type LS: Large vessel standard tip LX: Large vessel extended tip MS: Medium vessel standard tip SX: Small vessel extended tip SS+: Small vessel standard tip DS: Distal vessel standard tip
Vessel diameter (mm) 4.5–7.0 4.5–7.0 3.5–5.0 3.0–3.5 3.0–3.5 1.5–2.0
Zeller et al. also reported 2-year results of SilverHawk® atherectomy for infrapopliteal lesions. 25 Forty-nine lesions in 36 lower limbs were treated, 19 (53%) of these patients had CLI, and 11 (22%) lesions were total occlusions. Mean lesion length was 48 mm, and nine lesions (18%) were in-stent restenoses. Sixteen (33%) lesions were treated with predilation and 19 (39%) with post-dilation. Two of these lesions were stented. A residual stenosis < 30% was achieved in 48 (98%) lesions. The mean ankle–brachial index increased from 0.48 to 0.81 by discharge. Primary and secondary patency rates were 67% and 91% after 1 year and 60% and 80% after 2 years, respectively. In the US, Keeling et al.26 reported their early experience with the SilverHawk® catheter in patients with claudication or CLI, including clinical and duplex follow-up. Sixty-six limbs of 60 patients underwent 70 atherectomy, or plaque excision, procedures. Twenty-three of the 70 procedures (33%) were done for claudication but two-thirds of patients had CLI. Of the CLI patients, 22 of 70 (31%) had rest pain, and 25 of 70 (36%) had minor or major tissue loss. All of the patients had femoropopliteal lesions treated and 17 patients required plaque excision of tibial vessels. Mean lesion length was 8.8 cm, and femoropopliteal TASC27 criteria included 5 TASC A lesions, 14 TASC B lesions, 32 TASC C lesions, and 19 TASC D lesions. Adjunctive therapy was used in 17 procedures (24.3%), consisting of 14 balloon angioplasties and 3 stents. The mean increase in ankle–brachial index was 0.27. Duplex ultrasound surveillance was performed at 1, 3, and 6 months and annually. One-year primary, primary-assisted, and secondary patency was 61.7, 64.1, and 76.4%, respectively. Restenosis or occlusion was significantly more common in patients with TASC C and D lesions. Similar findings were seen in the TALON registry.23 Predictors of target lesion revascularization included increasing Rutherford–Becker score (HR 1.84, 95% CI 1.28 to 2.65, p = 0.0003) and multiple lesions (HR 1.37, 95% CI 1.11 to 1.70, p = 0.0019). Lesion lengths > 50 mm were associated with a 2.9-fold increased risk for TLR and lesion lengths > 100 mm were associated with a 3.3-fold increase in TLR. SilverHawk® for limb salvage CLI is usually caused by diffuse multi-level disease, often involving infrapopliteal vessels. These features might favor a strategy of plaque excision over plaque-displacement approaches. Yancey et al.28 described the outcome of 18 consecutive procedures in 17 limbs, all of whom had severe CLI and multi-level disease. All patients had femoropopliteal involvement with TASC C disease present. The clinical indication was tissue loss
Sheath compatibility (French) 7-F/8-F 8-F 7-F/8-F 7-F 7-F 6-F
in thirteen limbs and rest pain in four. Initial resolution of symptoms or complete healing was achieved in twelve limbs, and partial healing was achieved in two others. Early amputation was necessary in the remaining three patients, but this was felt most likely due to severe inframalleolar disease and advanced forefoot ischemia at the time of presentation. The mean ankle–brachial index improved from 0.39 to 0.75 postprocedure. However, at 6 months it had fallen to 0.48, and at 12 months, stenosis-free patency of the femoropopliteal segment was only 22%. Two patients required late amputation. A multi-center experience using SilverHawk® plaque excision for limb salvage was published by Kandzari et al.29 The study enrolled 69 patients with 76 ischemic limbs from 7 different institutions. A particularly severe cohort was selected, with all patients having tissue destruction, as defined as a Rutherford–Becker score of 5 or 6. Remarkably, amputation was already planned in 63% of patients prior to any attempt at salvage. Seventy-eight percent of patients had diabetes and 47% had renal impairment. All patients had multi-vessel and multilevel involvement. SilverHawk® plaque excision was performed in all patients, with procedural success of 98.7%. Adjunctive angioplasty was used in 13%, and 6% received stents. At 6 months, three patients required below-the-knee and three patients above-the-knee amputation. Eighty-two percent of patients had either avoided amputation completely or underwent lesser amputation than originally planned. Target lesion revascularization was 4% at 6 months. At our center, we reported on 57 consecutive patients with CLI treated with plaque excision.30 Forty-three patients (75%) had multi-level disease. An average of two lesions were treated per procedure. All patients had plaque excision. Adjunctive therapy was used in 20%, including angioplasty (16.5%), stent (1%), stent and angioplasty (2.5%), and rotational atherectomy and angioplasty (1%). Patients were followed up to 24 months, with a mean of 11 months (Table 10.2). The average Rutherford–Becker score was markedly improved at 6 months and 12 months. Of limbs with tissue loss, 80% showed visible healing; rest pain had resolved in 90% of patients with a Rutherford–Becker score of 4. One patient required above-the-knee and three required below-the-knee amputations. Overall, the limb salvage rate was 93%.
Special applications An argument for SilverHawk® plaque excision as the default strategy for most infrainguinal interventions is difficult until
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Table 10.2 Austin Heart PA single-center, critical limb ischemia experience. Data representative of 57 consecutive patients presenting with Rutherford–Becker (RB) scores ≥ 4. Of the five patients that did not show visible healing or resolution of rest pain; one went on to receive above-knee-amputation (AKA) and three below-knee-amputation (BKA). Furthermore, three patients died before 12-month follow-up Critical limb ischemia follow-up data
Preprocedure
6-month
12-month
Average RB score Limbs that showed visible healing Limbs with resolution of rest pain
4.45 ± 0.09 n = 33 (80% of those with RB < 4) n = 19 (90% of those with RB = 4)
1.45 ± 0.24
1.17 ± 0.35
Amputation AKA BKA Metatarsal or partial toe amputation
n n n n
= = = =
10 1 3 6
randomized data comparing it to other strategies are available. However, certain lesion locations are notoriously difficult to treat using plaque displacement technology. SilverHawk® plaque excision may offer a clear advantage in certain lesion subsets.31 Common femoral artery Endovascular treatment of common femoral lesions presents numerous challenges. Naturally, the lesions occur in a joint space making stenting unfavorable. They also often involve the bifurcation, and frequently are calcified and/or totally occluded. Access to reach the lesions may be difficult, and stent placement may prevent future access from this site. The frequent use of closure devices may have accelerated the prevalence of disease at this site. These challenges have made surgical endarterectomy often the best option to treat disease at this location, though this may also complicate future access. SilverHawk® plaque excision has the potential to perform as an “endovascular endarterectomy” in common femoral lesions.32 A vessel size of approximately 7 mm is easily treated with the LS device, the largest diameter cutter (see Table 10.1). As opposed to plaque displacement technologies, plaque excision does not compromise important branches. Instead, selectively choosing to place the wire in either the superficial or profunda femoral artery can facilitate delivery of the device to each wall to optimize plaque removal. The risk of major dissection (possibly leading to stent placement in this location) is minimized, especially compared to techniques like kissing balloons previously advocated. A specific indication for SilverHawk® may be in treating iatrogenic lesions created by femoral closure devices.33,34 Use of these closure devices has been associated with both acute limb ischemia, and subsequent claudication. Suturemediated closure devices can disrupt plaque within the femoral artery. Devices such as Angioseal (St. Jude, St. Paul, MN) may cause plaque disruption from the foot-plate, or the collagen plug may be inadvertently deployed within the artery. SilverHawk® plaque excision appears to be effective in treating either scenario. At our institution we have used SilverHawk® plaque excision to treat nine lesions with either stenosis or
17.5% 2% 5% 10.5%
occlusion 1 hour to 2 weeks following Angioseal deployment (Figure 10.2). The LS SilverHawk® platform was used in all cases. All procedures were technically successful and without complication. No patient has developed recurrent stenosis with more than 2 years follow-up including routine duplex surveillance. Profunda femoral artery The SilverHawk® device has performed well in ostial lesions, and is capable of treating profunda lesions of this type. A common scenario is the patient with SFA occlusion and stable claudication, who converts to severe symptoms with the development of an ostial profunda lesion. These resilient lesions exhibit recoil after dilation (even with cutting balloons) and stenting is discouraged because of the location. However, SilverHawk® plaque excision has proven effective for this lesion. The true reference vessel size may be difficult to estimate due to ostial location, early branching, and frequent post-stenotic dilation. The angle of the vessel take-off may also create the possibility of deep wall cuts. For these reasons we do not attempt to achieve angiographically “perfect” results (Figure 10.3). Postdilation is performed with greater frequency relative to other lesions. Even with low-pressure inflations, less recoil is evident after the lesion is “scored” with atherectomy. Popliteal artery The popliteal artery presents challenges to interventional therapy as it crosses a joint space that may experience extreme flexion. Stent placement with current stent technology is generally avoided. Distally, the trifurcation of the vessel presents further challenges, and tibial vessels may be compromised by angioplasty or stenting. Covered stents in particular may present risk as they occlude genicular collaterals, which may become critical if the intervention subsequently fails. Plaque excision is often capable of achieving technical success in popliteal lesions without the need for stenting and without compromising dependant branches (Figure 10.4). In some cases, rather than occluding important branches or collaterals, plaque excision may actually expose ostia to branches that previously had poor flow.
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(b)
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(e) Figure 10.2 (a) This patient underwent an angiographic interventional procedure via left common femoral access. The access site for this intervention was closed with an 8-French Angioseal; (b) four days later, the patient returned to the physician’s office with significantly elevated left-leg claudication and paresthesias. Angiographic results showed a total occlusion of the left common femoral artery at the previous arterial access site. A SilverHawk® atherectomy device was used to treat the lesion and provided excellent removal of thrombus and collagen material; (c) gross tissue samples removed from the SilverHawk® device were processed for histological analyses; (d) intimal plaque with collagen material removed from SilverHawk® device; and (e) collagen materials after collagen-specific stain. (See Color plates.)
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(a) Figure 10.3 alone.
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(b)
(a) Complex CFA stenosis involving the ostia of both the SFA and PFA; and (b) result after SilverHawk® plaque excision
In-stent restenosis In-stent restenosis in the lower extremities is often a diffuse proliferative process that responds poorly to repeated intervention. The SilverHawk® device is capable of excising a large amount of this tissue and may avoid repeated barotrauma. Although the device is not approved for this indication, we have found it to be invaluable in treating this common and difficult disease. Extremely large amounts of tissue may be removed in some cases (Figure 10.5) and adjunctive therapy is usually not necessary. Long-term patency may still be suboptimal in this difficult disease. Zeller et al. reported 1-year results of femoropopliteal lesions treated with SilverHawk® and compared de novo lesions to in-stent restenosis as well as non-stent restenosis. 35 Primary patency was defined as freedom from > 50% restenosis as defined by duplex ultrasound (proximal systolic peak flow velocity ratio > 2.4). Primary patency was 84% in the de novo lesions and 54% in the in-stent restenosis lesions (p = 0.002). Some of this difference may be explained by lesion length in that the mean lesion length was 43 mm in de novo lesions and 105 mm in in-stent restenosis lesions. The difficulty of treating in-stent restenosis remains one of the arguments against widespread use of stents for infrainguinal lesions.
Complications Device-related complications with SilverHawk® plaque excision are low. Major dissection, acute thrombosis, perforation, or late aneurysm formation occur in < 1% of cases in experienced hands.23 The complication that has received the most attention is distal embolization. Distal embolic protection devices catch debris in almost all peripheral interventions,36 including plaque excision.37 The clinical significance of these embolic particles is often inconsequential in the relatively tolerant peripheral bed as opposed to the cerebral or
coronary circulation. Furthermore, the incidence of embolization is probably directly related to operator experience and technique. For instance, in Zeller’s35 first eight SilverHawk® procedures, embolization was observed in five cases. However, the embolus was easily aspirated in each case without clinical sequelae. With further experience, using slower passes and taking care not to over-fill the collection chamber, there were no apparent emboli in the next 123 lesions treated. Clinically significant embolization has been a rare event in the 2000-plus lesions we have treated. We use embolic protection in less than 1% of cases, usually reserved for lesions with known thrombus, recent total occlusion, “coral reef ” calcification, or Angioseal occlusion. Patients with CLI and single-vessel run-off should be considered for embolic protection due the potential consequence of embolization and lack of reserve flow. Even in these higher-risk scenarios, the additional cost of the filter and technical challenges presented must be weighed against the risk of major embolization. Unfortunately, much of the argument for embolic protection has come from users with minimal device experience. With good operator technique (slow passes, frequent packing, avoiding over-packing), the risk of clinically significant embolization is low.
Future studies As with any new device, the first studies with the SilverHawk® device have attempted to define performance characteristics and outcomes across a broad range of clinical and lesion presentations. While these registry reports provide valuable information, trials randomizing SilverHawk® plaque excision against other strategies and employing rigorous core laboratory adjudication are needed. Design of these trials has been difficult as suitable control arms are lacking. Many investigators
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Figure 10.4 (a)–(d): Long superficial femoral artery occlusion (a) along with below the knee outflow (b) prior to treatment. Images were repeated at the prior site of occlusion (c) and below the knee (d) immediately following treatment with SilverHawk® athererctomy.
dismiss angioplasty as a suitable, or even ethical, control in long lesions and total occlusions. Approval from the FDA for a stent control arm is difficult as the stents currently favored by clinicians for femoropopliteal use are only approved for biliary use. Likewise, those often favored for infrapopliteal use are only approved for coronary use. The recent approval of standardized performance goals and endpoint assessments for evaluation of new devices in femoropopliteal intervention provides accepted benchmarks for comparison.38 A multi-center trial with the SilverHawk® in femoropopliteal lesions should commence soon. Follow-up will include meticulous clinical and duplex assessment for greater than 1 year. Arteries that appear to have restenosis by duplex ultrasound will undergo conventional or computed tomography angiography to confirm. All studies will have core lab adjudication.
A randomized multi-center study is currently enrolling patients with CLI and infrapopliteal disease. Many believe that distal bypass using a venous conduit is the accepted “goldstandard” for treating critical limb ischemia. The PROOF, (Plaque Removal Versus Open Bypass Surgery for Critical Limb Ischemia), study will enroll 304 patients at approximately 40 sites across the US. Patients with CLI are randomized to SilverHawk® plaque excision versus surgical bypass. SilverHawk® plaque excision provides the unique ability to readily remove and analyze plaque from multiple sites along with the freedom to provide subsequent treatments. Gross and histological information gained may impact clinical decisionmaking. Proteomic and genomic evaluation of the tissue has the potential to deepen the understanding of atherosclerosis. What are the characteristics of plaque and the features that predict recurrence? Within the same patient, how much
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or inter-patient plaque variability? What proteomic and gene expression changes can be measured when new systemic medications are started, and how soon do these changes occur? Most importantly, do these findings within plaque predict clinical success of the drug, leading to a markedly accelerated and more accurate pathway for drug development?
Summary
Figure 10.5 Tissue removed from SFA in-stent restenosis. A glistening white appearance and rubbery consistency are typical. (See Color plates.)
variability exists in plaque from one lesion to the next, from one vessel to the next, from one month to the next? Are there circulating biomarkers that correlate with either intra-patient
The SilverHawk® device offers a fundamentally different and more intuitive approach to solving the challenges presented by lower-extremity atherosclerosis. The mechanism of the device reduces barotrauma and achieves effective plaque excision that renders comparison to previous forms of atherectomy irrelevant. The device has particular utility in certain lesion subsets that have been notoriously difficult to treat with plaque-displacement technology. Results from single and multi-center registries are encouraging, but proof that SilverHawk® plaque excision should be the default strategy for infrainguinal disease needs to come from multi-center, randomized trials with operators skilled in using the device.
REFERENCES 1. 2. 3.
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5. 6. 7. 8.
9. 10. 11. 12. 13. 14.
15.
Agmon M, Scheinowitz M, Beitner S et al. The Bard Rotary Atherectomy System (BRAS): initial experience in patients with peripheral vascular disease. J Intervent Cardiol 1993; 6(1): 51–9 Mazur W, Ali N, Rodgers G et al. Directional atherectomy with the Omnicath: a unique new catheter system. Cathet Cardiovasc Diagn 1994; 31(1): 79–84 Dorros G, Iyer S, Lewin R et al. Angiographic follow-up and clinical outcome of 126 patients after percutaneous directional atherectomy (Simpson AtheroCath) for occlusive peripheral vascular disease. Cathet Cardiovasc Diagn 1991; 22(2): 79–84 Vroegindeweij D, Kemper F, Tielbeek A et al. Recurrence of stenoses following balloon angioplasty and Simpson atherectomy of the femoro-popliteal segment: A randomised comparative 1-year follow-up study using colour flow duplex. Eur J Vasc Surg 1992; 6(2): 164–71 Williams D, Fahrenbach M. Directional coronary atherectomy: but wait, there’s more. Circulation 1998; 97(4): 309–11 Thorpe P. Atherectomy tools for arterial treatment. Admin Radiol 1992; 11(2): 23, 25–88 Saland K, Cigarroa J, Lange R et al. Rotational atherectomy. Cardiol Rev 2000; 8(3): 174–9 Goldberg S, Berger P, Cohen D et al. Rotational atherectomy or balloon angioplasty in the treatment of intra-stent restenosis: BARASTER multicenter registry. Catheter Cardiovasc Interv 2000; 51(4): 407–13 Osula S, Ramsdale D. “Cutting Balloon and the Three Burrs”: treatment for ostial left anterior descending artery in-stent restenosis. J Invasive Cardiol 2002; 14(2): 93–5 Payne J. Alternatives for revascularization: peripheral atherectomy devices. J Vasc Nurs 1992; 10(1): 2–8 Kuan P. Clinical efficacy of transluminal extraction coronary atherectomy. J Formos Med Assoc 1992; 91(3): 323–8 Myers K, Denton M. Infrainguinal atherectomy using the Auth Rotablator: patency rates and clinical success for 36 procedures. J Endovasc Surg 1995; 2(1): 67–73 Sketch MH, Phillips HR, Stack RS et al. Coronary transluminal extraction-endarterectomy. J Invasive Cardiol 1991; 3(1): 13–8 Topol E, Leya F, Pinkerton C et al. A comparison of directional atherectomy with coronary angioplasty in patients with coronary artery disease: The CAVEAT Study Group. New Eng J Med 1993; 329(4): 221–7 Holmes DJ, Topol E, Califf R et al. A multicenter, randomized trial of coronary angioplasty versus directional atherectomy for patients
16.
17. 18.
19. 20.
21. 22. 23. 24. 25.
26. 27. 28.
with saphenous vein bypass graft lesions. CAVEAT-II Investigators. Circulation 1995; 91(7): 1966–74 Adelman A, Cohen E, Kimball B et al. A comparison of directional atherectomy with balloon angioplasty for lesions of the left anterior descending coronary artery. New Engl J Med 1993; 329(4): 228–33 Baim D, Cutlip D, Sharma S et al. Final results of the Balloon vs. Optimal Atherectomy Trial (BOAT). Circulation 1998; 97(4): 322–31 Lansky A, Mintz G, Popma J et al. Remodeling after directional coronary atherectomy (with and without adjunct percuta-neous transluminal coronary angioplasty): a serial angiographic and intravascular ultrasound analysis from the Optimal Atherectomy Restenosis Study. J Am Coll Cardiol 1998; 32(2): 329–37 Simonton C, Leon M, Baim D et al. ‘Optimal’ directional coronary atherectomy: final results of the Optimal Atherectomy Restenosis Study (OARS). Circulation 1998; 97(4): 332–9 Lansky A, Popma J, Cutlip D et al. Comparative analysis of early and late angiographic outcomes using two quantitative algorithms in the Balloon versus Optimal Atherectomy Trial (BOAT). Am J Cardiol 1999; 83(12): 1611–6 Tsuchikane E, Sumitsuji S, Awata N et al. Final results of the Stent versus directional coronary atherectomy randomized trial (START). J Am Coll Cardiol 1999; 34(4): 1050–7 Gammon R. Plaque excision treatment of infrainguinal PAD. Endovasc Today 2005; 6: 70–4 Ramaiah V, Gammon R, Kiesz S et al. Midterm outcomes from the TALON registry: Treating peripherals with SilverHawk®: Outcomes collection. J Endovasc Ther 2006; 13(5): 592–602 Rutherford RB, Beaker JD. Recommended standards for reports dealing with lower extremity ischemia: Revised version. J Vasc Surg 1997; 26(3): 517–38 Zeller T, Rastan A, Schwarzwalder U et al. Midterm results after atherectomy-assisted angioplasty of below-knee arteries with use of the Silverhawk device. J Intervent Radiol 2004; 15: 1391–97 Keeling W, Shames M, Stone P, et al. Plaque excision with the SilverHawk catheter: Early results in patients with claudication or critical limb ischemia. J Vasc Surg 2007; 45(1): 25–31 TransAtlantic Inter Society Consensus (TASC). Management of peripheral arterial disease (PAD). J Vasc Surg 2000; 30: 1–296 Yancey A, Minion D, Rodriguez C et al. Peripheral atherectomy in transatlantic intersociety consensus type C femoropopliteal lesions for limb salvage. J Vasc Surg 2006; 44(3): 503–9
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35. 36.
37. 38.
Zeller T, Rastan A, Sixt S et al. Long-term results after directional atherectomy of femoro-popliteal lesions. J Am Coll Cardiol 2006; 48(8): 1573–78 Wholey M, Toursarkissian B, Postoak D et al. Early experience in the application of distal protection devices in treatment of peripheral vascular disease of the lower extremities. Catheter Cardiovasc Interv. 2005; 64(2):227–35 Suri R, Wholey MH, Postoak D et al. Distal embolic protection during femoropopliteal atherectomy. Catheter Cardiovasc Interv 2006; 67(3): 417–22 Rocha-Singh K, Jaff M, Crabtree T et al. Performance goals and endpoint assessments for clinical trials of femoropopliteal bare nitinol stents in patients with symptomatic peripheral arterial disease. Catheter Cardiovasc Interv 2007; 69(6): 910–9
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I Henry, M Henry, and M Hugel
Introduction Balloon angioplasty alone or completed with stent implantation is the most effective procedure to treat peripheral arterial diseases. However, this technique is still limited by the complexity of certain lesions (e.g. calcified, long, bifurcated, diffuse, and those in small vessels). High-speed rotational ablation has been developed as a means of removing rather than simply displacing the occluding atherosclerotic material. It was postulated that this debulking process would improve results as compared to balloon dilatation. The RotablatorTM (Boston Scientific, Natick, MA) was developed by David Auth and used for the first time in humans by Zacca.1
Technique Description The Rotablator is a flexible, non-radio-opaque catheter fitted with a diamond-encrusted metal burr that selectively cuts away inelastic tissue during high-speed rotation. The catheter, which tracks coaxially over a 0.009-inch (0.23 mm) guidewire to prevent deflection, is encased in a 4.3-French sheath that protects the vessel wall during drive shaft rotation. Saline is infused through this sheath to lubricate and cool the catheter, burr, and guidewire. The drive shaft is connected to a compressed air turbine that rotates the burr at speed varying from 50,000 to 200,000 rpm. The diameters of available burrs range from 1.5 to 4.5 mm. Patient preparation On the day prior to the procedure, patients receive ticlopidine (500 mg) or clopidogrel (75 mg), aspirin (250 mg) and vasodilators (180 mg diltiazem and/or 60 mg nifedipine). In addition to the standard preangioplasty baseline testing, measurements of free hemoglobin (blood and urine), haptoglobin, and lactic dehydrogenase are made to monitor hemolysis that may be provoked by rotational ablation. During the procedure 5000 to 10,000 units of heparin are given. Approach techniques All procedures are carried out under local anesthesia and neuroleptanalgesia. The most frequently used access technique to
treat femoral, popliteal, or distal artery lesions is the ipsilateral antegrade femoral approach. An introducer is selected to accommodate the maximum size of the burr to be used (maximum size of the burr multiplied by 3 equals the French size of the introducer). For the percutaneous access, a 9-French is usually the largest sheath used in our facility (allows passage of a 3-mm burr). Once the introducer is in place, baseline imaging is conducted, including control angiography as well as endovascular ultrasound and/or angioscopy. The 0.009-inch guidewire is carefully passed through the lesion site(s) as far as possible down the artery so that any complications (spasm, distal embolism) may be dealt with promptly. If the femoral artery is tortuous or if there is a stenosis at the origin of the anterior tibial artery, a straight or angled 4-French catheter can be used to cross the proximal obstacles and/or to strengthen the guidewire. When selecting the first burr, the diameter is usually 75–85% of the arterial diameter below the stenosis. With the guidewire positioned, this burr is slowly advanced along the wire to about 1 cm above the stenosis (because the burr advances spontaneously when rotation begins). The rotational speed should not be allowed to dip below 2000–5000 rpm, and ablation sequences must be short (15–30 seconds) to reduce heat accumulation and ensure appropriate downstream dispersion of the particles produced. The total rotation time depends on the lesion (15–450 seconds in our experience), but a note of caution is warranted. Inasmuch as the total ablation time has a major influence on hemolysis, spasm frequency, and distal embolism, rotation time must be strictly limited. Once the lesion has been cleared with the Rotablator, the burr is withdrawn, and angiography is used to evaluate the results. If the remaining stenosis is > 50%, a larger burr is used. If < 20% luminal narrowing remains, the procedure is stopped. Residual stenoses between 20 and 50% are always treated by adjunctive balloon dilatation. As a rule the results of Rotablator therapy in the femoral segment are always insufficient, whereas in the distal arteries the outcome is almost always adequate. If a complementary dilatation is necessary, the balloon chosen is equal in diameter to the size of the nondiseased artery, and the inflation pressure must remain below 4–5 atmospheres. This low pressure is sufficient to remove the residual stenosis while avoiding a dissection. A completion angiogram documents the final results at the treatment site(s) as well as the distal run-off. If no thrombogenic incident occurred during the procedure, the introducer is immediately withdrawn, and 59
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the post-operative care of the patient ensues as for other peripheral angioplasties. However, in addition to clinical and Doppler surveillance, the hematologic tests must be repeated to check for hemolysis. If this occurs, the patient is hydrated, and a bicarbonate solution is infused. Other approach techniques may sometimes be used with the Rotablator. For example, the retrograde femoral procedure is required to treat iliac lesions. However, the size of this artery requires large burrs and introducers that increase procedural complications. The retrograde popliteal approach, on the other hand, is excellent for treating common femoral artery lesions and stenoses at the origin of the superficial femoral approach. In this technique, a 7-French or 8-French introducer is inserted to accommodate up to a 2.5 mm burr if long, calcified femoral lesions are to be treated. The procedure is the same as the one described above. Alternatively, the contralateral femoral approach can be used to treat lesions at the femoral bifurcation, in the common femoral artery, or at the origin of the SFA or profunda. An 8French or 9-French guiding catheter may assist in crossing the aortic bifurcation. The guidewire is placed far into the contralateral SFA or profunda, and the burr is gently advanced along the guidewire. In particular, this approach allows access to sites (e.g. femoral bifurcation) that were heretofore unapproachable by other standard techniques except surgery. The popularity of the radial or the brachial approach for balloon dilatation would appear feasible for rotational atherectomy treatment.
on the other hand, are always treated sequentially with a few days interval between treatments to minimize the side effects. In the case of an arterial occlusion, it is generally impossible to pass the Rotablator guidewire, and a channel must first be created through the obstruction. Currently, in 70–90% of cases, it is possible to recanalize with a hydrophilic guidewire, certain laser devices, or other recanalization devices. After creating a channel, the Rotablator guidewire can be inserted using a 4-French or 5-French catheter. Because even a recanalized calcified occlusion may not respond to balloon dilatation, the Rotablator can effectively debulk the lesion, reducing the delamination risk and possibly avoiding the need for a stent. It is preferable to use incrementally sized burrs to progressively pulverize the atheroma, and there should be no hesitation in using smaller burrs if resistance is encountered. Whereas recanalization of SFA occlusion remains controversial, the evolving Rotablator techniques for distal lesions require that the SFA remain open for access to these distal arteries. The immediate use of the Rotablator after angioplasty failure has not been investigated thoroughly. Poor radiological visibility may predispose to a high risk of complications, for example, dissection extension, perforation, or plaque embolism. Intraluminal imaging techniques, such as angioscopy or intravascular ultrasound, may assist in the decision to perform a simultaneous procedure; however, when there is doubt, it is preferable to wait until the lesion has healed before using this technique.
Special treatment scenarios Multilevel disease (Figure 11.1) in the femoropopliteal and distal segments may be treated concurrently with endovascular techniques. The Rotablator guidewire is placed down the leg artery, and proximal lesions are treated first. Bilateral lesions,
Personal experience
(a)
(b)
We have a large series of patients treated with Rotablator. Then we can draw some conclusions about indications, results, complications, and mid-term results of this technique.
(c)
Figure 11.1 (a) Arteriogram showing a very tight popliteal stenosis; (b) arteriogram at the origin of the anterior tibial artery; (c) after treatment with the Rotablator and balloon dilatation, both lesions show satisfactory flow.
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Percutaneous peripheral atherectomy using the Rotablator Table 11.1
Patient characteristics
Characteristics parameters
No. of patients
Risk factors: Diabetes Multivascular diseases (cerebral, coronary, renal, abdominal aorta) Previous vascular surgery Clinical stage: Moderate claudication Severe claudication Rest pain Minor tissue loss, no healing ulcer Run-off status: Number of occluded arteries: 3 2 1 0 Number of stenosed arteries (≥ 50%): 3 2 1 0
48 (32%) 128 (85%) 32 (21%) 16 (11%) 98 (65%) 28 (24%) 8 21 40 40 49 76 28 18 28
150 patients; mean age (years): 73 ± 1 (range 42–90) 94 male; mean age (years): 68 ± 1 (range 42–86) 56 female; mean age (years): 77 ± 1 (range 61–90)
Patient information A total of 150 patients (94 males, 56 females; mean age 73 ± 1 year, range 42–90) were candidates for percutaneous rotational ablation in the lower limbs. Details of the patient population are shown in Table 11.1. Thirty-two percent of the patients were diabetic, 85% had other atherosclerotic disease (cerebrovascular, coronary, renal). Twenty-one percent had undergone previous vascular surgery. Sixty-five percent had severe claudication, and one-quarter of the patients had rest pain and/or ulceration. Adequate run-off (no stenosis > 50% in three vessels) was present in only 28 patients (19%) and 51% of the patients had flow-limiting disease in all three distal arteries. Eighty-nine patients (59%) were being evaluated for failure to show improvement with other techniques (angioplasty, surgery, medical treatment), 39 patients (26%) for symptom progression or limb salvage, and the remainder for angioplasty restenosis or for the treatment of distal lesions in multilevel endovascular procedures. Techniques All 150 patients underwent rotational atherectomy using the Rotablator according to the methods described above. A total
Table 11.2
of 212 lesions were attempted in the iliac, femoral, popliteal, or distal arteries (Tables 11.2–11.4). There were 193 stenoses (91%) and 19 chronic occlusions; 93% were calcified, and 63% were located at important bifurcations or collateral branch origins. Fifty percent of the lesions were located below the knee. The length of the lesions varied from 1 to 20 cm, 17% of the treated lesions were longer than 7 cm, 25% were between 4 and 6 cm, and 58% were smaller than 3 cm. The lesions at the femoral level were significantly longer than those in other segments (5.70 ± 0.40 cm vs. 2.97 ± 0.30 cm) (p < 0.001). The maximum number of lesions treated in one patient was four. There was no difference between the male and the female population regarding the characteristics or location of the lesions, but the average number of treated lesions was lower in males (1.35 lesion per patient) than in females (1.53 per patient). The approach techniques used and incidences of concomitant procedures are listed in Table 11.5. One lesion in an anterior tibial stenosis was excluded when a guidewire failed to pass successfully. Rotational ablation alone was used to treat 16 patients (19%) at the femoral level, 9 (47%) at the popliteal level and 92 (87%) at the distal artery level. Adjunctive dilatation was necessary in 70 patients (81%) at the femoral level, 10 (53%) at the popliteal level, and 14 (13%) at the distal leg artery level (Figure 11.2). Figures 11.1 and 11.3–11.6 show some results at different locations. Procedural success Seven procedures failed subsequent to intra-procedural complications (see below). Therefore, the immediate technical success by lesion was 97% (95% by patient). Figure 11.7 summarizes the percentage stenosis before and after Rotablator and following adjunctive dilatation at the femoral, popliteal, and distal arterial levels. Residual stenosis after Rotablator was higher at the femoropopliteal levels (44%) than in the distal segment (p < 0.01), due to the burr-to-vessel diameter ratio, which was 80.8 ± 1.6% at the distal level but only 61.1 ± 2.6% at the femoropopliteal levels (p < 0.001). Complications There were 37 intra-procedural complications (25%) related to the Rotablator treatment (Table 11.6). Among these, arterial spasm (17 cases; 11%) comprised the majority of these events. It occurred more frequently in the distal arteries (15; 88%) than in the femoropopliteal segment (p < 0.02), but it was successfully treated in most patients (16/17). Twelve thromboses (8%) were encountered; eight were successfully treated by fibrinolysis. Dissections and perforations occurred
Lesion characteristics
Bifurcation or branches Calcified Occluded Stenosed
No.
Percent
134 192 19 193
63 93 9 91
61
Above knee (%) 62 98 14 86
Below knee (%) 64 87 4 96
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Lesion characteristics by location
Location
No.
Iliac Femoral Popliteal Tibioperoneal Trunk Posterior tibial Peroneal Anterior tibial Total Total
1 86 19 38 7 16 45 106 212
Mean length (cm)
Range
Mean % stenosis
Range % stenosis
12 5.7 ± 0.40 2.40 ± 0.30
1–15 1–6
84 ± 2 86 ± 3
100 60–100 75–100
2.6 ± 0.2 2.6 ± 0.6 2.4 ± 0.3 3.4 ± 0.6 2.9 ± 0.3 4 ± 0.2
1–6 1–5 1–4 1–20 1–20 1–20
85 79 82 82 83 83
± ± ± ± ± ±
70–100 70–90 75–99 60–100 60–100 60–100
rarely (3%), as did distal embolism (two cases; 1.3%), one of which was successfully treated by aspiration). Two instances of no-reflow phenomena were observed and treated. In the immediate post-operative period, there were seven (5%) cases of hemogloburinia and two cases (1.3%) of transitory renal insufficiency. They were resolved within 24 hours without any consequences. Follow-up The mean observation period for this population was 14.4 ± 1 months (range 1–51). One hundred and twenty-five patients were available for = 4-month follow-up evaluation (this cohort did not differ significantly in gender, age, risk factors, or location/type of lesions from the initial population). Of these, 114 patients underwent angiography at 4 months in addition to clinical evaluation and Doppler examination. Of the remaining 44 patients, 4 patients were lost to follow-up, 3 died, and 4 were excluded because they had stent implantation. In these 114 patients, 163 lesions (77% of original treatment group) were re-examined: 123 (76%) were patent with a residual percent stenosis of 17 ± 1.1%, and 40 arteries (24%) showed restenosis (= 50% luminal narrowing) of 82 ± 2.1%, as shown in Table 11.7, the restenosis rate was highest at the femoral level. Restenosis was more frequent for all lesions longer than 7 cm (p < 0.001) (Table 11.8) and at both the femoropopliteal level (55 vs. 19% of < 7 cm; p < 0.03) and the distal segment (80 vs. 18%; p < 0.01).
1 2 2 1 0.7 0.7
stretches the arterial wall. The Rotablator, on the other hand, does not crack the plaque or deform the vessel wall, as is shown by radiological, histological, angioscopic, and ultrasound studies.2–4 Rather, the Rotablator has an abrasive action that removes the obstructing material, preferentially ablating rigid, calcified atherosclerotic tissue while leaving healthy elastic tissue intact.4–5 This differential cutting produces a lumen that is smooth and polished in appearance. Despite the device’s preference for inelastic tissue, however, the endothelium adjacent to a lesion can suffer damage during progression of the burr. The same situation is encountered with a balloon whose length is greater than the stenosis; both may alter the endothelium on either side of a stenosis. As opposed to balloon treatment, however, the Rotablator rarely injures the media,2 an event that has been reported to be the impetus for intimal hyperplasia and restenosis. Whereas it is simple to select a balloon sized to match the lesion and artery, it is not so for rotational atherectomy. Using large-diameter introducers (> 9-French) to accommodate the percutaneous introduction of burrs > 3 mm would significantly increase the rate of access site complications. Dorros et al.,6 for example, used burrs up to 4.5 mm requiring a 14-French introducer for renal arteries. However, their incidence of local and systemic complications were considerable (e.g. 23% hematoma, 5% perforation, 63% hemoglobinuria). From our own experience and these early reports, we now treat only arteries < 6 mm in diameter using up to a 3-mm burr; this gives us residual stenosis of < 50%.
Discussion The mechanism of rotational ablation differs completely from that of balloon dilatation. In the latter, compression of the lesion promotes rupture of the atherosclerotic plaque and Table 11.4
Above knee Below knee Total
Lesion lengths by location < 3 cm
4–6 cm
> 7 cm
45 (42 %) 77 (72 %) 122 (58 %)
30 (28 %) 24 (23 %) 54 (25 %)
31 (30 %) 5 (5 %) 36 (17 %)
Table 11.5
Procedural details
Parameters Approaches: Ipsilateral femoral Contralateral femoral Popliteal Bilateral Atherectomy associated with: Femoral lesion dilatation Popliteal lesion dilatation Distal lesion dilatation
No. of patients 141 5 4 20 14 2 3
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151 patients 1 unsuccessful attempt 150 patients (212 lesions)
86 femoral
Alone 16 (19%)
Figure 11.2
19 popliteal
+PTA 70 (81%)
Alone 9 (47%)
Figure 11.3
Alone 92 (87%)
+PTA 14 (13%)
Treatment with Rotablator alone and with adjunctive balloon dilatation by vessel segment.
This interdiction against rotational ablation in arteries > 6 mm has necessarily limited our experience with the Rotablator at the iliac level. In the one iliac artery we have treated, the vessel was very calcified. Even though a hydrophilic guidewire passed the lesion, the balloon could not be advanced. In this case, we used the 3-mm Rotablator to debulk the lesion, producing a channel to facilitate balloon dilatation. In our experience, adjunctive dilatation is necessary at the femoral level to obtain satisfactory immediate results. This is not the case at the distal segment, where we have usually been able to introduce a burr equal to at least 80% of the arterial diameter. This burr-to-artery diameter ratio may explain our lower restenosis rate at the distal level (21%) compared to the higher rate in the SFA (36%), and in particular, when balloon angioplasty did not follow Rotablator ablation. At present, our series is too limited to offer conclusive proof, but it would seem that the use of adjunctive balloon dilatation might reduce the restenosis rate at the femoral level. Such an observation has been made at the coronary level by Bertrand et al.7 in a collaborative study of 129 patients treated
(a)
+PTA 10 (53%)
106 distal leg arteries
with the Rotablator alone, the rate was 46%, as opposed to only 30% when complementary balloon angioplasty was used. The same effect may occur at the peripheral level, but we have not studied this possibility. Insofar as determining an optimum technique for rotational ablation, we have used three treatment protocols: 1. Beginning the procedure with burrs and increasing the size until an optimal result is reached, with the burr size closely approaching that of the arterial diameter; 2. Initially using a single large burr equal to 75–80% of the arterial diameter; 3. Simply debulking the lesion using a small burr to remove inelastic material, then dilating the vessel at low pressure with a balloon that matches the diameter of the artery. Only for treatment of distal arteries have we developed a preference among these. We believe that it is advisable to use incrementally sized burrs that approach at least 80% of the artery’s diameter. This avoids the need for balloon dilatation and reduces the risk of dissection.
(b) (a) Multiple, severe, anterior tibial, and peroneal stenoses; and (b) the result after Rotablator therapy is excellent.
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(a)
(b)
Figure 11.4 (a) A very tight stenosis exists distal to a femoropopliteal bypass graft; and (b) satisfactory outflow has been re-established with the Rotablator.
The same opinion does not apply, however, to the femoropopliteal arteries or those with diameters > 3 mm. In these larger arteries, it would appear preferable to routinely complete the procedure with balloon dilatation to ensure residual stenosis of no more than 20% in order to limit the incidence of restenosis. Unlike balloon angioplasty, the Rotablator appears to be particularly well suited to deal with calcified and/or eccentric lesions and stenoses at bifurcations or in tortuous arteries. Further, the Rotablator may be useful for the treatment of severe, extensive lesions; by reducing the plaque burden,
(a) Figure 11.5
balloon dilatation may be applied with less risk of dissection. One situation in which the Rotablator must not be used is in the presence of thrombus; chronic thrombus tends to deflect away from the rotating burr, leading to suboptimal results. In terms of outcome, our procedural success with Rotablator therapy in the limb arteries has been high (97%). Other investigators have reported similar results in the 92–95% range.4,6,8,9 However, the published results of a multicenter trial (CRAG) of the Rotablator found only a 77% angiographic success in 107 lesions treated in 72 patients.10 This is not surprising when one considers that only half as
(b) (a) A severe lesion at a bifurcation; (b) results after Rotablator.
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(a)
(b)
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(c)
Figure 11.6 (a) Lesions in the superficial femoral artery and in the popliteal artery; (b) results after Rotablator; and (c) results after balloon angioplasty.
90
87
86
83
80 70 Before
60 50
After Rotablator After Dilatation 44
40
38
30 19
20 10
10
5
3
0 Femoral (n = 86)
Figure 11.7
Popliteal (n = 19)
Distal arteries (n = 106)
Percent stenosis before and after Rotablator and after adjunctive balloon dilatation.
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Table 11.6
Complications according to lesion location (above and below knee)
Ablation site: Spasm Thrombosis Dissection Perforation Distal emboli No reflow Total
Above knee
Below knee
No. cured/ No. total
2 6 1 0 1 2 12
15 6 2 1 1 0 25
16/17 8/12 3/3 0/1 1/2 2/2 30/37
many patients were treated by several physicians in three centers as represented in our single-center study. Clearly, the inevitable learning curve and operator inexperience with the technique probably contributed to these somewhat poorer procedural results. Moreover, their patient population had more advanced disease (56% limb-threatening ischemia vs. 24%), and the lesions treated were twice as long (9 cm average vs. 4 cm). Given that the Rotablator would often be applied in complex lesions unsuitable to other interventions, the complications inherent to the procedure seem acceptable, and most can be easily treated. Overall, in our study, no particular complication was statistically linked to gender, age, or lesion location. However, the frequency of complications at the ablation site seemed to be influenced by the length of the treated lesion (< 6 cm: 15%; > 6 cm: 85%). The most frequent complication we have encountered is arterial spasm (11%), which occurs more often in the distal arteries and for 2 or 3 cm proximal to the treatment site. Of particular note is the fact that the incidence of spasm appears to be related to operator experience. Indeed, spasms occurred at a rate of 14% during our first 50 procedures, decreasing to 8% over the next 50 cases, and finally ending at 2% (p < 0.05). Although some operators have postulated that arterial spasm may be caused by vibrations transmitted to the guidewire during rotation or to the liberation of vasoconstrictive substances contained with the plaque, endothelium, or blood cells, we are of the opinion that is dependent upon technique. In our experience, spasm appears most frequently when too large a burr is used, the rotation sequences are too long, or the rotation speed is too fast or too slow. Also, spasm will occur if the burr becomes entrapped in the wall or the drive
Table 11.7
shaft is deflected by a bent guidewire (the rotation drive shaft irritates the adjacent arterial wall). To prevent spasm, all patients are placed on vasodilators the day before the treatment. During the procedure, we routinely inject molsidomine and nitrates intra-arterially. If a spasm occurs, the same drugs are re-injected. If this medical treatment fails, low-pressure balloon dilatation is performed, which usually relieves the spasm in most arteries. Our acute thrombosis rate has been low (5.6%); almost half that reported in the multicenter trial.10 Moreover, most of these have been successfully treated either by thrombolysis, thromboaspiration, or thromboembolectomy. A number of factors may predispose to thrombosis: a residual stenosis, an intimal flap, elastic recoil, dissection, lengthy lesion, or vasospasm. Once the artery is reopened, low-pressure balloon dilatation may be attempted. The incidence of dissection, perforation, or angiographically visible flaps has been rare (< 2%), and these were encountered at the beginning of our experience. Because these complications are caused by the guidewire or the burr, they can be circumvented by cautious wire manipulation to prevent subintimal incursion and by prudently selecting the burr, avoiding a too-large diameter for the vessel. Although the Rotablator produces fine particles (5–180 µm) that are disseminated in the peripheral circulation,2,5 we have observed only two cases (1.3%) of distal embolism from particulate migration, and thromboaspiration was effective in treating one case. Other authors have experienced this complication at a much higher rate. Ahn et al.,8 for example, encountered emboli in 20% of their cases, but these were coincident to long lesion treatment with large burrs (4.0–4.5 mm). Not surprisingly, the CRAG trial reported a 10% incidence of emboli for the same reasons. Hemolysis, another complication related to rotational atherectomy, appears more or less constant with this technique, due to destruction of the red blood cells by the burr rotation. The intensity of this response is proportional to the ablation time, size of the burr, and length of the treated lesion. According to a study we performed following 54 patients at time intervals up to 24-hours post-atherectomy, we saw an increase in free hemoglobin, a drop in haptoglobin, and a rise in lactic dehydrogenase within the first 5 minutes following the procedure. The phenomenon was transitory, reversible, and usually without attendant complications, but in two of our cases, there was a slight transitory renal failure that resolved within 48 hours. Our 5% rate of hemoglobinuria is again less than half that reported in the CRAG trial (13%).
Number of location of restenosed and patent arteries in follow-up period (n = 163) Patent
Restenosed
No.
Femoral Popliteal Distal All
19 1 20 40
% stenosis 80 90 84 82 ± 2.1
Mean length 6.5 ± 0.8 2 4.9 ± 1.2 5.6 ± 0.7
No.
% stenosis
34 14 75 123
20 18 15 17 ± 1.1
Mean length 4.9 ± 0.5 2.1 ± 0.3 2.4 ± 0.2 3 ± 0.2
% restenosis 36% 7% 21% 24%
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Percutaneous peripheral atherectomy using the Rotablator Table 11.8
Relationship of restenosis to lesion length Femoral and popliteal
Mean length > 7 cm < 7 cm
67
p < 0.001
Distal artery
Restenosed
Patent
Percent
Restenosed
Patent
Percent
11
9 p < 0.03 39
55
4
80
19
16
1 p < 0.01 74
9
One other complication we encountered in two cases was slow flow or no reflow, a phenomenon seen in coronary angioplasty when the contrast agent ceases to flow, although no thrombus, flap, or spasm is visible. Several mechanisms have been proposed for this, from capillary obstruction by atherosclerotic or thrombotic embolism to interstitial edema. In the case of the Rotablator, however, cavitation may produce microbubbles that temporarily block outflow.11 Indeed, in our cases, stagnation of the contrast medium downstream in the popliteal artery followed successful atherectomy in the SFA. The phenomenon disappeared 2–3 minutes after the injection of molsidomine and nitroglycerine. No distal embolism was visible after contrast medium washing. As compared to the CRAG trial, our overall 25% complication rate is half what they observed, and the better part of our complications (46%) were due to spasm, a sequel the CRAG report did not even mention. This difference is particularly noteworthy when one considers that 21 of the 79 atherectomized limbs (27%) in their cohort required urgent or emergent surgical therapy, including two amputations. We have encountered nothing like this in our experience, and it is important to recognize that the CRAG trial was testing the gamut of Rotablator burrs in extremely long lesions (40 cm) requiring up to 35 minutes of rotation time! In these circumstances, neither their results nor their complication rates are surprising. Early in our experience, we recognized that protracted rotational ablation was inadvisable, and we restricted the rotation time whenever possible. Regarding our follow-up results, we have amassed angiographic data on 91% of our patients who were 4-months posttreatment. These data have shown that the restenosis rate is relatively low (24% overall), considering the severity of the initial pathology. This is comparable to the 66% primary patency at 6 months reported by Ahn et al.8 Both the site of the lesion and the length of the segment treated influenced restenosis. For lesions > 7 cm, the rate was very high, and complications were four times as frequent in lesions < 6 cm. This relationship between lesion length and restenosis is, however, not unique to rotational ablation. Other authors have reported a similar correlation for balloon angioplasty.12 Supported by these statistics, we feel that Rotablator therapy should be limited to lesions = 6 cm. If restenosis does occur, repeat treatment should be carried out without hesitation, either with the same procedure or a different technique. In our experience, this produces marked improvement in the secondary patency. This early re-intervention is possible only if regular follow-up is maintained to facilitate early diagnosis, thus avoiding or at least postponing surgery. It is difficult to compare the results of one technique with those of another because the lesions treated are often different.
18
Certainly, in terms of procedural success, the Rotablator is comparable to other atherectomy techniques4,8 and balloon angioplasty.12 However, perhaps the advantage of rotational ablation lies in its ability to enlarge the treatment potential for percutaneous interventions as a whole. Certain lesions cannot be treated by balloon dilatation alone, so the Rotablator is an important auxiliary technique that enhances our interventional capabilities overall. Further, the Rotablator allows percutaneous treatment of other lesions that until now had been impossible to treat non-surgically or posed higher risks with either endovascular or surgical techniques. Moreover, the potential to treat run-off vessels using this method should improve the long-term patency of iliofemoropopliteal bypasses and proximal angioplasties. Other techniques may make such claims as well. Lasers, either excimer or holmium, would also be capable of treating long, eccentric, calcified, ostial or bifurcation lesions.13,14 However, the complication rate appears to be no lower, particularly for spasms in excimer-treated arteries, and the costs of a laser are far greater than an atherectomy device. Moreover, long-term patency rates are disappointing as noted in the LACI trial. The holmium laser can be used in the presence of thrombus, which is an advantage over the Rotablator, but here again the expense of the laser versus the cost of thrombolytic therapy preliminary to Rotablator therapy is unquestionably greater. Directional atherectomy using the Simpson/Silverhauk atherectomy may be preferred to the Rotablator in certain cases of ostial or bifurcation lesions and in short eccentric lesions.16 Its manipulation is more taxing and particularly difficult in tortuous arteries. Moreover, the risks are greater, particularly at the distal level, and the restenosis rate is high.17 The transluminal extraction catheter (TEC) could compete with the Rotablator in certain disease pathologies, most notably for the treatment of focal stenoses and bypass lesions where thromboses are likely to be encountered. However, the device does not perform well in calcified vessels.18 The Rotarex catheter at the femoropopliteal level could also compete with the Rotablator but it is not proved that it is as effective for very calcified lesions.
Conclusion The treatment of long, diffuse, calcified femoropopliteal lesions remain challenging. Debulking with Rotablator could be very useful before angioplasty alone or maybe in the future before placing bare stents or stent grafts.
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The treatment of leg arteries in cases of critical limb ischemia remains a very challenging topic for interventionists. Among the tools available the rotational atherectomy appears to be a useful alternative to other techniques or surgical revascularization especially for the worst cases of infrainguinal occlusive diseases. Dormal et al. recently gave a review of the literature and analysis of their results,19 and underscore on the usefulness of this device for limb-threatening arterial occlusive disease. Also recently, Tamashiro et al. pointed out the role of the Rotablator to treat a patient in critical leg ischemia with long occlusion of the three infrapopliteal vessels.20 The anterior tibial artery was
treated with retrograde Rotablator atherectomy by an open approach though the pedal artery resulting in full patency of the anterior tibial artery and healing of the skin lesions. Our results and these recent data should encourage us to broaden the indications for this technique in leg arteries. The main limitation remains its cost; the catheters are expensive, and when multiple burrs are needed the procedural costs can rise. Without this drawback, it is probable that a far greater number of angioplasties would be preceded by rotational atherectomy. However, this enthusiasm must be tempered by the necessity for sound theoretical and practical knowledge of the device before approaching complex lesions.
REFERENCES 1. Henry M, Amor M, Ethevenot G et al. Percutaneous peripheral rotational ablation using the Rotablator: immediate and mid-term results. Single center experience concerning 146 lesions treated. Int Angiol 1993; 12: 213–44 2. Ahn SS, Auth DC, Marcus DR et al. Removal of focal atheromatous lesions by angioscopically guided high speed rotational atherectomy: preliminary experimental observations. J Vasc Surg 1988; 7: 292–300 3. Ahn SS. Angioscopic controlled atherectomy. In: White GH, White RA, eds. Angioscopy Vascular and Coronary Applications. Chicago: Year Book Medical Publishers, 1988: 114–22 4. Ahn SS, Eton D. The Rotablator high-speed rotary atherectomy: indications, technique, results and complications. In: Ahn SS, Moore WS, eds. Endovascular Surgery, 2nd edition. Philadelphia: WB Saunders, 1992: 295–307 5. McLean GK. Percutaneous peripheral atherectomy. J Vasc Intervent Radiol 1993; 4: 465–80 6. Dorros G, Iyer S, Zaitoun R et al. Acute angiographic and clinical outcome of high-speed percutaneous rotational atherectomy (Rotablator). Cathet Cardiovasc Diagn 1991; 22: 157–66 7. Bertrand ME, Lablanche JM, Leroy F et al. Percutaneous transluminal coronary rotary ablation with Rotablator (European experience). Am J Cardiol 1992; 69: 470–74 8. Ahn SS, Eton D, Yeatman LR et al. Intra-operative peripheral rotary atherectomy: early and late clinical results. Ann Vasc Surg 1992; 6: 272–80 9. White CJ, Ramee SR, Escobar A et al. High speed rotational ablation (Rotablator) for unfavourable lesions in peripheal arteries. Cathet Cardiovasc Diagn 1993; 30: 115–9 10. The Collaborative Rotablator Atherectomy Group (CRAG). Peripheral atherectomy with the Rotablator: a multicenter report. J Vasc Surg 1994; 19: 509–15
11. 12. 13. 14. 15.
16. 17. 18.
19. 20.
Zotz RJ, Erbel R, Philipp A et al. High-speed rotational angioplasty induced echo contrast in vivo and in vitro optical analysis. Cathet Cardiovasc Diagn 1992; 26: 98–109 Capek P, McLean GK, Berkowitz HD. Femoropopliteal angioplasty: factors influencing long-term success. Circulation 1991; 83(suppl I): I70–80 Litvack F, Grundfest WS, Adler L et al. Percutaneous excimer-laser and excimer-laser-assisted angioplasty of the lower extremities: results of initial clinical trial. Radiology 1989; 17: 331–35 McCarthy WJ, Vogelzang RL, Nemcek AA et al. Excimer laserassisted femoral angioplasty: early results. J Vasc Surg 1991; 13: 607–14 Laird JR. Peripheral excimer laser angioplasty (PELA) trial results. Paper presented at the Transcatheter Cardiovascular Therapeutic (TCT) Conference, September 24–28, 2005, Washington DC Gammo R. Plaque excision treatment of infrainguinal PAD. Endovasc Today 2005; 4: 70–4 Hinohara T, Selmon MR, Robertson GC et al. Directional atherectomy: new approaches for treatment of obstructive coronary and peripheral vascular disease. Circulation 1990; 81(suppl III): II79–III91 Wholey MH, Levitt RG, Fein-Millar D. The Transluminal Endarterectomy Catheter: indications, techniques, results and complications. In: Ahn SS, Moore WS, eds. Endovascular Surgery, 2nd edn. Philadelphia: WB Saunders, 1992: 308–15 Dormal PA, Afropoli AM, Dervaux P. Rotablator: a forgotten tool in limb ischemia. Acta Chir Belg 2005; 105: 231–34 Tamashira A, Villegas M, Tamashiro G et al. Retrograde Rotablator in limb salvage: a new technique using an open approach. Cardiovasc Intervent Radiol 2006; 29: 854–6
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A new rotational thrombectomy and atherectomy catheter: the Rotarex system I Henry, M Henry, and M Hugel
Introduction Balloon percutaneous transluminal angioplasty (PTA) has a major role in the treatment of coronary and peripheral significant stenoses and is now the first treatment to be proposed. Nevertheless, this technique alone has some limitations in its application to some specific subgroups of complex lesions, such as calcified, ulcerated, eccentric, long lesions, and thrombotic lesions with the risk of embolization. There is also the problem of restenosis, with a high restenosis rate in some locations (e.g. femoropopliteal arteries, small vessels, ostial lesions, lesions at bifurcations, long lesions, diabetic patients, etc). Several techniques have been proposed to reduce the restenosis rate and to treat some lesions not amenable to balloon angioplasty alone, such as stenting and debulking techniques with atherectomy devices. Atherectomy is defined as excision and removal of obstructive tissue, a concept first introduced by Simpson et al.1–3 The amount of plaque burden in the artery correlates with the restenosis rate. So, by creating a large, smooth lumen and by preventing elastic recoil, rather than increasing luminal diameter by arterial stretching and plaque fracture, as with balloon angioplasty, debulking could yield better clinical outcomes and short- and long-term patency rates. The first directional atherectomy procedure was performed in 1985 by Simpson et al. in a superficial femoral artery using a peripheral atherectomy device. This initial experience demonstrated the safety of directional atherectomy for peripheral vascular disease.4 It was approved by the US Food and Drug Administration (FDA) in 1987. This device was then adapted for coronary procedures and the directional coronary atherectomy (DCA) device was approved by the FDA in 1990 as the first non-balloon percutaneous coronary interventional device. In contrast to DCA, which relies on excision and tissue removal, the transluminal extraction–endarterectomy catheter (TEC) (Interventional Technologies Inc., San Diego, CA) was designed by Stack to cut and aspirate atheroma and debris. In 1989, this device was approved by the FDA for peripheral vascular disease, and in 1992 for revascularization of saphenous vein bypass grafts and native coronary arteries. Other devices have been proposed, for example the Rotablator,5 the Simpson AtherotrackTM,6 the Pullback Atherectomy Catheter,7 and more recently the SilverHawk® atherectomy device.8
A new device has been recently proposed, the Rotarex device (Straub Medical, Wangs, Switzerland), which is a rotational atherectomy catheter now in competition with other atherectomy devices. The device is also a rotational thrombectomy system combining two essential effects: mechanical clot fragmentation and removal of the fragmented material from the vessel under negative pressure, which purports to prevent peripheral embolization. This device is used to treat acute and subacute thrombotic occlusions of native vessels and bypass grafts. It competes with rheolytic thrombectomy catheters (e.g. Hydrolyser, Oasis, Angiojet) which employ a retrograde jet of fluid oriented toward the central lumen of the catheter to destroy clots by the Venturi effect, and with other devices which employ the vortex effect like the Amplatz thrombectomy catheter, the Arrow-Trerotola percutaneous thrombolytic device (PTD) or the Baxter percutaneous mechanical thrombectomy device (PMT) and which pulverizes thrombotic material in contact with the end of the catheter.9–20 We will describe these two applications of this new Rotarex system.
Rotarex system Description: equipment and mechanism of action The system has three components: ● ● ●
the Rotarex catheter; a 40 W D.C. electric motor drive; an electronic control unit.
Inside the whole length of the 8-French polyurethane catheter rotates a coated stainless steel spiral, which glides over a 0.020inch guidewire. The catheter head consists of two cylinders that fit over each other. The outer rotating cylinder is fixed to the spiral; the inner one is attached to the catheter shaft. Each cylinder has two oval slits. The blunt tip of the outer cylinder is perforated for the guidewire. The catheter and motor drive are connected by a magnetic clutch. The motor rotates the spiral at 40,000 rpm, resulting in 80,000 cuts/minute. The high frequency of revolution creates a negative pressure at the catheter head of 5.8 kPa (43.5 mmHg). When the catheter is activated, soft and solid occlusion material is caught in the 69
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Figure 12.1 drive.
The Straub Rotarex catheter attached to the motor
slits, transported by the spiral to the proximal side port and discharged into a plastic bag. No additional suction is required. The transport of the occlusion material is done exclusively by the rotating spiral. The catheter is for one-time use, while the motor drive and the connecting cable to the electronic control unit can be sterilized. Preclinical studies The catheter was tested in an arterial model made of silicon tubing of 4, 6, and 8 mm inner diameter and length 15–30 cm, allowing observation and video documentation of the catheter function. The tubes were bendable to test the behavior of the catheter at various angles. The tubing was filled with occlusion material of different consistencies: (1) bovine blood that was allowed to coagulate for 48 hours or 2 weeks and stored at 4°C; (2) stamp cylinders of “black pudding,” a mixture of thrombus, muscle, fat, and connective tissue, 4, 6, and 8 mm thick, and 15-mm-long, simulating organized thrombus; (3) strips of bovine arteries (3 cm long, 1 mm broad) sutured intraluminally to the vessel wall, imitating intimal flaps. The tubing was clamped at one end and connected to an infusion line on the other, where a mixture of saline and glycerol could be infused under a continuous pressure of 120 mmHg. In this infusion tube an 8-French sheath (Cook, Bjaerverskov, Denmark) was introduced, a 0.020-inch Tefloncoated guidewire threaded through the occlusion material, and the catheter advanced. In a second test series (n = 72), the silicon tubing was replaced by fresh bovine carotid arteries with an average length of 20 cm and a diameter of 6–7 mm. The side branches were ligated and the arteries filled with the above-mentioned occlusion material. During catheter activation, tube and arteries were either kept straight or bent at different angles up
Figure 12.2
Electronic control unit.
Figure 12.3
Schematic draining of the catheter head.
to 50°. Occlusion of the arteries was achieved by tightening a 5-mm-wide rubber band around the vessel, completely interrupting the flow of perfusate. The occlusion was passed with the catheter over the wire. All tests were recorded on video. The time of catheter activation was recorded, the volume of aspirated fluid measured and the fluid passed through different filters for analysis of particle size. The arteries were cut open and examined visually and histologically for remnants of occlusion material and possible intimal damage. Results The catheter removed 48-hour-old thrombi in silicone tubing of 4- and 6-mm diameter completely and regularly; the maximum working diameter was 8 mm. On average, 1 cm of thrombus was aspirated within 2 seconds. Thrombi stored in the refrigerator for 2 weeks often showed adherence to the wall of the tubing, but could also be easily aspirated, leaving occasionally a thin residual layer attached to the inner curvature if the tube was bent. Occlusion material of higher and inhomogeneous consistency, such as muscle, fat and connective tissue, was caught readily in the catheter head and transported to the outside by the spiral. Fluid was aspirated at a rate of 1.5 ml/second. While fresh thrombus was completely homogenized, more solid material was cut into particles of 100–500 µm. Strips of bovine arteries, sutured intraluminally to the vessel wall to imitate intimal flaps, were cut and fragmented, leaving only small stumps at the suture site. Bovine arteries
Figure 12.4 The rotating outer cylinder glides over the inner fixed cylinder with its oval slits. The guidewire runs inside the transport spiral, which is attached to the tip of the perforated head of the outer cylinder.
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A new rotational thrombectomy and atherectomy catheter: the Rotarex system filled with thrombi or “black pudding” could be cleared of the occlusion material without remnants. No intimal damage was noticed on visual examination or after staining. When the arteries were compressed to complete occlusion by a rubber band, the catheter drilled a lumen corresponding to its shaft size. When tubing or arteries were bent, the catheter followed the guidewire smoothly. No perforation was noticed. The catheter needed fluid (blood) for lubrication. Under experimental conditions the temperature of the catheter head rose by 1.5°C after rotating for 4 minutes at 40,000 rpm in a tube of 3-mm diameter perfused with a saline–glycerol solution (80 ml/minutes) at room temperature.
Clinical studies as thrombectomy devices First pilot study Based on the results of the preclinical tests, the Institutional Review Board of the Department of Internal Medicine, University Hospital, Basel, accepted the protocol of a pilot study for the evaluation of the device for the treatment of thrombotic occlusions in femoropopliteal arteries in humans.21 Ten patients (eight women and two men; 58–87 years of age, mean age 70.6 ± 10.1) with acute or subacute occlusion of the femoropopliteal artery with an estimated age < 4 weeks and patent proximal segments of lower leg vessels, were included in the study. All patients were informed in detail about the procedure and gave their written consent. Patients with aneurysms of the popliteal artery, severe coagulation disturbances or a history of adverse reactions to contrast media were excluded. Seven patients suffered from critical ischemia (rest pain) and three from peripheral arterial occlusive disease (PAOD) stage II (intermittent claudication). The estimated age of the lesions was between 2 and 28 days. The mean length of the occluded segments was 5.8 cm (range 2–15 cm). The diagnosis was established by clinical examination, oscillography, Doppler pressure recordings, duplex sonography9 and digital subtraction arteriography. Laboratory examinations included hemoglobin, free plasma arteriography, hematocrit and coagulation parameters, both before, immediately after, and 24 hours after thrombectomy. Non-invasive examinations (oscillography, Doppler pressure recordings, duplex sonography) were performed after 48 hours and after 3 months. Antegrade arteriography was performed via the common femoral artery to determine the length of occlusion and to document the collateral circulation and the peripheral run-off. Using the road-map technique, the occlusion was passed with a Teflon-coated 0.020-inch guidewire and its flexible tip placed in the distal popliteal artery. An 8-French sheath was introduced and 5000 units of heparin injected. The thrombectomy catheter was threaded over the guidewire. One centimeter proximal to the upper end of the occlusion, the catheter was activated by a foot switch and advanced through the occlusion in gentle forward and backward movements under fluoroscopic control. The continuous suction of blood and occlusion material into the reservoir bag was observed. After the catheter had passed the occlusion it was withdrawn in the
71
proximal femoral artery and angiography was repeated via the side port of the sheath. Depending on the result, thrombectomy was either terminated, repeated, or completed by PTA. The number and the duration of catheter passes, and the volume of aspirated fluid, were recorded. Extracted occlusion material was examined histologically. Results Thrombectomy was technically successful in all patients. A mean of 2.4 catheter passes (range 2–3) were required to recanalize the occluded segment, and 2.8 seconds on average were needed to reopen 1 cm of occlusion. Blood and detritus were aspirated at 1.1 ml/second; the total aspirated volume ranger from 20 to 90 ml, depending on the length and consistency of the lesion. In nine patients, an underlying residual stenosis was treated by PTA after the thrombectomy. Fortyeight hours after the reintervention no patient suffered from critical ischemia: eight patients were classified as PAOD stage I, and two patients as stage II. The ankle–brachial index (ABI) improved from 0.41 ± 0.18 (range 0.13–0.65) preinterventionally to 0.88 ± 0.15 (range 0.64–1.11) after the intervention (p < 0.0005). Three months after the intervention the mean ABI was 0.84 ± 0.20 (range 0.52–1.07). All patients received either oral anticoagulation or antiplatelet drugs and were assessed by duplex sonography 48 hours and 3 months after the intervention. The treated arterial segment remained patent in eight patients. Two patients had a reocclusion within 2 weeks after the intervention. In a 60-year-old woman with an occlusion 3 cm long in a smoothly outlined superficial femoral artery of 5 mm diameter and with three patent lower leg vessels, fresh thrombus was removed with the Rotarex catheter in two passes of 7 seconds. Complete vessel patency was restored, no peripheral embolism occurred and additional PTA was not considered to be indicated. As usual, the patient received 5000 units of heparin during the intervention and oral anticoagulation afterwards. After 48 hours duplex sonography revealed a reocclusion. At that time coagulation parameters were not in the therapeutic range, which might have contributed to the rethrombosis. The ABI, which improved from 0.61 to 0.71 after the intervention, remained at this level. The patient was classified as PAOD stage II without the need for a reintervention. The second patient was a 78-year-old diabetic woman with a history of claudication of several years, rest pain for 12 days and a 15-cm-long occlusion of the popliteal artery with poor lower leg outflow. Thrombectomy was primarily successful and complete vessel patency was restored after additional PTA. The ABI rose from 0.65 to 0.95 and duplex sonography showed a residual stenosis of < 50% diameter reduction. One week after hospital discharge the patient complained of recurrence of intermittent claudication and a reocclusion was documented. Since the patient was clinically in PAOD stage II, no further intervention was performed. Reduced outflow due to pre-existing lower leg artery occlusion was considered as a possible cause for rethrombosis. No patient had signs of mechanical damage to red blood cells. There was no increase in free plasma, hemoglobin, nor relevant changes in hemoglobin and hematocrit after thrombectomy. Histological examination of the aspirate showed mostly fresh thrombotic material and small components of fibrotic intima with sclerotic fragments. No serious
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complication occurred. In one patient a small embolus was detected angiographically within the proximal posterior tibial artery and lysed successfully by 100,000 units of urokinase. Other studies Berczi et al. reported a study of 19 limbs of 18 patients treated with the Rotarex device for acute or subacute occlusions of the middle or distal third of the SFA or the popliteal artery.22 Lesion length was 3–20 cm. Thrombectomy was technically successful in 15 of 19 vessels (79%). The primary procedural success including additional procedures such as angioplasty and/or stent graft placement in 17 limbs was 94%. Eight complications were observed (31.5%), two perforations, one arteriovenous fistula and three distal embolizations. Follow-up studies showed three early (4–11 days) and six late (1–6 months) reocclusions. The cumulative primary patency rate was 68% at 3 months, 39% at 6 months, and 12% at 19 months; the secondary patency 68% at 3 months and 53% at 6, 12, and 20 months. The authors concluded that this procedure is quick and effective but should not be used in calcified lesions due to the risk of perforation. Duc et al. published a series of 41 limbs in 38 patients with acute, subacute, or chronic femoropopliteal occlusions of 1–180 days duration (mean 31.6 days) treated with Rotarex. 23 Length of occlusion was 2–35 cm (mean 13.1). After an average of two passages, all but two limbs required PTA for residual stenosis > 25%. Five patients needed additional stenting. As complications, one arteriovenous fistula and ten distal embolizations occurred. Follow-up studies observed two early reocclusions after 1 day and two at 2 weeks. Primary and secondary patency rates were 62/84% at 6 months and 39/68% at 1 year. The amputation-free survival was 100%. The authors concluded that this technique is safe and effective, can be used in short and long occlusions with equal success provided the obstruction is not very calcified. Zeller et al. reported a series of 100 thrombotic lesions in 98 patients, measuring an average of 21 ± 11 cm long (2–40) treated with Rotarex.24 There were 33 acute (< 14 days) occlusions (group I), 58 subacute/chronic (> 14 days) (group II) and 9 acute bypass graft occlusions (group III). There were 4 ± 1.4 passes of the device performed. The amount of aspirated fluid was 240 ± 119 ml. Forty-eight percent of the arteries were stented. Primary success was achieved in 92%, 100% for the ipsilateral approach, and 56% for the crossover approach. Eighteen complications were reported: two amputations after unsuccessful intervention and one death, eight vessel perforations and seven peripheral embolizations. Thirty-day survival and limb salvage was 88% for group I, 100% for group II, 66% for group III. The 3-month restenosis/reocclusion rates were 9% for group I, 3% for group II and 29% for group III. The authors concluded that the technique is easy and useful, but the use of this device is limited by the 8-French diameter of the catheter and the limited capacity for crossover interventions.
Clinical study as atherectomy device: authors’ personal experience A second pilot study for evaluation of the device for the treatment of chronic atherosclerotic stenoses or in-stent restenoses
in femoropopliteal arteries in humans was conducted in our catheterization lab. Population Twenty-one patients (17 men and 4 women; 44–86 years of age, mean age 69.0 ± 11.9) with 26 lesions (tight chronic atherosclerotic stenoses or restenoses) of the femoropopliteal artery or tibioperoneal trunk were included in the study. All patients were informed in detail about the procedure and gave their written consent. Cardiovascular risk factors of these patients were: diabetes 3/21 (14.3%), high blood pressure 19/21 (90.5%), dyslipidemia 15/21 (71.4%), and tobacco 11/21 (52.4%). A history of coronary artery disease was present in 3/21 (14.3%) and previous peripheral transluminal angioplasty in 12/21 (57.1%). None of the patients had a history of femoropopliteal or distal bypass surgery. All the patients suffered from intermittent claudication and were in class IIb of Fontaine’s classification. None of them suffered from critical ischemia (rest pain). The estimated age of claudication varied between 2 months and 1 year. Pre- and post-procedure assessment Diagnosis was established by clinical examination, duplex sonography and digital subtraction arteriography. Duplex sonography was performed before, 24 hours and 6 months after the intervention. An arteriography was performed via the common femoral artery in all patients before the procedure to determine the characteristics of the lesions, to document the collateral circulation, the peripheral run-off and to decide the method of approach. Laboratory examinations included hemoglobin, hematocrit and coagulation parameters, both before and 24 hours after atherectomy. Characteristics of the lesions The characteristics of the lesions are summarized in Table 12.1. The mean arterial diameter of the artery was 5.4 ± 0.8 mm (range 3–6 mm) and the mean preintervention minimal lumen diameter (MLD) was 1.4 ± 0.6 mm (range 0–1.5 mm). The mean percentage diameter of the stenosis was: 83.5 ± 7.9% (range 70–100%) and the mean lesion length 31.1 ± 35.0 mm (range 10–150 mm). The majority of the patients had a good run-off (three distal leg vessel patency, seven patients; two distal leg vessel patency, eleven patients; one distal leg vessel patency, two patients). Technique Adjunctive medical therapy Adjunctive medical therapy for debulking with the Rotarex system is similar to PTA, including preprocedural aspirin (160 mg/day starting at least 1 day prior to the debulking procedure) and intraprocedural heparin (5000 units IV). Molsidomine was administered at the discretion of the operator to minimize vasospasm. The vascular sheath was removed immediately after the procedure. Heparin was given as enoxaperin (40 mg twice daily subcutaneously) for 24–72 hours at the discretion of the operator, depending on the
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Lesion characteristics
Characteristics Location Femoral Femoropopliteal Tibioperoneal trunk Etiology De novo Restenosis
Characteristics Calcifications Eccentricity Collaterals Ulceration
No. patients 19
No. patients Upper part Middle part Low part
4 9 6
Post-PTA In-stent restenosis
2 9
No. patients
6 1 15 11
Expander Palmaz Optimed
7 1 1
12 10 5 1
difficulties and the result of the procedure. All patients received aspirin 160 mg/day continuously after the procedure and clopidogrel 75 mg/day for 1 month. Technique of debulking We used the ipsilateral antegrade approach in most of the cases (19–21) and the contralateral retrograde approach in two cases to treat lesions of the upper part of the superficial femoral artery (SFA). An 8-French sheath was introduced in the femoral artery. In case of a stenosis, it was crossed with a Teflon-coated 0.020-inch guidewire and its flexible tip placed in the distal popliteal artery. In case of an occlusion, the lesion was first recanalized by a 0.035-inch guidewire through a 4-French catheter. The atherectomy catheter was threaded over the guidewire. One centimeter proximal to the upper end of the stenosis or occlusion, the catheter was activated by a foot switch and advanced through the lesion in gently forward and backward movements under fluoroscopic control. The continuous suction of blood and occlusion material into the reservoir bag was observed. After the catheter had passed the lesion it was withdrawn in the proximal femoral artery and angiography was repeated via the side port of the sheath. Depending on the result, atherectomy was either terminated, repeated, or completed by PTA, with or without stent. The number of catheter passes and the volume of aspirated fluid were recorded. Optimal atherectomy The end of the Rotarex procedure was based on angiographic appearance and was at the discretion of the operator. A technical success is defined as a post-procedural residual stenosis < 30% at angiography or a pressure gradient < 5 mmHg. In contrast to PTA, which often leaves moderate residual stenosis (20–50%) that requires stenting to enhance the result, the goal of optimal atherectomy was to create the largest possible lumen without complications, with a final residual stenosis < 30%, to avoid angioplasty and stenting. Optimal atherectomy could be achieved as follows: by debulking alone if the control angiogram demonstrates a residual stenosis < 30%, debulking followed by PTA ± stenting if the angiogram demonstrated a residual stenosis > 30% after
debulking. PTA was performed using a balloon-to-artery ratio of 1:1.2 and inflation pressure of 4–6 atmospheres. The “ideal” residual stenosis is unknown. In our study, we attempted to achieve a residual stenosis of < 30%. Results The immediate angiographic results are given in Figures 12.5–12.7 Technical success Atherectomy was technically successful in all patients and all lesions. One occlusion was first recanalized by a Terumo guidewire before the atherectomy with the Rotarex system. One very tight stenosis needed to perform an angioplasty with a small diameter balloon to enlarge the lumen before the Rotarex system could cross the lesion. A mean of 4.6 catheter passes (range 3–8) were required to enlarge the arterial lumen. Results in terms of MLD and percentage residual diameter stenosis after atherectomy with the Rotarex are shown in Table 12.2. Blood and detritus were aspirated at 1.1 ml/second; the total aspirated volume ranged from 40 to 100 ml, depending on the length and consistency of the lesion. In 19/26 lesions (73.1%), an underlying post-atherectomy significant residual stenosis (> 30%) was present and treated by PTA alone in 15/19 lesions (78.9%) and with PTA + stent in 4/19 lesions (21.1%). The mean residual stenosis after Rotarex was 36.8 ± 15.1% (range 5–55). Six stents were placed for significant residual stenosis (n = 4) or residual dissection (n = 2). The different types were: JoMed (JoMed France SARL, Voisins le Bretonneaux) in one patient; Optimed (Optimed Medizinische Instrumente GmbH, Ettlingen, Germany) in four patients; and Smart (Cordis Corp, Warren NJ) in one patient. The type of stent placed depended on the location, the diameter, and the length of the lesion. Final results after Rotarex and PTA + stent procedure are shown in Table 12.2. Angiographic complications The overall incidence of angiographic complications after the Rotarex procedure was 6/26 (23.1%). Dissection and abrupt closure: A small non-occlusive dissection, not compromising the arterial flow occurred in 15.4% of
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(a) Figure 12.5
(b)
(c)
(d)
(a) SFA calcified stenosis; (b) Rotarex; (c) result after Rotarex; and (d) final result after angioplasty.
cases (4/26 lesions) after the atherectomy procedure. It was treated by PTA (three cases, 75%), and stent (one case, 25%) without further revascularization. No abrupt closure was observed. Distal embolization and no-reflow: Distal embolization causing abrupt cut-off of the target vessel distal to the original target lesion has been seen in one case and treated successfully by thrombosuction. No emergency bypass was needed. This type of macroembolization was probably due to dislodgement of thrombus or friable plaque from the target lesion, or release or incomplete capture of tissue stored in the collection chamber of the device. Perforation: Artery perforation was observed in one case (3.8%) in a tibioperoneal trunk and treated with a covered JoMed stent after unsuccessful prolonged balloon inflations. Vasospasm: No severe vasospasm was observed after Rotarex. Side branch occlusion: No side branch occlusion occurred. Clinical outcomes A clinical success at 24 hours was observed in all patients (100%) with no major clinical complications, no vascular injury requiring blood transfusion or vascular repair. All patients were classified as class I of Fontaine’s classification. The ABI improved from 0.53 ± 0.12 (range 0.13–0.65) preinterventionally to 0.91 ± 0.13 (range 0.64–1.11) postintervention (p < 0.0005). All treated arterial segments remained patent with good results and no significant residual stenosis, except in one patient whose residual stenosis was evaluated to 50% and treated medically. No patient had signs of hemolysis. There were no relevant changes in hemoglobin and hematocrit after thrombectomy. Results are shown in Table 12.3. Follow-up Three months after intervention, the mean ABI was 0.84 ± 0.20 (range 0.52–1.07).
Restenosis and late outcome Three restenoses were observed. Two at 6 months: 2/21 patients, 2/26 lesions (two in-stent restenosis: one Expander and one Optimed). One patient treated by Rotarex and PTA alone for a severe long in-stent restenosis (90% in diameter stenosis, 100 mm in length, Optimed stent), had an occlusion of the left SFA at 4 months treated by femoropopliteal bypass surgery. The other patient was also treated by Rotarex and PTA alone for a severe in-stent restenosis (90% diameter stenosis, 30 mm in length, Expander stent) of the low part of the left SFA, and developed an occlusion at 6 months which was treated medically. The third restenosis occurred at 9 months in a patient who had been treated for a de novo lesion (75% diameter stenosis, 10 cm in length) in the mid part of a small left SFA (maximum lumen diameter 3 mm). This restenosis was treated by femoropopliteal bypass surgery at 9 months. At a mean follow-up of 9.6 ± 2.7 months, all patients were asymptomatic and in class I of Fontaine’s classification.
Discussion In the last decade, great efforts have been made to provide an alternative to time-consuming local fibrinolysis and surgical thrombectomy in the treatment of arterial thrombosis. Percutaneous aspiration thrombectomy through thin-walled, straight catheters is still a common, readily available, simple and cost-effective technique for the removal of fresh thrombi.25 Its restriction to loose – that is, not adherent – thrombi, the necessity of usually several passes, and the risk of plaque avulsion and antegrade dissection have, however, led to the construction of more sophisticated devices.26 Devices to debulk arteries with severe chronic atherosclerotic stenoses prior to angioplasty and stent have been developed. The expectancy was to decrease post-angioplasty residual stenoses and restenosis rates.
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(a)
(b)
(c)
(d)
(e)
(f)
75
Figure 12.6 (a) SFA in-stent restenosis; (b) Rotarex; (c) result after Rotarex; (d) ballon angioplasty; and (e-f) final result after balloon angioplasty.
The experience with the first catheter equipped with a fast-rotating, coaxially driven cam (Trac-Wright, formerly Kensey) was disappointing. The device was, however, the predecessor of several generations of rotational catheters,27,28 which can be roughly classified into two types of devices: ●
●
those using recirculation, e.g. pulverization of thrombi by a hydrodynamic vortex created either by a high-speed impeller1,29–31 or the Venturi effect;12,17,32 non-circulation catheters with concomitant suction, using either a rotating recessed propeller33,34 or rotating cutting blades35,36 and aspiration via a roller pump or any other suction modality.37
These devices are effective in clearing fresh thrombi, especially in arterial and hemodialysis grafts; however, their effectiveness decreases with the age of thrombi and their adherence to the vessel wall. Since many occlusions are “acute or chronic” thromboses, a thrombectomy device should have the potential to remove not only fresh but also underlying organized thrombi. Furthermore, it should track over a guidewire in order to prevent vessel perforation. Finally, it should transport the occlusion material to the outside without the risk of peripheral embolization. The new Rotarex catheter described here meets many of these requirements: its construction is relatively simple, using only one lumen for the spiral and coaxial guidewire. No extra channels for suction, lubrication, or cooling are needed.
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(a)
(b)
(c)
(d)
(e)
(f)
Figure 12.7 (a) SFA in-stent restenosis; (b) Rotarex; (c) result after Rotarex; (d) balloon angioplasty; and (e–f) final result after balloon angioplasty.
The transport of the occlusion material is done exclusively by the spiral. Some devices are easily obstructed by sticky occlusion material, especially by fibrin, which has to be transported through a narrow catheter over a distance of 80 to 100 cm. In the new catheter, this drawback was eliminated by a special coating of the spiral and by adjusting the rotational speed
Table 12.2
to 40,000 rpm. As with all rotating devices, heat caused by friction can be a problem.14 The new device needs blood for lubrication. Therefore, it should not be advanced continuously in an occlusion, but in gentle forward and backward movements, allowing the uninterrupted aspiration of blood and avoidance of running dry. Provided these precautions were observed, no
Angiographic results
Before atherectomy After atherectomy After procedure (PTA + stent)
Mean arterial diameter (mm)
Minimal lumen diameter (mm)
Mean stenosis (%)
5.4 ± 0.8 5.3 ± 0.9 5.4 ± 0.7
1.4 ± 0.6 3.2 ± 0.4 5.2 ± 0.8
83.5 ± 7.9 36.8 ± 15.1 2 ± 3.5
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A new rotational thrombectomy and atherectomy catheter: the Rotarex system Table 12.3 Hematocrit percentage and hemoglobin percentage before and after
Before After
Hematocrit (%)
Hemoglobin (g/dl)
40.0 ± 4.1 38.0 ± 4.3
13.5 ± 1.4 12.7 ± 1.5
undue warning of the catheter was noted. The average time for thrombectomy or atherectomy in these two pilot studies was short and did not exceed 90 seconds for occlusions up to 15 cm in length or long severe stenoses. Blood loss during thrombectomy or atherectomy is generally low, amounting to 80–90 ml/minute, depending on the composition of the occlusion material that has to be transported and the blood available in the artery. A useful parameter for the assessment of the efficacy of a thrombectomy catheter is the radial force coefficient; that is, the ratio of the lumen recanalized by thrombectomy to the catheter diameter. For this new catheter, the coefficient is 2 in vitro, meaning that the catheter with a diameter of approximately 3 mm clears a thrombus of 6 mm. In vivo the radial expansion coefficient depends on the composition of the occlusion material. It is about 2 in fresh thrombi but drops to 1 in solid material, which means that the reopened or debulked lumen corresponds to the diameter of the catheter head. Experimental data suggest use of the catheter for the treatment of obstructed vessels with a diameter up to 8 mm. These studies showed its feasibility and efficacy in superficial femoral or popliteal arteries of 5–7 mm diameter. Its applicability in larger vessels, such as pelvic arteries, vena cava, or pulmonary arteries, needs to be validated in further trials. Zeller et al.24 treated 16 iliac artery occlusions but was not able to remove all thrombi from the vessel. A disadvantage of the Rotarex catheter must be pointed out. It seems not well suited for lengthy occlusions bypass beginning near the origin of the SFA or femoropopliteal bypass grafts in the crossover technique. The catheter is too short, so the occlusion cannot be traversed throughout in its entire length. Furthermore, with an acutely angled aortic bifurcation the rotating spiral can be distorted so that it blocks up or breaks.2,4 Nevertheless, the Rotarex can be used in obtuse bifurcation angle as we showed in our series. Compared with other thrombectomy or atherectomy devices, the potential of the Rotarex catheter to remove not only fresh loose thrombus but also solid, organized occlusion material must be considered as an advantage. With fresh thrombi we may expect to remove all the material, but with organized occlusion it remains, in most cases, a residual stenosis, so we have to treat either by PTA alone or PTA plus stent. The catheter can also treat calcified plaques but seems less efficient than the Rotablation atherectomy catheter (Rotablator), in particular in small distal peripheral arteries.5 The risk of perforation is high in calcified arteries. Therefore, adjunctive PTA after atherectomy or atherectomy is often necessary to eliminate residual stenosis. We expect that debulking prior to angioplasty can avoid stenting in peripheral arteries and decrease the restenosis rate at follow-up, but we have no proof and further large-scale
77
randomized studies are needed. Debulking could be useful to treat long lesions of the SFA before angioplasty and before placing long covered stents, to have a good expansion of this stent. As shown in arterial models, the wire-guided catheter removes thrombus or atherosclerotic material without intimal abrasion, severe arterial dissection or perforation if the original caliber of the artery is larger than the catheter head. Consequently, the catheter in the 8-French version is not suitable for thrombectomy or atherectomy in vessels distal to the popliteal artery. For use in small vessels, a 5-French version is needed. Hemolysis occurs in recirculation catheters without aspiration, but its clinical effect seems minimal. In these small studies no change in hemoglobin or hematocrit was noticed after thrombectomy or atherectomy. Except for a small embolus on a posterior tibial artery after thrombectomy, which was removed by focal fibrinolysis, and one in a distal leg artery after atherectomy, treated successfully by thrombosuction, no relevant complications occurred. It can be assumed that the negative pressure built up by the catheter system is sufficient to avoid peripheral embolization. Nevertheless in other publications some embolizations were reported.22–24 As expected from the preclinical tests, the catheter was easy to handle and helped to save considerable time by shortening thrombectomy to a few minutes, thereby avoiding lengthy procedures such as local fibrinolysis or surgical intervention. The potential benefit of debulking could be to reduce the restenosis rate (we observed only three cases of restenosis in the 26 lesions treated, 11.5%) and treatment of some difficult lesions not well treated by PTA alone. Indications for treatment with the Rotarex system could be: ● ● ●
● ● ●
● ●
as a thrombectomy device; thrombotic lesions; acute and subacute occlusions and particularly femoropopliteal lesions; as an atherectomy device; in-stent restenosis; ulcerated, embolic, eccentric, ostial, and long lesions (either stenosis or occlusion); as we have seen, debulking long lesions could be useful before placing long stent; bifurcated lesions; calcified lesions (but the Rotablator, whose safety and efficacy has been well documented, could be better for this type of lesion, and particularly in small vessels). The risk of perforation seems higher in calcified lesions.
Due to the efficacy and safety, the potential benefit of such a debulking device for the treatment of peripheral stenoses or occlusions has to be well evaluated. The immediate, mid- and long-term results of this technique compared with those obtained with conventional therapy (PTA plus stent) in larger multicenter randomized series, show that use of this device greatly increases the duration and cost-effectiveness of the procedure. Theoretical advantages of debulking techniques are tissue removal, the stepwise controlled approach and reduced mechanical trauma to the vessel wall (less “overstretching”). Its limitations
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are specific complications (possibility of stent damage, perforation, dissection), duration of the procedure, and costs.
Conclusion The Rotarex system is a thrombectomy and atherectomy catheter, which is easy to handle. Its feasibility and efficacy has already been published for the treatment of acute and subacute occlusions avoiding or reducing lytic substances. Few publications were done on the treatment of chronic arterial occlusive disease using the Rotarex system. It appears feasible and safe in
arteries > 4–5 mm in diameter. The main limitation is the difficulty to treat long lesions beginning at the SFA origin, this device is not well suited for the crossover technique. Immediate and mid-term results are promising with a low restenosis rate. Indications for this device have to be determined but is seems that long lesions and in-stent restenosis could be better treated with this device than with PTA alone. Larger randomized studies (atherectomy vs. conventional angioplasty) are needed to evaluate if atherectomy before angioplasty could avoid stenting in arteries < 6 mm in diameter, reduce the restenosis rate, and improve the clinical outcome.
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Simpson JB, Johnson DE, Thapliyal HV et al. Transluminal atherectomy: a new approach to the treatment of atherosclerotic vascular disease. Circulation 1985; 72(suppl III): III-I I I-III-146 (abstract) Simpson JB, Robertson GC, Selmin MR. Percutaneous coronary atherectomy. J Am Coll Cardiol 1988; 11(suppl A): 100A (abstract) Simpson JB. Future interventional techniques. In: Califf RM, Mark DB, Wagner GS, eds. Acute Coronary Care in the Thrombolytic Era. Chicago: Year Book Medical, 1988: 392–404 Simpson JB, Selmon MR, Robertson GC et al. Transluminal atherectomy for occlusive peripheral vascular disease. Am J Cardiol 1988; 61: 96G–101G Henry M, Amor M, Ethevenot G et al. Percutaneous peripheral rotational ablation using the Rotablator: immediate and mid-term results. Single center experience concerning 146 lesions treated. Int Angiol 1993; 12: 231–44 Hoshino S, Midorikawa H. Clinical results of directional peripheral atherectomy. Nippon Geka Gakkai Zasshi 1996; 97: 568–73 White CJ. Peripheral atherectomy with the Pullback atherectomy catheter: procedural safety and efficacy in a multicenter trial. PAC investigators. J Endovasc Surg 1998; 5: 9–17 Gammo R. Plaque excision treatment of infrainguinal PAD. Endovascular Today 2005; 4: 70–4 Soulen MC; Zaetta JM, Amygdalos MA et al. Mechanical declotting of thrombosed dialysis grafts: experience in 86 cases. J Vasc Interv Radiol. 1997; 8: 563–7 Bildsoe MC, Moradian GP, Hunter DW et al. Mechanical clot dissolution: new concept. Radiology 1989; 171: 231–3 Schmitz-Rode TH, Adam G, Kilbinger M et al. Fragmentation of pulmonary emboli: in vivo experimental evaluation of two highspeed rotating catheters. Cardiovasc Intervent Radiol 1996; 19: 165–9 Bucker A, Schmitz-Rode T, Vorwerk D et al. Comparative in vitro study of two percutaneous hydrodynamic thrombectomy systems. J Vasc Interv Radiol. 1996; 7: 445–9 Reekers JA, Kromhout JG, Van Der Waal K. Catheter for percutaneous throombectomy: first clinical experience. Radiology 1993; 188: 871–874 Nazarian GK, Qian ZQ, Coleman CC et al. Hemolytic effect of the Amplatz thrombectomy device. J Vasc Interv Radiol 1994; 5: 155–160 Beyer Enke SA, Deichen J, Zeitler E. The long-term results after Hydrolyser-supported angioplasty – a prospective study (in German). Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr. 1999; 171: 126–9 Rousseau H, Sapoval M, Ballini P et al. Percutaneous recanalization of acutely thrombosed vessels by hydrodynamic thrombectomy (Hydrolyser). Eur Radiol. 1997; 7: 935–41 Henry M, Amor M, Henry I et al. Thrombectomy with the hydrolysing catheter. A propos de 50 cas (in French). Arch Mal Cœur Vaiss 1997; 90: 797–804 Pitton MB, Neufang A, Duber C. Therapy of thromboembolic blockages in the crural arteries: clinical experience with the Angiojet thrombectomy catheter (in German). Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr. 1999; 171: 380–5 Starck EE, Wagner HJ. Rotation aspiration thromboembolectomy (in German). Deutsch Med Wochen schr. 1991; 161: 1–6
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Höpfner W, Vicol C, Bohndorf K et al. Percutaneous transluminal hydrodynamic thrombectomy – the initial results (in German). Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr. 1996; 164: 141–5 Schmitt HE, Jäger KA, Jacob AL et al. A new rotational thrombectomy catheter: system design and first clinical experiences. Cardiovasc Intervent Radiol 1999; 22: 504–9 Berczi V, Deutschmann HA, Schedlbauer P et al. Early experience and mid-term follow-up results with a new rotation thrombectomy catheter. Duc SR, Schoch E, Pfyffer M et al. Recanalization of acute and subacute femoropopliteal artery occlusions with the Rotarex catheter: one-year follow-up, single center experience. Cardiovasc Interv Radiol 2005; 28: 603–10 Zeller T, Frank U, Burgelin K et al. Early experience with a rotational thrombectomy device for treatment of acute and subacute infra aortic arterial occlusions. J Endovasc Ther 2003; 10: 322–31 Brossmann J, Muller Hulsbeck S, Heler M. Perkutane thrombektomie und mechanische Thrombolyse. Fortschr Rontgenstr 1998; 169: 344–54 Kensey KR, Nash JE, Abrahams C et al. Recanalization of obstructed arteries with a flexible, rotating tip catheter. Radiology 1987; 165: 387–9 Triller J, Do DD, Maddern G et al. Femoropopliteal artery occlusion: clinical experience with the Kensey catheter. Radiology 1992; 182: 257–61 Bildsoe MC, Moradian GP, Hunter DW et al. Mechanical clot dissolution: a new concept. Radiology 1989; 171: 231–3 Pozza CH, Gomes MR, Qian Z et al. Evaluation of the newly developed Amplatz maceration and aspiration thrombectomy device using in vitro and in vivo models. AJR 1994; 162: 139 Uflacker R. Mechanical thrombectomy in acute and subacute thrombosis with the use of the Amplatz device: arterial and venous application. J Vasc Intervent Radiol 1997; 8: 923–32 Rilinger N, Görich J, Scharrer-Pamler R et al. Short-term results with the use of the Amplatz thrombectomy deice in the treatment of acute lower limb occlusions. J Vasc Intervent Radiol 1997; 8: 343–8 Guenther RW, Vorwerk D. A new aspiration thrombectomy catheter with propeller tipped rotating wire: in vitro study. J Intervent Radiol 1990; 1: 17–20 Guenther RW, Vorweck D. Aspiration catheter for percutaneous thrombectomy: clinical results. Radiology 1990; 175: 271–273 Yedlicka JW, Carlson JE, Hunter DW et al. Thrombectomy with the transluminal endarterectomy catheter (TEC) system. J Vasc Intervent Radiol 1991; 2: 343–7 Rillinger N, Görich J, Scharrer-Palmer R et al. Percutaneous transluminal rotational atherectomy in the treatment of peripheral vascular disease using transluminal endarterectomy catheter (TEC): initial results and angiographic follow-up. Cardiovasc Intervent Radiol 1997; 263: 267 Müller-Hülsbeck S, Schwarzenberg H, Bangard C et al. Saugpumpenunterstützte Aspirationthrombektomie: in vitro Vergleich mit einem. Thrombusfragmentierungsverfahren Fortschr Rontgenstr 1998; 162: 191–4 Gehani AA, Rees MR. Can rotational atherectomy cause thermal tissue damage? A study of the potential heating and thermal tissue effects of a rotational atherectomy device. Cardiovasc Intervent Radiol 1998; 21: 481–6
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Orbital atherectomy system: a novel means of peripheral vascular rotational atherectomy DT Cragen and RR Heuser
Introduction Balloon angioplasty and stenting in the peripheral vasculature is an immensely valuable tool that remains limited by the fact that the occlusive plaque is simply displaced and not removed. Long peripheral lesions or calcified lesions can present a significant challenge to the interventionist as they may not be easily displaced. Furthermore, restenosis rates continue to limit the success of percutaneous peripheral interventions and debulking the plaque with minimal injury to the vessel wall remains an elusive goal. The Orbital atherectomy system (OAS) (Cardiovascular Systems, Inc., St. Paul, MN) is a novel device utilizing a diamond-embedded, eccentrically mounted crown spinning at high rotational speeds to “sand” and debulk the lesion and provide safe, effective, and efficient atherectomy. Previous use of rotational atherectomy in the peripheral vasculature using a centrally mounted burr was limited by heat generated by the device, large access sheath sizes required to deliver large burrs, and inadequate atherectomy in many cases due to unavailability of burr sizes to match the lumens of larger vessels. The use of rotational atherectomy in the coronary bed with the currently available device, the Rotablator (Boston Scientific, Natick, MA), has also been limited by the heat generated by the rotating burr and by the occlusive burr which prevents antegrade flow while engaged with the lesion.
Device description The OAS uses an eccentrically mounted crown embedded with diamonds about its midsection to ablate tissue endovascularly (Figure 13.1). The OAS is advanced over a 0.014-inch guidewire to just outside the sheath. The OAS crown and sheath are then connected to a 0.9% saline bag and the nitrogen gas-based controller console. The sheath is flushed with the saline and the device is staged outside the body to deliver the desired level of revolutions per minute (rpm). Once appropriately staged, the device is then introduced through the sheath (all current crowns can be advanced through a 6-French sheath) and advanced to the site of stenosis. At the site of stenosis, the crown is activated. Multiple passes can be made through the lesion during each 30-second run. The crown is advanced and withdrawn using the drive shaft and handle with a maximum 7 cm excursion on each pass.
The eccentric position of the crown’s center of mass results in an orbital motion about the center of the wire and results in an achieved lumen that is significantly larger than the crown size itself (Table 13.1). Because the abrasive diamond particles are situated on the widest point of the device at its midsection, it can safely ablate tissue both on forward and backward motion of the device within the area of stenosis. At the end of each run, angiography determines whether further passes are necessary. As the device is operated and plaque is removed, the force exerted on the plaque decreases gradually as the radius of orbit increases. If a larger lumen is desired with the current crown, the rpm can be increased successively to 140,000 and maximally to 200,000. Each increase in driving speed results in an increased orbit of the device and an increased achieved lumen diameter. Increasing the speed of the device, also augments the force exerted on the atheroma, in addition to increasing the achieved lumen size. The crown can then be removed and exchanged for a larger crown if further atherectomy is required. Alternatively, angioplasty and stenting can proceed as indicated. The eccentric, semi-elliptical shape of the crown was designed in part to allow blood and saline infusions to pass while ablation is proceeding. This reduces heat build-up within the lesion, which has been shown to stimulate restenosis in coronary trials of the Rotablator device. The OAS drive shaft is powered by a compressed gas turbine (usually containing nitrogen). The speed of the drive shaft is regulated by a pressure valve located on the front panel of the OAS controller console (Figure 13.1). The pressure valve is adjusted with each crown before the device is introduced into the sheath to calibrate for the desired rpm. It can then be recalibrated in the body to adjust the speed as necessary. An electrical footswitch is used to control the flow of saline through the device’s sheath used for cooling and lubrication. The footswitch also activates and deactivates the gas turbine that drives the device.
Preclinical testing Significant preclinical testing was performed on the OAS in vitro, ex vivo, and in animals to document safety and efficacy.1 In vitro studies included characterization of the 79
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(a)
(b)
(c) Figure 13.1 OAS components: (a) single-use disposable catheter/crown device with controller console; (b) Orbital atherectomy device with handle and diamond-embedded crown tip; and (c) close-up of Orbital atherectomy sheath and crown showing the eccentric crown with a mid-crown band of abrasive diamond coating.
behavior of the different crown sizes at various speeds and determined the maximum orbits (Table 13.1). When large amounts of atheroma are removed and released into the bloodstream, distal microvasculature plugging can occur and lead to the no-reflow phenomenon (absence of flow with a patent vessel). Extensive testing of the OAS device was performed in ex vivo studies to quantify downstream particle size. Using explanted, artificially perfused porcine coronary arteries as the model, the downstream particles were collected and analyzed. A mean
particle size, regardless of the crown size used, of 1.7–3.1 µm was observed. Nearly 99% of the particles collected were < 5 µm and 99.7% were < 20 µm. Therefore, approximately 99% of all particles liberated during atherectomy with OAS are smaller than a red blood cell and should pass through the capillaries and be removed by the reticuloendothelial system. During animal studies, OAS was used on porcine peripheral arteries 1 month after injury by balloon angioplasty. There were no significant complications observed during treatment (i.e. no
Table 13.1 The three currently available crown sizes and their achieved maximal lumen diameters at the three recommended rotational speeds are shown. Note that all three crowns can be introduced through a 6-French sheath Crown size (mm) 1.2 1.7 1.9
Rotational speed (rpm) 80,000 140,000 200,000 80,000 140,000 200,000 80,000 140,000 200,000
Maximum lumen diameter (mm) 1.7 2.0 2.4 2.7 3.3 3.6 3.5 3.8 4.5
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(c) Figure 13.2 CaptionCase study: (a) Baseline angiography shows 8–9 cm total occlusion of the mid-distal right superficial femoral artery with extensive collateral vessel recruitment and flow; (b) the 1.9 mm crown is being passed through the lesion increasing the rotational speed with each pass; and (c) final results after atherectomy with resolution of the chronic total occlusion and much less prominent collateral vessels.
perforations, dissections, reflow, or significant distal embolization) and all debulking efforts were successful. Histopathologic examination of the explanted vessed showed no evidence of device-related vascular wall injury in the majority of treated arteries. The most severe injury observed was limited to the internal elastic lamina and did not extend to the adventitial layer.
Clinical studies In the US, a single-arm, prospective, multicenter trial is underway in patients with at least one treatable de novo stenosis < 10 cm in
length in an infrainguinal peripheral artery. The study is designed to establish both the safety and efficacy of the device and has nearly completed enrollment. The primary efficacy endpoint is the mean decrease in percentage diameter stenosis of the target lesions. The primary safety endpoint is the occurrence of severe adverse events at 30 days. Secondary endpoints include procedural success as quantified by angiography; overall clinical status of the patient at 1 and 6 months of follow-up; incidence of adverse events and 1 and 6 months; incidence of symptomdriven target lesion revascularization at 6 months; change in ankle–brachial index (ABI); and the degree of clinical improvement using Rutherford and Becker’s scale at 1 and 6 months.
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Currently, the OAS is only available in the US as an investigational tool within this ongoing study.
Case study A 75-year-old woman with a long history of tobacco use, hypertension, and hyperlipidemia and known to have peripheral vascular disease presented with rest ischemia of the right foot. An ABI of 0.1 was obtained in the right foot and 0.5 in the left foot. She was referred for angiography and endovascular intervention. Vascular access was obtained via a contralateral femoral approach and a 6-French access sheath was advanced across the aortic bifurcation to the right common femoral artery. An 0.035” Glidewire was then advanced across the chronic total occlusion and a 4-French GlideCath was advanced over the Glidewire to the popliteal artery. The Glidewire was then removed and replaced with a 0.009-inch atherectomy guidewire through the GlideCath which was then removed. A 1.7-mm OAS crown was then used to make three passes through the area of occlusion at 80,000, 140,000, and finally 200,000 rpm. Angiography still confirmed significant stenotic disease and we exchanged the crown for a 1.9-mm OAS crown and repeated three passes through the stenosis at the recommended three speed settings. Angiography then confirmed excellent antegrade flow with markedly fewer recruited collateral vessels. No further treatment was provided at the site of occlusion. The total OAS operation time was < 150 seconds. The patient had no significant complications and was discharged home the following day on aspirin and clopidogrel. The patient had immediate relief of her rest foot pain and her ABI improved significantly from 0.1 to 0.45. In this case, use of the OAS resulted in recanalization of a chronic total
REFERENCES 1.
Heuser RR, Safian R, Bosiers M, et al. Orbital Atherectomy. Endovasc Today 2006; (5)9: 20–6
occlusion with < 30% residual stenosis and relief of critical limb ischemia. There was no need for further angioplasty or stenting at the treated site.
Discussion Peripheral arterial disease is a serious, debilitating disease affecting millions of people worldwide. The OAS is a novel means of performing fast, efficient, safe, and efficacious debulking of the occlusive atheroma in the peripheral vasculature. Theoretically, its biggest advantages over currently available techniques include efficient removal of plaque, minimal injury of the vessel wall, and the ability to easily adjust the crown size and/or the rotational speed to obtain a larger vessel diameter. Previous attempts at rotational atherectomy in the peripheral arteries have been limited by inability to upsize the burr without upsizing the delivery sheath to match the burr size. The eccentric design of the OAS crown allows the operator to obtain lumens up to 4.5 mm through a 6-French sheath system and thereby minimize access-site complications. Furthermore, heat build-up at the site of ablation (which is associated with vascular restenosis) is decreased with the eccentric crown, which allows blood and saline to flow through the vessel while ablation is proceeding. The OAS is currently undergoing a clinical trial in the US to determine its safety and efficacy in the peripheral arterial system. In addition, the FDA has been petitioned to allow investigational use of the OAS system within the coronary arteries. Initial clinical results with the OAS in infrainguinal lesions have been promising and we eagerly await further safety and efficacy results from the ongoing trial.
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Subintimal angioplasty G Markose and A Bolia
Background It has been almost 20 years since subintimal angioplasty (SIA) was first described. This technique has now enjoyed broad clinical acceptance as well as a resurgence of interest and application. Originally used in the femoropopliteal segment, its role has been extended to the treatment of infrapopliteal lesions, including the recanalization of the trifurcation and long tibial occlusions, as well as in the iliac segment and occasionally in the subclavian artery. Experienced centers have repeatedly reported primary success rates of around 90% in the infrainguinal vessels, as well as 1-year limb salvage rates as high as 85–90%, and 5-year primary assisted patency rates of 64% while not interfering with subsequent vascular surgery. Indeed subintimal angioplasty has proved to be very effective in lower-limb ischemia management, both for intermittent claudication and critical ischemia. Currently the “gold standard” of management of peripheral arterial stenosis and occlusion is by restoration of the arterial flow by direct arterial revascularization using autogenous reversed saphenous vein grafts. However many patients with peripheral vascular disease usually have several other co-morbidities, such as heart disease, diabetes, and renal failure, that would put them at higher surgical and anesthetic risk. Surgery has been shown to be associated with increased mortality (30-day survival of 96 vs. 100% for angioplasty) and morbitidy.1 Vein harvest site and graft infections can be devastating when they occur. In addition, some patients may not have an adequate amount of saphenous vein to harvest to allow for autologous saphenous vein grafting, and alternative conduits are required. This, in turn, decreases graft patency and limb salvage rates, with 3-year limb salvage rates decreasing to 95% using arm vein and 75% using prosthetic materials for superficial femoral artery arterial disease.2 The techniques of Dotter3 and Gruntzig4 revolutionized the treatment of peripheral vascular disease, heralding the arrival of endovascular treatment techniques such as percutaneous transluminal angioplasty (PTA). PTA is now an established technique for the treatment of peripheral vascular disease, widely used in the treatment of stenotic and occlusive lesions in the lower-limb arteries. Unfortunately the primary success rates and long-term outcomes of PTA in the recanalization of long occlusions have been unsatisfactory. Subintimal angioplasty, sometimes described as percutaneous intentional extraluminal recanalization (PIER) was first introduced in 1987 to treat femoropopliteal occlusive disease in intermittent claudication.5 Since that time, this technique’s
success has seen its use extended to treatment of stenotic and occlusive lesions in the iliac and popliteal arteries, trifurcation, and crural vessels where it has found an important role in the management of critical limb ischemia. Recent studies have shown that SIA can produce good results not only in chronic critical limb ischemia but also in intermittent claudication. SIA can now help to extend the scope of endovascular therapy to include a large number of previously untreatable femoropopliteal and tibial occlusions and helps by increasing the long-term patency in these vessels. SIA can be attempted on those patients deemed poor candidates for surgery due to the anesthetic risks or because they have insufficient vein to allow bypass grafting, and also in patients with flush occlusions of the SFA. In addition SIA can be used to re-open occluded native vessels following graft occlusion.6,7 The technique is simple, inexpensive, has low complication rates, good primary success rates, and good long-term outcomes.
Indications SIA dramatically increases the limits of endovascular treatment compared to conventional PTA. These include: 1. Chronic occlusions that have hardened with time, and where an intraluminal approach would fail. A subintimal dissection plane in these circumstances is relatively easily made. 2. Long occlusions where an intraluminal position of the guidewire would be hard to maintain. 3. Previously failed PTA. 4. Flush SFA occlusions (with a very small stump or no stump at all). Conventional PTA is very difficult or impossible in these situations. 5. Long length stenoses that normally have poor outcome with PTA. 6. Heavily calcified vessels. Often these are difficult to treat by PTA, but can be more easily managed by SIA as the wire follows the path of least resistance along the subintimal plane. 7. Diffusely diseased vessels that frequently have occlusions that are not treatable intraluminally. 8. Occluded native artery in situations where the bypass graft has failed. 9. Popliteal occlusions that extend into the trifurcation vessels, allowing reconstitution of some or all of the run-off vessels. 83
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A = Atheroma L = True vessel lumen S = Subintimal channel
A
L
(e) Cross Sectional Representation of Artery
Pre angioplasty
L
(a)
(b)
(c)
A
Post angioplasty
S
A
(d )
Figure 14.1 Diagrammatic representation of subintimal dissection: (a) The guiding catheter is brought up to the occlusion and directed towards the vessel wall; (b) the guidewire and catheter are introduced into the subintimal space; (c) a loop is formed with the proximal end of the guidewire and advanced to dissect through the subintimal space; (d) the loop is then used to break back into the true lumen; and (e) the atheroma and other occluding material is displaced laterally following angioplasty creating a newly opened subintimal channel.
10. When an arterial perforation occurs during an attempt at PTA, a subintimal dissection channel can be used to exclude the perforation site.
Technique Technique for femoropopliteal lesions The aim of SIA is to intentionally dissect into the subintimal space, below the intima but above the media within the vessel wall, past any intraluminally sited occluding material, re-enter the vessel lumen distally, and dilate the whole length of the dissection with a balloon.5,8–10 In the treatment of SFA disease, usually an ipsilateral antegrade puncture is made in the common femoral artery for occlusions that begin close to the origin of the SFA. (A contralateral retrograde puncture can be used with an “up and over” technique across the aortic bifurcation, particularly in obese patients, but this allows less control.) Using SIA, only a very small stump (5 mm or less) of proximal vessel (e.g. SFA) is required to start the dissection plane. When a reasonable length of proximal SFA is available, then the puncture can be made selectively into the SFA itself. Catheters with an angled tip, such as a 4-French Bolia minicatheter (Terumo, Japan) or a 5-French Cobra-type catheter (Cook, UK) are useful to help direct the end of the guidewire towards the vessel wall to break into the subintimal space for proximal SFA lesions. Alternatively a 5-French Van Andel-type predilating catheter (Cook, UK)11 can be used. The catheter is antegradely introduced up to the origin of the occlusion. Heparin (3000–5000 units) is injected intra-arterially prior to
crossing the lesion. Tolazoline (5 mg), a vasodilator that helps to dilate the distal vessels and decreases the possibility of spasm during the procedure, can also be given intra-arterially. The catheter tip is brought up to the level of the occlusion (Figure 14.1a), and a curved tipped hydrophilic guidewire (Terumo, Japan) is used to enter the occlusion and then subsequently traverse the length of the occlusion (Figure 14.1b). The guidewire tip should be directed towards the vessel wall and away from any important collateral vessels that may be present. The guidewire, with the support of the catheter, is then advanced into the junction between the occluding material and vessel wall. In the majority of cases the guidewire advances into a dissection channel in the subintimal space, this being the path of least resistance. Entry into the subintimal space can be confirmed by injecting a small volume of dilute contrast medium. If a Bolia mini-catheter is used, once the initial dissection has been made, this can be exchanged for 5-French balloon catheter (usually 5–6 mm in diameter and 4 cm long). When it is in the subintimal space, the guidewire usually moves relatively freely with little resistance. Increased resistance is found in previously angioplastied vessels and sometimes in heavily calcified vessels. The guidewire is then manipulated to a form a U-shaped loop of ideally 3–5 cm in length (Figure 14.1c). The leading edge of the loop is then used to advance the dissection distally. The catheter provides support while it and the guidewire are advanced distally along the length of the occlusion. The guidewire is advanced first, followed by the catheter. If the guidewire fails to advance further, due to resistance, the catheter should then be advanced to provide support to one arm of the loop. This allows the dissection to be continued until the distal end of the occlusion is reached. Once this point has been reached, it is recommended
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(a)
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(d)
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Figure 14.2 (a–c) This patient has a moderate length occlusion of the SFA in the mid thigh with good distal run-off; (d, e) successful recanalization of the occluded segment was achieved subintimally.
to shorten the loop length to 2–3 cm. Further advancement of the guidewire can then result in the guidewire loop reentering the true lumen (Figure 14.1d). Adjunctive procedures such as a slight twisting or screwing action can help to re-enter the true lumen. Re-entry is marked by a sudden decrease in the resistance to forward pressure on the guidewire, and can be confirmed by advancing the catheter into the distal artery and injecting a small volume of contrast medium. A relatively disease-free vessel distal to the stenosis or occlusion is favorable to achieving re-entry. Occasionally the dissection channel has to be extended beyond the occlusion to obtain re-entry, usually as a result of diffuse vessel wall disease being present distal to the occlusion. Generally, extension of the dissection channel more distally is not significant, unless a major collateral becomes compromised and vessel lumen re-entry is not obtained. Because of this, it is advisable not to breach any major distal artery collaterals in the learning phase of this technique. In cases where luminal re-entry is problematic, IVUSguided (Pioneer, Medtronic, USA) and fluoroscopically guided (Outback, Cordis Corporation, USA) re-entry catheters are now available which are reported to have good success.12 If not already exchanged for a balloon catheter, once the lesion is crossed the guiding catheter is exchanged for a 5- or 6-mm-diameter 5-French balloon catheter. The entire length of the subintimal channel is then dilated, in a distal-to-proximal direction using short (5–10 seconds) inflations of approximately 10–12 atmospheres (Figures 14.2–14.4). Flow is assessed by the injection of small volumes of contrast medium, and flow impairment can be treated with repeated balloon inflation. Any residual stenosis of greater than 30% is repeatedly balloon dilated, including the use of higher inflation pressures. Refractory stenoses may require placement of a stent in the affected region.
Following successful recanalization, aspirin, if not contraindicated, is advised, usually 150 mg daily for at least 3 months. Oral anticoagulants such as warfarin or other antiplatelet agents do not have to be routinely given, unless already used for other clinical indications. Technique for tibial lesions SIA is useful in long (greater than 3 cm) occlusions of the tibial vessels. The technique is similar to that used for femoropopliteal lesions, with several modifications. A balloon catheter (usually with a 3-mm-diameter, 2-cm-long balloon on a 120-cm-long 5-French shaft) is used to primarily cross and dilate the lesion rather than using a guiding catheter. Of note, in treating tibial stenotic and occlusive disease, it is important to use a 0.035 guidewire system and catheters with a 5-French shaft. The resistance encountered when crossing a long tibial vessel occlusion (greater than 20 cm) can be substantial and this larger system has enough strength to allow the combination of catheter and guidewire to progress along the entire length of the occlusion. Again, a U-shaped loop is formed in the hydrophilic guidewire. The loop length is kept shorter (2–3 cm), so that only the soft part of the guidewire makes the leading edge of the loop. This decreases the likelihood of perforation in these smaller and more delicate vessels. The loop is used to achieve the dissection throughout the length of the tibial vessel and also to obtain distal true lumen re-entry. If resistance prevents passage of the guidewire/catheter system distally through the subintimal space, the system can be strengthened by the use of a half-stiff or stiff hydrophilic guidewire (Terumo, Japan). In the more distal arterial tree, the intima becomes thinner, and thus it is usually not difficult to enter the true lumen in
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(a)
(b)
(c)
(d)
Figure 14.3 (a, b) This patient has a full-length flush occlusion of the SFA in the thigh; (c, d) successful recanalization of the entire length of the SFA was achieved with subintimal angioplasty.
the distal tibial vessels. Once the lesion has been crossed, balloon dilatation is then performed similar to that in the femoropopliteal segment (Figures 14.5 and 14.6). Technique for iliac vessels SIA can be used for total occlusions of the iliac vessels. Ideally this should be done in a craniocaudal direction to prevent continuing the dissection plane into the aorta. This therefore requires either a contralateral (“up and over”) femoral approach, or a combined ipsilateral and contralateral femoral approach, or a combined approach via the brachial or axillary artery and the ipsilateral femoral artery. The latter allows the treatment of bilateral iliac artery occlusions. Using the contralateral femoral approach, either a SosOmni (Angiodynamics, USA), Simmons 1 or 2, or Renal (Cordis Corporation, USA) catheters can be used (depending on the angle of the aortic bifurcation) to cannulate the diseased (ipsilateral) iliac vessel and to then abut the occlusion. A loop is formed with a hydrophilic guidewire just proximal to the lesion and a subintimal dissection is performed, as described earlier, with the loop as the leading edge in a cranialto-caudal direction, followed by the catheter. As the end of the lesion is approached, the loop is shortened to allow easier reentry into the true lumen. True lumen re-entry is confirmed with a small test injection of contrast medium. If not already
done so, the catheter is exchanged for an appropriately sized balloon angioplasty catheter, and angioplasty performed. The presence of residual stenosis can be assessed by further injections of contrast medium. Any residual stenosis can then be re-dilated. Occasionally a resistant stenosis may require the insertion of a stent, which is placed in a similar way to conventional intraluminal stenting. Longer lesions may require a combined contralateral and ipsilateral approach.13 In addition to cannulating the diseased iliac vessel from the contralateral side and commencing a craniocaudal dissection, as described above, a caudocranial dissection is commenced from the ipsilateral side. The dissection channels then meet up, and one of the guidewires can then be passed through the whole length of the lesion. Sometimes a snare is required to capture the guidewire and pull it through the lesion from one side to another. Angioplasty is performed as described earlier, and occasionally stenting is required for refractory stenosis. Similarly, bilateral iliac vessel and distal aorto-iliac occlusions can be treated by commencing a craniocaudally directed subintimal dissection via a puncture in the left brachial or axillary artery, and retrograde caudocranial-directed subintimal dissections via the femoral arteries. The craniocaudal dissection requires placement of a sheath in the left axillary or brachial artery. A guiding catheter, such as a 5-French vertebral or Van Andel catheter, is then advanced over the wire to just cranial to the vessel occlusion. A loop is then formed with
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(e)
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Figure 14.4 (a–c) Further example of a full-length flush occlusion of the SFA with good distal run-off; (d–f) treated successfully with subintimal angioplasty. Note the relative smoothness of the subintimal channel unaffected by intraluminal debris.
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Textbook of peripheral vascular interventions Retroperitoneal hemorrhage The treatment of flush occlusions of the SFA by SIA sometimes requires a high antegrade puncture of the common femoral artery. This puncture needs to be high enough to allow catheter and guidewire manipulation into the occluded SFA, but not so high as to risk retroperitoneal hemorrhage. In these high puncture situations, the medical and nursing carers must be informed so as to be extra vigilant due to the higher risk of retroperitoneal hemorrhage. The risks of retroperitoneal hemorrhage are further increased in patients taking warfarin, heparin, multiple antiplatelet agents and in hypertensive patients. Vascular closure devices are being increasingly used in these circumstances to help reduce the risk of retroperitoneal hemorrhage.
Left
(a)
(b)
Figure 14.5 (a) An example of subintimal angioplasty in the tibial vessels. Note the occlusion of the popliteal artery, proximal occlusion of the anterior tibial artery and occlusion of the other tibial vessels; (b) successful subintimal angioplasty of the proximal anterior tibial artery allowing “straight line” arterial flow to the foot.
a hydrophilic wire proximal to the occlusion and a craniocaudally directed dissection is commenced, led by the loop of the wire closely followed by the catheter. The craniocaudal guidewire can then be fed, or pulled after being snared, through the lesion and out of the femoral sheath. This process is then repeated for the occlusion on the other side, so that a guidewire is passing through both of the occlusions simultaneously. These guidewires are then replaced with exchange wires and angioplasty of the occluded vessels can be performed, using a “kissing balloons” technique (Figure 14.7). The angioplasty balloons should ideally be delivered via the femoral route, thereby minimizing the size of sheath required in the left axillary or brachial artery. As before, refractory stenoses can then be re-angioplastied or stented. A similar anticoagulation protocol is used as for femoropopliteal lesions.
Complications The complications of SIA are similar to those of conventional PTA. Of these the four most significant complications are: retroperitoneal hemorrhage following a high puncture, peripheral embolism, vessel perforation, and elastic recoil.
Peripheral embolism There is a 5 to 8% risk of embolic complications following femoropopliteal SIA. In the majority of cases percutaneous aspiration thrombectomy can remove the majority of emboli, usually using large 5-French to 8-French non-tapered embolectomy catheters and a large (50 ml) suction syringe with adequate suction. If this fails, then another strategy would be the “push and park” concept.14 Here, the embolus is pushed using either the embolectomy or balloon catheter distally into one of the run-off vessels. Usually the embolus advances in a straight line into the common peroneal artery. This allows blood flow to the foot via the other tibial vessels. However, this technique is reliant on at least two run-off vessels being available. Rarely, surgical embolectomy is required to remove the occluding material following SIA. Vessel perforation Vessel perforation during SIA can occur either during the subintimal dissection or during the balloon inflation of the subintimal tract with an incidence of 5–8%. This approximates to be at least twice as common compared with conventional PTA. However the development of a perforation will not necessarily terminate the procedure, and over half of patients who develop an intra-procedural perforation can continue to have a successful SIA.15 In fact SIA can be used to treat vessel perforation as a result of conventional PTA. The associated risk factors for intra-procedural vessel perforation include increasing patient age, diabetes, and smoking. If a vessel perforation occurs, then the extent of injury should be evaluated. This will have to be done on radiological assessment, as it is not possible to directly measure the quantity of blood leaking through the perforation. Often (during the subintimal dissection) the perforation will seal by itself and no further action is required. If treatment is required, the perforation can be excluded by creating a new, alternative dissection channel on the contralateral vessel wall, starting proximal and extending distal to the site of perforation. This diverts the blood away from the perforation and further distally into the leg (following the path of least resistance), while at the same time shifting the atheroma to the damaged side of the vessel and compressing on the perforation site. If this treatment fails, or there is a large perforation as noted by large amounts of contrast medium extravasating into the surrounding tissues, then an embolization coil (usually of
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(b)
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Figure 14.6 (a, b) Extensive tibial vessel disease with only the anterior tibial artery patent proximally and just above the ankle joint; (c, d) the intervening anterior tibial artery is occluded. The entire length of the anterior tibial artery is recannulated following subintimal angioplasty.
3 mm diameter) can be placed in the subintimal tract immediately proximal to the site of perforation, to occlude the tract and stop the blood flow to the perforation. Many of these patients can then be recalled several weeks later for a repeat attempt. A new subintimal tract can then be created, bypassing the embolization coil. Vessel perforation as a result of balloon inflation tends to produce a large defect, which is usually difficult to treat by subintimal bypass. In this circumstance, balloon tamponade
(a)
(b)
(c)
Figure 14.7 (a) Aorto-iliac arterial disease with occlusion of the distal aorta; and (b) bilateral proximal common iliac arteries; (c) subintimal dissection allows reconstitution of the aortic bifurcation and common iliac arteries.
at the site of the perforation is attempted, using low balloon pressure (2–4 atmospheres) for 2–3-minute periods repeated up to four times if necessary. If this fails to close the defect, then either a covered stent may be used to seal the defect or embolization coils can be deployed proximal to the perforation to occlude the subintimal channel and the flow of blood to the perforation. In patients with deranged clotting or abnormality of platelet function, treatment of these large defects may require correction of their clotting abnormality or the use of adjunctive blood products (such as fresh frozen plasma or platelets) in addition to coil embolization of the dissection tract. Elastic recoil This complication is rare, occurring in less than 1% of cases. It is however very unpredictable. If the recanalized segment fails to remain open due to elastic recoil, an emergency situation can arise as a result of blood stasis and then thrombosis of blood within the segment as well as proximal or distal to the recanalized segment. This can be treated initially with repeated balloon inflations, administration of Tolazoline (5 mg) or glyceryl trinitrate (GTN) (50–250 µg) locally intraarterially. In refractory cases deploying long self-expanding stents at the site of the occlusion may be of help. However evidence suggests that the long-term patency of subintimally placed stents is poor.16 Surgical bypass is then sometimes required.
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Results and long-term outcomes Numerous publications over recent years have outlined the efficacy, safety, and cost-effectiveness of SIA. Unfortunately there has to date been no randomized control trial directly comparing bypass surgery with SIA, and many centers apply differing treatment choices. One thing that is certain is that SIA has a learning curve, and those centers with the most experienced practitioners have the best results, with initial technical success rates rising from 83 to 100% with increasing experience of the procedure.17 Once the procedure has been mastered, many centers have reported generally favorable results for both intermittent claudication and critical ischemia, with very low rates of surgical intervention, procedural complication, and mortality. Most importantly it is recognized that SIA does not compromise future surgical bypass. A recent study provides good long-term evidence for the efficacy of SIA in intermittent claudication with technical success in 87% of patients. Primary assisted patency rates on an intention to treat basis at 5 years was 54%, rising to 64% in successfully recanalized patients.18 This study also identified length of occlusion, male sex, and age as independent risk factors for re-occlusion. It also highlighted the usefulness of a duplex surveillance program, as all patients who underwent a successful procedure were placed on surveillance, so that restenoses were diagnosed and treated early. Evidence for the efficacy of SIA in critical ischemia, can be drawn from the results of Lipsitz et al. who looked at a group with severe lower limb ischemia treated with SIA.19 Of the 39 patients in the group, 25 had gangrene and 5 had rest pain. Whilst they had technical success rate of 87%, more significantly 84% of the patients with gangrene healed with SIA alone, and 100% had complete pain resolution. The cumulative 1-year patency rate following successful SIA was 74%. Surgery in technical failure group was not affected by the attempt at SIA. These are very respectable results for such a minimally invasive technique in a group of patients with very severe vascular disease. Treiman et al. reported that 92% of a group of high-risk patients with critical ischemia with no other treatment options available experienced clinical symptomatic improvement at 1 year following SIA.20 This outlines the benefit of SIA, particularly in this group of patients, with significant medical co-morbidities who would pose a significant anesthetic and surgical risk. There appear to be several factors that contribute to longterm patency. These include smoking, occlusion length, and the number of calf run-off vessels.21 The relationship of longterm patency with the number of calf run-off vessels was also identified in the group of patients studied by Laxdal et al.,22 and those studied by Lazaris et al.23 who also confirmed the
relationship between the length of occlusion and long-term patency with a hazard of reocclusion of 1.02 for every centimeter of occlusion. Therefore it is best to try to improve the run-off into at least one good caliber run-off calf vessel, and preferably into at least two run-off calf vessels to help maintain long-term patency. SIA in the infrapopliteal segment is currently only offered in a few centers, though it has been shown to be of benefit particularly in limb salvage. The most recent evidence reports technical success rate of infrapopliteal SIA of 86%, with a 3-year limb salvage rate of 94%, and with an 84% freedom from the symptoms of critical limb ischemia at 3 years.24 Vraux et al. reported an 81% limb salvage rate at 6 months in a group of patients who were all considered unsuitable for surgery either due to poor medical condition, extensive ulceration, swelling, or lack of sufficient vein for autologous bypass. A significant proportion, 68%, had occlusions greater than 10 cm long, which may help to explain the technical success rate of 78%.25
Conclusion SIA is a safe adjunct in the treatment of lower-limb occlusive disease. Most studies agree that it does not compromise further surgical management, and has decreased morbidity and mortality compared with surgical bypass. This is important in patients with vascular disease, since many of these patients have significant medical co-morbidities and reduced life expectancy. SIA, by extending the therapeutic range of conventional PTA, increases the treatment options in this group of patients, and can either delay or obviate the need for surgery. A learning curve does exist when performing SIA, and this most likely explains the better results from more experienced centers. The technique is however easy to learn, and does not require any extra equipment than used for conventional PTA. The development of a surveillance program, coupled with timely treatment of restenosis has been shown to be of significant benefit in maintaining long-term patency, and decreasing the need for surgery. Studies so far suggest better results for SIA in intermittent claudication compared to critical limb ischemia. This may in part be related to the absence of good calf run-off vessels in critical limb ischemia. However, there is good evidence that SIA can help prevent limb loss and allow ulcer/gangrene healing in critical limb ischemia. This may be as a result of SIA “buying time” for the development of collateral vessels. Given that this group of patients are usually very debilitated and can be very poor candidates for surgical bypass, attempting SIA could prove of dramatic benefit if successful, while generally not affecting future surgical management.
REFERENCES 1.
2.
Hynes N, Akhtar Y, Manning B et al. Subintimal angioplasty as a primary modality in the management of critical limb ischaemia: comparison to bypass grafting for aortoiliac and femoropopliteal occlusive disease. J Endovasc Ther 2004; 11: 460–71 Faries PL, LoGerfo FW, Arora S et al. A comparative study of alternative conduits for lower extremity revascularization: all
3.
autogenous conduit versus prosthetic grafts. J Vasc Surg 2000; 32: 1080–90 Dotter CT, Judkins MP. Transluminal treatment of arteriosclerotic obstruction: Description of a new technique and a preliminary report of its application. Circulation 1964; 30: 654–70
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Subintimal angioplasty 4.
5. 6. 7. 8. 9. 10. 11. 12.
13. 14.
Gruntzig A, Hopff H. [Percutaneous recanalization after chronic arterial occlusion with a new dilator-catheter (modification of the Dotter technique)] Dtsch Med Wochenschr 1974; 99: 2502–10, 2511. In German Bolia A, Brennan J, Bell PR. Recanalisation of femoropopliteal occlusions: improving success rate by subintimal recanalisation. Clin Radiol 1989; 40: 325 Nasim A, Sayers RD, Bell PRF, Bell A. Recanalisation of the native artery following failure of a bypass graft. Eur J Vasc Endovasc Surg 1995; 10: 125–7 Walker PR, Papavassiliou VG, Bolia A, London N. Subintimal angioplasty of native vessels in the management of occluded vascular grafts. Eur J Vasc Endovasc Surg 2001; 22: 41–3 Bolia A, Miles KA, Brennan J, Bell PRF. Percutaneous transluminal angioplasty of occlusions of the SFA by subintimal dissection. Cardiovasc Intervent Radiol 1990; 13: 357–63 Reekers JA, Bolia A. Percutaneous intentional extraluminal (subintimal) recanalisation: how to do it yourself. Eur J Radiol 1998; 28: 192–8 Reekers JA, Kromhout JG, Jacobs MJ. Percutaneous intentional extraluminal recanalisation of the femoropoliteal artery. Eur J Vasc Surg 1994; 8: 723–8 Bolia A. Subintimal angioplasty in lower limb ischaemia. J Cardiovasc Surg 2005; 46: 385–94 Jacobs DL, Motaganahalli RL, Cox DE, Wittgen CM, Peterson GJ. True lumen re-entry devices facilitate subintimal angioplasty and stenting of total chronic occlusions: Initial report. J Vasc Surg 2006; 43: 1291–6 Bolia A, Fishwick G. Recanalization of iliac artery occlusion by subintimal dissection using the ipsilateral and the contralateral approach. Clin Radiol 1997; 52: 684–87 Higginson A, Aleaddin F, Fishwick G, Bolia A. “Push and Park” an altenative strategy for management of embolic complication during balloon angioplasty. Eur J Vasc Endovasc Surg 2001; 21: 279–82
15.
16. 17. 18. 19. 20.
21. 22. 23.
24. 25.
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Hayes PD, Chokkalingham A, Jones R et al. Arterial perforation during infrainguinal lower limb angioplasty does not worsen outcome: results from 1409 patients. J Endovasc Ther 2002; 9: 422–27 Treiman GS, Treiman RL, Whiting JH. Results of percutaneous subintimal angioplasty using routine stenting. J Vasc Surg 2006; 43: 513–9 Yilmaz S, Sindel T, Yegin A, Luleci E. Subintimal angioplasty of long SFA occlusions. J Vasc Interv Radiol 2003; 14: 997–1010 Florenes T, Bay D, Sandbaek G et al. Subintimal angioplasty in the treatment of patients with intermittent claudication: long term results. Eur J Vasc Endovasc Surg 2004; 28: 645–50 Lipsitz EC, Ohki T, Veith FJ et al. Does subintimal angioplasty have a role in the treatment of severe lower extremity ischaemia? J Vasc Surg 2003; 37: 386–91 Treiman GS, Whitting JH, Treiman RL, McNamara RM, Ashrafi A. Treatment of limb-threatening ischaemia with percutaneous intentional extraluminal recanalisation: a preliminary investigation. J Vasc Surg 2003; 38: 29–35 London NJM, Srinivasan R, Sayers RD et al. Subintimal angioplasty of femoropopliteal occlusions: the long term results. Eur J Vasc Surg 1994; 8: 148–55 Laxdal E, Jenssen GL, Pederson G, Aune S. Subintimal angioplasty as a treatment for femoropopliteal occlusions. Eur J Vasc Endovasc Surg 2003; 25: 578–82 Lazaris AM, Salas C, Tsiamis AC et al. Factors affecting patency of subintimal infrainguinal angioplasty in patients with critical lower limb ischaemia. Eur J Vasc Endovasc Surg 2006; Sep 9; [Epub ahead of print] Ingle H, Nasim A, Bolia A et al. Subintimal angioplasty of isolated infragenicular vessels in lower limb ischaemia: long term results. J Endovasc Ther 2002; 9: 414–6 Vraux H, Hammer F, Verhelst R. Subintimal angioplasty of tibial vessel occlusions in the treatment of critical limb ischaemia: midterm results. Eur J Vasc Endovasc Surg 2000; 20: 441–6
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Recanalization devices for chronic total occlusions (including optical coherent reflectometry) G Baweja and RR Heuser
Introduction Chronic total occlusion (CTO) of peripheral arteries can cause disabling claudication or critical limb ischemia. In contrast to other vascular beds, occlusions are at least three times more common in the femoropopliteal arteries. For the patient with critical limb ischemia, multilevel disease with occlusion of some or all of the tibial arteries is typical. Patients with long infrainguinal occlusions generally tend to be sicker and bypass grafting in this population is often associated with a considerable procedure-related morbidity and mortality. Surgical intervention is usually reserved for patients with critical limb ischemia and consequently many patients with long, chronic superficial femoral artery (SFA) occlusions remain untreated, leaving them in pain and discomfort. While treatment of short CTO lesions of the iliac and femoropopliteal vessels with endovascular techniques has become the standard approach, longer complex lesion intervention can be extremely challenging and time-consuming. Iliac and femoropopliteal CTOs traditionally had high failure rate in the range 5–35%1,2 and 15–25%,3 respectively. Fortunately, with increasing complexity of the arterial occlusions, technical skills, and devices needed to successfully cross and treat the occlusion also continue to improve significantly. Nowadays, an initial endovascular approach can achieve limb salvage rates equivalent to surgical bypass.3,4
Pathology of total occlusion CTOs consist of various degrees of fibro-atheromatous plaque and thrombus depending on the mechanism of occlusion and its duration. A tough fibrous cap is often present at the proximal and distal margins of the CTO, with softer material in between. When the fibrous occlusion is long, densely organized, and homogenous, guidewire passage intraluminally is very difficult and subintimal approach in this type of lesion is likely to be more successful.
Patient selection Revascularization procedures are indicated for patients with disabling claudication, ischemic rest pain, or impending 92
limb loss. At the present time, for infrainguinal occlusions, the patency rates for long, complex disease are lower than the patency rates for open bypass.5 The rapid advances in interventional devices have inspired interest in tackling these long occlusions with an endovascular approach with the option of open surgery still remaining if the intervention later fails. Recently published guidelines state that the effectiveness of the use of stents, atherectomy, cutting balloons, thermal devices, and lasers for the treatment of infrainguinal lesions (other than to salvage a suboptimal result from balloon dilation) is not well established, and primary stent placement is not recommended in these arteries. In these guidelines, stent implantation is categorized under one broad definition and includes self-expandable, balloon-expandable, spiral-shaped, and covered stents.6 Lesion assessment Initial imaging of patients with iliac and femoral occlusions can be done with computed tomography angiography (CTA) or magnetic resonance angiography (MRA). This allows for excellent definition of the aortic, iliac, and femoral occlusions and the status of the femoral artery for access in case of iliac occlusions and helps in deciding on an antegrade versus retrograde contralateral femoral access for infrainguinal lesions. A limitation to percutaneous treatment is occlusive disease of the common femoral artery at the site of access. In this situation, open femoral access can be used when treating iliac or femoral–popliteal disease with endovascular techniques. In the catheterization laboratory, lesions should first be assessed with appropriate angiographic views, for example a 35∞ ipsilateral lateral angiogram. Most long SFA occlusions begin with a proximal stump followed by distal vessel reconstitution by collaterals from the profunda femoris artery. Special attention must be paid to the length of the proximal stump and the location of the distal reconstitution as it clearly influences device selection. A flush occlusion at the SFA origin or an extension of an occlusion to the popliteal trifurcation is not suitable for endovascular treatment, especially with antegrade approach.7 Diffuse, irregular, eccentric, calcified occlusions are much more difficult to recanalize and have less long-term success.8 Lesion length is an important factor when determining long-term success though it probably
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Recanalization devices for chronic total occlusions (including optical coherent reflectometry) plays lesser role in deciding between endovascular and surgical approach.
Crossing total occlusions Femoropopliteal CTOs are effectively treated with up-andover techniques, whereas iliac lesions are often best approached via ipsilateral retrograde femoral access. In order to provide the support needed to cross long infrainguinal lesions, a long 6- or 7-French sheath like Ansel or Raabe (Cook Inc., Bloomington, IN) is placed over the iliac bifurcation with the tip into the superficial femoral artery. Once the access is obtained, the patient is anticoagulated with either heparin or bivalirudin. We often use a combination of a hydrophilic guidewire such as a 0.035-inch Glidewire (Terumo, Somerset, NJ), and a support catheter such as the 4–5-French angled Glidecath as initial approach for crossing a CTO. The procedure from this point on requires road-map imaging to visualize the distal vessel as angiographic imaging through the support catheter is largely unhelpful. It is important that the hydrophilic guidewire enters the occlusion with the tip straight without any spiraling as this allows for the proper tip engagement into the lesion. At this point one can either attempt crossing intraluminally or looping the wire purposely to enter subintimal space. Despite the counterintuitive nature of starting a subintimal plane intentionally, the technique is relatively simple and usually more successful (70–90% of cases) than intentional true lumen passage for long-segment CTOs.9 Some interventionalists prefer retrograde approach over antegrade puncture for infrainguinal angioplasty. In a randomized study of 100 consecutive patients, retrograde puncture was found to be technically easier with a tendency to fewer complications like hematoma, but resulted in a higher radiation dose.10
Subintimal angioplasty Once wire enters the occlusion, it often loops back on itself for several centimeters with the 180∞ turn. One should try to maintain the width of the distal wire loop to remain smaller than or equal to the width of the native vessel as widening of the loop tip signifies more subintimal vessel dissection. This can limit successful re-entry of wire into the distal vessel true lumen. To avoid widening of the wire loop, one can push the support catheter to catch up over the proximal unlooped part of the Glidewire and then pull the wire back into the catheter to straighten the tip. After straightening the wire, it is readvanced with a small width loop as described previously.11 If the support catheter gets trapped in the subintimal space and does not follow the Glidewire, a smaller-diameter 0.035inch compatible catheter, such as the Quickcross catheter (Spectranetics Corporation, Colorado Springs, CO) may be used. Finally, the wire is re-entered into the distal true lumen under direct visualization. The support catheter is then advanced into the distal segment, beyond the occlusion, and confirmation of true lumen is done with contrast injection through this catheter. If there is difficulty in re-entering the true lumen, re-entry devices like the Outback or Pioneer
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catheters are used as described below. Alternatively, lowerprofile 0.014-inch torqueable stiff wires (e.g. confianza wire) with or without over-the-wire angioplasty balloon can sometimes be used successfully to achieve true lumen entry. It is preferable to try re-entry devices over vigorous attempts to reenter lumen with wire alone as this may lead to worsening of subintimal dissection and progression of dissection plane below the knee compromising distal collaterals. Primary patency rates of subintimal angioplasty range from 60 to 80% at 6 months and 60 to 70% at 12 months.12 In critical limb ischemia, limb salvage is achieved in approximately 80–90% of patients. Secondary interventions are usually quick and simple and approach does not interrupt subsequent bypass options.
Re-entry devices The key factor to subintimal success is having a relatively healthy, non-calcified target for re-entry in the distal vessel. Lesions with dense calcification, diffuse disease of the distal target, and small-caliber lumens often prove difficult to gain successful re-entry. In addition, in some cases re-entry is not achieved until subintimal passage to a site significantly remote from the level of patent vessel lumen. This causes subintimal angioplasty or stenting of an unintended target beyond the diseased segment and may jeopardize important collaterals. In these cases, re-entry tools such as the Pioneer catheter (Medtronic Vascular) or the Outback (Cordis, Miami, FL) can be used.13 It is important to remember that a 7-French sheath is necessary for these devices. Pioneer catheter The Pioneer catheter is a 7-French phased-array 20 MHz intravascular ultrasound (IVUS) catheter and is connected to a Volcano (Volcano Corporation, Rancho Cordova, CA) IVUS console. The catheter has two monorail 0.014-inch compatible wire ports, one with a curved retractable 24-gauge nitinol needle distally. The catheter is gently maneuvered under ultrasound guidance until the tip of the nitinol needle is oriented toward the true lumen and is lined up at the 12 o’clock position on the ultrasound image. The needle tip is then carefully advanced and deployed. A floppy-tip extra-support 0.014-inch guidewire is then passed through the needle into the distal vessel and is confirmed with angiography. The needle is then retracted, and the Pioneer catheter is removed, leaving the wire behind with distal end in the true lumen. At this point, secondary interventions are performed with standard techniques (Figure 15.1). Outback catheter The Outback catheter (Lumend Inc) is a 5-French multipurpose type catheter with 22-gauge nitinol canula that can be advanced or retracted from the end of the catheter to penetrate from the dissection plane to the true lumen. With the help of two orthogonal fluoroscopic views, the angle of the catheter is adjusted to point the end toward the true lumen. The proprietary locate, tune, and deploy technique is used to deploy the needle through the intima to the true lumen. A 0.014-inch wire is then advanced into the true lumen and the
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Figure 15.2
(a) A
B
C
D
(b) Figure 15.1 (a) Pioneer catheter with integrated 20 MHz phase array transducer and 24-gauge nitinol curved needle; (b) the Pioneer facilitating the true lumen re-entry: A. wire trapped in a subintimal location; B. Pioneer catheter is advanced to the target segment, where the needle is deployed under ultrasound guidance; C. guidewire is then passed through the needle into true distal lumen and the Pioneer is removed; D. lesion is treated successfully with an angioplasty device advanced over the wire.
Outback catheter is then removed. Secondary interventions are then performed either on this wire or after exchanging it with a 0.35-inch wire system (Figure 15.2).
Angioplasty and stenting Common iliac artery occlusions are routinely stented with balloon-expandable stents because of their high radial force and precise placement. In the external iliac, one can use either the balloon-expandable or self-expanding stents depending upon the lesion characteristics and location. Femoral or popliteal occlusions are treated with primary angioplasty with long balloons at nominal or greater pressures and longer inflations up to 2–3 minutes. If there is a presence of a flowlimiting dissection, then self-expanding bare nitinol stents should be deployed. Some interventionalists have also used laser, thermal, or atherectomy devices in this setting to treat residual lesions after angioplasty.
Outback catheter from Lumend.
needle deployments, but these devices are often used in complex difficult-to-cross lesions that have an increased risk of rupture with angioplasty. It is imperative that covered stents be available in the catheterization laboratory at the time of CTO intervention. The other important complication of intervening total occlusions is thromboembolism that can occur in 1–4% of cases. Adequate anticoagulation is therefore necessary during the procedure.
Chronic total occlusion devices Because of often complex and long occlusions, more than 80% of patients usually need a more specialized crossing technique over the standard technique. Recently, several devices have entered the market that may enable treatment of these difficult lesions. These devices cross the calcified plaque using different physical principles, such as blunt microdissection, optical coherence reflectometry, or laser. Some of the devices like magnum wires, rotational atherectomy, Kensey catheter, and Rotacs are already of historical significance only and will not be described any further in this chapter. Excimer laser The photoablative effect of an excimer laser can be used to recanalize total occlusions by debulking atherosclerotic and thrombotic material. In addition, it can facilitate subsequent balloon dilation at lower pressure to prevent dissection and reduce the risk of thromboembolic events. An excimer laser produces photons of ultraviolet light at a unique wavelength of 308 nm that is readily absorbed in human tissues, including atherosclerotic material and clots (Figure 15.3).
Complications The major complication related to the treatment of chronic total occlusion is vessel rupture secondary to catheter manipulation or angioplasty. Long or calcified occlusions are often more prone to such complications. The true lumen re-entry devices itself may not result in perforation related to the
Figure 15.3 (a) The Spectranetics CVX-300 excimer laser system and (b) TURBO elite laser ablation catheter (FDAapproved October 2006). (See Color plates.)
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Recanalization devices for chronic total occlusions (including optical coherent reflectometry) The activated laser catheter must be advanced very slowly, not exceeding 1 mm/sec. Fluoroscopic road mapping is used throughout to verify alignment of guidewires and catheters to the vessel lumen. Improvements in saline-infusion techniques with lasers have resulted in lower incidence of dissection. Thorough flushing of the vessel with saline effectively facilitates transmission of the laser light to the atherosclerotic tissue. In addition, effective removal of the contrast medium prevents formation of shockwaves that can result in dissections of the vessel wall. There also appears to be direct platelet aggregation inhibition with the use of excimer lasers, making it an attractive tool for treating chronic thrombotic lesions.14 The mid-term outcomes of patients with long chronic iliac artery occlusions after excimer-laser-assisted interventional recanalization were recently reported in 43 patients after 4year follow up. The primary technical success rate was 95.3%, with a major complication rate of 6.9% and clinical improvement in 97.6% of cases. The overall primary and secondary patency rate as determined by ankle–brachial index and duplex ultrasound was 86.1 and 95.4 % respectively.15 This is similar to the patency rates of short stenoses. In a study of laser-assisted recanalization of chronic SFA occlusions in 318 consecutive patients over 1 year, the primary and secondary patency rate was 83.2 and 90.5% respectively.16 There is data supporting use of lasers in the tibioperoneal region as well. In the LACI (Laser Angioplasty in Chronic Ischemia) prospective, multicenter, clinical registry patients with poor surgical risk with critical limb ischemia were treated with excimer laser in the SFA, popliteal and/or infrapopliteal arteries with adjunctive PTA, and optional stenting. Patency with distal flow to the foot was achieved in 89% of patients and the rate of limb salvage was 93% at 6 months.17 Blunt microdissection New catheter technology has recently been developed to recanalize CTOs through a process of blunt microdissection. The Frontrunner X39 CTO Catheter (LuMend Inc., Redwood City, CA) is a single-use catheter consists of an articulating, distal tip assembly. This tip features a crossing profile of 0.039 inches with actuating jaws that open to 2.3 mm and is remotely actuated by a manual rocker handle to facilitate blunt microdissection of the plaque (Figure 15.4). The Frontrunner catheter is commonly used in combination with the 4.5-French Frontrunner Micro Guide Catheter that provides additional support and acts as a conduit for a more
Figure 15.4
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rapid wire exchange once the frontrunner crosses the CTO. The microdissection can be performed in various planes to separate tissue in the target vessel segment. Though originally designed for coronary intervention, the Frontrunner CTO Catheter has now been used extensively to facilitate guidewire placement across peripheral CTOs. In a prospective study of 36 patients with 44 symptomatic CTOs (2 terminal aortic, 24 iliac, 16 femoral, and 2 popliteal), blunt microdissection was carried out with this type of catheter. Procedural success, evaluated angiographically, was achieved in 91% with no complications related to blunt microdissection itself.18
Vibration angioplasty Vibrational angioplasty is based on the concept of using highfrequency mechanical vibrational energy to help recanalize chronic total occlusions. The Crosser system consists of a generator, a transducer, and the single-use CROSSER catheter (Figure 15.5). The generator converts AC power into highfrequency current. This high-frequency current is then converted into vibartional energy by piezoelectric crystals contained within the transducer. The Crosser catheter is a nitinol-core standard 0.014-inch and 0.018-inch guidewires monorail catheter system with a stainless steel tip. Mechanical vibrations are transmitted to this stainless steel tip at approximately 20 kHz or 20,000 cycles per second. This vibrational energy provides mechanical impact at a stroke depth of approximately 20 µm and pulverizes the solid CTO tissue. In addition, high-frequency vibration creates vapor-filled micro-bubbles in the blood. These micro-bubbles expand and implode producing liquid jets that can break the molecular bonds and cause erosion of the CTO tissue helping recanalization of an occluded artery. This system has already been used safely and effectively in coronary artery total occlusions.19,20 Recently, the PATRIOT (Peripheral Approach To Recanalization In Occluded Totals) data on 40 patients was presented at the TCT 2006 meeting.21 The average CTO length was 10.6 cm with half of the attempted occlusions in the SFA and the remainder in the popliteal artery or below. CROSSER activation time averaged 2.5 min. Procedure time (PT) and fluoroscopy time were 2 h and 39 min respectively. There were no procedural complications and no clinical perforations. Technical success (successful passage of a guidewire into the true distal lumen) was achieved in 78% of the occlusions attempted. Improvement in
Schematic of blunt microdissection with Frontrunner device.
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Figure 15.5 (a) The Crosser system generator – high frequency current is converted into vibrational energy; (b) Crosser catheter – mechanical vibration at 20,000 cycles/second.
ABI (> 0.10) was achieved in 85% of patients with successful recanalization. (a) Optic coherence reflectometry with radio-frequency ablation All the new technologies described above are unable to see the true lumen of the vessel. Optical coherent reflectometry with radio-frequency ablative energy (Safe-Cross wire, Intraluminal Therapeutics, CA) is a forward-looking system that has been utilized to treat CTO.22 Using near infrared light, this guidewire system can distinguish calcified from noncalcified plaque and atherosclerotic lesions from arterial wall and display the signals on a monitor in real time. The green bar indicates lumen and radiofrequency ablative energy is enabled. The red bar means wire is against the vessel wall and radio-frequency energy is disabled (Figure 15.6). There are some technical limitations with the current system. The wire tip cannot be manually shaped or bent without risking the fracture of optical fibers inside the wire. The wire itself is not easily steerable, though this problem has been significantly improved in the latest generation of SafeCross wire. The GRIP registry study is one of the first peripheraldevice studies to focus on total occlusion recanalization with the Safe-Cross system.23 The device success rate, defined as the achievement of distal lumen position, was 76%, For the 56 lesions that were recanalized, the mean preprocedural ABI was 0.59; the mean post-procedural ABI was 0.86. In another study, Dippel et al. demonstrated a 72.7% success rate in recanalizing CTO in the peripheral vasculature following failure of conventional techniques.24
(b) Figure 15.6 (a) Safe-Cross system; (b) optical coherence reflectometry guided radio-frequency ablation-waveform display.
was undetermined in the majority of patients, 17 patients had arterial occlusions older than 2 years and half the patients had intermittent claudication from 8 months to 10 years. Surprisingly, 80% of CTOs including iliac and infrainguinal occlusions responded favorably to thrombolysis. Most arterial occlusions (more than a few centimeters in length) are associated with some degree of arterial thrombosis, and thus may be amenable to thrombolysis. Advances in the availability of smaller catheters (3 and 4 French) and development of an open-end injectable guidewire have increased the rate of success due to both a better delivery system and fewer complications. In the absence of bleeding complications, lytic therapy can be continued as low-dose prolonged infusion until complete clot lysis is achieved.
Thrombolytic therapy While thrombolytic therapy is still the treatment of choice in acute and subacute arterial occlusions and graft thrombosis, there are a few reports regarding thrombolytic therapy in chronic arterial occlusions.25–27 In a series reported by Motarjeme, 276 arterial occlusions (lesion length 3–66 cm) were treated in 268 patients with thrombolytic therapy. Though the duration of the occlusion based on angiography
Medical management Though the detailed medical management is beyond the scope of this chapter, the role of medical therapy in patients with advanced PVD should not be underestimated. Even in patients requiring invasive intervention, medical management has been proven to improve outcome, prolong the success of
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Recanalization devices for chronic total occlusions (including optical coherent reflectometry) the intervention, improve functional capacity, and prolong life. One must address all modifiable risk factors including smoking, hypertension, dyslipidemia, obesity, physical inactivity, and diabetes. In addition, the appropriate use of beta-blockers, antiplatelet therapy, angiotensin-converting enzyme (ACE) inhibitors, and statins are recommended for patients with peripheral vascular disease.
Future technologies There are many new innovative technologies on the horizon to treat chronic vessel occlusions. Omniwave technology using acoustic energy, Cronus stereotaxis wire for magnetic navigation28 and collagenase infusion29,30 are few of such novelties under investigation. Recent advances in rapid imaging, along with the development of special catheter devices visible under MRI, have made real-time MRI (rtMRI) guided therapeutic interventions feasible.31 Recently Raval et al. demonstrated successful real-time MRI-guided recanalization of a long peripheral artery CTO in a swine model.32 This technology
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may offer advantages in future human peripheral artery visualization during CTO traversal, while avoiding x-ray radiation and nephrotoxic contrast agents.
Conclusion At present, endovascular intervention is generally well accepted as an effective treatment modality in the majority of occlusive iliac artery lesions, but its role in the femoropopliteal region is still debatable. A successful intervention of chronic total occlusions depends a lot on operator’s patience, technique, and experience. New technologies, including the Frontrunner catheter, Safe-Cross system and re-entry catheters, have significantly improved our success of crossing long total occlusions. These innovations, along with ever-increasing operator experience, have considerably enhanced long-term patency in even the most complex chronic occlusions. In the future, more patients will have the opportunity for a less invasive treatment for their arterial disease.
REFERENCES 1. 2.
3.
4.
5. 6.
7. 8. 9. 10. 11. 12. 13.
14.
Uher P, Nyman U, Lindh M, Lindblad B, Ivancev K. Long-term results of stenting for chronic iliac artery occlusion. J Endovasc Ther 2002; 9(1): 67–75. Carnevale FC, De Blas M, Merino S, Egana JM, Caldas JG. Percutaneous endovascular treatment of chronic iliac artery occlusion. Cardiovasc Intervent Radiol 2004; 27(5): 447–52 Lofberg AM, Karacagil S, Ljungman C et al. Percutaneous transluminal angioplasty of the femoropopliteal arteries in limbs with chronic critical lower limb ischemia. J Vasc Surg 2001; 34(1): 114–21 Leville CD, Kashyap VS, Clair DG et al. Endovascular management of iliac artery occlusions: extending treatment to TransAtlantic Inter-Society Consensus class C and D patients. J Vasc Surg 2006; 43(1): 32–9 Yilmaz S, Sindel T, Yegin A, Luleci E. Subintimal angioplasty of long superficial femoral artery occlusions. J Vasc Interv Radiol 2003; 14(8): 997–1010 Hirsch AT, Haskal ZJ, Hertzer NR et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic). J Am Coll Cardiol 2006; 47(6): 1239–312 Saha S, Gibson M, Magee TR et al. Early results of retrograde transpopliteal angioplasty of iliofemoral lesions. Cardiovasc Intervent Radiol 2001; 24(6): 378–82 McLafferty RB. Patient selection: lesion characteristics and predictors of outcome. Perspect Vasc Surg Endovasc Ther 2006; 18(1): 25–9 Bolia A, Brennan J, Bell PR. Recanalization of femoro-popliteal occlusions: improving success rate by subintimal recanalisation. Clin Radiol 1989; 40: 325 Nice C, Timmons G, Bartholemew P, Uberoi R. Retrograde vs. antegrade puncture for infra-inguinal angioplasty. Cardiovasc Intervent Radiol 2003; 26(4): 370–4 Nadal LL, Cynamon J, Lipsitz EC et al. Subintimal angioplasty for chronic arterial occlusions. Tech Vasc Interv Radiol. 2004; 7: 16–22 Ingle H, Nasim A, Bolia A et al. Subintimal angioplasty of isolated infragenicular vessels in lower limb ischemia: long-term results. J Endovasc Ther 2002; 9: 411–16 Jacobs DL, Motaganahalli RL, Cox DE et al. True lumen reentry devices facilitate subintimal angioplasty and stenting of total chronic occlusions: Initial report. J Vasc Surg 2006; 43(6): 1291–6 Topaz O, Minisi AJ, Bernardo NL et al. Excimer laser effect on platelet aggregation. Am J Cardiol 2001; 87: 849–55
15. 16. 17. 18.
19. 20. 21. 22. 23.
24.
25. 26. 27. 28. 29.
Balzer JO, Gastinger V, Thalhammer A et al. Percutaneous laserassisted recanalization of long chronic iliac artery occlusions: primary and mid-term results. Eur Radiol 2006; 16(2): 381–90 Scheinert D, Laird JR, Schroder M et al. Excimer laser-assisted recanalization of long, chronic superficial femoral artery occlusions. J Endovasc Ther 2001; 8: 156–66 Laird JR. Late breaking clinical trials. LACI (laser angioplasty in chronic ischemia) trial. TCT Annual Meeting, September, 2002, Washington DC. Mossop PJ, Amukotuwa SA, Whitbourn RJ. Controlled blunt microdissection for percutaneous recanalization of lower limb arterial chronic total occlusions: a single center experience. Catheter Cardiovasc Interv 2006; 68(2): 304–10 Melzi G, Cosgrave J, Biondi-Zoccai GL et al. A novel approach to chronic total occlusions: the crosser system. Catheter Cardiovasc Interv 2006; 68(1): 29–35 Grube E et al. High frequency mechanical vibration to recanalize chronic total occlusions after failure to cross with conventional guidewires. J Invasive Cardiol 2006; 18: 85–91 Laird J. Recanalization of peripheral artery CTOs using the CROSSER catheter system: The PATRIOT feasibility study results. TCT Annual Meeting, September, 2006, Washington DC. Morales PA, Heuser RR. Chronic total occlusions: experience with fiber-optic guidance technology – optical coherence reflectometry. J Interv Cardiol 2001; 14: 611–6 Kirvaitis RJ, Heuser RR, Das TS et al. Usefulness of optical coherent reflectometry with guided radiofrequency energy to treat chronic total occlusions in peripheral arteries (the GRIP trial). Am J Cardiol 2004; 94(8): 1081–4 Dippel EJ, Shammas NW, Takes VS, Youngblut MM. Single center experience with the novel intra-luminal Safe-Cross wire for percutaneous treatment of peripheral vascular chronic occlusions. TCT-185. September 15–17. Am J Cardiol 2003: 82L Wholey MH, Maynor MA, Wholey MH et al. Comparison of thrombolytic therapy of lower extremity acute, subacute and chronic arterial occlusions. Cathet Cardiovasc Diagn 1998; 44: 159–69 Motarjeme A. Thrombolysis and angioplasty of chronic iliac artery occlusions. J Vasc Interv Radiol 1995; 6: 665–725 Motarjeme A. Thrombolytic therapy in arterial occlusion and graft thrombosis. Semin Vasc Surg 1989; 2: 155–78 Atmakuri SR, Lev EI, Alviar C et al. Initial experience with a magnetic navigation system for percutaneous coronary intervention in complex coronary artery lesions. J Am Coll Cardiol 2006; 47(3): 515–21 Strauss BH, Goldman L, Qiang B et al. Collagenase plaque digestion for facilitating guide wire crossing in chronic total occlusions. Circulation 2003; 108(10): 1259–62
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32.
Raval AN, Karmarkar PV, Guttman MA et al. Real-time magnetic resonance imaging-guided endovascular recanalization of chronic total arterial occlusion in a swine model. Circulation 2006; 113(8): 1101–7
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Catheter-directed intra-arterial thrombolytic therapy NN Khanna and RR Kasliwal
Introduction
In chronic limb ischemia:
Up until now, surgery was the only means of treating limb ischemia because of thrombosis in the peripheral arterial system. Acute lower limb ischemia (ALLI) is a surgical emergency and is associated with significant mortality and high rates of limb loss if there is delay in the treatment.1,2 Until now, surgical embolectomy had been the only approach but it is still associated with 10–18%3,4 amputation rate and 5–18% mortality.5,6 This is because surgical balloon thromboembolectomy (Fogarty embolectomy) causes endothelial damage and cannot de-clot small arteries of the leg and foot. Moreover, surgery carries a risk of infection and anesthesia. Catheter-directed intra-arterial thrombolytic therapy (CDTT) has been developed and perfected to treat thrombotic occlusion of the peripheral arteries. CDTT consists of direct intra-arterial infusion of a concentrated dose of fibrinolytic agents into the thrombus to restore blood flow to the ischemic limb. This uncovers underlying stenotic lesions which are then treated by an endovascular or surgical approach. Because the lytic agent is infused locally, the risk of bleeding is drastically reduced and the systemic affects of the drug are also reduced. In 1963, McNicol et al. and Verstraete et al. were the first to report their experience of local intra-arterial thrombolysis for peripheral arterial occlusions using intra-arterial streptokinase infusion. The father of interventional radiology, Charles Dotter9 proposed the basic presets of catheter-directed local delivery of thrombolytic agents directly at the sight of thrombosis. Dotter’s coaxial system led to larger arteriotomy size and resulted in a higher incidence of hemorrhagic complications. Subsequent refinement of the catheter design by Porstman10 and Gruntzig11 in 1970s and 1980s lead to a resurgence of peripheral intra-arterial thrombolysis in 1990s.
●
General goals of catheter-directed intra-arterial thrombolysis
●
●
to recanalize a chronic total occlusion; to soften the old clot which may then be treated by endovascular technique; to restore proximal vessel patency to facilitate distal bypass.
In this chapter, we will discuss the current status of catheterdirected intra-arterial thrombolytic therapy, including its indications, techniques, hardware, and results.
Thrombolytic agents The following thrombolytic agents are in general practice: ● ● ● ● ●
streptokinase (STK) urokinase recombinant tissue plasminogen activator (rtPA) anistreplase (APSAC) reteplase.
Urokinase and rtPA are commonly used in clinical practice. Although urokinase is very effective, its use has been banned in the US. rtPA is the only agent which is being used in that country. The pharmacokinetics, advantages and disadvantages of streptokinase, urokinase, and rtPA are given in the Table 16.1. Several new thrombolytic agents are under clinical trial. Recently, clinical studies in peripheral arterial occlusion have been published for recombinant urokinase,7 recombinant glycosylated pro-urokinase,8 and recombinant staphylokinase.9 Recombinant glycosylated pro-urokinase and recombinant staphylokinase have been shown to be effective without inducing fibrinogen depletion. Fibrin specificity of these agents appears to be an important advancement in CDTT because fibrinogen depletion is significantly (p < 0.01) related to hemorrhagic complications of urokinase and rtPA.10
In acute limb ischemia: ● ● ●
● ●
to restore antegrade flow by thrombolysis; to lyse thrombus in distal run-off vessels; to convert urgent surgical revascularization to elective surgical/endovascular revascularization; to limit the extent of surgical revascularization; to minimize the level of amputation when limb salvage fails.
Streptokinase (STK) In the early days of intra-arterial thrombolysis, STK was the most widely used agent. Hess et al.11 in 1982 originally proposed repeated intrathombus injection of 1000–3000 IU of STK with step-by-step advancement of catheter between two injections (stepwise infusion). However, this regimen was soon replaced by low-dose continuous infusion with the aid of 99
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Textbook of peripheral vascular interventions Table 16.1
Thrombolytic agents for CDTT
Dose:bolus Infusion Half-life Fibrin specificity Rate of lysis Hemorrhage Clinical success Immunogenic Platelet activation
rtPA
Urokinase
Streptokinase
— 0.5–2.0 mg/h < 5 min High Rapid 10% 90% No No
250,000 U 50,000–100,000 units/h 15 min Intermediate Slow 10% 75–90% Yes No
Empirical Empirical 23 min Low Slow 20% 60–70% Yes Yes
an arterial infusion pump at a rate of 5000 IU/hour following excellent results reported by Katzen in 1981.12 However, his results were not reproduced by MacNamara and other groups13 and in recent years, and rtPA has largely superceded and replaced streptokinase as the preferred agent in clinical use. Urokinase The dosage schemes varied initially, but now the low-dose concept is being gradually replaced with high-dose regimen. The most popular protocol was introduced by MacNamara13 and consists of initial infusion of 4000 IU/minute for 2 hours or until restoration of antegrade flow followed by 2000 IU/minute for the next 2 hours and 1000 IU/hour for the next 4–24 hours or until the lysis is completed. Systemic heparin infusion is continued during CDTT and is continued until definite endovascular or surgical treatment of underlying lesion is completed. MacNamara reported complete lysis in 75% cases.13 The average time for initial re-establishment of antegrade flow was 3.3 hours and for complete clot lysis was 13 hours. Significant bleeding complications were seen in only 4% of cases. Further analysis resulted in the following useful precepts: 1. Easy traversibility of the clot with non-hydrophilic guidewire (0.035-inch outside diameter) indicated that the thrombus was still not organized and predicted 100% success of thrombolysis (the wire traversal test) (Figure 16.1). 2. Significant lysis within the first 2 hours also predicted 100% likelihood of achieving complete clot lysis with continued infusion of urokinase. 3. Heparin infusion (maintaining APTT from 80 to 120 seconds) prevented pericatheter thrombus, distal embolization and was not associated with increased incidence of bleeding. 4. The final 10–20% of the clot is slow to lyse and can be often mistaken for an atherosclerotic plaque. PTA at this stage may lead to fragmentation and distal embolization of the thrombus resulting in acute ischemic insult of the leg and foot. 5. Underlying flow limiting lesion is present in 70% of the cases and surgery or PTA can be performed immediately after thrombolysis with no additional risk of bleeding.
Phase 1 of the Thrombolysis or Peripheral Arterial Surgery (TOPAS) trial compared the safety and efficacy of three dosage schemes of recombinant urokinase with the operative interventions in 213 patients with acute lower extremity ischemia. It concluded that 240,000 IU/hour for 4 hours and then 120,000 IU/hour to a maximum of 48 hours was the most appropriate regimen with a lytic efficacy of 71% and a bleeding risk of just 2%.14 Recombinant tissue plasminogen activator (rtPA) The range of usual dosage schemes for catheter-directed thrombolytic therapy has been 0.05–0.1 mg/kg/hour or 0.25–1.0 mg/hour. Usually either 0.05 mg/kg/hour or 1 mg/hour infusion is used. There are few prospective randomized trials comparing different thrombolytic agents. One open-ended trial compared intra-arterial STK with intra-arterial and intravenous tPA in 60 patients with recent onset or deterioration of pre-existing limb ischemia.15 Initial angiographic success
Figure 16.1
Wire traversal test.
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Catheter-directed intra-arterial thrombolytic therapy was 100% with intra-arterial tPA, 80% (p < 0.04) with intra-arterial STK, 45% (p < 0.01) with intravenous tPA. The 30-day limb salvage rates were 80, 60, and 45% respectively. In the Surgery versus Thrombolysis for Ischemia of the Lower Extremity (STILE) study, there was no difference in efficacy or bleeding complications in patients receiving tPA or urokinase.16
Dosage Table 16.2 summarizes the recommended doses of various thrombolytic agents for catheter-directed peripheral intra-arterial thrombolysis.
Delivery catheter systems Several catheters have been specifically designed for infusion of thrombolytic agents. Most of them are = 5 French in caliber and may have an end-hole or side-holes over different infusing lengths (5, 10, 15, 20 cm). They may or may not require an end-hole occluding wire. Recent designs incorporate a oneway valve at the distal end so that the tip-occluding wire is not needed during pulse spray infusion. Some people have also used a two-catheter system coaxially (e.g. 5-French outer with a 3-French inner) to bathe long segments evenly and to change the infusion length as the thrombolysis progresses. Some of the commercially available drug delivery catheters are: ● ● ● ●
Angiodynamic drug delivery catheter McNamara coaxial catheter Mewissen multi-side-hole catheter (Figure 16.2) Katzen infusion wire
Table 16.2
● ● ●
SOS infusion wire Cragg Convertible wire Dispatch catheter
However, till now there is no evidence that a particular infusion catheter or technique is superior to the other. Infusion methods Stepwise infusion This consists of stepwise advancement of the tip of infusion catheter as the thrombus dissolves. It is labor-intensive and requires the patient to remain in the angiographic suite. Graded infusion This refers to the protocol of periodic tapering of infusion rate. McNamara13 was the first to demonstrate the shortening of the duration and reducing the dose of lytic therapy by using this technique. Continuous infusion This is the most common method of catheter-directed thrombolysis. This may or may not be preceded by intrathrombus lacing. Pulse spray technique This refers to the technique of forcibly injecting thrombolytic agent into the thrombus to fragment it so as to increase the surface area available for the action of thrombolytic agents. It was originally developed for the potential of accelerating lysis.
Adjunctive technique Catheter suction thromboembolectomy (thromboaspiration), and mechanical thrombectomy by Possis Angiojet or
Recommended doses of various thrombolytic agents for CDTT
Agent
Infusion technique
Dose
Urokinase
Continuous infusion Graded infusion
120,000–240,000 IU/h McNamara protocol 4000 IU/min for 2 hours or up to restoration of antegrade flow followed by 2000 IU/min for 12–24 h or until complete lysis 60,000 IU followed by McNamara protocol 250,000 IU followed by 50,000 IU/h 5000 IU every 30 s for 20 min 2000 IU/cm occlusion length 1000–2000 IU/min in distal thrombus
Intrathrombus lacing Pulse spray
rtPA
Streptokinase Topas trial
Intraoperative thrombolysis Continuous infusion Pulse spray Intraoperative thrombolysis Continuous infusion Intraoperative thrombolysis
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0.05–0.1 mg/kg/h 3 × 5 mg (0.33 mg/ml) at 5–10 min interval) followed by 0.05 mg/kg/h infusion 0.1 mg every 30 s for 20 min 3 × 5 mg bolus over 30 min 3000–4000 every 3–5 5000–150,000 IU slow bolus or within 30 min 240,000 IU/h × 4 h 120,000 IU/h for up to maximum of 48 h
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(a)
(b)
(d)
(e)
(c)
Figure 16.2 (a) Acute thrombosis of right superficial femoral artery and popliteal artery; (b) result after 24 hours of thrombolysis; (c) mechanical thrombectomy with Oasis thrombectomy catheter; (d) final result after sequential thrombolysis with urokinase. Complete resolution of thrombus in right superficial femoral artery; and (e) final result: complete resolution of thrombus in popliteal artery.
(a)
(b)
(c)
Figure 16.3 (a) Acute thrombosis of left axillary artery; (b) catheter-directed intra-arterial thrombolysis (CDTT) using a multiple-hole Meweissen catheter placed in the entire length of thrombus; (c) final result after 18 hours of CDTT.
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Catheter-directed intra-arterial thrombolytic therapy Hydrolyser are adjunctive techniques to remove arterial clots. They may be used in conjunction with peripheral intra-arterial thrombolysis. Peri-procedural anticoagulation (heparin) is recommended until the underlying cause has been corrected. Aspirin therapy is also recommended.
Clinical indications The potential benefit of thrombolytic intervention with respect to alternative treatment modalities should be balanced against the potential risks of intra-arterial thrombolysis. The following are the indications of catheter directed intra-arterial thrombolytic therapy. Acute arterial occlusion Acute limb ischemia is a clinical challenge to clinicians. The problem presented by acute ischemia is compounded by the problems following revascularization due to reperfusion injury. In spite of several advancements in the management (both surgical and endovascular) acute limb ischemia continues to be associated with significant mortality and limb loss. Except in cases of profoundly ischemic limb where unacceptable delay in effective reperfusion is anticipated with thrombolysis, or in patients of irreversible limb ischemia, intra-arterial thrombolysis is the treatment of choice. If started early, it offers the greatest potential for saving lives and limbs. Therapeutic anticoagulation and correction of underlying lesion is also a part of overall management strategy in these patients. Surgical/Fogarty embolectomy has been associated with 10–30% mortality and limb loss. Intra-arterial thrombolysis followed by endovascular correction of the underlying lesion, on the contrary, is associated with just 1.6% 30-day mortality and 8% amputation rate.17 An interesting cost-effectiveness study by Kolassa et al. reported that CDTT is 47% more costeffective than immediate surgical intervention (based on the cost per life saved).18 Chronic arterial occlusion CDTT for chronic arterial occlusions is successful in 80% of the cases. However, it requires prolonged infusion. Chronic occlusions and chronic critical limb ischemia is often associated with extensively diseased vascular bed, advanced age, and coronary artery disease. The pioneering work of Amir Motarjeme19 revealed that even if one segment is recanalized the improvement in blood flow is sufficient to treat rest pain or ulcers. If the revascularized segment remains patent for 3 months, the non-healing ulcer will heal and interestingly the recurrence of this occlusion is not necessarily followed by the recurrences of the ulcer. However, for the treatment of gangrene, pulsatile blood flow to the foot is essential. Therefore, complete revascularization is advised. In a study of 238 patients, Mortarjeme reported 78% 5-year limb salvage rate and 60% 4-year primary patency rates with intra-arterial thrombolysis.20 Reocclusions are usually late and most of the time are associated with a benign course and less marked
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symptoms. They occur primarily in infrainguinal locations and can be prevented by regular duplex surveillance and timely treatment of restenosis (Figures 16. 4 and 16.5). Occluded bypass grafts Although open surgical procedure has been the traditional approach for bypass graft occlusion, intra-arterial thrombolysis has been advocated as an alternative means for restoring arterial patency. It is quite simple and effective, and successful CDTT unmasks the cause of bypass graft failure in the majority of cases thereby facilitating further treatment strategy. It also cleans clots in the distal outflow thereby reducing the chances of rethrombosis. Graft patency after successful CDTT and endovascular correction of the underlying stenosis is 89% at 1 year and 79% at the end of second year. Secondary patency is better for aortobifemoral bypass and venous grafts as compared to prosthetic grafts (24–69% vs. 29%) and below knee-vein grafts with thrombosis of small outflow vessels. Patients with graft occlusion of less than 2 weeks duration should be offered thrombolytic therapy as primary treatment modality. Thromboembolism Clinical diagnosis of arterial embolism in the leg is suggested on the basis of a sudden onset of clinical symptoms, the presence of an embolic source, and the absence of preceding claudication. Thrombolysis as well as thromboaspiration are the preferred lines of treatment as Fogarty’s thromboembolectomy is incomplete in 30% of cases. Full dose of intravenous heparin should be used in conjunction with intra-arterial thrombolysis. Thrombolysis is particularly useful in the setting of a fragmented thrombus which occludes many branches, and where it is complicated by a propagated thrombus (Figure 16.6). Peroperative thrombolysis Peroperative thrombolysis is used for residual thromboembolic material following mechanical thromboembolectomy or for thrombotic occlusion of small arteries in patients already undergoing an open surgical procedure. Thrombolytics are given as bolus or slow infusion as close as possible to the clot or within the thrombus itself. Acute occlusion following PTA Two to three percent of patients undergoing PTA have acute thrombotic occlusion. It is successfully managed by intra-arterial urokinase or rtPA infusion. Distal emboli can also be treated successfully by catheter-directed thrombolytic therapy. Thrombosed popliteal aneurysm These occur in association with an aortic aneurysm and usually present with acute ischemia. The aim of intra-arterial thrombolysis in these patients is only to restore patency of the thrombosed distal run-off vessels. The aneurysm itself is treated surgically.
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(a)
(b)
(d)
(e)
(c)
Figure 16.4 (a, b) Chronic thrombosis of left axillary artery, brachial artery, radial, and ulnar arteries; (c–e) complete resolution of thrombus in axillary artery, brachial artery, radial, and ulnar arteries and palmer arch arteries after 108 hours of CDTT.
Trash foot/blue toe syndrome Classically this was thought to be caused by cholesterol embolism from ulcerated plaque but is now thought to be due to thromboemboli. Intra-arterial thrombolysis is very effective in these groups of patients and usually changes the prognosis from amputation to no tissue loss. Heparin-induced thrombotic thrombocytopenia (HITT) Heparin induced thrombotic thrombocytopenia (HITT) was until now considered as absolute contraindication for intraarterial thrombolysis for the risk of bleeding complications. However, it is the only treatment available and represents an important breakthrough in the treatment of this condition as surgery is not possible because of the inability to use heparin. CDTT is not associated with unusual bleeding despite the thrombocytopenia. Acute ischemic stroke Intracranial microcatheter-directed thrombolysis by urokinase or rtPA has yielded 80% success in thrombus clearance
within 1 to 2 hours of infusion.21 Reports have suggested that the incidence of intra-cerebral hemorrhage is not significantly increased by intracranial thrombolysis. Thrombosed dialysis access grafts These are readily treated by thrombolysis and adjuvant PTA with 90% initial success. Secondary patency rates at 6 months and 1 year are 75 and 25%.22 The procedure is very fast and hemodialysis can be resumed within 2 hours. Therefore, these patients can remain on their hemodialysis schedule without the need for placing a temporary hemodialysis catheter and a surgical revision can be avoided for a long time. Bookstein’s strategy of pulse spray delivery of urokinase to declot the dialysis graft is very popular at the present time. Massive pulmonary embolism Massive pulmonary embolism (Figure 16.7) is a cardiac emergency and is best treated by CDTT using urokinase or TPA delivered directly into the clot in a pulmonary artery.
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(a)
(b)
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(c)
(d) Figure 16.5 (a) Chronic popliteal thrombosis (duration 3 months); (b) CDTT using multiple side-hole 4-French multipurpose catheter placed in the entire length of popliteal and proximal part of anterior tibial artery; (c, d) complete lysis after 76 hours of thrombolysis showing totally recanalized popliteal artery and anterior tibial artery.
Its results are better than that of IV heparin alone and thrombolysis is achieved much faster than with IV heparin. It is often accompanied by intrapulmonary artery hydrolytic thrombectomy by Angiojet or plain and simple thrombosuction.
●
● ● ● ●
Contraindications
● ●
Absolute ● established cerebrovascular accident (including TIAs within the last 2 months); ● intracranial trauma within the last 3 months; ● neurosurgery (intracranial, spinal) within the last 3 months; ● active bleeding diathesis; ● recent gastrointestinal bleeding (< 10 days). Relative cardiopulmonary resuscitation within the last 10 days; ● major non-vascular surgery or trauma within the last 10 days; ●
uncontrolled hypertension: > 180 mmHg systolic or > 110 mmHg diastolic; puncture of non-compressible vessel; intracranial tumor; hepatic failure, particularly those with coagulopathy; bacterial endocarditis; pregnancy; diabetic hemorrhagic retinopathy.
Complications Hemorrhage is the most common complication of CDTT. It may occur because of lysis of pre-existing hemostatic plug or loss of vascular integrity. Berridge et al.23 did a meta-analysis of ten prospective series of patients undergoing peripheral intra-arterial thrombolysis to determine the incidence of hemorrhagic complications. The overall risk of hemorrhagic stroke was 1% (14 out of 1401 patients). Major and minor bleeding occurred in 5.1 and 14.8% of patients. Recently Dawson et al.24 reported on the series of patients of the British Thrombolysis Study Group and found the incidence of
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(a)
(b)
(d)
(e)
(c)
Figure 16.6 (a, b) Massive thromboembolism in a patient of dilated cardio myopathy and atrial fibrillation resulting in saddle embolism of aortic bifurcation, total occlusion of left common iliac artery and left common femoral artery, partial occlusion of right common femoral artery, and saddle embolism at right common femoral bifurcation; (c) CDTT using 4-French pigtail catheter via left radial route placed at aortic bifurcation; and (d, e) complete resolution of thrombus after 12 hours of CDTT.
hemorrhagic stroke to be 2.3% (27 of 1157 patients) (half of which occurred during thrombolysis). STILE and TOPAS investigators (comparing surgery vs. thrombolysis) reported incidence of intracranial bleeding to be 1.2 and 2.1% respectively.7 Bleeding into the retroperitoneal space from the inadvertent posterior wall puncture may go undetected until hypotension develops or the patient presents with unexpected abdominal symptoms or back pain or sudden development of anemia without obvious blood loss. In cases of major hemorrhage, CDTT is discontinued and any coagulation defect if present is corrected. Irrespective of the site of major bleeding, management follows a standard pattern of discontinuation of CDTT and anticoagulation, replenishment of coagulation factors and blood, surgical evacuation of hematoma (if necessary), and rapid reversal of fibrinolytic state by tranexemic acid or epsilon aminocaproic acid (in cases of life-threatening hemorrhage). Distal embolization of a partially lysed clot is also a potential risk. Small emboli are clinically silent but large fragments that occlude distal tibial or foot arteries are potentially more harmful and may lead to clear clinical deterioration. However,
CDTT should be continued in this case. Additional measures to be considered are the repositioning of the infusion catheter more distally, increasing the dose or new boluses of thrombolytics, thromboaspiration, and angiojet. Allergic reactions can occur with STK and usually present with flushing, vasodilation, rash, hypotension, or anaphylaxis. Late reactions include serum-like illness and presents with joint pain, fever, and microscopic hematurea, usually 10–21 days after the thrombolysis. It has a benign outcome although permanent renal impairment has been reported.
Technique of catheter directed intra-arterial thrombolytic therapy (CDTT) Patient selection Patient selection is aimed at re-establishing blood flow. Best results are seen in thrombus which is less than 2 weeks old. However, lysis has been successful up to 90 days
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(f)
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Figure 16.7 (a) Massive pulmonary embolism leading to saddle embolism in main pulmonary artery and massive occlusive thrombus in bilateral pulmonary arteries; (b–e) Possis Angiojet thrombectomy of main pulmonary artery and right and left upper and lower lobe pulmonary arteries; and (f–h) excellent thrombolysis and recanalization of bilateral pulmonary arteries.
(although it takes longer time to lyse and the rate of success is low). The predictors of success are: ●
●
guidewire traversal test (if the guidewire traverses the clot, the chances of success are 100%); age of thrombus < 14 days (almost 100% success);
● ● ●
length of thrombus < 5 cm; good distal run-off; evidence of clot resolution within 2 hours (almost 100% success).
Patient selection is also aimed at minimizing the risk of bleeding or in other words excluding patients who are at a
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high risk of bleeding and ischemic complications and reperfusion injury. These contraindications are: ● ● ● ●
● ● ● ● ● ● ●
recent internal bleeding = 10 days; cerebrovascular accident < 6 months; transient ischemic attack < 2 months; history of gastrointestinal bleeding, cardiopulmonary resuscitation, major trauma, pregnancy < 6 months; systolic BP > 180 mmHg and diastolic BP > 110 mmHg; recent major surgery < 2 weeks; infective endocarditis; hepatic and renal failure; patients with intracardiac thrombus; established compartment syndrome or evidence of myolysis; patients with electrolyte imbalance, systemic acidosis, or left ventricular dysfunction.
Patient preparation Informed consent should be taken before the procedure and the risk and benefits of the procedure should be explained. Consent should also be taken for additional surgical or interventional procedure which may be required when underlying stenotic lesion is uncovered. Laboratory work should include complete blood counts, electrolytes, urea and creatinine, myoglobin, CPK, bleeding and coagulation time, blood grouping and cross-matching, prothrombin time, partial thromboplastin time, and activated clotting time (for monitoring heparin therapy). Some centers also assess parameters which reflect systemic lytic state (e.g. fibrinogen, fibrin degradation product (FDP), plasminogen levels). Very low levels of fibrinogen (< 10%) predicts bleeding complications. Technique The first step is to do an initial baseline angiography to map out the location and size of thrombus, the feeding collaterals and distal run-off vessels. Arterial access is then gained through antegrade ipsilateral approach or contralateral retrograde crossover approach. A 5-French or 6-French arterial sheath is placed. Then a guidewire transversal test is done to characterize the thrombus. Failure to cross the thrombus predicts a lower success rate and prolonged infusion time. In this situation the catheter is left proximal to the clot. In many cases the thrombus subsequently softens and can be crossed easily. After crossing the thrombus the infusion catheter is placed in the thrombus and the lytic agent is infused. Any of the previously described infusion methods can be adapted.
Monitoring the therapy Patients of catheter-directed intra-arterial thrombolytic therapy are kept under close observation in the intensive care unit. The ACT is kept between 200 and 250 seconds and the PTTK is kept between 2 and 2.5 times control. Continuous intra-arterial heparin is given through the side part of the arterial sheath to prevent clot formation around the catheter. Continuous hemodynamic and hematocrit monitoring is done for assessment of any
possibility of internal bleeding. The access site is closely observed and urine output is closely monitored. After completion of lysis the infusion catheter and the arterial sheath are removed and systemic anticoagulation is started after 4 hours. Angiographies are done frequently to assess the progress of thrombolysis and many the infusion catheter are advanced or readjusted regularly. After completion of thrombolysis underlying lesions are treated by PTA or stenting.
Experience at the Polyclinique Essey-Les-Nancy, France Our data for catheter-directed intra-arterial thrombolysis in 113 consecutive patients is reported below. Material and methods Eighty-three patients received intra-arterial thrombolysis between January 1999 and December 2005. The mean age of these patients was 60.6 ± 8.5 years (46–89 years). The majority of them were males and had thrombosis of the native arteries of the lower extremity. Thirty-nine had thrombosis of aortobifemoral or femoropopliteal bypass grafts. Eight-two of these 113 patients were referred to us within 15–90 days of the onset of thrombosis. The thrombolysis was done with intra-arterial infusion of urokinase according to McNamara’s protocol (4000 IU/minute for 2 hours followed by 2000 IU/minute for the next 2 hours and 1000–2000 IU/min until lysis completion. All patients received adjuvant aspirin and heparin infusion. Urokinase was delivered by Mewissen or thrombolysis catheter (Medicorp S.A., Villers-les-Nancy, France). The infusion catheter was positioned within the thrombus and advanced forwards as the fibrinolysis progressed. The patients were shifted to the CCU and brought back to the catheterization lab every 2–4 hours for angiographic reassessment of the progress of fibrinolysis, until the lysis was complete or there was no improvement. In most of the cases underlying stenosis was present and was treated. Patients with failure of lysis were either subjected to clot removal by thromboaspiration or were sent for surgery. All patients were followed up by angiography at 6 hours and by duplex scan at 1 day, 1 month and 6 months. Results One-hundred and thirteen consecutive patients with mean age of 60.6 ± 8.5 years underwent CDTT. Thrombosis was present in native arteries in 74 patients and in the bypass grafts in 39 patients. The duration of thrombosis was 1–4 days in 26 patients, 15–90 days in 82 patients and more than 90 days in 5 patients (Box 16.1) Complete clot lysis was seen in 80% of the patients (92/113). The mean duration of fibrinolysis was 18 hours. Incomplete lysis was seen in 19% of the patients (21/113). In the patients who failed to achieve significant clot lysis the majority had a more than 30-day-old thrombus. In seven of these patients the lysis was significant but still incomplete and
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Catheter-directed intra-arterial thrombolytic therapy Box 16.1 ● ●
No. of patients: Age
●
Male / Female
●
Bypass Grafts: Duration of thrombosis 䊊 1–14 days 䊊 15–90 days 䊊 ≥ 91 days Duratioin of fibrinolysis
●
●
Box 16.3 113 60.6 ± 8.5 (46–89) Aorticilicac : 30 Femoropopliteal: 41 Tibioperoneal : 3
25 82 5 18 hours
the residual clot was removed by thromboaspiration. The remaining 14 patients were sent for surgery. Significant underlying stenosis was present in 70 patients. Twenty-seven of them were treated with angioplasty alone while 43 patients received stent implantation. The success of CDTT was greater in patients of thrombosis of bypass graft (88%) (Box 16.2). Nineteen patients had minor complications in the form of local hematoma at the puncture site. Four patients had a major hematoma requiring surgery or blood transfusion. Distal embolism was seen in five patients and was successfully managed by increasing the infusion rate of urokinase and advancement of the infusion catheter near the emboli or by thromboaspiration. One patient died because of severe renal and cardiac failure. This patient had advanced chronic renal failure and severe coronary artery disease. None of our 113 patients had systemic or intracranial bleeding.
Discussion At six months, 63 of these 79 patients were followed up. Fifty-three had patent-treated arteries and grafts while restenosis
Complications
• Hematoma 䊊 Major: 4 䊊 Minor: 19 • Embolism: 5 • Death: 1 (Due to severe renal and cardiac failure) • Intracranial/systemic bleeding 0
was seen in ten patients. They were managed by repeat PTA in nine cases. One patient went for surgery because of personal preference. CDTT is very effective and saves the patients from limb loss or dying. It is better than surgery in most of the situations as surgery carries higher risk of complications. Ouriel reported lower in-hospital complications and mortality rates with fibrinolysis as compared to surgery (22 vs. 80%, p < 0.05).24? In the STILE trial at 6-months follow-up, patients who received PIAT had lower amputation rate (16 vs. 30%, p < 0.02) in comparison to those who went for surgery. The Rochester trial reported the results of a 12-month follow-up. The mortality rates in the thrombolysis group were 16 versus 58% in surgery group (p < 0.01). Conclusion PIAT is a safe, effective and alternative treatment modality for the treatment of thrombosis of native arteries and bypass grafts. The initial results are very encouraging and reports from various trials (STILE, TOPAS, ROCHESTER)4,5,6 suggest that it is perhaps better than surgery in terms of saving lives and limbs and is perhaps more cost-effective. Many advances have occurred in the CDTT technique and the experience is now growing in the interventional arena. The technique is now being picked up by cardiologist, radiologists, and vascular surgeons.
Box 16.2 Thrombolysis experience at the Polyclinique, Essey-les-Nancy, France Immediate results • Complete lysis: • Incomplete lysis: 䊊 Thromboaspiration: 䊊 Surgery: • Significant underlying stenosis:
Box 16.4 92 (81%) 21 (19%) 7 14 70
79% 88% 81%
Thrombolysis follow-up
113 Patients Day 1 Day 30
92 Patients F/U = 82 Patients 79 Patients
6 months
F/U = 63 53 patients
PTA (43 stents) • Success in 䊊 Native arteries: 䊊 Bypass grafts: 䊊 Occlusions 1–14 days: 䊊 Occlusions 15–90 days:
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21 incomplete lysis Lost to F/U: 10 3 occluded 2 surgery 1 PTA Lost to F/U: 16 10 Restenosis 1 surgery 9 PTA
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REFERENCES 1. Baxter-Smith D, Ashton F, Slaney G. Peripheral arterial embolism: a 20 year review. J. Cardiovasc Surg 1988; 29: 453 2. Linton RR. Peripheral arterial embolism: a discussion of the postembolic vascular changes and their relation to the restoration of circulation in peripheral embolism. N Eng J Med 1941; 224: 189 3. McPhail NV, Frastesi SJ, Barber GG et al. Management of acute thromboembolic limb ischemia. Surgery 1983; 93: 381–5 4. The STILE investigators. Results of a prospective randomized trials evaluating surgery versus thrombolysis for ischemia of the lower extremities. Ann Surg 1994; 220: 251–68 5. Macky WC. Peripheral embolization and thrombosis. In: Strandness DE Jr, van Berda A, eds. Vascular Disease: Surgical and Interventional Therapy. New York: Churchill Livingstone, 1994: 341–54 6. Ouriel K, Shortell CK, De Weese JA et al. A comparison of thrombolytic therapy with operative revascularization in the initial treatment of acute peripheral arterial ischemia. J Vasc Surg 1994; 19: 1021–30 7. For the TOPAS Investigators, Ouriel K, Veith FJ, Sasahara AA. Thrombolysis or peripheral arterial surgery (TOPAS): Phase 1 results. J Vasc Surg 1996; 23: 64–75 8. Hartmann JR, Enger EL, Villiard EM et al. Dose ranging trial of intra arterial r-prourokinase (A 74187) for thrombolysis of total peripheral arterial occlusions (abstr). J Am Coll Cardiol 1994; 23: Suppl: 95A 9. Collen D, Moreau H, Stockx L et al. Recombinant staphylokinase variants with altered reactivity. IV. Identification of variants with reduced antibody induction but intact potency. Circulation 1997; 95: 463–72 10. The STILE Investigators. Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischemia of the lower extremity: The STILE trial. Ann Surg 1994; 220: 51–68 11. Sullivan KL, Gardiner GA, Shapiro MJ et al. Acceleration of thrombolysis with a high dose transthrombus bolus technique. Radiology 1989; 173: 805–8 12. Katzen BT, Van Breda A. Low-dose streptokinase in the treatment of arterial occlusion. Am J Roentgenol 1981; 136: 1171–8
13. McNamara TO. Overview of thrombolysis for interventionalist. Ninth ETC Peripheral Course Book. Poieters: Europa, 1998, 105–21 14. Ouriel K, Shortell CK, De Weese JA et al. A comparison of thrombolytic therapy with acute peripheral arterial ischemia. J Vasc Surg 1994; 19: 1021–70 15. Berridge DC, Gregson RHS, Hopkinson BR et al. Randomized trial of intra arterial recombinant tissue plasminogen activator, intravenous plasminogen activator and intra-arterial streptokinase in peripheral arterial thrombolysis. Br Surg 1991; 78: 988–95 16. Allermand H, Wetergard-Nielsen J, Nielsen O. Lower limb embolectomy in old age. J Cardiovasc Surg 1986; 27: 440–2 17. Blaisdell FW, Steel M, Allen RE. Management of acute lower extremity ischemia due to embolism and thrombosis. Surgery 1978; 84: 822–34 18. Jivegard L, Holm J, Shresten T. The outcome in arterial thrombosis misdiagnosed as arterial embolism. Acta Chir Scand 1986; 152: 251–6 19. Motarjeme A. Thrombolytic therapy in arterial occlusion and graft thrombosis. Semin Vasc Surg 1989; 2: 155–78 20. Motarjeme A. Initial and long term results of thrombolysoangioplasty for limb salvage. American Roentgen Ray Society, New Orleans, Louisiana, April 1990, 4: 469–72 21. Mori E, Tabuchi M, Yoshida T, et al. Intracarotid urokinase with thromboembolic occlusion of the middle cerebral artery stroke. 1988; 19: 802–2 22. Kumpe DA, Cohen MAH. Angioplasty/thrombolytic treatment of falling and failed hemodialysis access sites: Comparison with surgical treatment. Prog Cardiovasc Dis 1992; 34: 263–79 23. Berridge DC, Niakin GS, Hopkinsom BR. Local l low dose intra arterial thrombolytic therapy, the risk of major stroke and haemorrhage. Br J Surg 1989; 76: 1230–2 24. Dawson K, Armon A, Braithwaite B et al. Stroke during intra arterial thrombolysis: a survey of experience in the UK (abstr). Br J Surg 1996; 83: 568
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Thromboaspiration and thrombectomy in peripheral vessels NN Khanna
Introduction Acute and subacute thromboembolic and local thrombotic lesions of the limbs are the most common cause of amputation. The standard surgical treatment of thrombotic occlusion below the inguinal ligament is the Fogarty embolectomy. However, multiple technical problems are associated with this procedure because of atherosclerotic blockages; for example, an inability to pass the obstruction, dissection, arteriospasm, and embolization of the thrombus distally in the vascular bed.1–3 Catheter-directed thrombolytic therapy (CDTT) is time consuming and expensive (requiring intensive care and repeated check angiograms) and is associated with a high risk of embolism and hemorrhage. In addition, local stenosis carries the risk of re-occlusion.4–13 The more recent catheter-directed techniques of removing a large chunk of thrombus in the peripheral arteries are: ● ●
thromboaspiration; catheter-based thrombectomy devices.
While thromboaspiration can only be used to aspirate fresh thrombi, thrombectomy devices can actually remove large chunks of fresh as well as 1- or 2-week-old thrombus. The first directional atherectomy procedure was performed in 1985 by Simpson et al. in a superficial femoral artery using a peripheral atherectomy device.14 This initial experience demonstrated the safety of directional atherectomy for peripheral vascular disease. It was approved by the US Food and Drug Administration (FDA) in 1987. In contrast to Directional Coronary Atherectomy (DCA), which relies on excision and tissue removal, the transluminal extraction–endarterectomy catheter (TEC) (Interventional Technologies Inc., San Diego, CA) was designed by Stack to cut and aspirate atheroma and debris. In 1989, this device was approved by the FDA for peripheral vascular disease. Soon, these atherectomy devices were being used as thrombectomy devices for removing large chunks of thrombus from peripheral arteries (Figure 17.1a–c). Thrombectomy devices work on the following three principles (Table 17.1): ●
●
Vortex principle. This fragments the thrombus without removing it: 䊊 Amplatz thrombectomy catheter (ATD, Microvena); 䊊 Arrow–Trerotola Thrombolysis System (Arrow). Bernouli/Venturi principle (rheolytic thrombectomy): 䊊 Hydrolyser (Cordis);
AngioJet (Possis Medical); Oasis (Boston Scientific). Mechanical clot fragmentation plus clot removal (a combination of the above two principles). 䊊 䊊
●
Straub-Rotarex (Straub Medical) This combines two essential effects: the mechanical clot fragmentation and removal of the fragmented material from the vessel under negative pressure with the theoretical effect of preventing distal embolization of thrombus. Initial model experiments,15 a single-center experience,16 and a multicenter study17 gave promising results. The Straub-Rotarex thrombectomy system This consists of three components: a 40-W electric motor connected to an 8-French/6-French, polyurethane thrombectomy catheter via an electromagnetic clutch. Within the catheter a coated steel spiral rotates at a speed of 40,000 rpm and produces a continuous vacuum (up to 5.8 kPa = 43 mmHg). The catheter tip consists of two superimposed cylinders, each having two lateral openings with the outer cylinder connected to the rotating spiral and the inner cylinder to the catheter shaft. The thrombus is first crossed with 0.035-inch Terumo wire and then a 4-French Multipurpose Terumo glide catheter (Terumo Corp., Leuven, Belgium) is used to exchange the Terumo guidewire with a 0.014-inch/0.018-inch guidewire. The device is advanced over the guidewire to remove the thrombus. Multiple passes are made until all thrombotic material is removed. The device removes approximately 10 cm of thrombus per minute. In a single-center series,18 technical success was 84% (defined as a remaining residual stenosis of < 50%). A residual stenosis of < 30% was achieved in 32% of these. This group reported a primary success rate after additional Percutenous Transluminal Angioplasty (PTA) to be 92%. The success rate in ipsilateral approach was 100% and in contralateral crossover approach 56%. The low success rate in contralateral approach is explained by the short length of the catheter (80 cm), which was not sufficient for complete recanalization of the superficial femoral artery. The complication rate with this device was 18%, of which only 8% were device-specific complications. The device-specific complications were perforation (which was sealed by PTA in three cases and covered in five cases) and retroperitoneal hemorrhage. 111
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(a)
(b)
(c) Figure 17.1 (a) Acute thrombosis of aorto renal graft; (b) DCA of thrombosed graft; and (c) final result: total recanalization.
Amputation-free survival without recurrence of critical limb ischemia after 1 year was better than in the TOPAS5 and STILE studies6 comparing surgery with local lysis, especially in native arteries. In the TOPAS trial, amputation-free survival was 65 and 69.9% for the urokinase group and the surgery
Table 17.1 Thrombolysis experience Polyclinique, Essay-les-Nancy, France No. of patients Male/female Vessels Bypass grafts Native vessels Iliac Femoral Popliteal Tibioperoneal trunk Ant. tibial Peroneal Occlusive thrombus
at
group, respectively. However, it was 95% in this cohort with comparable baseline characteristics. The main limitation of the Rotarex device is an inability to completely recanalize long lesions through a contralateral approach because of the short length of the catheter, an inability to completely remove thrombus from vessels of large diameter (e.g. iliac arteries), and a higher incidence of perforations.
the
85 47/29 85 11 74 14 38 14 6 1 1 33
The Hydrolyser This works using the Venturi effect and is a 6-French/7-French triple lumen catheter with a small injection lumen, a larger exhaust lumen, and a 0.020-inch guidewire lumen. The device is available in different lengths and is activated with a standard pressure injector filled with saline.19 For infrainguinal occlusion, the success rate is approximately 82% with positive clinical outcomes in 73% of native vessels and 53% of grafts. In about 50% of the successful interventions, additional local lysis is required to restore the distal outflow. Distal embolization of clot particles is seen in 15%. The catheter uses a high-velocity saline stream to microfragment and remove thrombus. It is available in 6, 8,
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and 10 French for use in hemodialysis access grafts and large vessels.
and results in less vessel injuries and a lower rate of distal embolization (Figure 17.3a–g).
Oasis (Boston Scientific Inc.) This is a 6-French thrombectomy system, very similar to the Hydrolyser device. It works on the Venturi principle and has just two lumens (Figure 17.2a–c).
The Amplatz Clot Buster (ATD) This is a 7-French 100-cm-long catheter based system that induces fragmentation of thrombus without removing it.21 The device leads to time-dependent transient hemolysis. The main disadvantage of this device is the fact that it cannot be guided over a wire. There is also a potential risk of vessel wall injury.
The Possis AngioJet The Possis AngioJet catheter tip consists of multiple holes that direct high-pressure water jets into the catheter lumen to remove fragmented thrombus by means of the Venturi effect. A special pump is necessary to provide a pressure of 70,000–105,000 kPa to the catheter. In a multi-center trial in infrainguinal application,20 success rate was 90%. Technical success was improved by adjunctive fibrinolysis in 30% and thromboaspiration in 18%. There was a 2% distal embolization rate and 4% rate of dissection. The advantage of this device is that it can also be used in calf arteries (also through a contralateral approach because of the longer catheter length)
(a)
The Trerotola device This is a low-speed, rotational device (5 French) primarily designed for venous thrombolysis in dialysis fistulae.22 A stainless-steel cable is connected to a self-expanding fragmentation basket made of nitinol. After passing the occlusion in a closed position, the basket is opened, activated, and slowly withdrawn through the clot leading to a fragmentation of the clot without removing it. The advantage of this device is low profile and simple handling. The main disadvantage of this device
(b)
(c) Figure 17.2 (a) Thrombosis of right SFA; (b) oasis thrombectomy; and (c) final result.
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(a)
(b)
(c)
(d)
Figure 17.3 (a) Massive pulmonary embolism; (b–e) extensive Possis AngioJet thrombectomy in each branch of the pulmonary artery and main pulmonary artery; (f) and (g) final result: significant thrombus removal.
is the limited length and potential risk of peripheral emboli with clot particles up to 3 mm in diameter. It can also potentially injure the walls of the blood vessels.
Thromboaspiration Over the last few years, this technique has become very popular among global interventionalists and cardiologists. It is a very simple technique of directly aspirating the clot with the help of a guiding catheter or sheath. It competes with Fogarty’s embolectomy. It is often better than Fogarty embolectomy because it is done under fluoroscopic guidance and can completely remove the clot, unlike the Fogarty method, which is successful in only 70% of the cases. Moreover, Fogarty is a blind procedure and is more traumatic. Thromboaspiration is an adjunctive technique to CDTT
when clot lysis is either incomplete or is complicated by distal embolism leading to deterioration of the limb ischemia. It is also an accepted technique for removing emboli in patients with mitral stenosis and atrial fibrillation.
Technique This consists of advancement of a 6-French/7-French (wide-lumen) guiding catheter or sheath under fluoroscopic guidance up to the level of the thrombus/emboli. The guidewire is then removed and the guiding catheter/sheath is attached to a 50-ml syringe. The thrombus/emboli is then aspirated manually and the guiding catheter/sheath is withdrawn under negative suction. The procedure is repeated several times until the thrombus is completely removed. Repeated angiograms are done to confirm the clot removal (Figure 17.4a–c).
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(e)
(f)
(g) Figure 17.3, cont’d.
(a)
(b)
Figure 17.4 (a) Acute arterial embolization of brachial artery; (b) final result after thromboaspiration.
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Experience at the Polyclinique Essey-les-Nancy, France (Tables 17.1 and 17.2) Eighty-five patients underwent thromboaspiration for clot removal at the Polyclinique Essey-les-Nancy between January 1997 and December 1998. Fifty-six were males and 29 were females. Seven patients had chronic atrial fibrillation. Thrombosis was present in 72 arteries/grafts while embolism was present in 13. Seventy-four patients had thrombosis in native arteries (14 in iliac arteries, 37 in femorals, 14 in popliteal, 6 in tibioperoneal trunk, 1 in anterior tibial and 1 in peroneal artery). Nineteen patients had residual thrombus after CDTT. Occlusive thrombus was present in 33 patients (Figure 17.5a and 17.5b). The procedure was successful in completely removing the clot in 78 patients (92%) and failed in 7 (8%) cases. The failure was due to distal embolization in the foot in four patients. In the majority of the cases underlying stenosis was present (52/85) and was treated with PTA in 12 patients, PTA plus stent in 33, Rotablator in 3, Laser in 4, Hydrolyser in 3, and
Table 17.2
Thromboaspiration results
Concomitant procedures Fibrinolysis Hydrolyser Possis AngioJet Laser Rotablation Stents (PTA + stent) PTA Success Failure
19 3 1 4 3 33 12 78 (92%) 7 (8%)
AngioJet in 1. There were no complications except a dissection in one case which was successfully treated with a stent.
Discussion Thromboaspiration is a safe, cost-effective, simple, and quick method of aspirating thrombi from native arteries/bypass grafts.
(a)
(b)
Figure 17.5 (a) Thrombus aspiration in occlusion of right SFA; (b) thrombus aspiration for acute occlusion of right popliteal artery.
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Thromboaspiration and thrombectomy in peripheral vessels It is particularly useful in cases of arterial embolism and residual clots after thrombolysis. In many cases it can also be used as a first line of management in acute limb ischemia (where urgent revascularization is warranted). It is better than Fogarty embolectomy as it is done percutaneously under fluoroscopic control and angiographic guidance. Fogarty on the other hand leaves behind
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residual clots in 30% of cases. We were successful in 92% of our cases with this technique and had no major complications. Anecdotal experiences are available in literature from various groups, but large-scale trials are awaited to clarify the exact place of thromboaspiration for successful clot removal from peripheral arteries.
REFERENCES 1. 2. 3. 4.
5.
6.
7. 8.
9.
10. 11.
Blaisdell FW, Stelle M, Allen RE. Management of acute lower extremity ischemia due to embolism and thrombosis. Surgery 1978; 84: 822–34 Gordon RD, Fogarty TJ. Peripheral arterial embolism. In: Rutherford RB, ed. Vascular Surgery, second ed. Philadelphia: WB Saunders, 1984: 451 Pemberton M, Varty K, Mydahl S, Bell PRF. The surgical management of acute limb ischaemia due to native vessel occlusion. Eur J Vasc Endovasc Surg 1999; 17: 72–6 Palfreyman SJ, Michaels JA. Vascular surgical society of Great Britain and Ireland: Systematic review of intra-arterial thrombolytic therapy for peripheral vascular occlusions. Br J Surg 1999; 86: 704 Ouriel K, Veith FJ, Sasahara AA. A comparison of recombinant urokinase with vascular surgery as initial treatment for acute arterial occlusion of the legs. Thrombolysis or Peripheral Arterial Surgery (TOPAS) Investigators. N Engl J Med 1998; 338 (16): 1105–11 Weaver FA, Comerota AJ, Youngblood M et al. Surgical revascularization versus thrombolysis for nonembolic lower extremity native artery occlusion: results of a prospective randomized trial. The STILE Investigators. Surgery versus Thrombolysis for Ischemia of the Lower Extremity. J Vasc Surg 1996; 24(4): 513–23 Lammer J, Pilger E, Neumayer K, Schreyer H. Intraarterial fibribolysis: long term results, Radiology 1986; 161: 159–63 Diffin DC, Kandarpa K. Assessment of peripheral intraarterial thrombolysis versus surgical revascularization in acute lower-limb ischemia: a review of limb-salvage and mortality statistics. JVIR 1996; 7: 57–63 Hess H, Mietaschke A, von Bilderling P, Neller P. Peripheral arterial occlusion: Local low-dose thrombolytic therapy with recombinant tissue-type plasminogen activator (rt-Pa). Eur J Vasc Endovasc Surg 1996; 12: 97–104 Tepe G, Lutz O, Hahn U, Pereira P et al. Gepulste Spraylyse mit Reteplase bei peripheren arteriellen Verschlussen – Technik aund erste Ergebnisse. Fortschr Rontgenstr 2000; 172: 780–84 Zahringer M, Heidel W, Gawenda M, Brochhagen HG, Landwehrr P. Akuter thrombembolischer Verschlub der A. Poplitea und
12. 13.
14. 15. 16. 17. 18. 19. 20. 21. 22.
Trifurkation aus einer als Anlageanomalie erhaltenen A, ischiadica. Fortschr Rontgenstr 1999; 171: 79–81 McNamara TO, Bomberger RA, Merchant RF. Intra arterial urokinase as the initial therapy for acutely ischemic lower limbs. Circulation 1991; 83(suppl 1): I–106, I–119 Meyerovitz MF, Goldhaber SZ, Reagan K et al. Recombinant tissue-type plasminogen activator versus urokinase in peripheral arterial and graft occlusions: a randomized trial. Radiology 1990; 175: 75–8 Simpson JB, Selmon MR, Robertson GC et al. Transluminal atherectomy for occlusive peripheral vascular disease. Am J Cardiol 1988; 61: 96G–101G Schmitt HE, Jager KA, Jacob Al et al. A new rotational thrombectomy catheter: system design and first clinical experiences. Cardiovasc Intervent Radiol 1999; 22: 504–9 Zeller T, Muller C, Frank U et al. Das Straub-Rotarex – thrombektomie-System: Erste Erfahrungen. Fortschr Rontgenstr 2001; 173: 626–31 Jager KA, Schmitt EM, Schmitt HE, Labs KH. Peripheral thrombectomy with the new Straub-Rotarex Catheter: A multicenter study. Intern Angiol 1999; (suppl. 1): 17A Zeller T. Recanalisation of thrombotic arterial and bypass occlusions using a mechanical thrombectomy device. The Paris Course on Revascularization 2003; 511: 522 Bucker A, Schmitz-Rode TH, Vorwerk D, Gunther RW. Comparative in vitro study of two percutaneous hydrodynamic thrombectomy systems. JVIR 1996; 7: 451–4 Trerotola SO, Lunc GB, Scheel PJ et al. Thrombosed dialysis access grafts: Percutaneous mechanical declotting without urokinase. Radiology 1994; 191: 721–6 Bildsoe MMC, Moradian GP, Hunter DW, Castaneda-Zuniga WR, Amplatz K. Mechanical clot dissolution: new concept. Radiology 1989; 171: 231–3 Tretola SO, Johnson MS, Schauwerker DS et al. Pulmonary emboli from pulsed-spray and mechanical thrombolysis: Evaluation with an animal dialysis-graft model. Radiology 1996; 200: 169–76
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The future of thrombolysis T McNamara
Increasing applications Stroke 1. The increasing age of the world’s population will increase the number of patients with stroke. 2. The triage will improve to bring patients in earlier. 3. Existing techniques will improve as follows: a. Combining ultrasound delivered through the tip of a catheter increases the effectiveness of lysis resulting in shorter times to re-establishment of flow without increasing the risk of bleeding. b. Giving a concurrent infusion of microbubbles (IV) should also shorten the time to achieve flow. c. Clinical trials of both of these additions to lysis are being conducted. d. Theoretically, combining these modalities would be additive (or synergistic) to clearing clot. This is not presently being trialed.
Myocardial infarction The above may also be applied to acute coronary occlusions to bring about faster lysis with a fraction of the dose of lytic now utilized. The result could be expected to achieve more complete lysis with less of the negative reflow phenomenon seen with balloon angioplasty alone; but without increasing the risk of bleeding. Venous occlusions At this time leg DVT is handled with systemic heparinization followed by 6–12 months of coumadin. This yields a high percentage of valvular insufficiency, and the sequelae of postthrombotic syndrome is in the region of 80%. The above techniques plus the pharmacomechanical combination obtained with the Trellis device, Rotarex, and the AngioJet could restore flow in a single setting with the ability of the patient to be quickly discharged (perhaps even on the same day), with valve function preserved. Pulmonary embolism Anecdotal reports of markedly improving the clearing of hemodynamically significant pulmonary embolism with both
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power pulse spray, and combination of ultrasound and lysis have been reported. At this time the applications are in patients who are having hemodynamic problems and whose clots have been resistant to systemic lysis and anticoagulation. A formal study to confirm the efficacy could result in a major change in the practice of medicine for this group of patients, resulting in a shorter ICU time, less morbidity, and some decrease in mortality.
Improved methods Pharmacomechanical The Trellis device combines trapping of the clot and lytic between two balloons, maceration of the clot by a rotating sinusoidal guidewire, and aspiration of clot fragments. The Rotarex utilizes a similar method with more emphasis on aspiration, while the AngioJet utilizes the Venturi effect to primarily aspirate, but has now been combined with an initial jet infusion of lytic into the clot followed by a dwell time of 20 minutes which has been associated with more rapid and complete clearing of clot. The EKOS system combines multiple ultrasound transducers within an infusion catheter. The ultrasound loosens the matrix of the cross-linked fibrin strands enabling easier and faster permeation of the clot by the lytic; resulting in faster lysis. Microbubbles In vitro and in vivo work has demonstrated faster lysis with the IV administration of microbubbles plus IV adminstration of lytic and then external ultrasound at the site of the clot. This can be expected to be true in humans, and to be augmented by the delivery of each modality directly into the clot.
Improved drugs Plasmin Instead of using the plasminogen activators to convert plasminogen to plasmin, the infusion of plasmin could result in faster lysis, and with the plasmin that escapes the region of the clot being quickly inactivated. This is theoretically attractive, and trials are now beginning.
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Endovascular treatment for acute and chronic lower extremity deep vein thrombosis PE Thorpe and FJ Osse
Introduction: treating acute deep vein thrombosis Deep vein thrombosis (DVT) is a medical condition which occurs with predictable consistency within the population despite innovations in therapy. Many cases of DVT are not diagnosed, since the signs and symptoms are either transient or vague. They are often misconstrued as muscle ache. Ultrasound has improved diagnostic capability, but only if the suspicion of thrombosis is perceived in the clinical presentation. The incidence of DVT appears to be increasing with an aging population. Statistics from the American Heart Association say up to two million Americans are affected annually by DVT and 200,000 die each year from the complication of pulmonary embolism.l As clinicians, we inconsistently utilize prophylaxis in high-risk patients whom we place
in high-risk circumstances.2 Furthermore, physicians are often slow to recognize early signs or symptoms of both extremity thrombosis and pulmonary embolus. The diagnosis is often made in the midst of a clinical crisis after both patients and doctors miss or ignore subtle clues that were present for days or weeks. Symptomatic DVT results from the presence of a critical mass of thrombus that supersedes collateral capacity and autolysis (Figures 19.1 and 19.2). The swelling and pain secondary to venous hypertension from the obstructed venous flow bring the patient to clinical attention. Whether in the emergency room, the physician’s office or in the hospital, clinical suspicion of DVT should prompt anticoagulation and investigation.3 More commonly, a patient with newly diagnosed DVT, other than phlegmasia, is treated as an outpatient. Upon duplex confirmation of thrombus in the deep venous system, the patient is treated with low molecular weight
Figure 19.1 Clinical appearance of a 22 year-old man one month after undergoing right hip-spur surgery. The patient had been a varsity football player in college and was very healthy otherwise. He was subsequently diagnosed with heterozygous Factor V Leiden mutation. The thrombus, most likely related to immobilization plus hypercoagulability, was approximately 3 weeks old when the patient was treated with mechanical thrombectomy, for debulking (Oasis by Cordis), and catheter-directed tPA for 48 hours. The initial right femoral venogram is seen on the right.
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Figure 19.2 Two images of the right femoral vein (prone) showing before and after catheter-directed tPA therapy. The 48 hour infusion was performed with 1mg/100 cc normal saline/hour. No angioplasty or stent was indicated.
heparin and sent home. We know that many do well. Others, despite adequate anticoagulation, progress to a symptomatic post-thrombotic syndrome. Ideally, symptomatic patients with occlusive or partially occlusive multi-segmental thrombus would be evaluated for the risks and benefits of actually eliminating the “clot burden” in addition to anticoagulation. The persistent presence of thrombus in the deep venous system can result in suboptimal venous flow and damage to the valves. The body attempts to resolve venous obstruction with a combination of autolysis and redirection of venous flow through collateral channels. If the extent of thrombus exceeds the compensatory effects of recanalization and collateralization, venous hypertension results and causes edema and/or discomfort. Chronic venous hypertension is associated with multiple symptoms (pain, cramping, limb heaviness, pruritis, parasthesias) and signs (edema, induration, venous ectasia, redness and calf tenderness, and stasis ulcers). A wide range of disability, clinical morbidity and deterioration of limb function can occur. The focus of this chapter is the spectrum of endovascular interventions available for thrombus removal in the clinical setting of acute DVT. In other words, we will discuss the interventional approach for treatment of acute thrombus in order to (1) re-establish deep venous flow to thereby reduce pain and edema; (2) preserve valve integrity; (3) remove thrombus that could embolize; and (4) prevent continued obstruction and valve damage that leads to post-thrombotic syndrome. An appreciation of the long-term sequella of persistent thrombosis, for example valve damage, venous hypertension, and post-thrombotic syndrome, hopefully prompts a clinician to consider the options of intervention with thrombolytic therapy, mechanical thrombectomy, and endovenous reconstruction. The long-term results of such interventions are limited to several series of 3–5 year follow-ups.4,5 In our follow-up of 1–10 years, patients treated with urokinase plus anticoagulation reported less pain and swelling compared to patients
treated with anticoagulation alone.6 Therefore, if endovascular intervention is a clinical consideration, we offer the following discussion about the techniques and available devices. It is a rapidly expanding area of innovation and industry focus with the frequent appearance of new tools which are intended to increase efficiency without sacrificing safety.
Diagnostic workup Patients referred with symptomatic acute DVT undergo a diagnostic workup including a history, hypercoagulability screening, physical exam, and baseline duplex exam. Attention to the difference of segmental flow velocities, as well as the waveforms, can provide clues to proximal venous obstruction. Common iliac occlusion and distal IVC obstruction are suggested by loss of phasicity and relatively low velocity at the femoral level. However, flow velocity may be deceptive if there are large collaterals or a prominent internal iliac system, but the waveform will still show little or no phasicity. An ascending phlebogram is obtained by manual injection of lowosmolar, non-ionic contrast through the pedal IV. A 22 g Jelco is placed in a dorsal pedal vein and secured with extension tubing and a distal-end 3-way stopcock. Using 60 cm3 syringes, contrast is pushed into the vein, observing for extravasation. This can be difficult and slow at the initial exam. It becomes easier as the venous resistance decreases. We advocate the phlebogram as a valuable baseline “road-map” of the state of venous flow in the extremity. Although some interventionalists avoid this study, due to the difficulty of placing an IV in an edematous foot, we find it valuable in several ways. First, it provides an access for infusion of thrombolytic drugs as well as contrast. Second, it is important to determine the flow status in the upper calf and popliteal region since these veins must be open for the calf-pump to function properly. Without continuity of flow from the calf into the deep system
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Endovascular treatment for acute and chronic lower extremity deep vein thrombosis of the thigh and pelvis, endovascular therapy rarely succeeds long-term. All patients referred for suspicion of DVT undergo duplex ultrasound. The standard examination does not include evaluation of valves. It also does not include iliac veins unless specifically requested. We find that iliac occlusions can remain undiagnosed for years, since duplex imaging of the common femoral vein shows flow. The loss of phasic flow, indicating a proximal obstruction, is often not recognized in an exam performed to rule out lower extremity thrombosis. Three-dimensional CT reconstructions and magnetic resonance venography (MRV) can provide information about pelvic vein and iliac compression. MRV has been compared with contrast venography and ultrasound in detection of DVT. All thrombi detected by contrast phlebograms were also detected with duplex and MRV. There was 98% correspondence in diagnosis of DVT with these modalities.7
Endovenous therapy Thrombolysis, balloon dilatation, and stent placement comprise the main elements of endovenous therapy for revascularization. Thrombectomy devices, useful in clearing dialysis fistulae, have not exclusively supplanted lytic therapy in the treatment of acute DVT. This is due in part to the limited size of the debulking channel, the fact that chronic thrombus often underlies acute obstruction, and that the devices work best with soft thrombus. Anticoagulation is required to prevent immediate rethrombosis. Duration of anticoagulation after the initial re-endothelialization phase may vary. Selected patients, without DVT, who are stented for iliac compression, may do well without warfarin.8 Our approach to endovascular therapy for thrombotic occlusion, for both acute and chronic occlusion, advocates the following philosophy. If one considers a limb as an “organ system,” in the sense that venous segments exist in continuity with smaller veins below and larger veins above, one can see that, ideally, they should not be treated in isolation. The run-off exam or knowledge of outflow is important in arterial disease. Similarly, continuity of venous flow is important for success in endovascular venous procedures. For example, flow in a stented iliac segment depends on flow from the femoral, popliteal, and infrapopliteal segments. If there is subacute and chronic DVT in the calf and thigh, treating only the superficial femoral vein without addressing the occlusive thrombus in distal veins, will result is suboptimal restoration of deep venous flow. If tibial flow is occluded, blood preferentially goes to the superficial veins. This pathway will persist even when the SFV is reopened because blood is being shunted to the saphenous system in the lower calf. The reopened SFV will not be the path of least resistance, due to persistent occlusion more distally. The limb will have diminished flow in the deep system, despite perforators, since the saphenous vein remains the path of least resistance. Ignoring strategic distal thrombus can cause early technical failure. A newly reopened femoral system is at greater risk for rethrombosis if there is little deep venous flow channeled into this segment. It is similar to placement of an arterial bypass graft above poor run-off. Patency will be less than in a limb with good run-off. In addition, residual distal thrombus can limit clinical improvement due to persistent hypertension in the calf. In both venous and arterial reconstruction,
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interaction among all segments must be taken into account to achieve optimal results. We have found a combination of catheter- and flow-directed therapy is most beneficial for treating multi-segmental thrombosis. Improving flow in the whole limb may be essential for good long-term clinical results in patients with thrombus located at every level.
Mechanical thrombectomy Thrombectomy refers to physical removal of soft, fresh thrombus. The idea of doing this is with a small, percutaneously inserted device that atraumatically “vacuums” the thrombus out of the vessel. Such a device would offer the speed of surgical intervention with the advantage of minimally invasive therapy. The Fogarty balloon, a standard tool for rapid thrombus debulking, requires a surgical incision. A number of new devices have emerged, and their design benefits and limitations are discussed in several review articles.9–12 The objective of the newer designs is thrombus removal with a small-profile, over-the-wire device that can be introduced percutaneously. Most devices provide a small pilot lumen that leaves a substantial amount of residual thrombus. The debulking ability varies according to the device as well as the thrombus composition. The devices do not perform well with organized thrombus.13 The devices are geared to vessels less than 10 mm in diameter. Both over-the-wire and wireless versions are available. They are not steerable. Residual mural thrombus persists in most vessels, particularly larger veins such as the iliac and cava. The endothelium can be injured and result in rethrombosis as well as intimal hyperplasia. The potential for valve damage has been studied in animals but it is hard to determine in humans.14 In general, the debulking seems most appropriate in patients who cannot receive thrombolytics. However, many of these patients, such as elderly post-op patients, cannot receive heparin either. Without anticoagulation, rethrombosis occurs rapidly. In our experience, the debulking process rarely decreases the overall time of the procedure, since additional thrombolysis is necessary to remove residual thrombus for optimal results. Some devices combine mechanical and pharmaceutical properties to accelerate restoration of flow.15 The TrellisTM (Bacchus, Menlo Park, CA) device is a combination bipolar balloon, infusion catheter and ossilating wire.16 The thrombolytic agent is delivered between the occluding balloons. The perfused thrombus is then subjected to gentle mechanical disruption by an oscillating sinusoidal wire positioned between the balloons. This allows contained thrombolysis, thus limiting systemic exposure to the lytic agent. The device allows rapid aspiration of lysed thrombus through the dual lumen design, but anticoagulation is still necessary. Isolated thrombolysis is most useful in treating acute VT in patients with contraindications to lytic therapy. The advantage of significantly limiting the systemic effect of the drug allows treatment of post-op patients and patients with other risks of bleeding. The “power pulse-spray” concept of the AngioJetTM(Possis, Inc., Minneapolis, MN) is also a combination of powerful delivery of a lytic agent with a thrombectomy catheter.17 The device has undergone several evolutions to create a more
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effective debulking channel. Despite the reported contributions of mechanical thrombectomy, we find there is generally still a need for overnight thrombolysis. The devices are expensive and require set-up time and a technologist familiarity with each design. The use of mechanical thrombectomy may shorten the time until flow is restored, and they may lessen the overall time to completion, especially if catheter-directed thrombolysis is not needed after the debulking process.
The role of thrombolysis While investigators have shown that early thrombolysis effectively removes thrombus and preserves valve integrity,18 the early published reports of the risk of bleeding complications has prevented widespread acceptance of catheter-directed thrombolytic therapy for acute DVT.19 Catheter-directed thrombolysis of acute DVT could decrease the number of patients who develop PTS.20 However, this position is more advocated by interventionalists than referring physicians precisely because of the fear of complications. The main principle in thrombolytic therapy is effective and efficient delivery of an agent to the thrombosed vascular segment(s). In larger axial veins, this is best achieved with catheter delivery utilizing multi-side-hole infusion catheters and wires. When there is thrombus in deep calf veins and the popliteal, simultaneous flow-directed infusion, utilizing tourniquets, serves to improve flow in these areas. It is most important to optimize venous flow in the distal deep system. Persistent diversion of distal flow into the superficial system will place the newly opened and stented proximal segments at greater risk for rethrombosis. Optimizing resting flow velocities, by re-establishing continuity of flow from the foot to the cava, has proven to give the best hemodynamic and clinical results. Between 1980 and 1999, peripheral vascular thrombolysis was largely performed with urokinase (Abbokinase, Abbott Laboratories, Chicago, IL). This agent was preferred over streptokinase and alteplase for the safety margin relative to bleeding complications.21,22 Problems centered on manufacturing protocols led to a shortage of urokinase and indefinite withdrawal of this agent from the US market. Urokinase has, however, returned to the market, but remains relatively expensive (ImaRx, Tucson, AZ). Alternative lytic agents such as retaplase or RetavaseTM alteplase or ActivaseTM, and tenecteplase or TNKTM (Genentech Inc., South San Francisco, CA) are available for peripheral interventions. In our experience, there remains an increase in bleeding complications with alternative lytic agents compared to urokinase. Dose adjustments for concomitant heparin are advocated, but the fibrin-specific drugs are less well suited to the longer venous infusions. We prefer the low-dose, high volume infusions for DVT therapy, and when urokinase was available more DVT patients received catheter-directed thrombolysis.23 The formula for urokinase is one million international units (IU) per liter of normal saline infused at 50–100 cm3/hour. The higher volume promotes percolation of the drug through the occlusive thrombus. By pushing the drug through the thrombus, the volume aids in exposure of the drug to the clot. A low volume infusion just “sits there” and the progress is slower. The risk of complications, the cost of ICU care, and the length of treatment led to less use of catheter-directed
thrombolysis as well as the evolution of thrombectomy devices and combination therapies. Now, pharmacomechanical thrombectomy has become the preferred method of treating acute DVT. The value of thrombolysis appears well accepted by the interventional community, and therefore remains an important tool in therapy. However, the methods of application have evolved to decrease the risks. This includes more use of mechanical debulking tools, temporary IVC filters and intravascular ultrasound (IVUS). The cost may not be decreased, but thrombolytic agents are used less. The fibrinolytic action of the drugs is clear in the case of acute DVT, but it is not immediately obvious nor well understood how thrombolytic therapy functions in the case of chronic venous occlusion. It does, however, make a difference. Physicians attempting to recanalize chronic thrombus frequently fail to advance the wire or stay intraluminal if they do not infuse a thrombolytic agent prior to and during the wire recanalization phase. Only sub-total occlusions can be readily treated without lytic therapy. Even in these cases, we find that a 24-hour infusion permits greater expansion of the residual lumen prior to stenting. In treating subacute and chronic occlusions, we share, with Semba and Dake,24 the impression that a thrombolytic infusion can “soften” more organized thrombus and thereby facilitate passage of wires and catheters. Although catheterdirected thrombolytic therapy has been shown to be most successful in removing acute thrombus, in chronic conditions, clinical improvement observed after thrombolytic infusion is often greater than the image would suggest. That is because improvement of venous flow, particularly in the calf, depends on the cumulative effect of many unnamed veins remaining patent. Restoring flow in these small conduits can make a significant clinical difference. Analysis of National Venous Registry (NVR) data suggested thrombolysis of chronic thrombus was unsuccessful.25 In truth, images of distal veins often look as abnormal after lytic infusion as they do before. Whereas comparison images show dramatic differences when lysing acute DVT, the phlebographic appearance of chronic venous obstruction changes less, even though the venous flow can improve significantly. Interpretation of static contrast images fails to explain the clinical improvement in patients after thrombolytic infusion for chronic obstruction. Reducing venous resistance, by augmenting small and medium size venous channels, does not dramatically alter the post-infusion images, but it is an important adjunct to stenting larger veins. Video/digital phlebography, as mentioned above, can demonstrate a clear difference in rate of flow/ contrast clearance after thrombolytic infusion. Vascular physiology and fluid dynamics studies show how flow in a tubular conduit is proportional to r 4, where r represents the radius. If we apply this concept to venous flow, we see that augmenting multiple occluded or tiny lumens from < 1 mm to > 2–3 mm, significantly increases venous flow despite minimal changes on radiographic images. According to this principle, Pousseille’s Law, delivery of thrombolytic agents to the extremity via catheter or flow-directed techniques, can promote flow by enlarging the residual lumen. Although not restored to original caliber, lysing acute and subacute thrombus, superimposed upon chronic organized thrombus, increases the luminal diameter. This may not produce a dramatic change on x-ray images, but the increase in flow can be documented with
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Endovascular treatment for acute and chronic lower extremity deep vein thrombosis duplex and correlated with post-treatment clinical improvement. Ambulatory venous pressure, as indirectly measured with air plethysmography, should decrease as resistance to flow decreases. However, in our exams, the numbers often do not reflect the degree of clinical improvement. Reasons for this are complex and most likely involve the effects of long standing obstruction on valves and the calf muscle pump.
Technical aspects of catheter-directed DVT thrombolysis When treating an acute iliofemoral DVT, the popliteal approach is generally selected (Figure 19.3). If necessary, a bilateral approach is used simultaneously. Certain cases may require access from the contralateral or jugular approach. The advantage of the popliteal approach is that a patient may sit in bed. The jugular sheath is not well-tolerated for extended treatment. Thrombus around the jugular sheath is prone to lysis with the continuous motion from carotid pulsation. This can result in miserable oozing. Therefore, we prefer to reserve the internal jugular vein for short-term access. Although the baseline phlebogram is performed with the patient supine, the endovascular procedure requires placement of the patient in a prone position. A urinary catheter is advised. Initial deep venous access is safest utilizing ultrasound guidance of a 21-gauge micropuncture needle into the back wall of the popliteal vein or a superficial tributary, (Figure 19.3). Successful entry into the vein, in continuity with occluded proximal deep venous segment(s), permits placement of a working sheath for catheter exchange and
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contrast injection. A thrombosed popliteal vein can be cannulated as well. However, a pedal infusion of lytic agent is recommended for simultaneous treatment of the calf and popliteal segments. Spasm and missed passes are significantly less with the combination 3–5.5-French, co-axial, micropuncture dilators and 0.018-inch nitinol wire than with standard intravenous catheters. An angled 4–5-French hydrophilic catheter, in combination with a 0.035-inch GlidewireTM (Boston Scientific, Na, MA) or 0.035-inch RoadrunnerTM (Cook Inc., Bloomington, IN), is carefully advanced from the popliteal level, through the superficial femoral vein to the common femoral level. During the initial 24–48 hours, the goal is to place a multi-side-hole catheter along the length of the abnormal segments traversed by the wire. An overnight infusion of thrombolytic agent will decrease the intraluminal resistance and set the stage for subsequent catheter advancement, balloon dilatation, and stent placement. Following passage of a wire into the normal vein above the occlusion, a stiffer exchange-length wire that is positioned as the working wire during dilatation, and stent deployment. If necessary, sequential predilatation in the stenotic areas is conducted, from proximal to distal, using 8–14-mm balloons (4 cm length). Balloon selection depends on the estimated size of the native vessel and the observed resistance to balloon expansion. Overdilatation is avoided. Some vessels are very tenacious while others dilate with relative ease. Great care is taken to “feel” the balloon as one slowly proceeds to expand the residual lumen. Since venous angioplasty can cause thrombogenic dissection, anticoagulation is key during and after this therapy. We have come to learn that spontaneous flow through an irregular vein is better than stasis in a nice-looking stent. Therefore, good judgment is required in determination of a therapeutic endpoint. Stasis of contrast and
Figure 19.3 Popliteal puncture site. This is generally visualized with duplex to avoid puncture of the artery with is directly anterior to the popliteal vein. The ultrasound shows the compressible vein above and slightly medial to the artery. The leg can be rotated slightly to separate the vessels. It is important to see the puncture. With contrast, the needle presses against the posterior wall and widens the vein, as shown here (arrow). The skin entrance is slightly above the crease behind the knee, but he needle entry site is close to the top of the patella when the patient is prone. Left image show Site-Rite™ with needle guide.
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persistent collateral flow indicate an outflow problem, whereas stasis alone may indicate sub-optimal inflow. Patients are systemically heparinized (PTT > 50 and < 80 seconds) throughout the period of thrombolysis with urokinase and prothrombin time > 40 but < 60 seconds with alteplase. Oral anticoagulation is tapered before therapy (2 days off coumadin before admission) and restarted 1 day prior to stent placement. This allows removal of the sheath before the INR is therapeutic. Upon completion of thrombolysis, heparinization is continued until oral anticoagulation is consistent; PT > 20 seconds; and INR of 2.5–3.0. Oral anticoagulation is monitored cooperatively with the referring physician for several months, as inadequate anticoagulation is the most frequent cause of early failure. Younger patients with chronic conditions may have a hypercoagulable state. Whereas a minimum of 6–12 months of warfarin is standard in acute DVT, patients with chronic disease and/or multiple stents are placed on indefinite warfarin. A single iliac stent with excellent venous flow, in a patient without thrombophilia may not require warfarin. Compression stockings or leggings are prescribed and fitted for all patients with documented reflux before discharge. Patients are followed with clinic visits and duplex exams upon completion and at 3-month intervals for 1 year and yearly thereafter. Bleeding complications can occur with prolonged thrombolytic infusions, but they are relatively uncommon in the post-thrombotic patient population compared to cardiac patients. In reviewing the complications reported in the literature, clearly the most common problem is minor bleeding at the sheath site. Major bleeding, requiring transfusion, has been reported in 1–25% of patients. This is more likely to occur in obese patients; and the use of ultrasound guidance for initial puncture is strongly recommended. Pulmonary embolus occurred one time in our series, and continued thrombolysis
resolved all symptoms. It has been reported in < 1% of all reported cases. Therefore, IVC filters are not routinely used with catheter-directed thrombolysis. However, with mechanical thrombectomy, temporary filters are used, despite the lack of any controlled studies. Among more than 1000 iliofemoral venous endovascular patients reported in the literature, death has occurred in < 1% due to PE (1), sepsis (1), retroperitoneal hematoma (1) and intracranial hemorrhage (2) and MI (1)(6). With the use of fibrin-specific lytic agents, such as alteplase and tenecteplase, we note many more soft-tissue hematomas at automatic blood-pressure cuff sites and at venapuncture sites. This observation did not accompany use of urokinase. Rethrombosis < 30 days is generally due to poor outflow or inflow and/or subtherapeutic anticoagulation. When this occurs, retreatment with thrombolysis and additional stents is effective. Intimal hyperplasia, causing symptomatic restenosis occurred in approximately 10–20% of stented veins, and can be effectively treated with angioplasty.26
Flow-directed thrombolysis for calf DVT This technique is reserved for treating thrombus located in the tibial, soleus, gatrocnemius, and popliteal veins. It is more prevalent than thought.27 It may be more important than many believe, given the strategic location of the majority of venous valves in this area.28,29 If the baseline venogram reveals preferential flow in the superficial veins of the calf, strive to acquire an idea of where the thrombus is located by injecting contrast with tourniquets in place (Figure 19.4). The duplex may underestimate the amount of thrombus in the upper calf. If there is no continuity of flow in the deep veins
Figure 19.4 Tibial thrombus in patient with acute pancreatitis. This was treated effectively with a urokinase infusion through a pedal access, with application of the ankle tourniquet as shown in the image on the right. Contrast and lytic agent can be re-directed to the deep veins of the calf by compressing the saphenous vein against the malleolus.
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(b)
Figure 19.5 (a) Acute left lower extremity DVT in a 38-year old man hospitalized with pancreatitis. Immobilization, due to bed rest, combined with a classic iliac compression (Figure 19.6), led to iliofemoral and femoral-popliteal thrombosis. Additional tibial vein thrombus (Figure 19.4) was treated with flow-directed thrombolysis. (b) Acute femoral thrombus. Very few collaterals are evident. The femoral vein is engorged with thrombus and contrast tracks along the edge of the obstruction.
of the calf and the thigh, a lytic infusion from the level can be effective in reopening veins that are untreatable with catheter technique. Acute failure has been attributed to residual thrombus in the popliteal vein, below the sheath entry site. Unfortunately, some interventionists have recognized the importance of treating the distal vein, especially the entire
(a)
popliteal, after rethrombosis of successfully lysed iliofemoral segments. For this reason, we recommend a baseline and completion venogram from the foot. Unfortunately, duplex does not provide the same understanding of flow patterns, in the lower extremity venous system as real-time contrast venography.
(b)
Figure 19.6 (a) Pelvic venograms (seen supine) following thrombolytic therapy to remove acute thrombus from the iliofemoral segments. The classic absence of the left common iliac segment is due to chronic fibrosis where the right iliac artery crosses the vein. Ascending lumbar collaterals (double arrows) and trans-pelvic, left-right collaterals are seen. (b) Venogram following placement of a 12 mm X 60 mm self-expanding stent across the focal common iliac occlusion.
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A 22-gauge intercath placed in a dorsal pedal vein for the purpose of performing the baseline venogram is used for the flow-directed infusion. A single puncture in a pedal vein below the ankle is desirable. Although multiple punctures cannot be avoided in certain patients, we attempt to work from a distal to proximal direction to avoid infusing urokinase below multiple punctures. A small clear plastic dressing is placed over the 22-gauge catheter to maintain visualization of the site throughout the procedure. It is important to loop the IV tubing to prevent inadvertent loss of the site. Infection and/or bleeding are not problems but, as always, care is taken to observe for any extravasation of contrast during each injection. A short, clear plastic connecting tube is used with a three-way stopcock to facilitate interval injection of contrast for follow-up evaluation of progress of lytic therapy. A saline infusion is maintained through the pedal site if urokinase is not being infused. A Velcro-elastic tourniquet (Tiger Surgical, Portland, OR) is placed at the malleolar level in combination with a small disc positioned to provide focal compression of the saphenous vein against the medial malleolus. Under fluoroscopic visualization, a small amount of contrast is injected to ascertain focal compression of the saphenous vein and redirection of flow through a communicating vein into the deep system. The disc position, as well as the upper and lower margins of the tourniquet, is marked on the skin. This allows a nurse to release the tourniquet once every hour and replace it in the correct position. A folded 4 × 4 gauze is placed under the disc to protect the skin from pressure. The pedal pulse is marked and monitored with blood pressure and pulse; the tourniquet provides adequate redirection of venous flow without any compromise of arterial flow. It is released 10 minutes every hour and reapplied at a specifically marked level, which assures proper disc position and tightness. Normally, blood flows preferentially from the superficial to the deep system. However, in the presence of DVT, one may see contrast reflux through the perforating veins into the superficial system in the mid calf or above. When this is fluoroscopically recognized, a second tourniquet is placed at the knee to compress the greater saphenous vein against the femoral condyle to promote redirection of flow into the tibiopopliteal veins.
The role of metallic stents The interventionalist must have a working knowledge of stent properties and be familiar with a wide variety of commercially available products. The number of stents now on the market has grown significantly over the past decade and currently there are more than 40 different stents available for coronary use and more than 20 for use in the periphery. Current lists are available at the Endovascular Today website <www.evtoday. com>. Significant improvement in patency rates has been observed in iliac lesions treated with stents in addition to angioplasty. In the NVR, at one year, 74% of limbs treated with stents remained patent compared to 53% of limbs not receiving stents (p < 0.001).25 No stent possesses all the qualities of an ideal stent, for example good radio-opacity, ease of positioning, flexibility, tractability, fidelity of shape, and low restenosis rate. Evaluation of the characteristics of the properties of metallic stents is gained with experience as new stents are introduced
and compared to those in use. Clinical use of stents in the iliac vein was first reported by Zollikofer et al. in 1988.30 Migration and intimal hyperplasia were documented with early use of the Gianturco Z stent.31 Modifications were made to prevent slippage; modular stent units were connected with nylon suture and small hooks were added. Migration has been a rare event with all stent designs. When this does occur, misplaced or migrated Palmaz and Wallstents can be effectively retrieved using endovascular techniques.32 All stents have been shown to become endothelialized and/or covered with neointima.33 Sawada reported this in all Z stents observed at autopsy.34 The neointima appears rapidly and the endothelialization process occurs within 2–6 weeks. The amount of intimal thickening has been correlated to design. More rigid stents, exerting greater axial force on the vessel wall, seem to accelerate intimal hyperplasia. In these animal studies, and our experience, the Wallstent is less likely to induce compromising intimal hyperplasia due to the small wire size, pliability, and longitudinal flexibility. Zollikofer noted two important observations in animal studies: (1) regression of intimal hyperplasia occurred with time; and (2) restenosis is more common at a site of high pressure flow, for example arteriovenous fistula.35 This appears true for stented and non-stented vein segments. Intravascular ultrasound (IVUS) has allowed us to examine symptomatic patients and document restenosis caused by intimal hyperplasia. The majority of interventionalists use the Wallstent for venous stenting. In the common iliac location, with extrinsic pressure a factor in causing compression, flexibility and selfexpansion may give the Wallstent an advantage. A study comparing long-term patency of self-expanding versus balloon expandable stents, placed in the common iliac vein, has never been done. However, the general consensus is that the flexibility of the self-expanding stents is suited to the pelvic veins. The choice of lengths and diameters make this design suitable for 1–2 cm vein diameters. The newer nitinol stents have less foreshortening than the Wallstent, but they are less visible under fluoroscopy, especially in large patients. Currently available stents are used “off label”, as the 8–16 mm diameter stents are only FDA approved for biliary and iliac artery use. Covered stents, suitable for repair of venous tears, are generally not needed or recommended. In a low-pressure system, our limited use of covered stents has led to thrombosis. Another stent limitation is length. Many of the venous occlusions are long, and reconstruction requires tandem stent deployment. The fully expanded stent length ranges from 4.0 to 10.0 cm. Stents remain correspondingly longer if full expansion is not achieved. As in the arterial system, crossing the origin of branch vessels does not appear to be associated with problems. We have closely followed iliac vein Wallstents, in place for over 14 years, with duplex imaging. There is no indication of strut fracture or failure. Occasionally, we see separation of two stents by 1–2 cm. Patients with recurrent symptoms of edema or leg pain are scheduled for stent dilatation. Duplex imaging does not usually discern in-stent restenosis. This is better seen with IVUS. Approximately 15% of patients may return with intimal hyperplasia that can be effectively dilated. Clinically, they improve after this intervention. It is done via the jugular approach without reversal of warfarin. Although the majority of patients encounter restenosis within 12–24 months after
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Endovascular treatment for acute and chronic lower extremity deep vein thrombosis the initial procedure, we have treated patients anywhere from 2–10 years after the stents were placed. Progressive venous hypertension in the limb can be a sign of restenosis or rethrombosis. If there is no sign of thrombus, we advocate stent dilatation. Several technical points regarding venous stenting should be emphasized. Firstly, complete stenting of diseased segments promotes re-established continuity of deep venous flow which is imperative to stent patency. Under-stenting should be discouraged in view of the observation that tributary flow passes through Wallstent interstices and traversing the inguinal ligament with overlapping, self-expanding metallic stents is well tolerated (Figure 19.7). It is also important to not ignore stasis of contrast when stenting. This is a sign of inadequate spontaneous flow. This can be due to a sheath blocking flow, but contrast can obscure stenoses and dissections on digital imaging. So, stasis must be respected as a sign of poor flow which could cause the stents to fail. Moreover, neither the initial venographic appearance, the extent of the lesion nor the duration of the symptoms is a predictor of success or failure of guidewire passage through a venous obstruction. Some very chronic lesions are almost impossible and some are very easy. There must be genetic issues we do not yet recognize.
Acute left leg DVT: iliac compression or May–Thurner syndrome When Zollikofer first placed a stent in the iliac system, the indication was treatment of intimal hyperplasia, at the proximal anatamosis of a common femoral-to-common iliac bypass graft.30 Since then, stents have been shown to be an effective adjunct to surgery and balloon dilatation, particularly in the
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left common iliac segment.36 As in arterial disease, “culprit” lesions are frequently discovered after removal of acute thrombus. Verhaeghe et al. reported discovery of an underlying anatomical anomaly or lesion in 13/19 (68%) of limbs treated with catheter-directed rtPA for iliofemoral thrombosis.37 Ten of the venous lesions (77%) were unknown before lysis and eight (62%) were treated with stent therapy. For the most part, the condition is diagnosed in association with thrombosis, and as Cockett observed, early on, in acute cases, “mere removal of the clot does little good in these cases as it does not deal with the real cause of venous obstruction (i.e., the stricture).”38 Although the majority of large vein thromboses recanalize sufficiently, a certain percentage of iliofemoral DVT patients do not recover satisfactorily. Following standard therapy of heparin, bed rest, and oral anticoagulation, they remain symptomatic with pain and/or edema. Some develop ulcers. Unfortunately, it is not possible to predict which patients will develop a severe post-thrombotic syndrome. Cockett and Thomas, identified the relative lack of iliac recanalization and associated post-inflammatory perivenous scarring, as the main etiologies of serious post-thrombotic sequellae. The degree of uncompensated residual obstruction causes venous claudication, and the cutaneous changes associated with persistent venous hypertension. Patients in this category were among those first considered for surgical bypass.39 Left iliac compression (LIC) explains why deep vein thrombosis predominantly affects the left leg. Many persons with occult left iliac compression or occlusion are, in fact, asymptomatic. Prethrombotic venous hypertension may be present, but remains largely undiagnosed. Subtle asymmetry in leg or foot size may be noticed, but is mostly ignored. Iliac compression patients frequently present with associated femoral thrombosis. In fact, the condition should be suspected in anyone with acute left extremity DVT and/or symptoms of venous insufficiency. The youngest patient in whom we have seen venous claudication and edema, with a normal saphenous vein and Phlebographic confirmation of left iliac compression, was a 12-year-old girl. In addition, we have treated three young women, between 17 and 24 years old, with iliac stents to alleviate symptoms caused by May–Thurner compression not yet complicated by thrombosis. In their study of 94 patients with suspected iliac vein obstruction, Neglen and Raju have reported on primary stenting of May–Thurner compression as well as the prevalence of non-thrombotic iliac obstruction among patients with chronic venous insufficiency.40,41
Clinical experience: iliofemoral and iliocaval obstruction
Figure 19.7 Understenting demonstrated in the CTA scan. The aorta and iliac arteries are clearly seen the stent position is too low to open the common iliac vein. When the compression is tight, the large diameter, short stent can slip caudal if the leading upper edge is not deployed above the stenosis. Approximately one-two centimeters of stent must be positioned in the IVC to bridge the lesion. The lesion is very narrow in an AP diameter and wide in the transverse diameter.
In 1997, Bjarnason et al. reported on treatment of 77 patients. The majority of the patients, mean age 47 years (range 14–78 years) presented with acute DVT symptoms of < 14 days duration (69/86, 78%), while 9 (10%) had subacute thrombus (14–28 days) and 9 (10%) had thrombus older than 28 days. The mean length of symptoms prior to thrombolysis was 15 days (range 0–256 days). The average dose of urokinase was 10.5 million IU (range 4–24 million IU) and the average infusion time was 75 hours (range 8–247 hours). They reported greater technical success in treating iliac veins (79%) versus femoral veins (63%). We have seen this pattern as well. It reflects the
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fact that subclinical thrombosis is present prior to clinical presentation with acute iliofemoral DVT. Even though the initial technical success was similar between patients undergoing stent placement versus those who did not, it was less for patients with thrombus older than 4 weeks than those with more acute conditions. Thrombosed superficial femoral veins are often poorly recanalized and respond poorly to thrombolysis, alone. Eighty-six stents were placed in 38 (44%) of the 87 limbs treated for iliofemoral thrombosis. Seventy-five Wallstents were placed in 36 limbs and 11 Gianturco stents were placed in two limbs. Interestingly, they found a lower 6-month primary patency rate between stented (60%) and non-stented (75%) iliac veins and 54 vs. 75% at 1 year (p = 0.011). At one year, the secondary patency rate was 76% for stented and 82% for non-stented vessels (p = 0.46). They hypothesized that patients requiring stents presented with more severe chronic venous disease, accounting for the poorer long-term results. Stented patients were not uniformly maintained on warfarin longer than 6 months. An important report in the literature regards the National Venous Registry (1994–97).25 This was a multicenter registry that collected data on 473 iliofemoral DVT patients treated with endovascular techniques. The study included 287 patients with adequate follow-up. The majority had acute presentation of iliofemoral thrombosis (70%). The average dose of urokinase was 7.8 million IU and nearly 50% required placement of an iliac stent. Technical success, including placement of 104 stents, was 97%. Results were reported in terms of lysis grade. Complete lysis was achieved in 60% of patients presenting with acute thrombus (< 10 days). Among this group, 90% remained patent at 12 months compared to 70% of those with less than complete lysis. Patients were maintained on warfarin for 4–6 months. The study revealed greater 1-year patency in limbs with iliac stenosis treated with angioplasty
plus stent (74%) versus angioplasty alone (53%). A remarkably lower patency rate (20% at 2 months) was observed in the five stents placed in femoral segments. In our experience, stenting lower segments require careful assessment of flow patterns and intimal hyperplasia. The study was based on analysis of pre-and post-phlebograms and duplex ultrasound with minimal follow-up of 12 months. Between 1988 and 99, 116 patients received urokinase for lower extremity DVT at Creighton, in Omaha, NE. Eightyfour underwent endovascular therapy for chronic lower extremity thrombosis. The mean age was 47.5 years (range 12–90 years). Patients received a mean dose of 8.7 million IU (range 2–27 million IU with a minimum 24 hour infusion of urokinase (range 24–120 hours). Persistent venous stenoses, after thrombolysis, required stent placement in 53% (62 patients and 71 limbs) (Figure 19.8–19.10). Among these patients, 32 (51% of those stented and 28% of the total) had stents placed in the common femoral and/or superficial femoral veins. Sixteen patients had a single iliac stent placed for focal common iliac compression associated with acute thrombosis (L/15,R/1). In this subgroup, there is 100% primary patency with median follow-up of 24 months (range 8–50 months). Three patients have developed intimal hyperplasia within the stented segment causing increase in edema and discomfort compared to post-stenting. This occurred between 6 and 12 months and all were treated with balloon dilatation resulting in resolution of symptoms. All patients treated for chronic iliofemoral and iliocaval occlusion were examined before and after lysis/stenting with ultrasound. In 16 patients, peak velocities in diseased and non-affected iliac and femoral veins were suitable for analysis. We found the median common iliac velocity in the normal limb to be 44 cm/second (n = 16). Comparison of pre-stent mean (7.25 cm/second) and post-stent mean (41.3 cm/second)
Figure 19.8 Post thrombotic syndrome in a 42 year-old woman. Her right leg DVT first occurred 3 weeks after her first pregnancy, and reoccurred after her second delivery. She has a heterozygous prothrombin gene mutation. Following endovascular stent therapy, five years after the initial DVT, the right leg is significantly improved two weeks after discharge. Four years later, she remains Therapeutically anticoagulated and clinically improved with no further interventions.
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Figure 19.9 Early images (prone) during endovascular recanalization of the chronically occluded left common femoral and iliac segments. Left: Large iliolumbar and extensive hypogastric collaterals seen on day 3. Right: Finally, the close view of the classic narrowing of the common iliac segment. Several days of low-dose catheter delivered tPA required for traversing the common femoral vein.
common iliac vein velocity demonstrated a significant difference (p = < 0.0001) whereas the mean stented left iliac vein velocity (41.3 cm/second) was not significantly different from the untreated right iliac vein mean velocity (47 cm/second) (p = 0.4569).6 Bjarnason et al. also reported that velocities of less than 25 cm/second in the stented iliac segment correlated with poor patency.42 Further analysis of stented patients showed 19 required two iliac stents, 20 received three stents and three large patients (> 250 pounds) had more than three stents placed in the left iliac vein. Overall, 1-year primary patency of patients with iliac stents, including those with femoral stents, is 80% (57/71). Rethrombosis occurred within 30 days in 8/71 (11%). Six of these patients were retreated with thrombolysis and additional stents to improve inflow. This group included the three large patients with more than three stents in their long iliac veins. Symptomatic restenosis was documented and dilated in 6/71 (9%) limbs. In all, the restenosis became clinically apparent between 6 and 12 months. One-year secondary patency was 94% (67/71).
Neglen and Raju have reported on several large endovascular series in which thrombolysis was not used in treating chronic venous obstruction.36 They treated a highly selected group of patients suspected of having iliac vein occlusion. They reported placement of 118 Wallstents in 77 iliac veins, 43 of which were diagnosed with non-thrombotic iliac occlusion or stenosis. In the remaining limbs, there was evidence of prior DVT. As in the other large patient series, technical success was high (97%). Eighty-seven limbs were treated with a 1-year primary patency of 82% and assisted and secondary patency of 91 and 92%, respectively. Their data support the Creighton finding that focal iliac vein stenoses or occlusions can be opened effectively and safely stented with good 1-year patency rates. Clinical improvement usually parallels technical success. However, in severe chronic DVT, involving multiple venous segments, relief of large vein obstruction can produce clinical improvement even when chronic venous insufficiency remains. Raju reported similar experience with percutaneous recanalization of totally occluded iliac veins in 38 limbs and
Figure 19.10 Pelvic venograms (prone) pre and post-stent placement in the 42 year-old woman with a 5-year history of post thrombotic syndrome. Clinical improvement included decreased edema and resolution of right groin pain, leg heaviness and discoloration (Figure 19.8).
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Figure 19.11 IVC occlusion and endovascular reconstruction. The 40 year-old woman patient did not suspect IVC obstruction when she presented with a 2 year history of a non-healing right ankle ulcer. Her initial DVT occurred. After undergoing bilateral therapy for iliocaval occlusion, the ulcer healed in less than 4 weeks. She presented with recurrence of the ulcer two years after stent placement. Balloon dilatation of the right-side in-stent hyperplasia corrected the venous hypertension an allowed the ulcer to heal. Deep valve reflux, in the right femoral veins contributes to venous hypertension, as well. The patient remains anticoagulated.
the occlusion extended into the infrarenal IVC in nine cases.43 Two cava had an occluded filter. The median length of the occluded segment was 22 cm. The median number of 14– 16 mm diameter stents used per patient was three. Diffuse distal chronic venous changes were noted in 88% of treated limbs. The chronic, non-occlusive DVT involved femoral, popliteal, and tibial segments in 62% versus a single segment in 9%. However, distal segmental occlusions were noted in 52% of the limbs; the majority of such tandem occlusions were femoral. Distal femoral lesions were not stented. Mean follow-up was 24 months. He reported actuarial primary, assisted, and secondary patency rates of 49, 62, and 76%, respectively. Clinical improvement was gauged with the pain scale where a significant decrease from level 4 to level 0 (p < 0.0001) was reported. Sixty-six percent of limbs showed resolution of open ulcers or stasis dermatitis at 1 year. Reflux was documented in 87% of treated limbs and involved both superficial and deep systems in 65% of these individuals. Perhaps the differences in the long-term ilio-caval stent patency rates among separate series reflect variable treatment of distal and tandem obstructions as well as selective use of anticoagulation. We reported our initial IVC series at the American Venous Forum (AVF) in 1996 and in the Handbook for Venous Disorders.6 Then, 10 years later, the IVC occlusion patient data were presented at the AVF with long-term follow-up (Figure 19.11). Between Oct 1995 and June 2005, 26 patients (20 male/6 female, average age 41 years, range 17–73 years) underwent endovascular repair for IVC occlusion. Two patients with malignancy-related caval obstruction were successfully treated with relief of venous hypertension, but both died of their malignancy. Twenty-one patients had benign, chronic total infrarenal IVC obstruction and three had acute thrombotic occlusion of a partial, chronic caval stenosis. Mean duration of symptoms was 12.1 years (range 1–25 years). Six filters were occluded; Greenfield (3), Simon Nitinol (1) and Trapese (1). Three chronically occluded filters were successfully stented open. All patients had bilateral lower limb venous hypertension with the exception of two individuals aged 17 (left only) and 26 (right only). Thirteen out of twenty-four (54%) had a history of pulmonary embolus and 14/24 (58%)
had caval interruption with a filter (12) or surgery (2). The 48 limbs included prior BKA for venous disease and the following classifications: CEAP 1 (2), CEAP 3 (11), CEAP 4 (19), CEAP 5 (9), and CEAP 6 (5). The entire IVC was occluded in 7/24 (29%) and infrarenal in 16/24 (67%). Mean follow-up is currently 4 years (range 8 months–10 years). Primary patency among 22 surviving patients is 71%; seven patients have been redilated. Assisted patency is 23/24 (96%) and secondary patency is 100%. We concluded that endovenous reconstruction of the chronically occluded IVC can be accomplished with low morbidity and excellent technical and long-term clinical results.
Summary The success of endovascular therapy for venous occlusion is well known to a select group of interventionalists who care about patients with venous disease. It is a reality that venous disease continues to be regarded by too many physicians as a condition that is treated with anticoagulants or compression stockings. Venous disease treatment with new technology and pharmacotherapy represents an area of pioneering spirit among vascular specialists. While the majority still focuses on arterial disease, a few keep trying to teach the rest that chronic venous disease is far more prevalent than peripheral arterial disease. The growing awareness of possible treatments is slowed by the lack of randomized clinical trials. Many referring physicians consider the endovascular venous reconstruction and pharmacomechanical thrombolysis for acute DVT as anecdotal, unless level I data can substantiate recommendations for care. There are ongoing efforts to organize and fund such trials.44,45 In the meantime, the American Venous Forum and the European Venous Forum, along with other groups and industry, are expanding annual screening events and public awareness to diagnose and teach about venous disease. And, in the age of the Internet, patients search for solutions to their conditions. Still, the magnitude of venous disease remains overshadowed and underappreciated in the clinical arena. It truly is an important frontier in vascular medicine.
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Stents RR Heuser, KL Waters, CW Hatler, and LM Kelly
Introduction Peripheral artery disease is characterized by diffuse disease affecting 12% of the adult population and up to 20% of elderly persons. These patients have significant functional disability. Although effective, the concept of treating with focal stents or focal balloon angioplasty clearly is not the panacea for this clinical problem nor is it the panacea for coronary artery disease. Endovascular stenting does avoid the problem of early elastic recoil, residual stenosis, and flow-limiting dissection after balloon angioplasty. Judicious use of stents in the peripheral tree can be the treatment of choice for many of the challenges of treating peripheral arterial disease.1,2 When describing this stent technology, it would be preferable if one stent would be effective for all of these applications. Please see the appropriate chapter for the vessel location application of specific anatomic stent applications. See Table 20.1 where we have compiled a list from manufacturers on many of the peripheral stents available and approved in the US. The ideal stent would have the following characteristics: ● ● ●
●
● ● ●
●
low profile, perhaps a few microns in diameter; high tensile strength; highly radio-opaque (but not so radio-opaque to obscure arteriographic images); highly compatible with MRI and totally visible with imaging modalities; pharmacologically coated to inhibit intimal hyperplasia; no polymer covering; torque resistant and fracture resistant to thousands of pounds of pressure; biodegradable, reabsorbable (there should be absolutely no inflammatory reaction when it breaks down and the degradation can be modified after placement of the stent).
It can be surmised from this list, that not one stent meets all of the ideal characteristics. Peripheral vascular lesions are even more heterogenous than coronary lesions. Furthermore, each application will have to be modified for the anatomy.
10 mm or greater in diameter. The balloon’s expandable nature makes it possible to be more accurate in placement to make sure there is no extension of the stent into the aorta or across the vertebral or internal mammary artery. The expansible strength of a self-expanding stent may make this more durable. For the aorta, many stents are not large enough and in a patient with stenosis combined with an aneurysm, an aorta cuff as part of an endoluminal graft may be a better option.
Renal, iliac, femoral, and popliteal arteries When treating renal artery lesions, balloon expandable stents are preferred over the self-expanding stents since accuracy of placement is necessary. It must be noted that a main renal artery stenosis differs from the ostial lesion. The ostial lesion will not only need to be treated with a device with significant radial strength but length must be taken into consideration. Many manufacturers have made the shorter stents to accommodate many of these lesions that are quite minimal in length. The iliac arteries have been treated with both selfexpanding and balloon expandable stents. For lesions effecting the bifurcation, the kissing balloon technique necessitates a balloon expandable stent, but in areas not affected by branches, the self-expanding stent is quite adequate. Iliac stents require the ability to dilate up to 8–9 mm. The femoral artery in many cases is not amenable to stenting simply because of the length of lesions. However recent studies suggest focal stenting with nitinol devices are preferable to balloon angioplasty.2,3 The popliteal arteries in general are usually not treated with stents unless a flow-limiting dissection is present.4–7 The anterior tibial, peroneal, and posterior tibial arteries in general are not treated by stenting. If so, coronary stents are usually applied although dedicated peripheral stents for these applications are used by some investigators.
Coronary stents for peripheral arteries Carotid, subclavian and aortic arteries Carotid arteries have traditionally been treated with selfexpanding stents. In the subclavian, balloon expandable stents are necessary and should be dilated to at least 8 mm up to even 132
The coronary stent application in the peripheral arteries is limited. Coronary stents have to be fairly large. The drug-eluting stent in particular would not be large enough. In lieu of the current controversy about coronary thrombosis, drug-eluting stents may prove not to be an ideal alternative to consider. There may
Table 20.1
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(a) Biliary stents; (Reproduced with permission Diagnostic & Invasive Cardiology, published by Reilly Communications Group (www.dicardiology.net))
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(a) Biliary stents; (Reproduced with permission Diagnostic & Invasive Cardiology, published by Reilly Communications Group (www.dicardiology.net))—cont’d
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Stents Table 20.1 (b) Carotid stents; (Reproduced with permission Diagnostic & Invasive Cardiology, published by Reilly Communications Group (www.dicardiology.net))—cont’d
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(c) Peripheral stents; (Reproduced with permission Diagnostic & Invasive Cardiology, published by Reilly Communications Group (www.dicardiology.net))
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Table 20.1
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(c) Peripheral stents; (Reproduced with permission Diagnostic & Invasive Cardiology, published by Reilly Communications Group (www.dicardiology.net))—cont’d
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Table 20.1
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Stents be situations where a carotid dissection in the internal carotid may be small enough that only a coronary stent can make the turn or make access possible. With the renal arteries, the vessels are too small for consideration of coronary stents and the tensile strength is not great enough with current coronary devices. Below the knee, it is not advantageous to use coronary stents; however, in patients with critical limb ischemia or patients with flow-limiting dissections, these can be very effective.
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Conclusion In the case of peripheral stenting it is clear that neither one size nor one type of stent fits all. In peripheral arterial disease stenting needs to be modified toward the patient’s arteriosclerosis with a common knowledge that the diffuse nature of peripheral vascular disease makes stenting an adjunct and not always a requirement.
REFERENCES 1. 2. 3. 4.
Yadav J, Wholey M, Kuntz R et al. Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med 2004; 351: 1493–501 Schillinger M, Sabeti S, Loewe C et al. Balloon angioplasty versus implantation of nitinol stents in the superficial femoral artery. N Engl J Med 2006; 354: 1879–88 Cejna M, Turnher S, Illiasch H et al. PTA versus Palmaz stent in femoropopliteal artery obstructions: a multicenter prospective randomized study. J Vasc Interv Radiol 2001; 12: 23–31 Vroegindeweij D, Vos LD, Tielbeek AV, Buth J, van de Bosch HC. Balloon angioplasty combined with primary stenting versus balloon angioplasty alone in femoropopliteal obstructions: a comparative randomized study. Cardiovasc Intervent Radiol 1997; 20: 420–5
5. 6.
7.
8.
Grimm J, Muller-Hulsbeck S, Jahnke T et al. Randomized study to compare PTA alone versus Palmaz stent placement for femoropopliteal lesions. J Vasc Interv Radiol 2001; 12: 935–42 Zdanowsmki Z, Albrechtsson U, Lundin A et al. Percutaneous transluminal angioplasty with or without stenting for femoropopliteal occlusions? A randomized controlled study. Int Angiol 1999; 18: 251–5 Becquemin JP, Favre JP, Marzelle J et al. Systematic versus selective stent placement after superficial femoral artery balloon angioplasty: a multicenter prospective randomized study. J Vasc Surg 2003; 37: 487–94 Reilly Communications Group. Diagnostic & Invasive Cardiology Sept/Oct 2006; 46(5), www.dicardiology.net.
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Role of covered stents in peripheral arterial diseases M Henry, I Henry, and M Hugel
Introduction During the past 40 years, surgery has been established as a reliable treatment for peripheral diseases in all peripheral regions. Endovascular therapy is a relatively new field of vascular medicine and has continued to expand over the past two decades, thanks to the advancement of technical developments. This new concept has become widely recognized and accepted. The applications of endovascular procedures have been expanded dramatically throughout the human body for both occlusive and aneurysmal diseases, not only at iliac and femoropopliteal levels but also at aortic, renal, and supra-aortic levels. Angioplasty is now the first treatment proposed for peripheral vascular diseases and the treatment of choice for simple arterial lesions. Yet angioplasty alone is limited and has several complications (dissections, acute thromboses, etc.). The problem of restenosis remains and for long lesions the initial success and the long-term results are not as good as they are for short lesions, particularly in femoropopliteal arteries, in which surgery is often preferred.1–3 The concept of vascular stenting originated with Charles Dotter in 1969,4 but it did not become a clinical reality until the late 1980s. Expandable metallic stents have proved their usefulness in the management of complications related to angioplasty and possibly restenosis;5,6 for the later, however, this benefit is debated. Stenting is controversial, particularly at infrainguinal location. Its use is considered acceptable in the aortoiliac vessels and in the majority of published series in the literature, and the immediate and long-term results are encouraging.7–14 A primary or a direct stenting could be envisaged for these lesions if we consider the meta-analysis reported by Bosch and Hunink.15 Nevertheless, stenting is more in dispute for the femoropopliteal vessels and the results are very disparate in the literature with a primary patency between 22 and 77%.16–24 Three randomized trials showed no difference between PTA alone vs. PTA and stent,25–27 and according to TASC recommendation 36,28 femoropopliteal stenting as a primary approach to the interventional treatment of intermittent claudication or arterial limb ischemia is not indicated. Stents may have a limited role in salvage of acute PTA failure or complications. These recommendations were based on studies performed with the old generations of stents and it is the same with the randomized studies. New stents are now available, nitinol and covered stents, which seem to give better results.28–31 140
Endoluminal stent grafts and covered stents are now being investigated for treatment of both aneurysmal and occlusive peripheral arterial diseases.32–45 For occlusive diseases, it is postulated that an endoluminal bypass with a stent graft may limit the ingrowth of intimal hyperplasia along the length of the treated segment thereby improving patency as compared to conventional angioplasty and stenting. For an aneurysmal disease, the stent graft may be used to bridge the aneurysmal segment and therefore occlude the aneurysm from the native circulation. Several covered stents are either currently available or in clinical experiment: ●
● ●
● ● ●
● ●
The Cragg Endopro System 1/Passager (Boston Scientific, Natick, MA) The Corvita endoluminal graft (Boston Scientific) The Hemobahn or the new Viabahn (WL Gore & Associates, Flagstaff, AZ) The Wallgraft (Boston Scientific) The Jostent (Jomed International AB, Helsinberg, Sweden) The aSpire covered stent (Vascular Architects, San José, CA) The Cordis covered nitinol stent (Cordis, Warren NJ) The Adventia V12 (Atrium Medical Corporation, Hudson, NH)
We describe below these different covered stents, the results obtained, and their clinical applications in different locations.
The different types of covered stents: description and techniques of implantation The Cragg Endopro System 1/Passager Stent-graft construction The Cragg Endopro System 1/Passager (Figure 21.1) consists of a flexible, self-expandable nitinol stent covered with ultrathin woven polyester fabric. It has the property of shape memory.46–48 The design and construction of the stent have been previously described.47–50 The fabric is of low porosity and is attached to the stent framework by polyester ligatures. The stent graft is presented in a compressed form in a loading cartridge. Stent grafts range from 5 mm to 12 mm in diameter
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Figure 21.1
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Cragg/Passager.
and from 3 cm to 10 cm in length. They are delivered through 50-cm-long introducer sheaths ranging in diameter from 7French to 10-French, depending on the size of the stent-graft to be implanted. Stent-graft introduction technique Device delivery is usually accomplished using an ipsilateral retrograde or antegrade femoral artery approach. A retrograde popliteal approach has been used in cases in which femoral artery access was not possible. The rigidity of the delivery device limits the possibilities of implantation using contralateral access. For occlusive disease, balloon angioplasty is always performed first in order to enlarge the arterial lumen. Occasionally, debulking techniques such as rotational atherectomy are used in case of calcified arteries. The stent graft is delivered through the 50-cm-long introducer sheath, which is placed across the lesion to be treated. The stent-graft diameter is usually selected to be equal to or 1 mm greater than the nominal arterial diameter. The stent graft is positioned fluoroscopically across the treated segment. Platinum markers at each end of the stent assist in positioning the device. Once the stent graft is in position, the sheath is withdrawn, and an internal positioning catheter is used to fix the stent graft in place. The stent graft expands using the thermal memory characteristics of its nitinol frame. The graft is usually then dilated with an angioplasty balloon at high pressure (14–16 atmospheres); this fixes the graft against the arterial wall and helps unwrinkle the fabric. When several grafts are needed to cover a long lesion, it is important to overlap the prostheses by at least 5–10 mm so that the fabric portion of the graft covers the entire arterial lumen. In the middle part of the femoral artery, an overlapping of 1 cm may be better to avoid disjunction of the stents. The Corvita endoluminal graft51 This prosthesis was formerly developed by Schneider/Boston Scientific but is no longer available. Stent-graft construction The Corvita Endoluminal Graft (Figure 21.2) is a self-expanding endoluminal vascular prosthesis with an introducer system that makes it a low-profile device and permits percutaneous delivery and deployment. The integrated endoluminal graft consists of two components:
Figure 21.2
● ●
Corvita covered stent.
a self-expanding cylindrical wire structure; a highly porous and elastic coating of spun 13-µm-thin Corethane (polycarbonate urethane; The Polymer Technology Group Inc., Berkeley, CA) fibers in which blood can coagulate and seal the Corvita endoluminal graft to form a new blood-tight vessel wall. The Corethane coating is glued on the inside of the metallic structure.
Stent-graft implantation The endoluminal graft can be cut to length by the user with surgical scissors and mounted in the tip of an introducer sheath. For that purpose, the Corvita endoluminal graft is manually compressed to one-fifth or one-sixth of its original, expanded diameter and simply inserted by the user into the introducer sheath. Then it is loaded into and deployed from a delivery system consisting of an internal sheath and a coaxial catheter, which is introduced inside the sheath and therefore helps to release the endoluminal graft precisely at the predetermined placement site. The introducer sheath with the compressed Corvita endoluminal graft in the tip can be introduced transfemorally as well as over a guidewire into the arterial system and advanced under continual fluoroscopic visualization to the site of the lesion. The Corvita endoluminal graft can be released from the introducer sheath at the intended site by coaxial introduction of a “holding” catheter and by slowly withdrawing the introducer sheath. The exact placement of the Corvita endoluminal graft can still be corrected during the initial release process. The flexibility of this device allows its implantation using various approaches such as the ipsilateral femoral, the contralateral, or the popliteal approach, and in tortuous arteries. The Hemobahn/Viabahn (Gore and Associates, Flagstoff, AZ) This endoprosthesis (Figure 21.3) is constructed with a durable, reinforced biocompatible, expanded polytetrafluoroethylene (PTFE) liner attached to the external nitinol stent structure. This self-expanding prosthesis is designed to allow
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Figure 21.4
Figure 21.3
Viabahn covered stent.
relining of luminal surfaces in tortuous arterial anatomy. Its extreme flexibility enables it to better traverse tortuous areas such as the SFA and conforms more closely to the complex anatomy of the artery. Along with its superior flexibility, the Viabahn endoprosthesis is engineered for exceptional strength and durability. Radio-opaque markers enhance visualization to facilitate accurate placement. The catheter-based system allows for rapid, accurate deployment without device lengthening or shortening. The Viabahn is compressed and attached to a dual-lumen polyethylene delivery catheter available in lengths of 75 cm and 110 cm. The device is available in diameters from 4.5 mm to 13 mm and lengths of 25, 50, 100, and 150 mm. The delivery system is ≤ 10 French in diameter and it requires a 0.025-inch or 0.035-inch guidewire. The deployment consists of untwisting and slowly pulling the deployment knob. After deployment, the device must be smoothed against the arterial lumen wall by inflating an appropriately sized angioplasty balloon within it. The flexibility of the device allows easy contralateral approach. In comparison with Hemobahn, Viabahn has some refinements (0.035-inch guidewire instead of 0.025-inch and deployment from proximal to distal). The Wallgraft endoprosthesis This endoprosthesis (Figure 21.4) is composed of a braided polyester graft, which is bonded to the outside of a commercially available Wallstent with a thin layer of a Corethane (Boston Scientific Corporation). Radio-opaque tracer wires are braided with the stent wires to distinguish the Wallgraft from a Wallstent under fluoroscopy. This design configuration is flexible and self-expanding. The Wallgraft is available in diameters of 6 mm to 14 mm and lengths of 20, 30, 50, and 70 mm. The premounted Wallgraft is available on a Unistep Plus delivery system. The delivery system is equal to or less than 11 French in diameter, has a 90-cm working length and a central lumen that can accommodate a 0.035-inch guidewire.
Wallgraft covered stent.
The deployment is achieved by withdrawing the protective sheath. The self-expandable endoprosthesis is then expanded further by inflating the appropriately sized angioplasty balloon. The flexibility of this prosthesis allows its use in tortuous arteries, even through a contralateral approach. Its shortening, however, may render precise placement difficult. The Jostent stent The Jostent stent (Figure 21.5) is a balloon-expandable prosthesis. It is available in lengths ranging from 28 mm to 58 mm and its expansion diameter ranges from 5 mm to 10 mm. It consists of double thin stainless steel prosthesis. There is a PTFE coating between the two prostheses. An implantation in a flexion area such as the popliteal artery should be avoided because of potential compression and its rigidity. The aSpire covered stent (Vascular Architects, San José CA, USA) This stent (Figure 21.6) is a double-spiral helical nitinol selfexpanding stent completely covered by a thin layer of PTFE, which provides significantly greater vessel wall coverage than metallic stents. Unlike other covered stent grafts, the aSpire stent preserves many of the native vessel’s desired elements including side-branch access. It is available in lengths of 2.5, 5.0, and 10.0 cm and in diameter from 6 mm to 14 mm.
Figure 21.5
Jostent peripheral stent graft.
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●
Figure 21.6
aSpire covered stent.
It provides good radial strength, flexibility, and conformability. The spiral design preserves smooth laminar flow, maintains natural compliance, and withstands torsional stress. If the stent position is not in optimal position it can be “wrapped down,” repositioned, and re-expanded. Cordis covered nitinol stent (in experiment) The Cordis covered nitinol stent is a PTFE tube encapsulated between two nitinol self-expanding, laser-cut stents. The PTFE graft material is located on the inner lumen of the outer stent and is cuffed and bonded at the ends of the outer stent framework. The inner framework supports the inner lumen of the graft to prevent any draping or sagging. Covered stents were available in lengths between 40 mm and 80 mm and diameters between 6 mm and 10 mm. Stents were constrained in a 9French or 10-French delivery system consisting of an inner shaft and an outer sheath designed to accept a 0.035-inch guidewire. Radio-opaque markers were located on the inner shaft at the proximal and distal ends of the undeployed stent and at the tip of the outer sheath for monitoring stent deployment. New stents Other stents will be developed by different companies: ●
The Advanta V12 covered stent (Atrium Medical Corporation, Hudson NH). It is a low-profile balloon-expandable
Figure 21.7
Bard Fluency covered stent.
143
stent made of stainless steel with low foreshortening, covered with a microporous PTFE film for improved biocompatibility and to protect the blood from undesirable vessel wall lesions. It controls tissue prolapse and helps to minimize in stent restenosis due to vascular wall injury. It is available in diameters from 5 mm to 12 mm and fit through 6-French and 7-French introducers. We are waiting for the first studies in peripheral field. The Fluency developed by Bard Peripheral Vascular Inc. (Tempa, AZ, USA) (Figure 21.7). It is a low-profile selfexpanding stent with an ultrathin PTFE covering, exceptional radial force, highly radio-opaque stent graft ends, a soft atraumatic tip, and minimal shortening. It has an excellent trackability, pushability, and flexibility allowing implantation in the main peripheral arteries, with placement accuracy with an 8-French or 9-French delivery system.
The different locations for covered stents Iliofemoropopliteal angioplasty and stenting: results with the different covered stents Cragg Endopro System 1/Passager (Figures 21.8–21.12) Our experience Patient population. One hundred and fifty-six patients (134 males, 22 females), mean age 63.4 ± 10.5 years (range 38–88 years) were selected for treatment with the stent graft. According to Rutherford’s classification, 136 patients were in grade I (8 in category 2, 128 in category 3), 12 patients in grade II, and 8 in grade III (category 5). The mean ankle–brachial index (ABI) was 0.56 ± 0.11. Three tibial vessels were patent in 72, two in 74, and one in 10 patients. Results. Table 21.1 shows the locations and the types of lesions. Ninety-three lesions were heavily calcified (21 were treated with rotational atherectomy), and 17 ulcerated. Tables 21.2 and 21.3 detail the lesion characteristics including the mean lesion length, the mean percentage stenosis before angioplasty and graft placement, and the mean arterial diameter. A total of 266 stent grafts were placed. Lengths ranged from 3 cm to 10 cm and diameters ranged from 5 mm to 10 mm. Indications for stent-graft placement were postangioplasty residual stenoses (n = 70), dissections (n = 22), restenoses (n = 21), ulcerated lesions (n = 17), and aneurysms (n = 26).
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STENT FEMORAL G.
(a) Figure 21.8
(b)
(a) Long SFA occlusion; (b) recanalization: final result after Cragg/Passager stent implantation.
Technical success was achieved in all cases but one at the iliac level (98%) and the femoropopliteal level (99%) (83 cases of 84). In this one case, the patient had a large femoral aneurysm, and partial success was achieved but with persistent arterial leak at the distal part of the aneurysm. This patient was in poor general condition and died from an acute myocardial infarction 4 days after the procedure. Post-angioplasty percent stenoses decreased from 43 ± 3.9% to 0.6 ± 3% after stent-graft implantation, with no significant difference in the iliac and femoropopliteal location (Table 21.4). No significant residual stenosis was seen even in calcified lesions. The mean length of stent segments was significantly greater at the femoropopliteal level in comparison with the iliac level for occlusions and stenoses (Table 21.5).
The mean stent-graft length for all lesions was 114.7 ± 65.7 mm. Immediate clinical success was obtained in all uncomplicated cases with an increase in the ABI from 0.56 ± 0.11 to 0.95 ± 0.14. All patients were given ticlopidine (250 mg/day) or clopidogrel (75 mg/day) and aspirin (100 mg/day) for 1 month, and aspirin alone thereafter. Complications. In the first 30 days there were 18 major complications. At the puncture site, five complications occurred: ● ● ●
two hematomas, one requiring surgery; two pseudoaneurysms both requiring surgery; one local thrombosis treated by thrombolysis.
At the iliac level, four complications occurred (6.2%): ●
●
●
One stent-graft thrombosed within 24 hours (this was associated with distal embolization, treated by surgical thrombectomy). One patient who had two stent-grafts placed for treatment of a right iliac occlusion presented 15 days post-procedure with left-leg claudication. Angiography demonstrated partial obstruction of the left common iliac artery by one of the stent grafts, which protruded slightly into the aorta. A new stent-graft was placed in the left common iliac artery with a good result. Two arteries thrombosed and were treated with success by new PTA.
At the femoropopliteal level: (a)
(b)
Figure 21.9 (a) Total occlusion right iliac artery; diffuse stenoses left iliac artery; (b) final results after Cragg/Passager stent implantation.
●
One patient developed distal embolization after recanalization of an 8-cm-long femoral occlusion, treated by thrombolysis and thromboaspiration. This patient died from an acute myocardial infarction on the third postoperative day.
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(a) Figure 21.10
(b)
(c)
AFTER STENTING
(a) Popliteal artery aneurysm; (b) Cragg/Passager covered stent; and (c) final result after Cragg/Passager stent implantation.
(a) Figure 21.11
CRAGG/PASSAGER
(b)
(a) SFA aneurysm; (b) treatment with Cragg/Passager stent.
BEFORE ANGIOPLASTY
RUPTURE OF THE ARTERY AFTER ANGIOPLASTY
AFTER STENTING
CRAGG/PASSAGER
(a) Figure 21.12
(b)
(c)
(d)
(a, b) Right external iliac artery stenosis; (c) arterial rupture after angioplasty; and (d) treatment with Cragg/Passager stent.
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Lesion characteristics: locations and types of lesions
Location
No.
Iliac Femoral Popliteal Total
64 82 10 156
Stenoses
Occlusions
Aneurysms
33 28 1 62
18 46 4 68
13 8 5 26
Table 21.2 Location
Calcified
Ulcerated
27 63 3 93
10 6 1 17
Lesion characteristics: mean lesion length Stenoses
Iliac 52.2 ± 26.4 Femoral 112.5 ± 69.8 Popliteal 80
Occlusions
Aneurysms
Range
86.7 ± 36.1 161.1 ± 85.3 67.5 ± 15
38.5 ± 13.9 125 ± 93.3 114 ± 80.5
20–150 20–300 30–200
Table 21.3 Lesion characteristics: mean percentage stenosis before PTA and mean arterial diameter Mean percent stenosis before PTA SFA Iliac Popliteal Mean arterial diameter SFA Iliac Occlusion Stenosis Popliteal
Table 21.4
70–100% 70–100% 75–100%
5.95 ± 0.6 mm
5–7 mm
7.8 ± 1.1 mm 7.9 ± 1.1 mm 5.5 ± 0.6 mm
6–10 mm 7–10 mm 5–6 mm
Results before and after PTA
Global population Iliac Femoral Popliteal
Table 21.5
93 ± 4.1% 89 ± 3.7% 92 ± 4.6%
Stenosis before PTA
Stenosis after PTA
Stenosis after stent
92 ± 3.7 89 ± 3.7 93 ± 4.3 92 ± 4.6
43 ± 3.9 48 ± 4.3 45 ± 3.8 37 ± 2.7
0.6 ± 0.3 0 0.8 ± 0.8 0.8 ± 0.8
Results before and after stent Lesion length before stent (mm)
Global population Iliac Femoral Popliteal
104.1 59.2 140.9 92
Stented lesion length (mm) 114.7 63.8 155.2 112
Mean percent of covering (%) 110.2 107.8 110.1 121.7
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●
Seven stent-graft thromboses occurred within 24 hours of the procedure. Three were treated by thrombolysis and thromboaspiration and four required surgical bypasses. Five of the lesions were longer than 15 cm. One stent-graft thrombosis occurred on day 8, requiring surgical bypass.
Finally, a complication that appears to be directly linked with this type of endoprosthesis is the rapid development of fever along with pain in the region of the implant that can last from 2 to 3 weeks; however no infection has been found in these cases. Consequently, the etiology of this phenomenon is still uncertain. This was observed 29 times (18.6%): 25 times at the femoropopliteal level (occlusion n = 15, stenosis n = 7, aneurysm n = 3) and 4 times at the iliac level (occlusion n = 1, stenosis n = 3). There could be a relation between this phenomenon and lesion length, as it appears to be more frequent as the lesion length increases; however, the condition appears to be self-limiting. Follow-up. All patients were followed up by duplex scan on day 180 and every 6 months thereafter. At 6 months, a followup angiography was performed. The maximum follow-up was 60 months, the mean follow-up 36.9 ± 17.9 months. Restenosis. At the iliac level, one restenosis occurred outside the stent and was treated with success by new PTA. At the femoropopliteal level eight patients (8.6%) developed a restenosis, regardless of the stents placed at this extremity. Restenosis inside the stent was not observed. Of these eight restenoses, seven were treated by new angioplasty and three had an additional stent-graft placement. One patient was treated surgically with a bypass. Pseudoaneurysms. In three patients small pseudoaneurysms were detected at the end of the stent graft. In two cases they were treated by the placement of an additional short stent graft. The third patient, however, was only monitored medically due to the small size of the aneurysm. Late thrombosis. At the iliac level, no late thrombosis was observed. At the femoropopliteal level, 18 patients (19.6%) had graft thrombosis. One was recanalized percutaneously, three were treated by surgical thrombectomy, ten required bypass graft placement, and four refused surgery and were treated medically. Of these lesions, twelve were longer than 15 cm. Long-term follow-up. The long-term patencies at 60 months are summarized in Table 21.6. In the literature Several series were published with the Endopro/Passager. Scheinert et al.52 analyzed the primary and long-term results of 48 endoprostheses implanted in iliac artery in 39 patients for long iliac occlusions (n = 22), aneurysms (n = 16), perforation (n = 1). The primary patency was 89.7% at 6 months, 87.1% at 12 months and 84.2% at 24 months. The secondary patency was 94.9% at 6, 92.1% at 12 and 24 months, respectively. Link et al.53 treated an iliac occlusion and 15 high-grade iliac stenoses with a cumulative patency rate of 71% at 12 months. Dorffner et al.54 reported a series of 15 aneurysms in 13 patients (common iliac artery n = 6, external iliac artery: n = 1, hypogastric artery: n = 1, femoral artery: n = 2, popliteal artery: n = 4). In all cases, the aneurysm was successfully
Table 21.6
147
Long-term patencies at 60 months Primary patency (%)
Iliac Global Lesions ≥ 10 cm Lesions > 10 cm Occlusions Stenoses Aneurysms Femoropopliteal Global Lesions ≥ 10 cm Lesions < 10 cm Occlusions Stenoses Aneurysms Femoral Popliteal
Secondary patency (%)
88 85 89 88 92 84
100 100 100 100 100 100
62 51 75 61 63 55 65 40
70 59 85 72 73 55 73 50
occluded after stent implantation. The primary and secondary patency rates at 6 months were 93 and 100% respectively. An arterial rupture of the external iliac artery during balloon angioplasty was treated successfully with the prosthesis by Formichi.55 Beregi JP et al.56 reported a series of 19 aneurysms (iliac: n = 7, subclavian: n = 5, femoral: n = 3, popliteal: n = 3, carotid: n = 1) treated with the same prosthesis with a successful aneurysm occlusion in 18 of 19 patients. At 1 year, the stent was patent in 13 patients (68%) and the aneurysm excluded in 17 (89%). Scheinert et al.32 reported a series of 48 iliac aneurysms treated with 53 endoprostheses. Complete occlusion of the aneurysm was achieved in 47 of 48 cases (97.9%). Primary patency rates were 100% after 1 year, 97.9% after 2 years, 94.9% after 3 years and 87.6% after 4 years. No secondary leaks were observed. Cormier et al.33 treated 34 iliac aneurysms (mean diameter 42 mm). Three procedures were carried out under emergency conditions after acute rupture. The technical success was 97.6%. Scheinert et al.34 reported a series of 20 catheter-included iliac artery injuries treated with these covered stents. An immediate exclusion of the lesion was achieved in all cases, but within 24 hours after, fever (55%), elevations in white blood cell count (50%) and C-reactive protein (65%) were seen in the majority of patients. Two restenoses appeared at the outlet of the endografts and were successfully treated with balloon angioplasty, achieving primary and secondary patency rates of 87 and 100% respectively for a median 21-months follow-up. Ahmadi et al.35 reported a series of 30 patients who underwent covered stent implantation because of post-PTA recurrent stenosis in the SFA. Technical success was 100%. At 6, 12, 36, and 72 months, respectively primary patency rates were 27, 23, 17, and 17%, and secondary patency rates were 63, 60, 34, and 34%. All these published series showed much better long-term results at iliac level than at femoropopliteal level, but for some types of lesions the results appear encouraging.
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The Corvita endoluminal graft (Figure 21.13–21.16) Our experience Population. Sixty-four patients (51 males, 13 females), mean age 65.1 ± 9.8 years (range 39–86) were treated with the Corvita endoluminal graft. According to Fontaine’s classification, 10 were in stage IIa (patients with aneurysms), 52 were in stage IIb, and 2 were in stage III. At the distal arterial level, 6 patients had only 1 patent leg vessel, 36 had 2 patent vessels, and 22 had 3 patent vessels. Lesion characteristics. Table 21.7 summarizes the localization of the lesions following their etiology. We treated 27 stenoses (iliac n = 18, femoropopliteal n = 9), 20 occlusions (iliac n = 8, femoropopliteal n = 12), and 17 aneurysms (iliac n = 12, femoropopliteal n = 5) (Figure 21.6–21.13). The mean length of the lesions was 80.5 ± 55.2 mm (range 20–300). At the iliac level, the mean length was 60.5 ± 28.3 (range 20–150) and at the femoropopliteal level it was 109.7 ± 70.7 (range 20–300). Long-term follow-up. Primary patency and secondary patency rates at 3-year follow-up are listed in Table 21.8. The Hemobahn/Viabahn stent An initial feasibility study36 addressing iliac and femoral artery occlusive disease was performed at three investigational sites in the US and in twelve European centers. In total, 93 patients had 100 lesions treated (iliac n = 58, femoral n = 42). The current mean implant duration was 5.4 months. The primary technical success in this group was 99%. The primary and secondary iliac patency at 1 month (n = 49), 3 months (n = 43), and 6 months (n = 24) was 96% at all intervals. The primary patency for treated femoral arteries at 1 month (n = 37), 3 months (n = 24) and 6 months (n = 7) was 100%, 91%, and 80% respectively. The corresponding secondary patency in the femoral region was 100, 94, and 82% at 1 month, 3 months, and 6 months of follow-up. Our experience We have implanted ten prostheses in the SFA to treat nine long occlusions (mean length 14.5 cm) and one aneurysm with good short- and mid-term results. All the prostheses remain patent at a mean of 12.5-month follow-up.
(a) Figure 21.13
BILATERAL ILIAC ANEURYSM
(b)
In the literature Procedure-related complications have included distal embolization in 5%, groin hematoma in 2%, and iliac artery rupture in 1%. The last case was successfully managed with deployment of a second stent graft without clinical sequelae. Lammer et al.57 reported a study of 127 patients treated for symptomatic peripheral arterial occlusive disease (iliac, n = 61 limbs; femoral, n = 141 limbs). Endoprosthesis deployment was successful in all patients. Primary patency rates in iliac arteries were 98 ± 3% and 91 ± 4% at 6 and 12 months respectively, and at femoral level 90 ± 3% and 79 ± 5% at 6 and 12 months respectively. Secondary patency rates were 95 and 93% for iliac and femoral arteries respectively at 12 months. Bauermeister37 treated 25 patients with long segment occlusions of the femoropopliteal arteries with the Hemobahn stent graft (median occlusion length 22 cm). Primary and secondary patency rates were 73.2 and 82.6% respectively at 1 year. Bleyn38 reported a series of 65 patients (67 limbs) with a mean femoral occlusion length of 14.3 cm. The primary patency rates were 80% at 1 year and 55.6% at 4 years; secondary patency rates were 88.7% at 1 year and 77.8% at 4 years. Saxon et al.39 published a 70% primary patency rate and 93% secondary patency rate at 4-year follow up for lesions of SFA with an average length > 10 cm using Hemobahn or Viabahn. Jahnke et al.40 reported a series of 63 Hemobahn stents used in 52 patients with occlusion (82.7%) or stenosis (17.3%) of the SFA. Mean length of vessel segments covered 10.9 cm ± 5.1. Technical success was 100%. Primary patency rate at 12 and 24 months were 78.4 and 74.1% respectively. Secondary patency was 88.3% at 12 months and 83.2% at 24 months. Chopra et al.41 reported a series of 60 patients (70 lower limbs) with SFA lesions. A total of 158 Hemobahn/Viabahn were implanted. Mean lesion length was 20 cm (2.38 cm). Technical success was 98%. The primary patency rates at 6, 12, 18, and 24 months were 97, 93, 89, and 87% respectively.
RESULT AFTER STENTING
(c)
RESULT AFTER 1 YEAR
(a) Bilateral iliac aneurysm; (b) result after placement of Corvita stents; and (c) results after 1 year.
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(a) Figure 21.14
(b)
(d)
(a) Long SFA occlusion; (b) recanalization; (c, d) final results after covered stents implantation (Corvita).
The secondary patency rates were 99, 96, 91 and 89% respectively. Recently, Fisher et al.42 reported a series of 57 patients treated with 82 Hemobahn or Viabahn for stenoses (13%) or occlusions (87%) of the SFA in 60 limbs. The average length of the treated lesions was 10.7 cm (3–34). Technical success was 98%. Early thrombosis (within 30 days) occurred in 10%. Late thrombosis or reocclusion was observed in 22 arteries (37%) up to 5 years after prosthesis placement (14 in the first year). Primary–secondary patency rates were 90, 95% at 30 days, 67–81% at 1 year, 57–80% at 2 years and 45–69% at 5 years. In a subgroup analysis of 48 patients with “optimal” conditions for implantation (no heavy calcifications, popliteal obstruction, or complete SFA occlusion) minimum 1 vessel run-off, and adequate antiplatelet therapy or anticoagulation, the primary-secondary patency rates were 80–91% at 1 year, 71–89% at 3 years, 62–90% at 5 years. The authors concluded
(a)
(c)
149
(b)
Figure 21.15 (a) SFA popliteal aneurysm; (b) treatment with Corvita covered stent.
that this prosthesis seems to be suitable for SFA so long as ideal indications and prophylaxis against secondary thrombosis are strictly observed. All these reported data with Hemobahn/Viabahn showed good long-term results even at femoropopliteal level. Primary and secondary patencies were similar to those reported for open synthetic femoropopliteal bypass procedures. The Wallgraft stent (Figure 21.17) Our experience We have used this prosthesis in 11 patients to treat occlusive or aneurismal diseases in the iliac (n = 3), femoral (n = 4), popliteal (n = 2), radial (n = 1) and carotid (n = 1) arteries. All prostheses remain patent at a mean of 16 months follow-up (3–41 months). In the literature Steinkamp et al.43 implanted 24 prostheses in 16 patients in iliac arteries to treat large dissections (n = 9), arterial perforations (n = 4), and aneurysms (n = 3). The secondary patency rate was 94.1%. Kumins et al.44 successfully treated three iliac embolic lesions responsible for blue toe syndrome with no recurrence after 16 months. Rzucidlo et al.45 reported the results of stent grafting to treat diffuse aortoiliac occlusive diffuse. Thirty-four patients were treated (Wallgraft: 88%, Hemobahn: 12%). Mean lesion length 13.7 ± 8 cm. Technical success was 100%. At 1 year primary patency was 70% and primary assisted patency 88%. For the authors, early results of stent graft placement to treat this type of lesion appear better than with stenting alone. The Wallgraft was also used to treat traumatic vascular injury as reported by White et al.58 Sixty-two patients were treated: iliac (n = 33), subclavian (n = 18), and femoral (n = 11). Post-procedure exclusion was achieved in 93.5%. One-year exclusion rates were 91.3% iliac, 90% subclavian and 62.3% femoral. One year primary patency rates were 76.4% iliac, 85.7% subclavian, and 85.7% femoral. Freedom from bypass was achieved in 74.3% iliac and 100% femoral and subclavian injuries. The Wallgraft for the treatment of traumatic arterial injuries offers a promising alterative to conventional operative
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(a)
(b)
(c)
(d)
Figure 21.16 (a) Left external iliac artery occlusion; (b, c) recanalization after fibrinolysis/ angioplasty; and (d) final result after stent implantation (Corvita).
The Jostent stent This balloon-expandable stent (Figures 21.18 and 21.19) is useful to treat small lesions at different locations and particularly in emergency to solve complications, which could appear after any PTA. Our experience We have implanted this stent with success in the iliac and femoral arteries in 20 patients to treat ulcerated plaques, small aneurysms, arterial perforations or ruptures, and pseudoaneurysms. In the literature Liistro et al.61 reported a case of thrombus containing iliac lesion treated with a Jostent stent with good follow-up at 6 months.
repair with comparable patency and less major morbidity and mortality. Femoropopliteal aneurysms have been treated with this prosthesis. Howell et al.59 reported a series of 17 patients with a technical success of 100% for femoral aneurysms and 92.3% for popliteal aneurysms. The one-year primary and secondary patency rates were both 100% for femoral, and 69 and 92% respectively for popliteal aneurysms. Lagana et al.60 published a series of 17 femoropopliteal aneurysms (14 treated with Wallgraft) with a 3-year primary patency of 63% and an assisted primary patency of 73%.
Table 21.7
Corvita endomunial graft: lesion characteristics
Location
No.
Iliac Femoral Popliteal Bypass Total
38 22 3 1 64
Stenoses 18 8 — 1 27
Occlusions 8 12 — — 20
Aneurysms 12 2 3 — 17
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Role of covered stents in peripheral arterial diseases Table 21.8 Primary patency & secondary patency at 3-year follow-up Primary patency (%) Global Iliac Global Lesions ≥ 10 cm Lesions > 10 cm Occlusion Stenoses Aneurysms Femoropopliteal Global Lesions ≥ 10 cm Lesions < 10 cm Occlusions Stenoses Aneurysms
Secondary patency (%)
74
86
87 100 85 88 83 92
95 100 94 88 94 100
55 55 54 31 78 57
72 64 82 64 78 78
Cil et al.62 published a case of arteriovenous fistula, which occurred after femoral arterial catheterization and treated with a Jomed stent, with an excellent result at 4-year follow-up. The aSpire covered stent Rosenthal et al.63 reported the results of remote SFA endarterectomy in conjunction with distal aSpire stenting in 210 patients. Mean length of endarterectomized SFA: 28.3 ± 6.2 cm (15–43). At 33 months the primary patency was 60.6% and the primary assisted patency 70.2%. Lenti et al.64 published a multicentric study including 152 patients (168 limbs) with 118 occlusions and 50 stenoses of the SFA. The mean length of the vessel segments covered was 104.35 ± 73.7 mm. The primary patency rates at 12 and 24 months were 64 and 57% respectively and the primary assisted patency rates 76 and 71% respectively. These studies showed good mid-term results but a high number of reinterventions were necessary in order to obtain an optimal assisted primary patency.
(a) Figure 21.17
(b)
(c)
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The Cordis covered nitinol stent Wiesinger et al.65 reported a multicenter prospective nonrandomized COVENT study involving 98 patients who received 130 stents in 107 arteries (60 iliac and 47 SFAs) after predilatation. Mean lesion length was 50 mm in the SFA and 45 mm in the iliac arteries. Technical success was 99%. Primary patency rates were 92% at 6 months and 89.8% at 1 year for the entire cohort. Secondary patency rates were 98 and 95.6% respectively. No statistically significant differences were observed in the primary patency rates for the SFAs (89.3% at both 6 and 12 months) versus the iliac arteries (94.3% at 6 months and 90.7% at 12 months). Carotid angioplasty and stenting: indications for covered stents Self-expandable stents have been providing excellent results when treating most cases of carotid stenosis. With cerebral protection, the neurological complication rate is reduced by 60%. However, brain embolisms may occur even with brain protection, and delayed embolic post-procedure events may also occur. With soft plaques we may have protrusion of cholesterol material through the net of the metallic stent. The migration of the plaque material through the mesh may go on for several days after the insertion of the stent, and produce these delayed embolisms and strokes. Covered stent grafts have been proposed to treat these high-risk embolism plaques.66 They can seal the plaque completely and also eliminate the risk of the stent being crossed by the cholesterol material. Covered stents can also exclude thrombi from the lumen of a vessel.61 Several covered stent grafts may be used. The Jostent stent graft is a balloonexpandable stent and its precise delivery makes it preferable when treating lesions at the ostium of the common carotid and brachiocephalic trunk. Self-expandable stents such as Wallgraft are more resistant to external compression and adapt better to areas where flexion may occur such as carotid bifurcation. Moreover, if this stent is delivered across the bifurcation, the flow of the external carotid artery may be jeopardized. Designs are therefore being developed to provide partial covering of the stent, which
(d)
(a, b) Ulcerated SFA lesion; (c–e) treatment after Wallgraft stent implantation.
(e)
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(a) Figure 21.18
(b)
●
carotid aneurysms with their risk of brain embolism;68 carotid pseudoaneurysms which are more common than true aneurysms, being usually iatrogenic or posttraumatic.69,70
(a) Figure 21.19
(d)
Jostent peripheral stent graft; (a,b) ulcerated, aneurismal lesions; (c,d) treatment with Jostent stent.
will maintain the flow toward the external carotid artery, while sealing the internal carotid plaque.66 Recently, Schillinger et al.67 published a study done to investigate when filter-protected carotid angioplasty stenting using a covered self-expanding stent reduces the risk of cerebral embolization. A significant reduction in ipsilateral microembolic signals by transcranial Doppler was observed with the covered versus the bare stent but a restenosis occurred in 38% of patients treated with covered stents, and none treated with bare stents. The trial was stopped. So, covered stents potentially reduce the risk of cerebral embolism but the problem of in-stent restenosis has to be resolved. Covered stents have also been proposed in other indications: ●
(c)
(b)
A covered stent has also been used to seal a pseudoaneurysm, which had developed at the site of an infected anastomosis between the carotid and the subclavian artery71 as well as in the following situations: ● ● ● ●
severe or extensive disruption of the vessel wall;72 arteriovenous carotid to jugular fistula;73 aneurysms in Behcet’s disease;74 dissection, which may occasionally follow iatrogenic catheter injury or spontaneous trauma.
Subclavian and vertebral angioplasty and stenting: indications for covered stents Covered stents may be indicated to treat specific lesions of the subclavian and vertebral artery: ●
(c)
aneurysm74 or pseudoaneurysm;75
(d)
(a, b) Left iliac artery complex lesion (stenosis + ulceration); (c) treatment with Jostent covered stent.
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traumatic artery injury;76 spontaneous arterial rupture or dissection.77
Other indications for covered stents Covered stents may be indicated for: ●
●
●
Renal arteries in case of aneurysms not involving a large collateral branch, or pseudoaneurysm or arteriovenous fistula, or in case of arterial rupture during renal angioplasty.78 We have used a Jomed covered stent to treat successfully three cases of rupture of a renal artery avoiding surgery. Digestive visceral arteries with the same indications as for renal arteries.79 Hemodialysis access. Covered stents are effective in controlling angioplasty-induced rupture and sometimes for maintaining patency after restenosis in another stent like a Wallstent, but they do not prevent restenosis for de novo lesion. Aneurysm or pseudoaneurysm of hemodialysis access may also be treated with covered stents.
Techniques and treatment The role of covered stents in the treatment of arterial occlusive diseases is controversial, but the last generation of prostheses seems to give promising results, which are competitive with surgery even for long occlusions of the SFA where a primary patency greater than 80% has been reported in several series at long-term follow-up. Stent grafts have potential advantages. They may help to improve the technical success rate by permanently compressing atheromas, repairing obstructive flaps or dissections, and preventing elastic recoil. In the long term the stent structure may prevent remodeling and the fabric tube may prevent tissue infiltration and intimal hyperplasia.42 The latter hypothesis had been proven in several studies and particularly by Virmani et al.80 who found 75% endothelialization of the flow surface in PTFE nitinol stents after 3 months and almost complete coverage after 6 months. The main disadvantage of these endoprostheses is their thrombogenicity, particularly in the first months. Reocclusions can occur suddenly and mostly during the first month, whereas the mean occlusion time of bare stents is a few months or years. In addition the progression of atheromatous lesions outside the stent increases the possibility of reocclusion. In-stent restenosis and stenosis at the distal end of the stent may occur which can also lead to reocclusion. To expect good results and good patency with these prostheses, it is important to know some important variables to optimize stent graft use. Our technique for graft placement has evolved with practice. The following are important points that we have learned during our initial stent-graft experience. Prior to stent-graft implantation, the target lesion should be predilated with a balloon approximately 1 mm larger than the nominal arterial diameter. In some cases, such as calcified fibrous lesions, it could be useful to debulk the arteries before balloon angioplasty. Atherectomy devices, like the Rotablator
153
may be used. It is important to cover the entire lesion with the stent graft and, if possible, to implant a long stent graft so that both ends are implanted in a relatively normal segment of the artery. Angioplasty should not be performed outside the target lesion to avoid restenosis. Accurate placement of the endoprosthesis can be obtained with some prostheses like Cragg Endopro System I/Passager and the Hemobahn/Viabahn due to the minimal shortening, but can sometimes be difficult with other stents because of significant shortening during expansion. After stent implantation, it is important to dilate the stent graft to its nominal diameter. This helps to fully expand the stent and to remove any wrinkles in the fabric that may have occurred during compression and delivery of the graft. An aggressive balloon dilatation is preferable and requires high pressures to achieve the true diameter of the graft within the vessel. High-pressure angioplasty with shorter (2–4 cm) balloons allows for improved deployment and outcomes over long 10-cm balloons. When long lesions must be treated with several prostheses, grafts should overlap by approximately 10–15 mm to prevent them from separating from each other. Separation may lead to a false aneurysm that could thrombose. Adequate inflow to the proximal graft is of utmost importance. Thus it appears important to place a stent graft only after ensuring that proximal iliac and common femoral disease has been adequately addressed. The patency status of the run-off vessels has been shown to affect both surgical bypass and endovascular procedure patency. Patency of tibial vessel run-off has been shown to be a strong predictor of long-term success in endovascular procedures, with two or three vessel run-off associated with two or three times the patency of patients with zero to one vessel runoff. Fischer et al.42 found significantly lower patency in patients with poor run-off. However for Hartung et al.81 poor run-off does not affect the long-term patency because most of the time outflow lesions are improved during catheter intervention. The fact that reocclusions mostly occur in the first year after stent graft placement correlates with the nearly complete endothelialization after 12 months.80 About 71% of all reocclusions occur in the first year after graft implantations, 21% in the first 30 days, which underscores the importance of consistent antiplatelet therapy. A powerful anti-aggregant protocol associating ticlopidine or clopidogrel and aspirin given several days before the procedure seems to have limited early thromboses. Aspirin plus ticlopidine or clopidogrel for 3–6 months are recommended. The treatment of aneurysms with covered stents in the iliac and femoropopliteal arteries seems rather easy. The results of our series are very favorable at the iliac level but less favorable at the femoropopliteal level, regardless of the graft used. The simplicity of their use should make these covered grafts the treatment of choice for aneurysmal lesions. We wish to insist that even after a stent occlusion at the femoropopliteal level, there have been no serious ischemic complications or limb loss in our experience. The phenomenon of pain and fever encountered after implantation of Cragg Endopro System/Passager is a complication that we still do not fully understand. The phenomenon does not seem to be related to local infection, but it is clearly an inflammatory response to graft implantation. It is likely that the stent graft itself or one of its fabric or metal components may be an inducer of cytokinins from neutrophils.
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We have seen that covered stents may also have good specific indications at other levels: supra-aortic vessels, renal and abdominal arteries, and hemodialysis fistula. More specific devices should be developed to enlarge their indications. The indications for covered stents are still debated; however, the following indications are not debatable: aneurysms; arteriovenous fistulae; arterial traumas; arterial rupture.
● ● ● ●
Covered stents should be available in all catheterization laboratories in order to quickly treat arterial ruptures that may occur during an angioplasty procedure and thus avoid surgical repair. Certain indications are more questionable, such as long occlusions or stenoses, long dissections, and ulcerated lesions. Fischer et al.42 pointed out patients with “optimal” conditions for a good long-term arterial patency: no heavy calcifications, popliteal obstruction or complete SFA occlusion, minimum one vessel run-off, and adequate antiplatelet therapy or anticoagulation.
Results obtained with covered stents seem encouraging and the use of new prostheses, with lower thrombotic risks, should allow the treatment of long lesions with success rates and results that are at least as good as those obtained with surgery, and results obtained with the Hemobahn/Viabahn stent seem promising. A continuous follow up is necessary to prevent reocclusions owing to poor compliance or progression of atheromatous disease. Intensive surveillance using objective testing followed by prompt repeat intervention are mandatory to maintaining patency and quality of life.
Conclusion Covered endoprostheses allow the operator to perform true internal bypass using percutaneous access. The indications for their use should broaden and they could become an alternative to surgery. Improvements should come about, particularly with respect to thrombogenicity and the method of implantation. Randomized studies versus surgery and other types of stents are expected in order to confirm the interest of these new prostheses and their place as compared to non-covered prostheses.
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Mewissen M. Nitinol stents in the femoropopliteal arterial segment. Endovasc Today 2005; 4: 29–34 Scheinert D, Schroder M, Steinkamp H et al. Treatment of iliac artery aneurysms by percutaneous implantation of stent grafts. Circulation 2000; 102: 253–8 Cormier F, Alayoubi A, Laridon D et al. Endovascular treatment of iliac aneurysms with covered stents. A Vasc Surg 2000; 14: 561–566 Scheinert D, Ludwig J, Steinkamp HJ et al. Treatment of catheter induced iliac artery injuries with self-expanding endografts. J Endovasc Thur 2000; 7: 213–20 Ahmadi R, Schillinger M, Maca T et al. Femoropopliteal arteries: immediate and long-term results with a Dacron-covered stent graft. Radiology 2002; 223: 345–50 Dake MD, Semba CP, Kee ST et al. Hemobahn: Results of a multicenter feasibility study. Presented at the International Symposium on Vascular Diagnosis and Intervention. Miami, January 11–15, 1998 Bauermeister G. Endovascular stent grafting in the treatment of superficial femoral artery occlusive disease. J Endovasc Thur 2001; 8: 315–20 Bleyn J. Superficial femoral artery stenting with Hemobahn. International Stenting Congress XV. Scottsdale, February 2002 Saxon AR, Coffman JM, Gooding JM et al. Endograft used in the femoral and popliteal arteries. Tech Vasc Interv Radiol 2004; 7: 6–15 Jahnke T, Andresen R, Muller-Hulsbeck S et al. Hemobahn stentgrafts for treatment of femoropopliteal arterial obstructions: midterm results of a prospective trial. J Vasc Interv Radiol 2003; 14(1): 41–51 Chopra P. Use of the Viabahn stent graft for PVD in the femoropopliteal arterial segment. Endovasc Today 2005; 5(Suppl): 4–8 Fisher M, Schwabe C, Schulte KL. Value of the Hemobahn/Viabahn endoprosthesis in the treatment of long chronic lesions of the superficial femoral artery: 6 years of experience. J Endovascular Ther 2006; 13: 281–90 Steinkamp HJ, Werk M, Seibolds et al. Treatment of arterial traumas by the Wallgraft endoprosthesis. Rofo Fortschr Geb Roentgenstr Nerren Bildgeb Verfahr 2001; 173: 97–102 Kumins NH, Owens EL, Oglevie SB et al. Early experience using the Wallgraft in the management of distal microembolism from common iliac artery pathology. Ann Vasc Surg 2002; 16: 181–6 Rzucidlo EM, Powell RJ, Zwolak RM et al. Early results of stentgrafting to treat diffuse aorto iliac occlusive disease. J Vasc Surg 2003; 37: 1175–80 Cragg AH, Lund G, Rysavy JA et al. Non-surgical placement of arterial endoprostheses: A new technique using nitinol wire. Radiology 1983; 147: 261–83 Cragg AH, De Jong SC, Barnhart WH et al. Nitinol intravascular stent: Results of pre-clinical evaluation. Radiology 1993; 189: 775–8 Cragg AH, Dake MD. Percutaneous femoropopliteal graft placement. J Vasc Intervent Radiol 1993; 4: 445–63 Henry M, Amor M, Ethevenot G, et al. Initial experience with the Cragg Endopro System 1 for intraluminal treatment of peripheral vascular disease. J Endovasc Surg 1994; 1: 31–43 Henry M, Amor M, Cragg A et al. Occlusive and aneurismal peripheral arterial disease: assessment of a stent-graft system. Radiology 1996; 201: 717–24 Dereume JP, Ferreira J El Douaihy M et al. Clinical experience with an integrated self-expandable stented graft (Corvita) for the treatment of various arterial lesions. In Veith FJ, ed. Current Critical Problems in Vascular Surgery, Vol. 6. St. Louis: Quality Medical Publishing, 1995 Scheinert D, Ragg JC, Vogt A et al. The value of a fabric coated selfexpanding stent in iliac arterial occlusions or aneurysms. the primary and long-term results. Rofo Fortschr Geb Roentgenstr Nerren Bildgeb Verfarh 1998; 169: 302–9 Link J, Muller-Hulsbeck S, Hackethal S et al. Midterm follow up after Cragg stent placement in iliac arteries. Rofo Fortschr Geb Roentgenstr Nerren Bildgeb Verfarh 1997; 167: 412–7 Dorffner R, Thurnher S, Puig S et al. Treatment of arterial aneurysms of the pelvic leg vessels using dacron covered nitinol stents. Rofo Fortschr Geb Roentgenstr Nerren Bildgeb Verfarh 1998; 168: 275–80 Formichi M, Raybaud G, Benichou H et al. Rupture of the external iliac artery during balloon angioplasty: endovascular treatment using a covered stent. J. Endovasc Surg 1998; 5: 37–41 Beregi JP, Prat A, Willoteaux S et al. Covered stents in the treatment of peripheral arterial aneurysms: Procedural results and mid-term follow up. Cardiovasc Intervent Radiol 1999; 22: 13–9
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Lammer J, Dzkr MD, Bleyn J et al. Peripheral arterial obstruction, prospective study of treatment with a transluminally placed selfexpanding stent graft. Interventional Trial Study Groups. Radiology 2000; 8: 315–20 White R, Krajcer Z, Johnson M et al. Results of a multicenter trial for the treatment of traumatic vascular injury with a covered stent. J Trauma 2006; 60: 1189–95 Howell M, Kracjer Z, Diethrich EB et al. Wallgraft endoprosthesis for the percutaneous treatment of femoral and popiteal artery aneurysms. J Endovasc Ther 2002; 9: 76–81 Lagana D, Carrafiello G, Mangini M. Endovascular treatment of femoropopliteal aneurysms: a five years experience. Cardiovasc Intervent Radiol 2006; 29: 819–25 Liistro F, Stankovic G, Dimario C et al. Covered stent to exclude intravascular thrombus. J Endovasc Ther 2002; 9: 246–49 Cil BE, Akmangit I, Peynircioglu B et al. Iatrogenic femoral arterioveinous fistula: endovascular treatment with covered stent implantation and 4 year follow-up. Diagn Interv Radiol 2006; 12: 50–2 Rosenthal D, Martin JD, Smeets L et al. Remote superficial artery endarterectomy and distal aSpire stenting: results of a multinational study at three year follow-up. J Cardiovasc Surg 2006; 47: 385–91 Lenti M, Cieri E, Derango P et al. Endovascular treatment of long lesions of superficial femoral artery: results from a multicenter registry of aSpiral covered PTFE stent. Vascular Annual Meeting. Baltimore, May 30–June 4, 2006 Wiesinger B, Beregi JP, Oliva VL et al. PTFE covered self-expanding nitinol stents for the treatment of severe iliac and femoral artery stenoses and occlusions: final results from a prospective study. J Endovasc Ther 2005; 12: 240–46 Inglese L, Calabrese E. Extracranial carotid aneurysm: Interventional treatment. In: Henry M et al, eds. Angioplasty and Stenting of the Carotid and Supra-aortic Trunks. London: Martin Dunitz, 2004 Schillinger M, Dick P, Wiest G et al. Covered versus bare self-expanding stents for endovascular treatment of carotid artery stenosis: a stop randomized trial. J Endovasc Ther 2006; 13: 312–9 Mukherjee D, Roffi M, Yadav JS. Endovascular treatment of carotid artery aneurysms with stent grafts. J Endovasc Cardiol 2002; 14: 269–72 Simionato F, Righi C, Melissano G et al. Stent-graft treatment of a common carotid artery pseudoaneurysm. J Endovasc Ther 2000; 7: 136–40 Scavee V, De Wispelaere JF, Mormont E et al. Pseudoaneurysm of the internal carotid artery: treatment with a covered stent. Cardiovasc Intervent Radiol 2001; 24: 283–5 Battaglial, Barolucci R, Minacci S et al. Stent graft repair the rupture of the subclavian artery secondary to infection of a subclavian carotid bypass graft. Ann Vasc Surg 2001; 15: 474–76 Parodi JC, Ferreira LM, Bergan J. Endovascular stent-graft treatment of traumatic arterial lesions. Ann Vasc Surg 1999; 13(2): 121–9 Geremia G, Bakon M, Brennecke L, et al. Experimental arteriovenous fistulae: treatment with silicone-covered metallic stents. Am J Neurorad 1997; 18(2): 271–7 Eggebrecht H, Bruch C, Haude M et al. Transluminal exclusion of a subclavian artery aneurysm with stent graft implantation. Z Kardiol 2000; 89: 761–5 Hernandez JA, Pershad A, Laufer N et al. Subclavian artery pseudo aneurysm: successful exclusion with a covered self expanding stent. J Invas Cardiol 2002; 14: 278–9 Stecco K, Meier A, Seiver A et al. Endovascular stent graft placement for treatment of traumatic penetrating subclavian artery injury. J Trauma 2000; 48: 948–50 Chiaradio JC, Guzman L, Padilla L et al. Intravascular graft stent treatment of a ruptured fusiform dissecting aneurysm of the intracranial vertebral artery: technical case report. Neurosurgery 2002; 50: 213–16 Schneidereit NP, Lee S, Morris DC et al. Endovascular repair of ruptured renal artery aneurysms. J Endovasc Ther 2003; 10: 71–4 Larson RA, Solomon J, Carpentier JP. Stent graft repair of visceral artery aneurysms. J Vasc Surg 2002; 36: 1260–63 Virmani R, Kolodgie FD, Dake MD et al. Histopathologic evaluation of an expanded polytetrafluoroethylene nitinol stent endoprosthesis in canine ilio femoral arteries. J Vasc Interv Radiol 1999; 10: 445–56 Hartung O, Oterd A, Dubuc M et al. Efficacy of Hemobahn in the treatment of superficial femoral artery lesions in patients with acute or critical ischemia: a comparative study with claudicants. Eur J Vasc Endovasc Surg 2005; 30: 300–6
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Embolic protection devices M Henry, I Henry, A Polydorou, and M Hugel
Introduction Percutaneous endoluminal interventions have revolutionized the contemporary management of atherosclerotic arterial disease in a variety of vascular beds. Beginning with coronary circulation and quickly spreading to the peripheral and cerebral vessels, balloon angioplasty, with and without stenting, has been remarkably successful in treating arterial occlusive disease, and is currently the first treatment to be proposed to patients suffering from atherosclerotic diseases. Over the past few years, the vascular interventionist has managed to treat increasingly complex lesions in high-risk patients using a combination of new techniques and new devices. One of the problems remaining is the occurrence of embolic debris liberated during vascular manipulation. It is now clear that atheroemboli are the rule in any intervention in atherosclerotic disease and seem the root cause of many procedural complications whenever atherosclerotic lesions are treated. Contrary to earlier beliefs that atheroembolization is a “non-issue” during percutaneous catheter intervention, there is now mounting evidence that distal atherosclerotic debris commonly embolize from lesions in many vascular territories during percutaneous intervention. The role of distal embolization was well demonstrated at first in coronary arteries, saphenous vein grafts1,2 and in carotid angioplasty,3–14 but has been increasingly demonstrated in other territories such as the renal15–19 and peripheral arteries.20–23 Embolic protection devices (EPD) have been developed to reduce the complications due to atheroembolism in different territories. These EPDs currently on the market or in clinical experiments can be classified under three main groups, each with its own working principle: ● ● ●
distal occlusion devices; distal filters; proximal occlusion devices.
These three types of EPD can be used in carotid angioplasty stenting (CAS), yet there are some specific cases or locations for which a certain type is more advantageous when compared to the others. This article lists the main EPDs and outlines our device selection criteria. 156
Different types of EPDs Distal occlusion The different devices The concept here is based on blockage of distal blood flow by placement of a sealing balloon downstream from the lesion of interest and inflated at low pressure. This redirects blood flow towards the external carotid artery (ECA) and results in a stagnant column of blood during intervention. The brain is protected from any embolic migration during the occlusion and the potential embolic debris trapped within it can be removed before releasing downstream occlusion. These debris generated by the dilatation and stent placement are then eliminated using one or two techniques such as aspiration or cleaning depending on the device used. Three devices employ this approach. The Percusurge Guardwire (Medtronic Inc., Santa Rosa, CA) (Figure 22.1) ●
This device has been widely used in CAS24–28 and more recently in renal angioplasty stenting.15–17
Description. The Percusurge GuardWire system is constructed as a 0.014-inch hollow nitinol (nickel–titanium alloy) wire with a shapeable floppy distal tip (190 or 300 cm). Proximal to the floppy tip is a compliant elastomeric polyurethane occlusion balloon with a maximal crossing profile of 0.036-inch when deflated. Once the stenotic lesion is crossed with the GuardWire, the occlusion balloon is inflated to a variable size, ranging from 3 to 6 mm in diameter, using the handheld Microseal Adaptor and EZ Flator. The handheld system is then removed from the proximal end of the wire while the occlusion balloon remains inflated. This coaxial exchange set-up allows for over-the-wire (OTW) delivery of angioplasty balloons and stent systems. Any embolic particles released during this portion of the procedure remain in the stagnant pool of blood below the occlusion balloon in the distal internal carotid artery (ICA). This column of blood is aspirated through the large bore lumen of the Export catheter connected to a vacuum syringe. Two or three aspirations can be done through the stent and below the balloon to eliminate the maximum of debris. At the conclusion of the procedure, the occlusion balloon is deflated with the handheld device. Total occlusion times typically range from 5 to 15 minutes.
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Figure 22.1 Rosa, CA).
157
The Percusurge Guardwire (Medtronic Inc., Santa
Published results. The PercuSurge GuardWire currently has US FDA approval for use in the treatment of degenerated saphenous vein grafts following coronary artery bypass surgery. In 1999, we reported our initial experience treating 53 carotid stenoses on 48 patients.24 Immediate technical success rate was 100% with mean balloon occlusion time of 542 ± 243 seconds. One patient developed amaurosis, yielding an overall neurological event rate of 1.8%. More recently, we published our midterm results, 268 procedures performed under cerebral protection on 242 patients.25 Technical success rate was 99.3%, mean occlusion time was 410 ± 220 seconds, five patients suffered neurological events (1.9%) for a combined 30-day stroke, and death rate was 2.3%. With the EPD, visible debris were extracted from all patients. Mean diameter was 250 µm (52–2652 µm), with the mean number per procedure being 74 (7–145). Different types of particles were found: atheromatous plaques, cholesterol crystals, calcified crystals, necrotic cores, fibrin, recent and old thrombi, platelets, macrophage foam cells, lipoid masses, and acellular material. Al-Mubarak and colleagues reported their results following stenting of 37 patients with carotid stenosis. One patient suffered a non-disabling stroke and another died from consequences of hyperperfusion syndrome resulting in a peri-operative combined stroke and death rate of 5.4%. The same group has also reported the occurrence of ipsilateral cerebral embolization via ECA collaterals using the distal balloon protection system.27,28 We have used the Percusurge Guardwire in renal angioplasty stenting in 46 patients. We aspirated visible debris in all patients. The mean particle number was 98.1 ± 60 (13–208) and the mean particle diameter 201 ± 76 m (38–6206). The Tri Active FX (Kensey Nash, Exton, PA) (Figure 22.2) This device has the ability to block, flush, and aspirate the debris generated during CAS. It consists of a 0.14-inch hypotube attached to an inflatable balloon (3–5 mm). This hypotube, like the PercuSurge Guardwire, serves as the interventional guidewire over which balloon and stents can be placed. The current version of the Triactive FX system uses a rapid CO2 exchange system, allowing for quick inflations and deflations. This allows for rapid re-establishment of antegrade flow. After the procedure is completed, the stagnant column of blood is removed using a distal saline infusion catheter (Flushcath) and active extraction. This active flush system allows for more aggressive particle removal from the walls of the vessel, stent struts, and area surrounding the distal balloon before the downstream vasculature is exposed
Figure 22.2
The Tri Active FX (Kensey Nash, Exton, PA).
to restoration of flow. Recently, Franke29 reported a prospective, non-randomized multicenter pilot study. Fifty patients were included with a procedural success of 94 and 2% of neurological complications at hospital discharge (one minor stroke). The Guard Dog (Possis Medical Inc., Minneapolis MN) (Figure 22.3) This was recently approved for work in the periphery and consists of a 0.035-inch guidewire that incorporates a 3–6-mm CO2-filled compliant balloon at the tips. The balloon requires 0.7 atmospheres of pressure to be inflated and is used to seal off the distal vasculature. Removal of debris can then be performed using another device (Possis Angiojet) as desired. The Twin-One (Minvasys, Gennevilliers, France) (Figure 22.4) This new system was recently proposed by Theron and is an evolution of his cerebral protection concept described many years ago.30–32 For this author, as well as for Castriota et al.,33 the only moment of a real risk of embolic complication is the time of post-dilatation of the stent when the plaque is broken. The goal of this new protection device is therefore to focus the problem on the carotid bifurcation and to concentrate, from the beginning to the end of the procedure, all manipulations on a very limited anatomical space (Figure 22.4a). The various phases of the technique are as follows: ●
●
●
●
●
After having positioned the guiding catheter in the common carotid artery, the stenosis is passed with a 0.014inch wire (Figure 22.4b). When a predilatation is necessary, it is performed with a 2-mm balloon without cerebral protection (Figure 22.4c). The stenosis is passed with the stent without cerebral protection. The stent is auto-expandable and its length is 4 cm or more. It can be rapid-exchange or over-the-wire. Its diameter is 7–9 mm according to the artery. It is a delicate moment and the manipulations must be extremely soft (Figure 22.4d). The stent is deployed without cerebral protection. It is positioned covering the origin of the external carotid (Figure 22.4e). The guiding catheter is introduced in the stent (Figure 22.4f).
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(b) Figure 22.3
●
●
(c)
The Guard Dog (Possis Medical Inc., Minneapolis MN).
The delivery system of the stent and the wire are withdrawn (Figure 22.4g). The protection system is introduced (TwinOne) in the stent. It is a device combining a catheter loaded with an occlusion balloon with a rapid exchange angioplasty catheter. Introduced as one tool, it is possible – after peeling away the sheath – to move each catheter separately to ensure the best positioning of each item. There is no wire and the progression is particularly fast and simple when continuous frame stents are used. For the open cell stents, a torquer facilitates the progression of the balloon.
4a
4b
4h
Figure 22.4
4c
4i
●
●
●
●
The system is positioned at the distal extremity of the stent (Figure 22.4h). The occlusion balloon is inflated in the stent and the angioplasty balloon is positioned at the narrowing of the stent (Figure 22.4i). An angiographic series is performed. Contrast should be gently injected to avoid forcing the contrast around the occlusive balloon and give a false impression of incomplete occlusion. The contrast must remain at the origin of the internal carotid if the closure is efficient (Figure 22.4j). The post-stenting dilatation is achieved.
4d
4j
The Twin-One (Minvasys, Gennevilliers, France).
4e
4k
4f
4l
4g
4m
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●
The angioplasty balloon is pulled back and withdrawn from the femoral or radial introducer. The guiding catheter is repositioned when necessary on the site of the angioplasty and blood (one or two 20-cm3 syringes) is aspirated quickly through the guiding catheter (Figure 22.4l). A flush is not performed. The occlusion balloon is deflated and retrieved. The mean occlusion time is less than 5 minutes in most cases and may reach only 3 minutes in some cases. The guiding catheter is positioned, again in the common carotid artery, and control angiographic series are performed (Figure 22.4m).
●
A first series of 45 CAS performed with this technique has been reported without complications and without any cerebral intolerance. This system can be used via a femoral or radial approach. Advantages of distal occlusion These devices have a very low crossing profile ( 250 to 300 seconds is recommended. The filter may cause spasm or dissection of
Figure 22.11
The Rubicon Filter (Rubicon, Salt Lake City, UT).
the distal ICA, which could possibly lead to restenosis. Closure and retrieval of filters can dislodge their content collected during the procedure. Some difficulties in retrieving the filters have been reported, for example in 8.4% of cases.4 We may have difficulties getting the retrieval catheter in and the filter could get caught on the struts of the stents during retrieval. These problems occur more frequently with open cell stent design. As with occlusion balloons, filters cannot prevent all neurological embolic events. The filter can protect the brain only after the filter has crossed the lesion and has been deployed. This maneuvre and the initial positioning of the guide catheter in the CCA can release embolic material. Some emboli may occur during the procedure if the filter is not well deployed or if the diameter of the filter is not sufficient during systole and diastole, and after predilatation of the lesion, which could increase the flow and the diameter of the artery. It is important to deploy the filter in a straight part of the vessel to have a good wall apposition of the filter to avoid embolism. Inadequate filter vessel apposition is not always angiographically detectable and complete protection from embolization may not be possible in oval or eccentric vessels. A filter can generally retrieve debris > 100 µm, most of the devices have a pore size of 100 µm or larger, which can allow smaller particles to go to the brain with the possibility of micro infarcts. Only a small number of particles are removed43 and macroscopically visible particles are retrieved in only 35.0–83.7% of the filters.42,44 Filters reduce the risk of brain embolism as demonstrated by TCD or diffusion weighted magnetic resonance imaging (DW-MRI) but do not prevent all emboli from reaching the cerebral circulation. Asymptomatic or “silent” ischemic lesions detected with DW-MRI have been reported more frequently after CAS than after endarterectomy.45–47 Recently, Flach et al.48 published
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Embolic protection devices a 9% frequency of new hyperintense lesions in surgically treated patients and a 43% frequency in the CAS group. Although the clinical importance of silent lesions is yet unclear, Vermeer et al. recently found that silent brain infarcts are associated with cognitive dysfunction in the general population. An increased frequency of dementia, and neuropsychomatic changes could also be a consequence of these lesions.49–52 With all protection devices, all stents we may observe periprocedural or delayed embolic events. Most of the time, these complications are due to plaque protrusion through the stent struts and embolization of plaque material. To avoid these problems, we can aspirate this debris inside the stent and below the filter with an aspiration catheter or the guiding catheter. It is better to aspirate and clean the dilated area for at least all symptomatic lesions and all echolucent plaques. Other issues have been demonstrated with current EPD. Recently, Vos et al.53 published interesting data showing that the role of some filters is unclear and associated with potential problems. By means of TCD, he detected a higher number of microemboli during filter-protected CAS but the number of particulate macroemboli was higher in the unprotected group. Distal thrombus formation occurred only in patients with filter protection. MacDonald et al.54 published similar data with the EmboShield filter. New generation of filters (Figure 22.12) To overcome some problems encountered with current filters, a new filter was recently proposed and is in experiment. This filter, the FiberNet (Lumen Biomedical Inc., Plymouth, MN) consists primarily of polyester fibers located coaxially around the distal tip of a guidewire assembly. This filter is soft, conformable and when activated, expands radially to fill the vessel, providing excellent apposition to the vessel wall. Contained and captured emboli are recovered/removed both by aspiration through the retrieval catheter and also by retention within the filter fibers when the filter is closed and retracted into the retrieval catheter. Aspiration is achieved through the retrieval catheter using vacuum syringes to provide suction. This filter enables capture of emboli as small as 40 µm without compromising the flow through the filter, and can be delivered as a standard coronary guidewire.
Figure 22.12
New generation of filters.
163
The possibility of suction through the retrieval catheter during device removal is probably one of the major improvements with this device, allowing cleaning of the dilated area and of the inner part of the stent. This technique allows aspiration of the debris, which can protrude through the struts of the stent after stent placement and dilatation and which could be one of the causes of the delayed embolic events. We performed the first human study in carotid and renal arteries with this new protection device. Fifty-three patients (49 carotid and 4 renal) were treated. Visible debris comprising atheroma was detected in each case. It is important to state that nearly 30% of the debris was aspirated from inside the stent, which could potentially reduce delayed embolic events. We compared this device with other filters. With the FiberNet, we removed five times more debris. Thirty-four patients underwent CT or MRI before and at 30-day post-procedure. No changes were noted in the follow-up tests when compared to the baseline.55
Flow reversal technique Parodi antiembolization catheter (Gore and Associates Inc., Flagstaff, AZ) (Figure 22.13) Description of the device56,57 The Parodi antiembolization catheter (PAEC) is a guiding sheath with an occlusion balloon attached at the distal end of the catheter. The main lumen has an inner diameter of 7.3 French that allows the passage of balloons and stents. Once the PAEC has been inserted in the CCA, a Parodi external balloon (PEB) is inserted and inflated in the ECA. Then, the occlusion balloon attached on the outer surface of the PAEC is then connected to a sheath that is percutaneously inserted into the femoral vein to create a temporary arteriovenous shunt. This shunt, along with the PEB, creates reversal of flow in the ICA. The deployment of the PEB is required to prevent retrograde flow from the ECA, which may cause prograde flow in the ICA. Particles of all sizes flow through the PAEC and are captured by a filter placed at the arteriovenous connection. The new device is 9-French-sheath compatible. The working length of the Gore balloon sheath (0.035-inch-guidewire compatible) is 91 cm.
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GORE Balloon Wire GORE Balloon Sheath
Figure 22.13
Parodi antiembolization catheter (Gore and Associates Inc., Flagstaff, AZ).
Advantages ●
●
●
● ●
● ●
●
Complete protection can be achieved before manipulating the lesion. The risk of complications is reduced by never crossing the lesion unprotected. The lesion can be crossed with any guidewire of our choice under protection, avoiding brain embolism during this step. Embolization to the brain is not possible during reversed flow. Particles of all sizes can be captured. Tight, tortuous lesions, and stenosis with limited landing zone can be treated with any wires. The PAEC provides a treatment option for patients whose anatomy is unsuitable for the use of a distal filter. No damage is caused to the fragile intima of the distal ICA. The technique avoids flushing through the ECA with the risk of brain embolization in the case of collateral circulation between the ECA and ICA or vertebral artery. Complications associated with filter retrieval and filter related vasospasm in the ICA are eliminated.
Disadvantages and limitations ●
●
●
●
The interruption of flow during protection may not be tolerated in some patients (5%), as with distal occlusion balloon. The new generation of PAEC need a 9-French introducer. With the previous device a larger puncture side-hole was needed (11-French). The technique has the potential to cause spasm or dissection in the ECA or CCA. As with other protection devices, a brain embolism may occur during placement of the catheter in the CCA. This step cannot be protected.
Seatbelt and airbag technique This technique was described by Parodi et al.58 in two patients. They used a flow-reversal system (Parodi anti-embolism system), which was first placed with a 260-cm exchange wire in the CCA 3 cm below the carotid bifurcation. Flow reversal was achieved by inflating the balloon in the ECA and CCA. Via an external connector a guidewire and an E Trap Filter (MSD, Pittsburgh, PA) were delivered to the distal ICA with active suction from a syringe on the PAES catheter. Once the filter was above the stenosis, the flow reversal was discontinued and the procedure proceeded under cerebral protection with the filter. The combination of these existing cerebral protection devices could, at least in theory, achieve what neither of them could independently. Moreover, it may be feasible to avoid some drawbacks of the various systems. Because distal protection devices must cross the lesion, which may account for about 12% of all emboli generated during a procedure,12 Parodi et al. sought to provide protection during this step by initiating flow reversal through the ICA to prevent distal embolization. No cerebral embolization has been demonstrated on TCD monitoring during these procedures. This technique could be indicated for carotid stenoses that demonstrate a high potential for embolization or in patients with an aberrant or a non-functioning circle of Willis or contralateral ICA occlusion, which may be intolerant to balloon occlusion.
MOMA Device MOMA Device is a “proximal flow blockage” cerebral protection device. Cerebral protection occurs by interruption of antegrade blood flow from the common carotid artery and
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Embolic protection devices retrograde blood flow through the ipsilateral ECA. This is achieved by a low-pressure balloon occlusion of the two vessels by means of a single device integrating the two occlusive balloons and a working channel for the delivery of interventional devices to the target lesion. One balloon occludes the ECA and the second balloon the CCA, so that passing the target lesion with the embolic protection system before starting the procedure can be avoided. Debris are thus stopped at the carotid bifurcation and prevented from dislodging to the brain. Removal of debris is performed by spot (active) syringe aspiration which can be performed any time during the intervention through the working channel of the device.
Choice of the protection device Device selection for carotid angioplasty and stenting Table 22.1 summarizes advantages and disadvantages of the different protection devices. We know that all CAS should be performed under cerebral protection. The choice of the protection device depends on the interventionist, the lesion, the anatomy of the different vessels (aortic arch, carotid arteries, etc.), the intracranial circulation and the collateral circulation. Before deciding which protection device to use it is indispensable to assess carefully the anatomy at intracerebral level, the access site and the lesion itself. Intracerebral circulation To decide on which protection device to use, a good angiography of the intracranial circulation is mandatory with fourvessel angiography and a good assessment of the collateral circulation. Without sufficient collateralization, only distal filters can be used. Distal and proximal occlusion systems should not be used because cerebral perfusion will be inadequate during the procedure and intolerance episodes could happen. It could be the case in patients with severe contralateral carotid stenosis or occlusion. Distal occlusion is also contraindicated in patients with anastomosis between ICA, ECA, and vertebral territories. With sufficient collateralization distal occlusion can be used. Access site assessment Patients presenting with tortuous vessels, or type III aortic arch, require low-profile flexible protection systems, as it is
Table 22.1
165
difficult to reach the lesion site. Low-profile, steerable, flexible devices should be used, like the distal occlusion system, and some filters we have to choose carefully. But proximal occlusion systems seem inadequate due to their larger profile. Lesion site assessment ●
●
●
●
Severe stenoses and irregular lesions can be treated under any kind of protection but we have to choose very lowprofile, steerable devices. With a very tortuous ICA, a severely angulated ICA or when there is little space between the lesion site and the cerebrum, with lake of landing zone for the device, it is better to use proximal occlusion devices. If thrombotic lesion or thrombi are suspected, proximal occlusion devices are the only possibility of avoiding a brain embolism. Some authors advise proximal occlusion system to treat plaques with very high risk of brain embolism (soft, dishomogenous plaques, plaques with GSM < 25). However, very low-profile, flexible, soft-tipped filters or distal occlusion systems can be used and the generation of protection devices like FiberNet seems also very promising for these lesions with a greater tendency to embolize.
Device selection for renal angioplasty and stenting We have the choice between distal occlusion and filters. The limitation with filters as in CAS is the pore size with the possibility of small emboli going to the kidney. The landing zone is also a concern. For these reasons, the new three-dimensional filter FiberNet seems a good indication. Device selection for peripheral angioplasty Any filters of distal occlusion systems can be used in peripheral arteries. Device selection for vertebral artery If a protection is indicated for a vertebral angioplasty stenting, low-profile, flexible filters or occlusion balloons can be used and placed in the vertebral artery. Another possibility is to place a Parodi device at the ostium of the subclavian artery to block the flow and create a reversal flow inside the vertebral artery.
Advantages and disadvantages of the different concepts
Embolization Flow ICA Ability to during decrease protection perform guidewire/catheter from angiography lesion crossing emboli during protection Filters +++ + + Occlusion ++ ++ ++ Flow reversal –– +++ +++ ECA: external carotid artery; ICA: internal carotid artery
Embolization through ECA
Potential Tolerance Easy to spasm/damage use to ICA
+++ –– +++
–– +++ ––
+++ +++ ––
+++ + +
+++ ++ +
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Conclusion Several protection devices have been developed and are currently available on the market. All are not equivalent and have some limitations and drawbacks. When performing CAS it is mandatory to have a good knowledge of the three kinds
of protection device to choose the best system suited to the patient, the lesion, and the anatomy to avoid some problems, which can lead to dramatic neurological complications. New generations of protection devices are proposed. They should widen the indications of CAS and other peripheral angioplasties and limit their potential complications.
REFERENCES 1. 2.
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Piana RN, Paik GY, Moscucci M et al. Incidence and treatment of “no-reflow” after percutaneous coronary intervention. Circulation 1994; 89: 2514–18 Grube E, Gerckens U, Yeung AC et al. Prevention of distal embolization during coronary angioplasty in saphenous vein grafts and native vessels using porous filter protection. Circulation 2001; 104: 2436–41 Bicknell CD, Cowling MG, Clark MW et al. Carotid angioplasty in a pulsatile flow model: factors affecting embolic potential. Eur J Vasc Endovasc Surg 2003; 26: 22–31 Bicknell CD, Cheshire NJ. The relationship between carotid atherosclerotic plaque morphology and the embolic risk during endovascular therapy. Eur J Vasc Endovasc Surg 2003; 26: 17–21 Roubin GS. Carotid Angioplasty and Stenting under Cerebral Protection: The Standard of Care. International Congress XV. Scottsdale, February 11–14, 2002 Ohki T, Veith FJ. Carotid stenting with and without protection device: Should protection be useful in all patients? Semin Vasc Surg 2000; 13(2): 144–52 Ohki T, Roubin GS, Veith FJ, Iyer SS, Brady E. Efficacy of a Filter Device in the Prevention of Embolic Events during Carotid Angioplasty and Stenting. An ex-vivo Analysis. J Vasc Surg 1999; 30(6): 1034–44 Wholey MH, Al-Mubarak N, Wholey MH. Updated review of the global carotid artery stent registry. Cathet Cardiovasc Interv 2003; 60: 259–66 Reimers B, Schlueter M, Castriota F. Routine use of cerebral protection during carotid artery stenting: results of a multicenter registry of 753 patients. Am J Med 2004; 116: 217–22 Kastrup A, Groschel K, Frapf H et al. Early outcome of carotid and stenting with and without cerebral protection devices: a systematic review of the literature. Stroke 2003; 34(3): 813–19 Henry M, Polydorou A, Henry I, et al. Carotid angioplasty under protection with the Percusurge Guardwire device. In: Henry M and Ohki T, eds. Angioplasty and Stenting of the Carotid and Supraaortic Trunks. London: Taylor and Francis, 2004; 485–96 Ohki T, Veith FJ. Embolization during carotid stenting: experimental models and results. Carotid Intervent 2000; 3: 66–74 Ohki T, Marin ML, Lyon RT et al. Ex vivo human carotid artery bifurcation stenting: correlation of lesion characteristics with embolic potentials. J Vasc Surg 1998; 27: 463–71 Henry M, Polydorou A, Henry I et al. Carotid angioplasty and stenting under protection. Techniques, results and limitations. J Cardiovasc Surg 2006; 47: 519–46 Henry M, Klonaris C, Henry I. Renal stenting with the Percusurge Guardwire device: a pilot study. J Endovasc Ther 2001; 8: 227–37 Henry M, Henry I, Klonaris C et al. Renal angioplasty and stenting under protection. The way for the future? Catheter Cardiovasc Interv 2003; 60: 299–312 Henry M, Henry I, Polydorou A et al. Renal angioplasty and stenting: long-term results and the potential role of protection devices. Expert Review Cardiovasc Ther 2005; 3: 321–34 Holden A, Hill A. Renal angioplasty and stenting with distal protection of the main renal artery in ischemic nephropathy: early experience. J Vasc Surg 2003; 38: 962–68 Holden A, Hill A, Jaff MR et al. Renal artery stent revascularization with embolic protection in patients with ischemic nephropathy. Kidney Int 2006; 70: 948–55 Freeman HJ, Rundback JH. Embolic protection in femoropopliteal artery intervention. Endovasc Today 2006; 5: 65-70 Wholey MH, Toursarkissian B, Postoak D et al. Early experience in the application of distal protection devices in treatment of peripheral vascular disease of the lower extremities. Catheter Cardiovasc Interv 2005; 64: 227–35 Siablis D, Karnabatidis D, Katsanos K et al. Outflow protection filters during percutaneous recanalization of lower extremities arterial occlusions: a pilot study. Eur J Radiol 2005; 55: 243–49
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Konig C, Pusich B, Tepe G et al. Frequent embolization in peripheral angioplasty: detection with an embolism protection device (Angioguard) and electron microscopy. Cardiovasc Intervent Radiol 2003; 26: 334–9 Henry M, Amor M, Henry I et al. Carotid stenting with cerebral protection: First clinical experience using the Percusurge Guardwire system. J Endovasc Surg 1999; 6: 321–31 Henry M, Henry I, Klonaris C et al. Benefits of cerebral protection during carotid stenting with the Percusurge Guardwire system: Mid-term results. J Endovasc Ther 2002; 9: 1–13 Mehran R, Roubin GS, New G et al. Neurologic events after carotid stenting with distal protection using an occlusion balloon: final results from the café USA trial. AHA Meeting, Anaheim, November 12, 2001 Al Mubarak N, Roubin GS, Vitek JJ et al. Effect of the distal-balloon protection system on microembolization during carotid stenting. Circulation 2001; 104: 1999–2002 Al Mubarak N, Vitek JJ, Iyer S et al. Embolization via collateral circulation during carotid stenting with the distal balloon protection system. J Endovasc Ther 2001; 8: 354–7 Franke J, Bauer C, Ghamzemzadeh A5L5 et al. Distal occlusion with flushing and aspiration: the Kensey Nash device. Presented at the ICCA 06, Frankfurt, November 23–25, 2006 Theron J, Cosgrove R, Melançon D, Ethier R. Embolization with temporary balloon occlusion of the internal carotid artery and vertebral arteries, Neuroradiology 1986; 28: 246–53 Theron J, Raymond J, Casasco A et al. Percutaneous angioplasty of atherosclerotic and post-surgical stenosis of carotid arteries. ANJR 1987; 8: 495–500 Theron J, Courtheoux P, Alachkar F, Maiza D. New triple coaxial catheter system for carotid angioplasty with cerebral protection. ANJR 1990; 11: 869–74 Castriota F, Manetti R, Liso A et al. Cerebral protection: can only the poststenting dilatation phase be protected? In: Henry, Ohki, Polydorou, Strigaris, Kiskinis, eds. Angioplasty and Stenting of the Carotid and Supra-aortic Trunks. Informa, London, 2004, 381–90 Eskandari MK. Design and development of mechanical embolic protection devices. Expert Rev Med Devices 2006; 3: 387–93 Wholey MH. The ARCHER trial: prospective clinical trial for carotid stenting in high surgical risk patients, preliminary thirtyday results. Presented at the 52nd Annual Meeting of the American College of Cardiology, Chicago, IL, March 30, 2003 Yadav JS, Wholey MH, Kuntz RE et al. Protected carotid artery stenting versus endarterectomy in high-risk patients. N Engl J Med 2004; 351: 1493–501 Ouriel K. SAPPHIRE study. Vasc News 2004; 22: 1–2 White CJ, Iyer SS, Hopkins LN et al. Carotid stenting with distal protection in high surgical risk patients: the Beach Trial 30 day results. Catheter Cardiovasc Interv 2006; 67: 503–12 Whitlow PL. SECURITY: Multicenter registry in high-risk symptomatic and asymptomatic carotid disease with the Abbott Xact stent and MedNova filter. Presented at Transcatheter Cardiovascular Therapeutics (TCT), Washington, DC, September 15–19, 2003 Cremonesi A. The Spider Embolic protection device performance evaluation in the carotid artery during percutaneous transluminal angioplasty and/or stenting. J Invasive Cardiol 2005; 17: 463–67 Castriota F, Cremonesi A, Manetti R. Carotid angioplasty and stenting with and without cerebral protection: single center experience in 275 consecutive patients. International Congress XV, Scottsdale, February 11–14, 2002 Reimers B, Corvaja N, Moshiri S et al. Cerebral protection with filter devices during carotid artery stenting. Circulation 2001; 104: 12–15 Coggia M, Goeau-Brissonnière O, Duval JL et al. Embolic risk of the different stages of carotid bifurcation balloon angioplasty: an experimental study. J Vasc Surg 2000; 31: 550–7
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Angelini A, Reimers B, Dellabarbara M. Embolized debris during carotid artery stenting with cerebral protection device: a histopathologic survey. AHA Meeting, Anaheim, 13 November 2001 Jaeger H, Mathias K, Drescher R et al. Clinical results of cerebral protection with a filter device during stent implantation of the carotid artery. Cardiovasc Interv Radiol 2001; 24: 249–56 Barth A, Remonda L, Lovblad KO et al. Silent cerebral ischemia detected by diffusion-weighted MRI after carotid endarterectomy. Stroke 2000; 31: 1824–8 Tomczak R, Wunderlich A, Liewald F et al. Diffusion weighted MRI: detection of cerebral ischemia before and after carotid thromboendarterectomy. J Comput Assist Tomogr 2001; 25: 247–50 Flach H, Ouhlous M, Hendricks J et al. Cerebral ischemia after carotid intervention. J Endovasc Ther 2004; 11: 251–57 Vermeer SE, Prins ND, Den Heijer T et al. Silent brain infarcts and the risk of dementia and cognitive decline. N Engl J Med 2003; 348: 1215–22 Heyer EJ, Adamas DC, Somon RA et al. Neuropsychometric changes in patients after carotid endarterectomy. Stroke 1998; 29: 1110–15 Heyer EJ, Sharma R, Rampersad A et al. A controlled prospective study of neuropsychological dysfunction following carotid endarterectomy. Arch Neurol 2002; 59: 217–22 Vanninen E, Vanninen R, Aikia M et al. Frequency of carotid endarterectomy related subclinical cerebral complications. Cerebrovasc Dis 1996; 6: 272–80
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Vos AJ, Vandenberg JC, Ernst SM. Carotid angioplasty and stent placement: comparison of transcranial Doppler vs data and clinical outcome with and without filtering cerebral protection devices in 509 patients. Radiology 2005; 234: 493–9 MacDonald S, Cleveland TJ, Evans D, Griffiths PD, Gaines PA. A comparison of the high-intensity signal rate using transcranial Doppler during unprotected and protected carotid stenting (Neuroshield) with a randomised controlled trial. Presented at the Annual Meeting of the Cardiovascular and Interventional Radiology Society of Europe, Antalya, Turkey, September 20, 2003 Henry M, Polydorou A, Henry I et al. New distal embolic protection device. The FiberNet 3-dimensional filter. First carotid human study. Cath Cardiovasc. Intervent (in press) Parodi JJC, Lamura R, Ferreira LM et al. Initial evaluation of carotid angioplasty and stenting with three different cerebral protection devices. J Vasc Surg 2000; 32: 1127–36 Parodi JC, Bates MC, Schonholz C. Parodi embolization system: description and first results. In: Henry M, T. Ohki, eds. Angioplasty and Stenting of the Carotid and Supra-aortic Trunks. Taylor & Francis, London, 2004; 523–30 Parodi JC, Schonholz C, Ferreira MC et al. Seat belt and airbag technique for cerebral protection during carotid stenting. J Endovasc Ther 2002; 9: 20–4
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Vascular closure devices ZG Turi
Introduction After Seldinger contributed a method for percutaneous puncture of the femoral artery a half century ago,1 relatively little changed in vascular access and closure until the late 1970s. Standard percutaneous femoral access technique required multiple passages through the skin and thigh muscles by catheters over exchange wires, a method that occasionally resulted in loss of access, accumulation of debris in the tips of catheters, and a variety of secondary complications. Most importantly, repeated passage of catheters through the femoral puncture site resulted in fraying of the arteriotomy edge. The introduction of vascular sheaths was a significant step forward,2 allowing simultaneous pressure monitoring through a Y connector (or later a sidearm), and resulted in smoother arteriotomy edges because it eliminated the need for multiple catheter introductions though the vessel wall. Closure was entirely by external compression (Figure 23.1), largely manual but in some laboratories with mechanical compression devices, several of which remain in use (Figure 23.2). The state of the art for vascular closure remained largely unchanged for four decades. Patients undergoing percutaneous access, whether from the arm or leg, typically had compression applied, while open arteriotomy was accompanied by suture closure. The paradigm shifted in the early 1990s with the introduction of VasoSeal (Datascope, Montvale, NJ), a collagen plug device, which was the first of the vascular closure devices (VCDs) to be commercialized. Vascular closure is now a 500-million-dollar medical device market, accounting for some 30–40% of femoral catheterizations in the US, but < 10% of vascular closure in the rest of the world. The evidence base to justify routine use of VCDs is extremely limited, and adoption has been largely by physician and patient preference. Nevertheless, these devices are an important consideration in the everexpanding armamentarium of endovascular technologies.
Vascular access The sine qua non of vascular closure is good vascular access. Although not the primary focus of this chapter, good vascular access technique can prevent most of the vascular complications associated with femoral procedures and with VCDs. Four techniques that may reduce complications, facilitate access, and prevent VCD complications are largely 168
ignored by much of the vascular intervention community. These include: ●
●
adjunctive use of fluoroscopy and/or ultrasound for access to the common femoral artery, with confirmation that needle position is below the center of the femoral head and over the medial half of the bone prior to arterial entry (Figure 23.3); arterial puncture in the “safe zone” for vascular access (Figure 23.4);
Figure 23.1 The most common closure technique, manual compression, is utilized in 70% of cases in the US and well over 90% in the rest of the world, despite the need for prolonged bed rest, greater patient discomfort and delay in ambulation and discharge. Besides cost considerations, the perception of a higher complication rate with vascular closure devices has resulted in continued preference for manual compression by most hospitals and operators.
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(a)
(b)
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(c)
Figure 23.2 Three types of mechanical compression: (a) the Compressar (Advanced Vascular Dynamics, Portland, OR) has an adjustable arm and a flexible hinged diaphragm deployed on top of the arteriotomy; (b) the FemoStop (Radi Medical Systems, Uppsala, Sweden) utilizes a bladder inflated to sufficient pressure to control hemorrhage; and (c) SafeGuard combines an inflatable bulb and a sterile dressing to apply local pressure to the arteriotomy site (Datascope, Montvale, NJ).
above the bottom of the femoral head eliminates approximately 75% of punctures into the femoral bifurcation vessels;3 䊊 puncture below the middle of the femoral head eliminates much of the retroperitoneal bleeding risk because it nearly guarantees arterial entry below the inguinal ligament;4 angiography to assess femoral artery size, location of puncture, and presence of disease in the common femoral or low external iliac artery, regardless of whether VCDs are used; 䊊
●
(a)
●
avoidance of anticoagulation if the femoral puncture is outside the “safe zone,” most importantly if it is above the inferior reflection of the inferior epigastric artery (IEA).5 This means that in elective or ad hoc intervention cases, the patient should be brought back for intervention in a separate sitting if the femoral puncture is suboptimal.6
Use of a single anatomic landmark for femoral puncture, most commonly the inguinal crease, is not optimal, since the inguinal crease is on average 6 mm below the femoral bifurcation and
(b)
Figure 23.3 (a) Hemostat placed over the medial portion of the femoral head just below the center identifies a landmark for targeting the common femoral artery prior to skin puncture; (b) after skin puncture and advancement of needle until pulsation is felt just prior to arterial entry, repeat fluoroscopy is used to ascertain that the tip is over the target (light blue circle) at a point just below the centerline of the femoral head (dashed red line). (See Color plates.)
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Manual compression
Figure 23.4 The safe zone for femoral access. Note the location of the bottom loop of the inferior epigastric artery (IEA, red arrow) and the femoral bifurcation (back arrow). The safe zone begins above the femoral bifurcation or at the bottom of the femoral head (whichever is higher) and extends to a point below the IEA’s lowest excursion. About one-quarter of patients have the femoral bifurcation above the bottom of the femoral head. Since neither the location of the femoral bifurcation or IEA is known at the time of puncture, we recommend a site approximately where the light blue circle is shown. This image is in the RAO view for clarity – the blue circle would be over the common femoral artery in the AP view. (See Color plates.)
not, as generally assumed, over the center of the common femoral artery.7 Nevertheless, the inguinal crease remains the most common landmark (Figure 23.5), resulting in femoral puncture being outside the “safe zone” in a large percentage of patients (74% in our series3). Puncture outside the “safe zone” is associated with a significant increase in closure complications,
Pulse/Bone 7%
All Three 1%
Crease/Bone 1% Crease/Pulse 13%
Crease 40%
Manual compression (MC) is invariably effective if adequate compression is applied proximal to the femoral puncture, the femoral puncture is located over the femoral head and below the inguinal ligament, the clotting cascade and platelet function are intact, the compression is carried out over a long enough period of time, the fenestration is small, and only a single anterior wall puncture of the artery has occurred. Because all of those criteria are frequently not met, and because the technique has inherent limitations, a complication rate for MC of approximately 2% for diagnostic catheterizations and 4% for interventions remains in the modern era.8 These rates may also represent an underestimation (see the later section on “Complications”). MC itself lends to certain complications related to prolonged compression, including venous stasis and potential venous thrombosis, and there is evidence, albeit weak, that deep vein thrombosis and pulmonary embolism may be related to prolonged groin holds and immobilization.9 The technique is also painful, and engenders significant delay before patients are allowed to ambulate. The delay is exacerbated in the setting of periintervention anticoagulation; most laboratories do not allow sheaths to be pulled until the activated clotting time has decreased below 150–180 seconds. This leads to patients leaving the catheterization laboratory with indwelling vascular sheaths, potentially causing a variety of complications in addition to bleeding, including infection. Nevertheless, the lowest complication rates have typically been associated with MC, and it remains the standard of care for the majority of diagnostic and interventional cases, with wide geographic variation. An alternative to MC, assisted compression with a variety of compression devices (Figure 23.2), has a good safety record, although some devices have been associated with pain, occasional injury from tissue necrosis owing to excess and prolonged compression of the skin, and some infrequent but rare complications primarily associated with incorrect placement or inadequate attention to the puncture site during device deployment, among others.10 Comparison between MC and compression devices have generally favored the latter,11 and between compression devices and VCDs have been equivocal,12–14 although design issues limit the applicability of these studies and the findings have not been consistent.15
Closure devices
Bone 13%
Pulse 25%
Figure 23.5 Results of a survey of 200 interventional radiologists and cardiologists asking what landmarks they use for femoral puncture. Note that the inguinal crease is the primary landmark, an unfortunate choice (see text). Based on data from Grier et al.7 (See Color plates.)
It is helpful to categorize VCDs by their mechanism of action and mechanical properties. In general devices can be classified as invasive or non-invasive based on whether they are introduced through the skin into the tissue track or applied topically. Active approximation of the arteriotomy edges, either by bringing the edges of the fenestration together with sutures, clips or staples, or sandwiching the arteriotomy closed, is differentiated from devices deployed only outside the artery; the latter works by passive approximation. For active
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Angio-Seal Clotting/Sealing
No C/S
Clotting/Sealing
No C/S
Intraluminal Active Approximation
Passive
Extraluminal Perclose
StarClose
Boomerang
Permanent Foreign Body
Invasive
No Foreign Body
No Foreign Body
EpiclosePlus
Temporary Foreign Body
Temporary Foreign Body
VasoSeal
(a)
No C/S
Clotting/Sealing
No C/S
Passive
Active Approximation
Syvek Patch
Noninvasive
Therus
No Foreign Body
(b)
No Foreign Body
FemoStop
Figure 23.6 (a) The invasive vascular closure devices can be subcategorized by whether or not they provide active or passive approximation, incorporate a clotting or sealing agent, reside intra- or extraluminally, and whether or not a temporary or permanent foreign body is left behind. By way of an example, among the invasive closure devices shown, Angio-Seal is an active approximator, incorporates a clotting agent, leaves behind an intraluminal anchor, and resorbs over time, thus it is a temporary foreign body; (b) the non-invasive vascular closure devices include topical patches, compression devices, and a novel experimental ultrasound closure system.48 C/S = clotting or sealing agent. (See Color plates.)
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approximators, devices can be differentiated by whether a foreign body is left inside the arterial lumen (intraluminal) as opposed to buried in the vessel wall only (extraluminal). Further subclassification depends on whether a sealing or thrombosing agent is used. Finally, some devices leave behind a foreign body, which either resorbs (temporary) or remains permanent. Figure 23.6 shows an algorithm for classification and an example of each of the subcategories described above. Thrombosing agents in VCDs have been either collagen or a thrombin–collagen mixture. The use of collagen for hemostasis was well established in the surgical literature16 prior to its introduction by Datascope as a vascular closure plug in the early 1990s.17 Collagen exerts its thrombotic effect by inducing both platelet adhesion and activation.18 Collagen is also part of the vessel wall, ordinarily protected from blood by an endothelial layer but triggering clotting when endothelial disruption occurs. Gelatin foam has been used in lieu of collagen as a VCD thrombosing agent. Sealing agents are being utilized in several devices in lieu of collagen; these do not actively promote thrombosis, potentially decreasing the risks associated with inadvertent intravascular placement. In general, closure devices have required a system for ascertaining the exact depth of the arteriotomy. An inner locator has been common to virtually all of the devices with the exception of first-generation VasoSeal, a device that used a clip placed on the original needle used for femoral access to mark the arteriotomy depth. The locator used in various devices has been in the form of an anchor, wings, or a balloon. The diameter of these locator devices is an important consideration given the relatively small size of the common femoral artery. The minimal luminal size varies with demographics: for women the mean is approximately 5.0 mm, and for men approximately 6.3 mm (Figure 23.7). The 5.0–6.0 mm size of most locator devices (the notable exception is the smaller profile of the Angio-Seal anchor) used inside the common femoral artery can be seen to eliminate a fair percentage of women (particular those with diabetes) and a minority of men from safe VCD deployment.
Closure devices either deploy through the procedural sheath or require placement of a separate assembly in exchange. The former approach has two advantages: first, it allows introduction of the closure device through an existing conduit rather than through a new exposure of the tissue tract, simplifying the procedure and perhaps decreasing infection risk. Second, it avoids upsizing of the tissue tract, a drawback of most available VCDs that likely increases complication rates due to bleeding and trauma, especially when the arteriotomy itself is upsized.19
Passive approximators (Figure 23.8) VasoSeal, a passive collagen plug, was relatively effective in diagnostic catheterization and to a lesser degree in interventional procedures. When compared with MC in metaanalyses, it had a higher failure rate than other devices20 and was associated with an overall higher complication rate.21 The device, and possibly the passive closure approach in general, may have intrinsic drawbacks, particularly in interventional cases with full anticoagulation and antiplatelet therapy. However, much of the VasoSeal literature is from an earlier intervention era, when larger sheaths, excessive anticoagulation, post-procedure heparin, and non-weight adjusted heparin were widely used – all markers for increased vascular complications, particularly bleeding.22 In addition, there is an overall learning curve associated with vascular closure generically as well as individual closure devices; complication rates during the first 50 deployments have been shown to be up to four times higher than seen after 100 cases23 with an inflection point for decreasing complications requiring as many as 350 cases in individual institutions24 (see “Complications”). VasoSeal, as the first device to market, suffered a disproportionate disadvantage in these respects and is no longer actively marketed. A similar fate was suffered by the Duett (Vascular Solutions, Minneapolis, MN), which remains available from
n=200
25
Study population %
20
15
10
5
0 2
3
4
5 6 7 8 9 Femoral artery minimal luminal diameter (mm)
10
11
12
Figure 23.7 Minimal luminal diameter of the common femoral artery in 200 patients undergoing diagnostic cardiac catheterization. Superimposed are three vascular closure device technologies, with a dotted line showing the minimal luminal diameter for deployment. Note that a 4-mm locator wing would exclude a relative minority of primarily female patients while a 6-mm-diameter balloon would potentially exclude the majority of women in the particular population studied. Adapted from Schnyder G et al.3 (See Color plates.)
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(b)
(c)
(e)
(f)
173
(d)
Figure 23.8 A gallery of passive approximation vascular closure devices: (a) Syvek patch; (b) VasoSeal; (c) Duett; (d) Boomerang ClosureWire; (e) Mynx (previously Finale); and (f) ExoSeal*. * = Not FDA approved as of fall 2007. (See Color plates.)
the manufacturer. This device features a procoagulant combination of thrombin mixed with collagen, deposited in the tissue track through the sheath used for the procedure after the latter is withdrawn to just outside the artery. The delivery system was relatively complex, and it carried an inherent risk of intra-arterial injection of thrombin with consequent iatrogenic arterial occlusion25 with rare but occasional catastrophic consequences. A review of the FDA MAUDE database demonstrates a small but disproportionate percentage of complications associated with arterial occlusion due to injection of thrombin/collagen into the vessel. Because the resorption rate of the coagulant foam is relatively rapid, this device has rarely been associated with infection. The marker balloon deployed inside the arteriotomy, 6 mm in diameter, limits the use of this device to arteries that are relatively large. Like VasoSeal, it does not actively approximate the arteriotomy edges. Several other passive approximators using sealants rather than thrombosing agents are currently under investigation or recently FDA approved. These include the Mynx (AccessClosure, Mountain View, CA) and ExoSeal (Johnson and Johnson, New Brunswick, NJ). The former utilizes a polyethylene glycol wafer, while the latter incorporates a biopolymer. Although pivotal trials of polyethylene glycol sealant were performed in the US and Europe, and were reported as successful in abstract presentations, these have not been published to date. Another passive approximator, the Boomerang Closurewire (Cardiva Medical, Mountain View, CA), works by a novel approach: a nitinol disk is deployed inside the blood vessel and brought back against the arteriotomy; traction is then applied until hemostasis occurs, at which point the disk is collapsed and removed from the tissue track. The device leaves no foreign body behind. The inherent disadvantage in the
concept, the withdrawal through the freshly formed clot, is mitigated to an extent by the low profile of the collapsed disk as it is withdrawn, but it does require additional compression at that point. It has been evaluated primarily for diagnostic catheterizations,26 although it is FDA-approved for intervention as well. A large number of topical patches are available. These accelerate hemostasis by a variety of mechanisms, with the active agents being a wide range of substances with apparent procoagulant properties. The ability of these devices to facilitate clotting inside the tissue track down to the arteriotomy level has not been demonstrated convincingly, and despite wide availability and some 20% of the vascular closure market, no significant evidence base for effectiveness exists.
Active approximators (Figure 23.9) Angio-Seal, the second VCD to be released, could be characterized as a “belt and suspenders” VCD. It provides active rather than passive approximation, sandwiching the arteriotomy between a resorbable anchor and a collagen plug held together by a cinched resorbable suture. In addition, the collagen plug serves as a thrombosing agent. Overall, it has a high (and possibly the highest overall) success rate of deployment and closure with a short learning curve.23,27 Potential disadvantages relate to the anchor, particularly inside an atherosclerotic femoral artery, causing vascular obstruction; in addition there is rare dislodgement of the anchor resulting in obstruction of the infrainguinal vessels. The device leaves a foreign body inside the tissue track to serve as a potential nidus for infection, and on occasion the collagen sponge has been
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(b)
(c)
(e)
(f)
(d)
(g)
Figure 23.9 A gallery of active approximation vascular closure devices: (a) Angio-Seal; (b) Perclose; (c) StarClose; (d) AngioLink; (e) SuperStitch; (f) Therus*; and (g) Epiclose Plus*. * = Not FDA-approved as of fall 2007. (See Color plates.)
inserted inside the artery resulting in arterial thrombosis. It dominates the VCD market with over two-thirds of the VCDs used. Perclose was the next of the VCDs released. It provides active approximation with suture. It has a high success rate, but somewhat lower than Angio-Seal28 (large true randomized device-to-device comparisons without major design flaws are essentially non-existent). Because there is no clotting or sealing agent, oozing from the tissue track in interventional cases is the most common disadvantage. Unlike Angio-Seal, there is a permanent foreign body in the form of suture material; however the intra-arterial profile of the suture is substantially less than that of the Angio-Seal anchor. The learning curve for earlier generations was substantial,24 but modifications in design have largely eliminated this issue. The device has significant advantages for “preclosure.” Use of the preclosure technique as well as a version of the device designed for large caliber arterial punctures has been successful for a variety of interventions with devices > 18 French, including abdominal aortic endograft placement.29 Preclosure of large bore venous access sites is also effective,30 although care should be taken with this technique, since inadvertent trans-section of the common femoral vein can occur; the latter is both highly morbid and difficult to treat. Perclose has held about onequarter of the vascular closure market. Similar to Perclose is the Sutura SuperStitch (Sutura, Fountain Valley, CA). A new class of active approximators, the percutaneous metal arterial closure devices, have several features in common. Both StarClose (Abbott Vascular, Redwood City, CA) and AngioLink (Medtronic, Santa Rosa, CA) actively approximate the arteriotomy edges, and both are designed to penetrate only as far as the media, with no metal exposure inside the arterial lumen. The StarClose device is a nitinol clip while AngioLink is a titanium staple; both result in upsizing, with StarClose upsizing the tissue tract to 12 French but leaving the arteriotomy itself intact, while AngioLink upsizes the arteriotomy to 10 French. Neither incorporates a thrombosing
or sealing agent, and both leave a permanent foreign body behind. StarClose has taken an increasing portion of the VCD market, primarily from Perclose; both devices share the same classification system (and manufacturer) except for the extraluminal nature of StarClose. Finally, two novel concepts of active closure, both acting by heating of the arterial puncture site to denature collagen and seal the vessel, are under development. Therus (Therus, Seattle, WA) beams ultrasound energy at the arteriotomy from the skin surface using tracking technology to identify the exact location of puncture. Epiclose Plus (Cardiodex, TiratHacarmel, Israel) uses a balloon placed inside the tissue track on top of the arteriotomy to deliver local heat for the same purpose. Several issues remain to be clarified in this promising approach, most prominently the effectiveness of the targeting algorithms and reliability of heat sealing in fully anticoagulated patients.
Complications In general, the causes of vascular access complications, whether or not related to VCDs, have been variable across studies. A number of common though not consistent associations include female gender, small or very large body habitus, diabetes, presence of peripheral vascular disease, aggressive anticoagulation (high doses, non-weight-based dosing, postprocedure continuation of anticoagulation), poor access techniques (multiple, high, low, or back wall punctures), large sheath size, small vessel size, poor sterility control, glycoprotein IIb/IIIa use, and operator learning curve. The specific role of VCDs in these complications is muddled. Because the clinical trials are generally flawed by a weak evidence base31 that includes changing device platforms, selection bias, cohort mismatch, learning curve issues and lack of essential information such as predeployment femoral angiography and extent of anticoagulation, the answer to whether or not the
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Vascular closure devices complication rate of VCDs is higher has been elusive. Compared with MC, the complications of VCDs have been variously reported as equivalent,20,32 greater,33,34 or lower overall,21,35 with meta-analyses and propensity scoring having been used to attempt to address the poor quality of the evidence base (Figure 23.10). The issue is also confounded by varying definitions, including what constitutes a hematoma. The common use of a 10-cm threshold underestimates the complication rate8 while a threshold as small as 2 cm tends to overestimate it.11 The most common complication has been minor bleeding and hematoma, and the most serious has been retroperitoneal bleeding, the latter associated with a mortality between 4% and 6%.4,36 Retroperitoneal bleeding occurs in < 1% of interventional cases, though the percentage appears to have increased in the era of glycoprotein IIb/IIIa inhibitors. The use of VCDs increases retroperitoneal hemorrhage risk36,37 by odds ratios as high as 3:1; in the earlier Cleveland Clinic analysis, retroperitoneal hemorrhage after VCD use was 1.2–1.8%37 compared to 0.2% with MC. The phenomenon may be due to two likely causes: first, VCDs are deployed while the patient is fully anticoagulated, whereas MC is only used when the ACT has normalized. This all but guarantees greater bleeding risk with VCD use in patients who have undergone percutaneous intervention, though the effect of rapid resolution of anticoagulation with an agent like bivalirudin may help mitigate this.38
Second, in the setting of high punctures, the transversus abdominis muscle may lie between the skin site of puncture and the external iliac artery, and may prevent the collagen plug, knot, or staple/clip from descending all the way down to the arterial surface (Figure 23.11). The second most morbid complication is infection secondary to VCD use. The incidence appears to be < 0.3%, but the co-morbidities are significant, and a 6% mortality has been reported.39 Mycotic pseudoaneurysm is found in nearly half of cases, positive blood cultures (predominantly S. aureus) in nearly 90%. The median time of occurrence is 8 days, but in our experience, can first present as late as one month. Because VCDs can serve as a wick for bacterial passage to the arteriotomy site, and provide a foreign body focus for abscess formation, surgical intervention is required in half or more of patients and conservative management typically requires prolonged and usually parenteral antibiotic therapy. Several other complications are worth noting. Vascular occlusion occurs in < 0.2% of cases and has several causes: first, direct closure of the vessel by active approximation of the front and back walls, typically by suture or clip/staple devices. Second, and more commonly, insertion of a thrombosing agent into the vessel, usually the Angio-Seal collagen plug, causing acute or subacute thrombosis. Third, the Angio-Seal anchor has resulted in a localized reaction or on occasion has migrated distally and been trapped in a diseased superficial
No. (%) vascular complications All procedures (n = 21,841)
VCD
MC
0.1
1
10
Propensity score adjusted OR (95%CI)
(n = 8,807)
(n = 13,034)
Any VC
120 (1.36)
188 (1.44)
0.87 (0.68-1.13)
Major VC
67 (0.76)
99 (0.76)
0.96 (0.68-1.35)
Minor VC
76 (0.86)
140 (1.07)
0.75 (0.55-1.02)
(n = 3,600)
(n = 9,524)
Any VC
31 (0.86)
118 (1.24)
0.81 (0.54-1.22)
Major VC
18 (0.50)
63 (0.66)
0.94 (0.54-1.62)
Minor VC
19 (0.53)
92 (0.97)
0.64 (0.38-1.06)
(n = 5,207)
(n = 3,510)
Any VC
89 (1.71)
70 (1.99)
0.92 (0.66-1.28)
Major VC
49 (0.94)
36 (1.03)
0.99 (0.63-1.56)
Minor VC
57 (1.09)
48 (1.37)
0.84 (0.56-1.26)
Diagnostic caths (n = 13,124)
PCI's (n = 8,717)
175
VCD protective
VCD harmful
Figure 23.10 Propensity score adjusted analysis of vascular complications in over 20,000 patients undergoing diagnostic or interventional catheterization. Complications were compared for patients receiving VCDs (Angio-Seal, Perclose, or VasoSeal) and those undergoing manual compression. In general the complications straddle the null hypothesis. As with virtually all of this literature, there is an absence of randomized, intention-to-treat data, hence the use of propensity score adjustment to attempt to account for selection bias. MC = manual compression. VCD = vascular closure device. From Applegate et al.32
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Textbook of peripheral vascular interventions I
"high" entry
Inguinal ligament
Usual entry Fascia of Camper Fascia of Scarpa Obliquus externus abdominis Obliquus internus abdominis
Femoral artery
Transversus abdominis
External iliac artery
Deep inferior epigastric artery Tamper
II
Collagen plug Fascia of Camper Fascia of Scarpa Obliquus externus abdominis Femoral artery
Obliquus internus abdominis Transversus abdominis
Deep inferior epigastric artery
External iliac artery
Figure 23.11 The relationship of the external iliac artery site of entry to surrounding structures in the setting of a high stick. Note the interposition of the transversus abdominis muscle between the skin and the arterial puncture site, resulting in interference with deployment of the Angio-Seal collagen plug onto the arterial surface. Presumably as a result, retroperitoneal hemorrhage in the setting of Angio-Seal use has an odds ratio of 2.8:1. From Ellis et al.36
femoral artery, or obstructed the smaller lumens of the popliteal, tibioperoneal trunk, or lower circulation. The latter have typically occurred several days to 2 weeks after device deployment, although progressive claudication has been reported in some cases to take many months to fully develop.40 Neural injury caused by suture or clip/staple entrapment probably occurs, although the evidence base is murky, with only anecdotal reports of surgery to relieve nerve entrapment. Pseudoaneurysms or AV fistulae do not seem to correlate with VCD use.
The importance of femoral angiography The instructions for use for VCDs call for femoral angiography prior to device insertion despite which a significant percentage of operators, particularly outside the US, continue to avoid this practice.6 Femoral angiography provides essential information for safe deployment. Low punctures, particularly into the bifurcation vessels, should dictate avoidance of VCD use.40 A significant percentage of VCD complications, in particular vessel obstruction, result from low puncture40,41 or deployment into atherosclerotic vessel segments. High puncture is associated with up to a 17:1 higher risk of retroperitoneal hemorrhage.36 If femoral angiography through the sheath is performed as soon as access is obtained, and the puncture is seen to be above the origin of the IEA,
prudence dictates avoiding intervention and anticoagulation in that setting.
Issues for peripheral vascular interventions VCDs have specific advantages and drawbacks in the setting of peripheral vascular interventions. Early ambulation can be particularly helpful for patients with peripheral vascular disease, since early discharge, one of the potential benefits of VCD use, is more likely to occur after peripheral than after coronary interventions. MC or compression devices used upstream from ipsilateral access is undesirable, inasmuch as they result in prolonged blood stasis at the fresh angioplasty or stent site downstream from the puncture. Although potentially more hazardous, device closure, in particular Perclose, has been effective in anecdotal series,42 including one randomized trial comparing Perclose to MC in the setting of peripheral vascular disease.43 VCD closure of antegrade femoral punctures has been reported with both Perclose and Angio-Seal.44,45 Similarly, compression upstream or over a synthetic graft may cause stasis and thrombosis, and some interventionalists have advocated off-label Perclose use in this setting. Finally, VCDs have been utilized for a variety of non-femoral access sites,46 though the evidence base is thin and care should be taken to avoid infection risk if the arteriotomy is close to the skin surface.
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Cost considerations
Conclusion
Vascular closure devices are expensive. Without a clear evidence base to show superior outcomes or lower complication rates, their use remains a question of preference and economics. The argument has been made that costs can be offset by earlier ambulation with less requirement for post-procedure nursing care and potentially earlier discharge from the hospital.47 These considerations do not apply in many parts of the world, and resistance to adoption of VCDs remains high in those areas.
VCDs substantially increase the comfort and convenience of patients and allow earlier ambulation. These benefits come at a price of a possibly higher rate of complications and the cost of the devices themselves. Until a more substantial evidence base is developed, or the economic arguments become more compelling, the use of VCDs will remain largely an issue of physician and patient preference. A new generation of VCDs may provide for a more compelling risk/benefit/cost ratio to mandate use of these devices.
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Seldinger SI. Catheter replacement of the needle in percutaneous arteriography; a new technique. Acta Radiol 1952; 39: 368–76 Barry WH, Levin DC, Green LH et al. Left heart catheterization and angiography via the percutaneous femoral approach using an arterial sheath. Cathet Cardiovasc Diagn 1979: 5: 401–9 Schnyder G, Sawhney N, Whisenant B et al. Common femoral artery anatomy is influenced by demographics and comorbidity: implications for cardiac and peripheral invasive studies. Catheter Cardiovasc Interv 2001; 53: 289–95 Farouque HM, Tremmel JA, Raissi SF et al. Risk factors for the development of retroperitoneal hematoma after percutaneous coronary intervention in the era of glycoprotein IIb/IIIa inhibitors and vascular closure devices. J Am Coll Cardiol 2005; 45: 363–8 Sherev DA, Shaw RE, Brent BN. Angiographic predictors of femoral access site complications: implication for planned percutaneous coronary intervention. Catheter Cardiovasc Interv 2005; 65: 196–202 Turi ZG. Optimizing vascular access: routine femoral angiography keeps the vascular complication away. Catheter Cardiovasc Interv 2005; 65: 203–4 Grier D, Hartnell G. Percutaneous femoral artery puncture: practice and anatomy. Br J Radiol 1990; 63: 602–4 Chandrasekar B, Doucet S, Bilodeau L et al. Complications of cardiac catheterization in the current era: A single-center experience. Catheter Cardiovasc Interv 2001; 52(3): 289–95 Gowda S, Bollis AM, Haikal M et al. Incidence of new focal pulmonary emboli after routine cardiac catheterization comparing the brachial to the femoral approach. Cathet Cardiovasc Diagn 1984; 10: 157–61 Jackson A, Beards SC, Gillespie JE. Possible hazard associated with the use of the “FemoStop” groin compression device. Br J Radiol 1993; 66: 748 Pracyk JB, Wall TC, Longabaugh JP et al. A randomized trial of vascular hemostasis techniques to reduce femoral vascular complications after coronary intervention. Am J Cardiol 1998; 81: 970–6 Juergens CP, Leung DY, Crozier JA et al. Patient tolerance and resource utilization associated with an arterial closure versus an external compression device after percutaneous coronary intervention. Catheter Cardiovasc Interv 2004; 63: 166–70 Amin FR, Yousufuddin M, Stables R et al. Femoral haemostasis after transcatheter therapeutic intervention: a prospective randomised study of the angio-seal device vs. the femostop device. Int J Cardiol 2000; 76: 235–40 Chamberlin JR, Lardi AB, McKeever LS et al. Use of vascular sealing devices (VasoSeal and Perclose) versus assisted manual compression (Femostop) in transcatheter coronary interventions requiring abciximab (ReoPro). Catheter Cardiovasc Interv 1999; 47: 143–7 Benson LM, Wunderly D, Perry B et al. Determining best practice: comparison of three methods of femoral sheath removal after cardiac interventional procedures. Heart Lung 2005; 34: 115–21 Vistnes LM, Goodwin DA, Tenery JH et al. Control of capillary bleeding by topical application of microcrystalline collagen. Surgery 1974; 76: 291–4 Kuhn C, Sumpelmann D, Geiger B et al. [Early hemostasis after coronary therapeutic interventions by using a collagen plug]. Z Kardiol 1993; 82: 515–20
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Farndale RW, Sixma JJ, Barnes MJ et al. The role of collagen in thrombosis and hemostasis. J Thromb Haemost 2004; 2: 561–73 Kahn ZM, Kumar M, Hollander G et al. Safety and efficacy of the Perclose suture-mediated closure device after diagnostic and interventional catheterizations in a large consecutive population. Catheter Cardiovasc Interv 2002; 55: 8–13 Nikolsky E, Mehran R, Halkin A et al. Vascular complications associated with arteriotomy closure devices in patients undergoing percutaneous coronary procedures: a meta-analysis. J Am Coll Cardiol 2004; 44: 1200–9 Tavris DR, Dey S, Albrecht-Gallauresi B et al. Risk of local adverse events following cardiac catheterization by hemostasis device use – phase II. J Invasive Cardiol 2005; 17: 644–50 Blankenship JC, Balog C, Sapp SK et al. Reduction of vascular access site bleeding in sequential abciximab coronary intervention trials. Catheter Cardiovasc Interv 2002; 57: 476–83 Warren BS, Warren SG, Miller SD. Predictors of complications and learning curve using the Angio- Seal closure device following interventional and diagnostic catheterization. Catheter Cardiovasc Interv 1999; 48: 162–6 Balzer JO, Scheinert D, Diebold T et al. Postinterventional transcutaneous suture of femoral artery access sites in patients with peripheral arterial occlusive disease: a study of 930 patients. Catheter Cardiovasc Interv 2001; 53: 174–81 Katsouras CS, Michalis LK, Leontaridis I et al. Treatment of acute lower limb ischemia following the use of the Duett sealing device: Report of three cases and review of the literature. Cardiovasc Intervent Radiol 2004; 27: 268–70 Doyle BJ, Godfrey MJ, Lennon RJ et al. Initial experience with the cardiva Boomerangtrade mark vascular closure device in diagnostic catheterization. Catheter Cardiovasc Interv 2006; 69: 203–8 Applegate RJ, Sacrinty M, Kutcher MA et al. Vascular complications with newer generations of angioseal vascular closure devices. J Interv Cardiol 2006; 19: 67–74 Applegate RJ, Grabarczyk MA, Little WC et al. Vascular closure devices in patients treated with anticoagulation and IIb/IIIa receptor inhibitors during percutaneous revascularization. J Am Coll Cardiol 2002; 40: 78–83 Quinn SF, Kim J. Percutaneous femoral closure following stentgraft placement: use of the Perclose device. Cardiovasc Intervent Radiol 2004; 27: 231–6 Mahadevan VS, Jimeno SS, Benson LN et al. Pre-closure of femoral venous access sites used for large sized sheath insertion with the PercloseTM device in adults undergoing cardiac intervention. Heart; 2006; Published online 3 November 2006 Schnyder G, Turi ZG. Complications of vascular closure devices— not yet evidence based. J Am Coll Cardiol 2002; 39: 1705–6 Applegate RJ, Sacrinty MT, Kutcher MA et al. Propensity score analysis of vascular complications after diagnostic cardiac catheterization and percutaneous coronary intervention 1998–2003. Catheter Cardiovasc Interv 2006; 67: 556–62 Koreny M, Riedmuller E, Nikfardjam M et al. Arterial puncture closing devices compared with standard manual compression after cardiac catheterization: systematic review and meta-analysis. JAMA 2004; 291: 350–57 Dangas G, Mehran R, Kokolis S et al. Vascular complications after percutaneous coronary interventions following hemostasis with manual compression versus arteriotomy closure devices. J Am Coll Cardiol 2001; 38: 638–41
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Textbook of peripheral vascular interventions Arora N, Matheny ME, Sepke C et al. A propensity analysis of the risk of vascular complications after cardiac catheterization procedures with the use of vascular closure devices. Am Heart J 2007; 153: 606–11 Ellis SG, Bhatt D, Kapadia S et al. Correlates and outcomes of retroperitoneal hemorrhage complicating percuta-neous coronary intervention. Catheter Cardiovasc Interv 2006; 67: 541–5 Cura FA, Kapadia SR, L’Allier PL et al. Safety of femoral closure devices after percutaneous coronary interventions in the era of glycoprotein IIb/IIIa platelet blockade. Am J Cardiol 2000; 86: 780–2 Lincoff AM, Bittl JA, Harrington RA et al. Bivalirudin and provisional glycoprotein IIb/IIIa blockade compared with heparin and planned glycoprotein IIb/IIIa blockade during percutaneous coronary intervention: REPLACE-2 randomized trial. JAMA 2003; 289: 853–63 Sohail MR, Khan AH, Holmes DR, Jr. et al. Infectious complications of percutaneous vascular closure devices. Mayo Clin Proc 2005; 80: 1011–15 Dregelid E, Jensen G, Daryapeyma A. Complications associated with the Angio-Seal arterial puncture closing device: intra-arterial deployment and occlusion by dissected plaque. J Vasc Surg 2006; 44:1357–59 Jang JJ, Kim M, Gray B et al. Claudication secondary to Perclose use after percutaneous procedures. Catheter Cardiovasc Interv 2006; 67: 687–95
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Mackrell PJ, Kalbaugh CA, Langan EM, III et al. Can the Perclose suture-mediated closure system be used safely in patients undergoing diagnostic and therapeutic angiography to treat chronic lower extremity ischemia? J Vasc Surg 2003; 38: 1305–8 Starnes BW, O’Donnell SD, Gillespie DL et al. Percutaneous arterial closure in peripheral vascular disease: a prospective randomized evaluation of the Perclose device. J Vasc Surg 2003; 38: 263–71 Biondi-Zoccai GG, Fusaro M, Tashani A et al. Angioseal use after antegrade femoral arteriotomy in patients undergoing percutaneous revascularization for critical limb ischemia: A case series. Int J Cardiol; 2006 Mukhopadhyay K, Puckett MA, Roobottom CA. Efficacy and complications of Angioseal in antegrade puncture. Eur J Radiol 2005; 56: 409–12 Bilecen D, Bongartz G, Ostheim-Dzerowycz W. Off-label use of Angio-Seal vascular closure device for brachial artery puncture closure-deployment modification and initial results after transbrachial PTA. Eur J Vasc Endovasc Surg 2006; 31: 431–3 Resnic FS, Arora N, Matheny M et al. A cost-minimization analysis of the angio-seal vascular closure device following percutaneous coronary intervention. Am J Cardiol 2007; 99: 766–70 Turi ZG. Overview of vascular closure. Endovasc Today 2007; 6: 93–9
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Other techniques of percutaneous intervention: retrieval devices, embolization therapy, and angiogenesis JA Silva and JS Jenkins
Percutaneous retrieval of foreign bodies
available including the loop-snare retrieval systems, biopsy forceps, baskets, and others.
The use of indwelling catheters as well as the application of percutaneous diagnostic and revascularization procedures has grown exponentially over the past decade. As a result, endovascular therapists are sometimes confronted with the problem of misplacement or migration of some of these devices into unintended and potentially dangerous anatomical locations. The rate of serious complications associated with foreign body embolism has been reported to be as high as 71% with a mortality rate ranging from 24 to 60%.1 Consequently, non-surgical removal of misplaced intravascular foreign bodies is desirable. In the last few years, there have been several reports regarding the successful percutaneous retrieval of these devices. Some of these experiences are discussed in the present section. The first report of successful percutaneous retrieval of an intravascular foreign body was published in 1964.2 Following that case report, Dotter et al.3 published their multi-center experience on endovascular retrieval of foreign bodies and described successful percutaneous removal of intravascular foreign bodies in 29 cases. In 1978, Bloomfield conducted an international survey and published the results of 180 cases of non-surgical retrieval of intracardiac foreign bodies, suggesting that percutaneous retrieval yielded a very high success rate.4 Since then several case reports or small case series have described the successful non-surgical extraction of intravascular foreign bodies.5–7 In 1986, Uflacker and coworkers7 described their experience on the successful extraction of 19 of 20 intravascular foreign bodies. In this experience, 70% of the fragments were the sheared-off tips of through-the-needle venous catheters. Compared to that early experience3–7 which included the extraction of catheter fragments in the majority of the cases, metal stents, embolization coils, and vena cava filters encompass the majority of foreign bodies removed in more contemporary clinical practice. In addition, technologic innovations and the introduction of new retrieval devices available for extraction of intravascular foreign bodies have enhanced the intravascular recovery rate. Many retrieval tools are currently
Loop-snare retrieval systems Loop-snare devices are frequently among the first choice when attempting percutaneous removal of a foreign body because they are safe and easy to use.8 One loop-snare retrieval system described in the literature is the Welter retrieval loop catheter (Cook, Letchworth, UK), which consists of a wire snare operated from the proximal handle. This device has radio-opaque markers at the catheter tip and the origin of the loop, which facilitates visualization during manipulation and retrieval (Figure 24.1). The Retriever snare (Target Therapeutics, Fremont, CA) consists of an adjustable platinum loop that can be visualized during fluoroscopy and allows retrieval of different-sized objects. It has a low profile (6-French guiding catheters), which allows access to distal and tortuous vessels (Figure 24.2). More recently, the Amplatz gooseneck snare (Microvena Corp, White Bear Lake, MN), which has a nitinol 90° snare loop to shaft orientation has been shown to be of great utility in percutaneous retrieval of foreign bodies (Figure 24.3).9 Compared to other loop-snare techniques in which parallel-opening, self-made, or early wire snares limit foreign body capture,10 the nitinol gooseneck micro-snare has a rightangle design which maximizes engagement and capture of the foreign body. Cekirge et al.,11 described the successful retrieval of intravascular foreign bodies in 13 patients (11 venous, 2 arterial: 10 catheter fragments, 1 stent, 1 coil, 1 guidewire) using nitinol gooseneck snares. Egglin and his colleagues12 attempted removal of 35 intravascular foreign bodies (30 venous and 5 arterial: 16 catheter fragments, 6 embolization coils, 5 metal stents, 4 guidewires, 2 vena cava filters, 1 balloon catheter fragment) in 32 patients. The retrieval devices included nitinol gooseneck snares (n = 28), flexible grasping forceps (n = 5), pigtail catheters (n = 4), and tip-deflecting wires (n = 2) with more than one retrieval system required in 25% of the cases. The retrieval success rate was 97% in this series. In a report of 45 patients using nitinol gooseneck snares in 78% of the cases, retrieval of foreign bodies (12 endovascular stents, 14 catheter fragments, 11 embolization coils, 4 guidewire fragments, 179
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Figure 24.3 permission.
Figure 24.1 permission.
The Welter retrieval loop. Reproduced with
The Amplatz gooseneck snare. Reproduced with
It is important to understand that the free end of the foreign body must be present if loop-snare retrieval is to be attempted. Different techniques have been reported to obtain free end of entrapped foreign bodies. A double-curve catheter or a pigtail may be used to dislodge the target object in a remote vessel or may be used to pull or rotate them exposing an adequate profile or free end for entrapment by a snare.15
3 vena cava filters, and 1 cardiac valve fragment) was successful in 91%.13 More recently, Koseoglu et al.14 reported retrieval of 15 intravascular foreign bodies in 15 patients using nitinol gooseneck snares, with a procedural success rate of 100% and no complications. Interestingly, the authors were capable of successfully retrieving foreign bodies in potentially dangerous locations such as the carotid and middle cerebral arteries.
Retrieval baskets Several baskets for retrieval of foreign bodies have been described in the literature: the Dotter retrieval catheter,16,17 the mini-basket, and the Dormia stone catheter or other stone basket retrieval catheters (Figure 24.4).18–20 These consist of an outer sheath enclosing movable parallel metal wires which can be opened or closed by a sliding cone in and out of a coronary catheter. In a
Figure 24.2
Figure 24.4 permission.
The Retriever snare. Reproduced with permission.
The Cook retrieval forceps. Reproduced with
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Other techniques of percutaneous intervention: retrieval devices, embolization therapy, and angiogenesis report on retrieval attempt of 12 intravascular foreign bodies,19 10 were successfully removed with the stone basket retrieval catheter (Bard Inc., US). Eight of the 10 cases were from major veins. In a recent series of 26 patients with intravascular foreign bodies (8 stents, 4 embolization coils, 9 guidewires, 1 pacemaker lead, and 4 catheter fragments), retrieval was successful in 25 patients (96%) using the Dormia basket without in-hospital or long-term procedural complications.20 Retrieval basket devices appear to be of particular importance for the removal of relatively large objects from the great veins, intracardiac chambers, and the arterial circulation when the objects have reached large arteries or the aorta.21 Biotope and grasping forceps Different types of forceps have been utilized for the retrieval of intravascular foreign bodies.13,22–24 The Cook retrieval forceps is a 3-French profile device operated from a proximal handle and includes a distal spring coil to minimize vascular trauma. The Cordis biopsy forceps (Cordis Corp., Miami, FL), although used to obtain myocardial biopsies, have also been used to remove intravascular foreign bodies. This catheter is relatively large and rigid which enhances the likelihood of vascular trauma and procedural complications. Miscellaneous techniques A variety of improvised retrieval techniques have been utilized to retrieve lost foreign bodies from the vasculature. Doubling an exchange-length wire at its mid-section and inserting it into a 4-French probing catheter can create snares. Alternatively, looping the distal 5 cm of a standard-length wire or tying together the flexible ends of two 0.014-inch wires may build a snare.25,26 The probing catheter is then passed through the guide catheter and positioned just proximal to the retained fragment. The loop is front-loaded through the probing catheter and then passed over the object. Once the object is trapped, the wire ends are pulled firmly to secure the object against the catheter tip and removed through the femoral sheath. Inflated or deflated balloon catheters may be used to drag fragments physically from the vessel into the guide catheter in the coronary circulation.27,28 There are also reports on the use of pigtail catheters to snare and retrieve catheter fragments.29,30 These last techniques have the potential of causing vascular damage necessitating operator care if attempted.
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Coil embolization The delivery of embolization coils has the purpose of inducing selective and “controlled” thrombosis, leading to interruption of vascular flow in a specific target vessel. This endovascular technique has been shown to have important clinical applicability for the treatment of many vascular territories and conditions. It is beyond the scope of this discussion to address the use of embolization coils in every clinical scenario, but instead to provide a general view of their potential applications. Embolization coils are useful for the treatment of patients with patent ductus arteriosus (PDA), systemic-topulmonary artery shunts, and pulmonary arteriovenous (AV) malformations. In addition, coil embolization therapy has become an important treatment modality for intracranial aneurysms, mesenteric aneurysmal disease, gastrointestinal bleeding, iatrogenic vascular perforation in the coronary and peripheral circulation, and others (see below). Most coils consist of preshaped, stainless steel or platinum wire covered with Dacron fiber that are advanced through standard angiographic catheters or microcatheters and delivered to the vessel to be occluded. They are available in different lengths, diameters, and configurations, including straight, helical, or conical shapes (Figure 24.5). The coils are delivered into the target vessel by pushing them through the catheter with an introducer, guidewire, or saline flush and detaching them from an introducing wire after they are placed in the target vessel. The nominal coil diameter is determined by the effective diameter of the extended coil, and range from 0.018to 0.052-inch size. Nester coils are soft, long, platinum-fiber coils which are excellent for packing large vessels or arteriovenous connections and are available in 0.018- and 0.035-inch diameters. Therapeutic embolization of unwanted thoracic vessels was first reported in 1974.31 Vascular occlusion techniques using coil embolization for the treatment of patients with PDA is an attractive and an effective therapeutic modality. Approximately 95% of PDAs smaller than 2.5–3.0 mm can be completely occluded with a single coil. Larger PDAs can also be occluded but require multiple coils.32–35 Coil embolization therapy has also been successfully utilized for the closure of aortopulmonary collaterals, arteriovenous malformations, Blalock–Taussig shunts, venous collaterals, venae cavae, and coronary artery fistulas.36–39
Embolization therapy: coils and occlusive agents There are clinical conditions in which selective interruption of blood flow by inducing thrombosis of the vessel is desirable or necessary to decrease the patient’s morbidity and mortality. These include vascular malformations, arteriovenous fistulas, aneurysms, and spontaneous or iatrogenic bleeding. Endovascular catheter-based therapy with selective embolization of coils, occlusive agents, and sclerotherapy appears to be very useful for the treatment of many of these conditions.
Figure 24.5 permission.
Different embolization coils. Reproduced with
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Over the past 15 years the use of embolization coils has dramatically changed treatment of intracranial aneurysms. The development of the Guglielmi detachable coil led in 1995 to the approval of this technique by the Food and Drug Administration for the treatment of intracranial aneurysms.40 Many prospective and retrospective studies have now confirmed that coil embolization is a feasible alternative treatment to surgery, which carries 5–10% morbidity, negligible mortality and the achievement of complete or near-complete occlusion of > 90% of patients with unruptured intracranial aneurysms.41–43 Likewise coil embolization has been shown to be a feasible alternative to surgery for the treatment of aneurysms in other anatomical locations, such as the renal, mesenteric, coronary, and peripheral circulation in selected patients.44–50 Pseudoaneurysms in the coronary and noncoronary circulation or those that result as a complication of arterial vascular access have also been successfully treated with coil embolization therapy.51–53 Severe gastrointestinal bleeding, retroperitoneal hemorrhage, and iatrogenic complications of percutaneous interventions can be treated with coil embolization after the source of bleeding has been identified.54–56 Occlusive agents Occlusive agents that induce thrombosis and interruption of blood flow are divided into embolization agents such as polyvinyl alcohol foam and gel foam; sclerosing agents such as ethanol, tetradecyl ethanolamine, polydocanol, doxycycline, and others which produce irritation, endothelial damage and thrombosis of the vessel; and more recently, natural procoagulants such as thrombin.57 These occlusive agents are used for treating arteriovenous malformations, arteriovenous fistulas, hemangiomas, venous and lymphatic malformations,57–60 and acquired or iatrogenic bleeding complications after percutaneous coronary and peripheral vascular interventions (Figure 24.6).61–64 In the treatment of arteriovenous malformations the results are mixed and patients often require
several treatment sessions due to recurrence of the condition. Treatment of bleeding and iatrogenic complications is limited to case reports. When treating these conditions the operator must keep in mind potential complications such as tissue necrosis, nerve injuries, and thrombosis of non-targeted vessels, pulmonary embolism, and others.57
Angiogenesis Symptomatic patients with significant peripheral vascular disease should be considered for percutaneous or surgical revascularization therapy. A proportion of these individuals are not suitable for either revascularization strategy due to poor target vessels, inability to cross chronic total occlusions, or other comorbidities, and often require amputation. Angiogenesis is the process of new blood vessel development (neovascularization) from pre-existing vasculature. Vasculogenesis refers to blood vessel formation from endothelial progenitors that differentiate in situ. Until recently, angiogenesis was considered the only means of adult neovascularization and vasculogenesis was thought to be limited to embryologic development. The existence of bone marrow-resident and/or circulating endothelial progenitor cells (EPCs) has provided evidence that postnatal vasculogenesis also occurs in adults. Based on promising preclinical studies and the abundant information of their biological properties, the potential of EPCs to regulate angiogenesis as a therapeutic modality for saving tissue from ischemic damage has been suggested.65,66 Based on this recent research, investigators have explored therapies aimed at promoting the development of new vessels in the coronary and peripheral circulation as a way to enhance perfusion to the ischemic tissue with promising results.67–70 In a murine model of limb ischemia, successful induction of angiogenesis was accomplished by transplantation of peripheral blood mononuclear cells and platelets.70 In patients with critical lower-extremity ischemia, the pioneer work of
Figure 24.6 Retroperitoneal bleeding caused by laceration of the inferior epigastric artery, successfully treated with balloon catheter-delivery of thrombin. Reproduced with permission from Silva JA et al. Catheter Cardiovasc Interv 2004; 62: 230–3.
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Other techniques of percutaneous intervention: retrieval devices, embolization therapy, and angiogenesis Tateishi-Yuyama et al.71 showed that transferring bone marrow-derived mononuclear cells (BM-MNCs) into ischemic limbs dramatically decreased ischemic symptoms, increased ankle–brachial index (ABI), enhanced the transcutaneous oxygen pressure, and prolonged exercise tolerance. The safety, feasibility, and clinical benefits of
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this form of therapy have recently been confirmed by other investigators.72–74 Angiogenesis appears to be a promising revascularization strategy in patients who are poor candidates for conventional surgical or percutaneous revascularization, and is at present undergoing intense research.
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Richardson JD, Grover FL, Trinkle JK. Intravenous catheter emboli experience with 20 cases and collective review. Am J Surg 1974; 128: 722–8 Thomas J, Sinclair SB, Bloomfield D et al. Nonsurgical retrieval of a broken segment of steel spring guide from right atrium and inferior vena cava. Circulation 1964; 30: 106–8 Dotter CT, Roesch J, Bilbao MK. Transluminal extraction of catheter and guide fragments from the heart and great vessels: 29 collected cases. AJR Am J Roentgenol 1971; 111: 467–72 Bloomfield DA. The non-surgical retrieval of intracardiac foreign bodies: an international survey. Cathet Cardiovasc Diagn 1978; 4: 1–14 Zollikofer C, Nath PH, Castaneda-Zuniga WR et al. Non-surgical removal of intravascular foreign bodies. ROFO 1979; 130: 590–3 Rubinstein ZJ, Morag B, Itzchak Y. Percutaneous removal of intravascular foreign bodies. Cardiovasc Intervent Radiol 1982; 5: 64–8 Uflacker R, Lima S, Melichar AC. Intravascular foreign bodies: percutaneous retrieval. Radiology 1986: 160: 731–5 Furui S, Yamauchi T, Makita K, et al. Intravascular foreign bodies: loop snare retrieval system with a three-lumen catheter. Radiology 1992; 182: 283–4 Nazarian GK, Myers TV, Bjarnason H, et al. Applications of the Amplatz snare device during interventional radiologic procedures. AJR Am J Roentgenol 1995; 165: 673–8 Savander SJ, Brodkin J, Osterman FA. In-situ formation of a loop snare for retrieval of a foreign body without a free end. Cardiovasc Intervent Radiol 1996; 19: 298–301 Cekirge S, Weiss JP, Foister RG et al. Percutaneous retrieval of foreign bodies: experience with the nitinol goose neck snare. J Vasc Interv Radiol 1993; 4: 805–10 Egglin TKP, Dickey KW, Rosenblatt M et al. Retrieval of intravascular foreign bodies: experience in 32 cases. AJR Am J Roentgenol 1995; 164: 1259–64 Gabelmann A, Kramer S, Gorich J. Percutaneous retrieval of lost or misplaced intravascular objects. AJR Am J Roentgenol 2001; 176: 1509–13 Koseoglu K, Parildar M, Oran I et al. Retrieval of intravascular foreign bodies using the goose neck snare. Eur J Radiol 2004; 49: 281–5 Seong KC, Kim JK, Chung JW et al. Tubular foreign body or stent: safe retrieval or repositioning using the coaxialsnare technique. Korean J Radiol 2002; 3: 30–7 Steele PM, Holmes DR, Mankin HT et al. Intravascular retrieval of broken guidewire from the ascending aorta after percutaneous transluminal coronary angioplasty. Cathet Cardiovasc Diagn 1985; 11: 623–8 Bellamy CM, Roberts DH, Ramsdale DR. Ventriculo-atrial shunt causing tricuspid endocarditis: its percutaneous removal. Int J Cardiol 1990; 28: 260–2 Lassers BW, Pickering D. Removal of an iatrogenic foreign body from aorta by means of uretric stone catheter. Am Heart J 1967; 73: 375–8 Yang FS, Ohta I, Chiang HJ et al. Non-surgical retrieval of intravascular foreign body: experience of 12 cases. Eur J Radiol 1994; 18: 1–5 Sheth R, Someshwar V, Warawdekar G. Percutaneous retrieval of misplaced intravascular foreign objects with the Dormia basket: an effective solution. Cardiovasc Intervent Radiol (2007; 30: 48–53; published on line) Grech ED, Ramsdale DR. Percutaneous removal of retained foreign bodies. In: Grech ED, Ramsdale DR, eds. Practical Interventional Cardiology, second edition. London: Martin Dunitz, 2002, 425–40 Foster-Smith KW, Garratt KN, Higano ST et al. Retrieval techniques for managing for managing flexible intracoronary stent misplacement. Cathet Cardiovasc Diagn 1993; 30: 63–8
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Eeckout E, Stauffer J, Goy J. Retrieval of a migrated coronary stent by means of an alligator forceps catheter. Cathet Cardiovasc Diagn 1993; 30: 166–8 Roberts DH, Bellamy CM, Ramsdale DR. Removal of a fractured temporary pacemaker electrode using endomyocardial biopsy forceps. PACE 1989; 12: 1835–6 Bogart DB, Earnest JB, Miller JT. Foreign body retrieval using simple snare device. Cathet Cardiovasc Diagn 1990; 19: 248–50 Tatsumi T, Howland WJ. Retrieval of a ventriculoatrial shunt catheter from the heart by a venous technique. J Neurosurg 1970; 32: 593–6 Krone RJ. Successful percutaneous removal of retained broken coronary angioplasty guidewire. Cathet Cardiovasc Diagn 1986; 12: 409–10 Feldman RL, Trice WA, Henneman WW et al. Retrieval of a fractured USCI probe tip from a diseased coronary artery using another fixed-wire balloon catheter, the Cordis Orion. Cathet Cardiovasc Diagn 1990; 19: 257–63 Auge JM, Orial A, Serr C et al. The use of pigtail catheters for retrieval of foreign bodies in the vcardiovascular system. Cathet Cardiovasc Diagn 1984; 10: 2635–638 Bessoud B, de Baere T, Kuoch V et al. Experience at a single institution with endovascular treatment of mechanical complications caused by implanted central venous access devices in pediatric and adult patients. AJR Am J Roentgenol 2003; 180: 527–32 Zuberbuhler JR, Dankner E, Zoltum R et al. Tissue adhesive closure of aorto-pulmonary communications. Am Heart J 1974; 88: 41–46 Moore JW, Cambier PA. Transcatheter occlusion of patent ductus arteriosus. J Intervent Cardiol 1995; 18: 517–31 Cambier PA, Kirby WC, Wortham DC et al. Percutaneous closure of small (< 2.5 mm) patent ductus arteriosus using coil embolization. Am J Cardiol 1992; 69: 815–6 Lloyd TR, Raymond F, Mendelsohn AM et al. Transcatheter occlusion of patent ductus arteriosus with Gianturco coils. Circulation 1993; 88: 1412–20 Akagi T, Iemura M, Tananari Y, et al. Simultaneous double or triple coil technique for closure of moderate sized (> or = 3.0 mm) patent ductus arteriosus. J Interv Cardiol 2001; 14: 91–6 Perry SB, Radtke W, Fellows KE, et al. Coil embolization to occlude aortopulmonary collateral vessels and shunts in patients with congenital heart disease. J Am Coll Cardiol 1989; 13: 100–8 Perry SB, Rome J, Keane JF et al. Transcatheter closure of coronary artery fistulas. J Am Coll Cardiol 1992; 20: 205–9 Okamoto M, Makita Y, Fujii Y et al. Successful coil embolization with assistance of coronary stenting in an adult patient with a huge coronary arterial-right atrial fistula. Intern Med 2006; 45: 865–70 Guo H, You B, Lee JD. Dilated cardiomyopathy caused by a coronary-pulmonary fistula treated successfully with coil embolization. Circ J 2006; 70: 1223–5 Vinuela F, Duckwiler G, Mawad M, MASH Study Group. Guglielmi detachable coil embolization of acute intracranial aneurysm: preoperative anatomical and clinical outcome in 403 patients. J Neurosurg 1997; 86: 475–82 Pouratian N, Oskouian RJ Jr, Jensen ME et al. Endovascular management of unruptured intracranial aneurysms. J Neurol Neurosurg Psychiatry 2006; 77: 572–8 Koebbe CJ, Veznedaroglu E, Jabbour P et al. Endovascular management of intracranial aneurysms: current experience and future advances. Neurosurgery 2006; 59: S93–S102 van Rooji WJ, Sluzewski M. Procedural morbidity and mortality of elective coil treatment of intracranial aneurysm. AJNR Am J Neuroradiol 2006; 27: 1678–80 Nosher JL, Chung J, Brevetti LS et al. Visceral and renal artery aneurysms: a pictorial essay on endovascular therapy. Radiographics 2006; 26: 1687–704
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Hammer FD, Boon LM, Mathurin P et al. Ethanol slerotherapy of venous malformations: evaluation of systemic ethanol contamination. J Vasc Interv Radiol 2001; 12: 595–600 Yoo BS, Yoon J, Lee SH, Kim JY, Lee HH, Ko JY, Lee BK, Hwang SO, Choe KH. Guidewire-induced coronary artery perforation treated with transcatheter injection of polyvinyl alcohol form. Cathet Cardiovasc Intervent 2001; 52: 231–4 Dixon SR, Webster MWI, Ormiston JA, Wattie WJ, Hammett CJK. Gelfoam embolization of a distal coronary artery guidewire perforation. Cathet Cardiovasc Intervent 2000; 49: 214–7 Fischell TA, Korban EH, Lauer MA. Successful treatment of distal coronary guidewire-induced perforation with balloon catheter delivery of intracoronary thrombin. Cathet Cardiovasc Intervent 2003; 53: 370–4 Silva JA, Stant J, Ramee SR. Endovascular treatment of a massive retroperitoneal bleeding. Successful balloon catheter-delivery of intra-arterial thrombin. Cathet Cardiovasc Intervent 2005; 64: 218–22 Elsheikh P et al. Only a specific subset of human peripheral-blood monocytes has endothelial-like functional capacity. Blood 2005; 106: 2347–55 Zambides ET. Blood-forming endothelium in human ontogeny: lessons from in utero development and embryonic stem cell culture. Trend Cardiovasc Med 2006; 16: 95–101 Isner JM, Vale PR, Symes JF et al. Assessment of risks associated with cardiovascular gene therapy in human subjects. Circ Res 2001; 89: 389–400 Ferrara N, Alitalo K. Clinical application of angiogenic growth factors and their inhibitors. Nat Med 1999; 5: 1359–64 Urbanek K, Torella D, Sheikh F et al. Myocardial regeneration by activation of multipotent cardiac stem cells in ischemic heart failure. Proc Natl Acad Sci USA 2005; 102: 8692–7 Iba O, Matsubara H, Nozawa Y, et al. Angiogenesis by implantation of peripheral blood mononuclear cells and platelets into ischemic limbs. Circulation 2002; 106: 2019–25 Tateishi-Yuyama E, Matsubara H, Murohara T et al. Therapeutic angiogenesis for patients with limb ischaemia by autologous transplantation of bone-marrow cells: a pilot study and a randomized controlled trial. Lancet 2002; 360: 427–35 Higashi Y, Kimura M, Hara K et al. Autologous bone-marrow mononuclear cell implantation improves endothelium-dependent vasodilation in patients with limb ischemia. Circulation 2004; 109: 1215–8 Saigawa T, Kato K, Ozawa T et al. Clinical application of bone marrow implantation in patients with arteriosclerosis obliterans, and the association between efficacy and the number of implanted bone marrow cells. Circ J 2004; 68: 1189–93 Huang P, Li S, Han M et al. Autologous transplantation of granulocyte colony-stimulating factor-mobilized peripheral blood mononuclear cells improves critical limb ischemia in diabetics. Diabetes Care 2005; 29: 2155–60
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SECTION III Neurovascular
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Epidemiology and pathophysiology of neurovascular disease C Klonaris, A Papapetrou, and A Katsargyris
Historical background The great importance of carotid artery in cerebral blood perfusion was recognized by the ancient Greeks. The name “carotid” comes from the ancient Greek word “caroun” (‘καρου´ν’), which means “to plunge into deep sleep,” or “to stupefy,” because compression of these arteries is said to produce carus or stupor. The correlation of carotid artery disease and cerebral ischemia was first described in 1856, when Savory found carotid artery occlusion at postmortem examination1 of a patient with neurological symptoms. Later, Chiari1a described cerebral emboli arising from an ipsilateral carotid lesion; Hunt suggested that cerebrovascular ischemic symptoms were similar to claudication symptoms in the lower extremities and that both manifestations were due to reduced blood flow.2 In 1927, Moniz2a developed the technique of cerebral angiography for assessment of carotid circulation and visualized four cases of carotid thrombus associated with ipsilateral cerebral infarction. The first attempt to restore blood flow to the ischemic brain was made by Carrea and his colleagues in 1951, but their work was not reported until 1955.3 They excised the proximal part of a diseased internal carotid artery (ICA) and performed an end-to-end anastomosis of the external carotid artery (ECA) to the distal part of the ICA. A different carotid bifurcation reconstruction had been performed earlier in 1918 by Lefèvre for a neck gunshot injury.4 In 1954, Eastcott and colleagues reported the first operative procedure in which the diseased carotid bifurcation was resected to relieve transient ischemic attacks and the common carotid artery (CCA) was anastomosed to the ICA.5 DeBakey performed a carotid endarterectomy (CEA) in 1953 and published a 19-year follow-up report in 1975.6
Epidemiology Stroke is the third leading cause of death in the developed countries. The age-adjusted annual death rate from strokes is 116 per 100,000 population in the US and about 200 per 100,000 in the UK, some 12% of all deaths. It is more common in males and in black African populations, and uncommon in ages under 40 years. Death rate following a stroke is 25%. One-third of stroke survivors require prolonged inpatient rehabilitation, and 70% of disabled patients fail to recover
normal cerebral function.7,8 The annual cost of stroke in the US exceeds $7 billion in medical expenses and lost productivity. Prevention of thromboembolic cerebral ischemia is the goal of carotid artery disease treatment. Considering that the extracranial carotid-disease-derived stroke counts for more than one-third or half of all strokes, depending on the author, it is obvious that the management of carotid artery disease has important health care and socioeconomic implications through stroke reduction. Carotid endarterectomy is one of the most common vascular procedures; more than 100,000 of such operations were performed in 1984 in the US.9 In the mid-1980s, several large multicenter trials answered important questions about the appropriate indications and the efficacy of CEA and contributed to better understanding of the nature of carotid artery disease. Later, advances in endovascular procedures came to add a significant weapon in the armamentarium of vascular surgery, but also raised debates and controversies about the “gold-standard” technique.10 Vertebrobasilar circulation is the other component of cerebral perfusion and the management of vertebrobasilar insufficiency (VBI) is of great interest. Hemodynamic compromise is considered to be the most common mechanism causing symptoms due to VBI, in contrast to the carotid-diseasederived symptoms that mainly are of embolic origin. The nature of VBI and the complexity of evaluation of such cases have raised several controversies in the field of treatment.
Pathophysiology Carotid artery Atherosclerotic carotid artery disease is one of the major causes of neurovascular events. Atherosclerosis is a complex inflammatory process characterized by the accumulation of lipid, macrophages and smooth muscle cells in intimal plaque. The vascular endothelium plays a critical role in maintaining the vascular integrity. Mechanical shear stress (e.g. hypertension), biochemical abnormalities (e.g. diabetes mellitus, hyperhomocysteinemia, elevated Low Density Lipoprotein (LDL)), inflammation and genetic alteration may contribute to the initial endothelial “injury” or dysfunction, which is believed to trigger atherogenesis. Atherosclerotic plaques have been long known to form at bifurcations or branching sites. Carro et al.11 were the first to suggest that the decreased shear stress was associated with 187
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subintimal thickening and atherosclerosis initiation. One of the first explanatory mechanisms suggested that the relative stagnation of blood resulted in prolonged “residence time,” which promoted the harmful interaction of atherogenic substances of the blood with the endothelial cells. In addition, many studies revealed that there is a major biological response of the endothelial cells under low shear stress, which alters cell morphology, increases cell proliferation, and triggers the expression of several vasoconstrictor agents.12–14 Consequently, the endothelium is no longer considered as a simple alignment of cells, but as a unique actively responsive vascular structure.15–20 Interestingly, sites with reduced shear stress are located at the lateral wall of a flow divider and this explains the anatomical observation of the preferential location of plaques on the lateral wall of the carotid bulb.21 Endothelial dysfunction is the initial event that promotes arterial wall permeability and accumulation of oxidized lipoproteins, which are taken up by macrophages of the endothelium at low shear stress sites producing lipid foam cells. Macroscopically, this is seen as flat yellow dots or lines called “fatty streaks.” These lesions are present in the human arteries from the early years of life. A complex mechanism of extracellular lipid accumulation, along with proliferation and migration of smooth muscle cells and macrophages result in the formation of an “advanced or elevated fibrolipid atheromatous plaque.” This plaque consists of the core (fat deposit, foam cells, lymphocytes, phagocytes, smooth muscle cells) and the fibrous cap (smooth muscle cells and collagen). The “vulnerable” plaque The fate of the “advanced” atherosclerotic plaque has been at the center of interest of several studies that attempt to clarify the nature of carotid artery disease. Such a lesion may grow slowly and encroach to the lumen, or become “unstable” and cause embolization, thrombosis, and blood flow obstruction. Several features of the “vulnerable” plaque have been identified. A plaque with a thin fibrous cap with inflammation is more prone to rupture than the one with a thick cap. The ratio between the lipid contents and calcification may also affect plaque stability.22 Lately, many inflammatory factors such as MMPs (matrix metalloproteinases) and hsCRP (highsensitivity CRP), neovascularization and genetic factors have been also claimed to affect plaque stability.23–28 Asymptomatic carotid stenosis An atheromatous plaque in the carotid bifurcation can be either asymptomatic or symptomatic. The slow progress of a plaque may result in a silent total occlusion of the internal carotid artery causing no symptoms. The collateral blood flow to the brain via the circle of Willis, in harmonization with the autoregulation of the intracerebral circulation, is an extremely efficient system compensating for the lack of flow from the occluded ipsilateral carotid artery. However, asymptomatic carotid plaques undoubtedly put patients at risk for transient ischemic attacks (TIAs) or stroke. Stenosis degree, plaque composition, and the progress of the lesion during follow-up determine the risk for cerebrovascular events.29 The physician should consider all these factors, as
Figure 25.1 Transverse section of a carotid plaque causing 95% stenosis (eversion technique) in a symptomatic patient with ipsilateral TIAs and contralateral carotid occlusion. Arrow indicates the residual lumen.
well as the clinical status and life expectancy of the patient, before coming to any treatment decision. Symptomatic carotid stenosis The benign scenario of a stable plaque comes in contrast to the devastating results of a complicated plaque (Figure 25.1). Several mechanisms have been described for the process that leads to the formation of “unstable” plaques. One involves superficial endothelial injury, which results in connective tissue matrix denudation and formation of a thrombus adherent to the vessel wall. A deeper injury of the fibrous cap may also result in a symptomatic plaque. The cap of the plaque ruptures, the contents of the core are washed to the circulation and platelets enter the residual plaque. The remaining ulcer is extremely thrombogenic and stimulates thrombus formation, which can either remain adherent to the lumen causing occlusion or be embolized to the distal circulation (Figure 25.2). Another presentation is the intraplaque hemorrhage, which although “protected” from the circulation by the intact fibrous
Figure 25.2 Atherosclerotic carotid plaque from a symptomatic patient with ipsilateral TIAs. Note the thrombus in the nidus of the ulcer (arrow).
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Epidemiology and pathophysiology of neurovascular disease cap, can cause sudden narrowing of the artery and result in hemodynamic compromise. Some definitions describing the cerebrovascular events are valuable in understanding the mechanisms involved and explaining the variety of the clinical presentations. ●
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Transient ischemic attack (TIA) is defined as a focal neurological deficit that is completely resolved within a few seconds to 24 hours. It is usually of sudden onset. It has a tendency to recur and is a herald of thromboembolic stroke. When it recurs with a more severe presentation it is called “Crescendo TIA.” TIAs are usually the result of passage of microemboli to the cerebral circulation. The principal sources of these emboli are debris and thrombi from the great vessels of the aortic arch or the heart chambers (i.e. atrial fibrillation). TIAs may be also caused by a decrease in cerebral perfusion (i.e. postural hypotension or decreased flow through stenosis of carotid or vertebral arteries). Autoregulation comes to protect the cerebral circulation and usually averts infarction of the brain. Stroke is defined as a focal neurological deficit due to a vascular lesion lasting longer than 24 hours. Completed stroke occurs when the deficit is maximal within 6 hours from the onset of symptoms. Stroke-in-evolution is an event under progress within the first 24 hours from the onset of symptoms Minor stroke implies that the patient recovers without a significant deficit usually within a week.
Vertebral and basilar arteries Vertebral arteries (VA) contribute to cerebral perfusion supplying blood to the circle of Willis via the posterior circulation (intracranial union of VA to form the basilar artery, which separates to two branches the posterior cerebral arteries that are anastomosed to the circle of Willis with the posterior communicating arteries). In addition to the anterior and posterior circulation, the autoregulation of cerebral perfusion maintains a constant cerebral flow independently of perfusion pressure. This is achieved by the immediate response of small intracerebral arteries to pressure gradient changes across the vessel wall. Symptoms related to posterior circulation insufficiency include bilateral visual disturbances and transient vertigo with diplopia, dysarthria, dysphagia, or ataxia. Occlusion of the posterioinferior cerebelar artery, the largest intracranial branch of vertebral artery, is presented with a severe clinical condition due to ischemia of the brain stem and particularly of the lateral medula (Wallenberg syndrome). Anatomic variations of vertebral arteries are not rare. Aberrant left VA originating from the aortic arch is found in 6–10% of individuals, while VAs of different diameters (with the left VA being usually the larger “dominant” vessel) is also a common finding. Vertebrobasilar insufficiency (VBI) may be due to either (i) thromboembolic events or (ii) hemodynamic compromise. The most frequent etiology of distal embolization is intraluminal thrombus formation secondary to spontaneous or traumatic dissections/aneurysms. In contrast to carotid artery disease, thromboembolic events due to atherosclerotic plaque rupture are not common, because of the smooth nature of the
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plaques developed in the VA. Atherosclerotic plaques however, can cause hemodynamic compromise of the posterior circulation, which in combination with dysautoregulation are considered to be the primary cause of VBI. There are several factors involved in the pathophysiology of VBI including anatomic variations of the posterior circulation (e.g. formation of basilar artery from one VA, absence of one or both posterior communicating arteries), the competitive nature of anterior and posterior circulation in the circle of Willis, the small diameter of the branches of basilar artery supplying the hindbrain, the loss of cerebral autoregulation (especially in the elderly), cardiac insufficiency, and rheologic factors. Assessment of VBI is relatively complex and the use of advanced imaging modalities (e.g. SPECT) have been recruited to assess the percentage of regional perfusion attributed to vertebrobasilar circulation.30–33 The variety of factors involved in the pathogenesis of VBI explains the complexity of evaluation and the difficulty in decision-making regarding the treatment of these patients. The physician has to assess both carotid and vertebral circulation and consider the cerebral perfusion on the balance of anterior and posterior circulation before management planning. Spontaneous dissection of carotid and vertebral arteries Spontaneous dissections of carotid and vertebral arteries are responsible for only 2% of all ischemic strokes.34,35 However, when we confine strokes in young and middle-aged groups, the carotid or vertebral artery dissection accounts for 10–25% of ischemic events. It is estimated that the annual incidence of spontaneous carotid dissection in the community ranges from 2.5 to 3.0 per 100,000 and the annual incidence of vertebral spontaneous dissections are halved.36 Extracranial carotid and vertebral arteries are more prone to spontaneous dissection than their intracranial segments or other arteries of similar size throughout the body. This is explained by the greater mobility of the cervical arteries and their anatomical proximity to rigid bony structures that potentially can cause intimal trauma.37 Dissection of carotid and vertebral arteries usually begins from an intimal tear and results in entrance of blood into the vessel wall forming an intramural hematoma called false lumen. A false lumen close to the intima causes stenosis, whereas close to the adventitia causes aneurysm formation.38 Several factors have been implicated in the etiology of spontaneous dissection including inherited structural deficiencies of the vessel wall (e.g. Ehlers-Danlos IV, Marfan syndrome), fibromuscular dysplasia, cystic medial necrosis, etc. Specific movements causing hyperextension or rotation of the neck, especially when they are sudden, may cause intimal injury of carotid artery. Up to 25% of patients with unexplained stroke after trauma will be found to have dissection of the carotid artery. The classic clinical manifestation of carotid dissection includes neck pain and ipsilateral headache, Horner syndrome, lower cranial nerve palsy, and cerebral ischemia symptoms. The clinical presentation of vertebral dissection consists of pain in the back of the neck followed by ischemia of the vertebrobasilar circulation.
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Table 25.1 Risk factors for stroke in symptomatic patients managed medically (data from NASCET)39 Risk factors: Age > 70 years Systolic blood pressure > 160 mmHg Diastolic blood pressure > 90 mmHg Recent cerebrovascular event Diabetes mellitus Smoking Hyperlipidemia Intermittent claudication Plaque stenosis > 80% Ulcerated plaque Stroke risk at 2 years: Low risk (0–5 risk factors): 17% Moderate risk (6 risk factors): 23% High risk (> 6 risk factors): 39%
Risk factor modification and stroke prevention Atherosclerosis risk factors have been extensively examined. Many studies have attempted to correlate risk factor modification and protection from stroke and important conclusions have been drawn delineating guidelines for prevention of cerebrovascular events. Data from the North American Symptomatic Carotid Endarterectomy Trial (NASCET) shown in Table 25.1 characteristically present the implication of risk factors for stroke in medically treated symptomatic patients.39 Differential diagnosis The differential diagnosis of acute cerebrovascular ischemia include cardiac, hematologic, intracranial, and arterial etiologies. The most important are outlined in Table 25.2.
Conclusion Regardless of the treatment options of the lesions of cervical arteries (pharmaceutical, endarterectomy, bypass, balloon
Table 25.2 Differential cerebrovascular ischemia
diagnosis
of
acute
1. Carotid artery disease Atherosclerotic occlusive disease Ulcerative plaque Dissection (traumatic, spontaneous) Fibromuscular dysplasia Carotid aneurysm 2. Cardiac Atrial arrhythmia (fibrillation/flutter) Valvular disease (mitral valve prolapse, aortic stenosis) Mural thrombus (ventricular aneurysm, cardiomyopathy) Atrial myxoma 3. Hematologic disorders Polycythemia, platelet disorders Lupus anticoagulant 4. Intracranial Brain tumor Subdural hematoma, subarachnoid hemorrhage Focal seizure Ruptured berry aneurysm 5. Miscellaneous Inflammatory arteritis Giant cell (temporal arteritis, Takayasu’s arteritis) Infectious (tuberculosis, syphilis, fungus) Induced by drugs Rheumatologic (lupus erythematous)
angioplasty) several questions remain to be answered. What causes a plaque to become unstable? Can we transform an unstable plaque to a stable one? Is there a role for genetic intervention in the treatment of these lesions? Undoubtedly, there is still a lot for research teams to do; answers to these questions will help to understand further the nature of the disease and will probably open new horizons for the treatment of patients with neurovascular disorders.
REFERENCES 1.
Savory WS. Case of a young woman in whom the main arteries of both upper extremities and of the left side of the neck were throughout completely obliterated. Med Chir Trans London 1856; 39: 205–35 1a. Wein TH, Bornstein NM. Stroke prevention: cardiac and carotidrelated stroke. Neurol Clin 2000; 18(2): 321–41 2. Hunt JR. The role of the carotid arteries in the causation of vascular lesions of the brain with remarks on certain special features of the symptomatology. Am J Med Sci 1914; 147: 704–13 2a. Lowis GW, Minagar A. The neglected research of Egas Moniz of internal carotid artery (ICA) occlusion. J Hist Neurosci 2003; 12(3): 286–91 3. Carrea R, Mollins M, Murphy G. Surgical treatment of spontaneous thrombosis of the internal carotid artery in the neck. Carotidcarotideal anastomosis. Report of a case. Acta Neurol Latinoam 1955; 1: 71–8 4. Lefèvre MH. Sur un cas de plaie du duble carotidien per balle, traitèe par ligature de lacarotid primitive et l’anastomose bout à bout de la carotid extreme avec la carotid interne. Bull Mem Soc Chir 1918; 44: 923–8 5. Eastcott HHG, Pickering GW, Rod C. Reconstraction of internal carotid artery in a patient with intermittent attacks of hemiplegia. Lancet 1954; 2: 994–6
6. 7. 8. 9. 10. 11.
12. 13.
DeBakey ME. Successful carotid endarterectomy for cerebrovascular insuficiency: Nineteen year follow up. JAMA 1975; 233: 1083–5 Matsumoto N, Whisnant JP, Kurland LT, Okazaki H. Natural history of stroke in Rochester, Minnesota, 1955 through 1969. Stroke 1973; 4: 20–9 The National Survey of Stroke. National Institute of Neurological and Communicative Disorders and Stroke. Stroke 1981; 12(2 Pt 2 suppl 1): 11–91 Barnett HJ, Plum F, Walton JN. Carotid endarterectomy [Editorial]. Stroke 1984; 15: 941–3 Brott T, Thalinger K. The practice of carotid endarterectomy in a large metropolitan area. Stroke 1984; 15: 950–5 Caro CG, Fitz-Gerald JM, Schroter RC. Atheroma and arterial wall shear: observation, correlation, and proposal of a shear dependent mass transfer mechanism of atherogenesis. Proc R Soc Lond B Biol Sci 1971; 177: 109–59 Rieder MJ, Carmona R, Krieger JE, Pritchard KA Jr, Greene AS. Supression of angiotensin-converting enzyme expression and activity by shear stress. Circ Res 1997; 80: 312–9 Mondy JS, Lindner V, Miyashiro JK et al. Platelet-derived growth factor ligand and receptor expression in response to altered blood flow in vivo. Circ Res 1997; 81: 320–7
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Epidemiology and pathophysiology of neurovascular disease 14.
15. 16. 17. 18. 19. 20. 21.
22. 23.
24.
25.
26.
Walpola PL, Gotlieb AI, Langille BL. Monocyte adhesion and changes in endothelial cell number, morphology, and F-actin distribution elicited by low shear stress in vivo. Am J Pathol 1993; 142: 1392–400 Davies PF. Flow-mediated endothelial mechanotransduction. Physiol Rev 1995; 75: 519–60 Malek AM, Izumo S. Control of endothelial cell gene expression by flow. J Biomech 1995; 28: 1515–28 Gimborne MA Jr. Vascular endothelium: an integrator of pathophysiologic stimuli in atherosclerosis. Am J Cardiol 1995; 75: 67–70 Traub O, Berk BC. Laminar shear stress: mechanisms by which endothelial cells transduce an atheroprotective force. Atheroscler Thromb Vasc Biol 1998; 18: 677–85 Nerem RM, Alexander RW, Chappell DC et al. The study of the influence of flow on vascular endothelial biology. Am J Med Sci 1998; 316: 169–75 Chien S, Li S, Shyy YJ. Effects of mechanical forces on signal transduction and gene expression in endothelial cells. Hypertension 1998; 31: 162–9 Ku DN, Giddens DP, Zarins CK, Glagov S. Pulsatile flow and atherosclerosis in the human carotid bifurcation. Positive correlation between plaque location and low and oscillating shear stress. Arteriosclerosis 1985; 5: 293–302 Hunt JL, Fairman R, Mitchel ME et al. Bone formation in carotid plaques. A clinicopathological study. Stroke 2002; 33: 1214–9 Johnson JL, George SJ, Newby AC, Jackson CL. Divergent effects of matrix metalloproteinases 3, 7, 9, 12 on atheroscleroticplaque stability in mouse brachiocephalic arteries. Proc Natl Acad Sci USA 2005; 102: 15575–80 Morgan RA, Reikasem K, Gallagher PJ et al. Differences in matrix metalloproteinase-1 and matrix metalloproteinase-12 transcript levels among carotid atherosclerotic plaques with different histopathological characteristics. Stroke 2004; 35: 1310–15 Choi H, Cho DH, Shin HH, Park JB. Association of high sensitivity C-reactive protein with coronary heart disease prediction, but not with carotid atherosclerosis, in patients with hypertension. Circulation 2004; 68: 298–303 Dosa E, Rugonfalvi-Kiss S, Prohaszka Z et al. Marked decrease in the levels of two inflammatory markers, hs-C-reactive protein and fibrinogen in patients with severe carotid atherosclerosis after eversion carotid endarterectomy. Inflamm Res 2004; 53: 631–5
27. 28. 29. 30.
31.
32.
33.
34. 35. 36. 37. 38. 39.
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Fleiner M, Kummer M, Mirlacher M et al. Arterial neovascularization and inflammation in vulnerable patients: early and late signs of symptomatic atherosclerosis. Circulation 2004; 110: 2843–50 Flex A, Gaetani E, Papaleo P et al. Proinflammatory genetic profiles in subjects with history of ischemic stroke. Stroke 2004; 35: 2270–5 O’Holeran LW, Kenely NM, McClurken M, Johnson JM. Natural history of asymptomatic carotid plaque. Five year follow up study. Am J Surg 1987; 154: 659–62 Baron JC, Bousser MG, Rey A et al. Reversal of focal “misery perfusion syndrome” by extracranial arterial bypass in hemodynamic cerebral ischemia. A case study with 15 O positron emission tomography. Stroke 1981; 12: 454–9 Herold S, Brown MM, Frackowiak RS et al. Assessment of cerebral hemodynamic reserve: corelation between PET parameters and CO2 reactivity measured by the intravenous 133xenon injection technique. J Neurol Neurosurg Psychiatry 1988; 51: 1045–50 Kanno I, Uemura K, Higano S et al. Oxygen extraction fraction at maximally vasodilated tissue in the ischemic brain estimated from regional CO2 responsiveness measured by positron emission tomography. J Cereb Blood Flow Metab 1988; 8: 227–35 Knop J, Thie A, Fuchs C, Siepmann G, Zeumer H. 99m TcHMPAO-SPECT with acetazolamide challenge to detect hemodynamic compromise in occlusive cerebrovascular disease. Stroke 1992; 23: 1733–42 Leys D, Moulin TH, Stoijkovic T, DONALD Investigators. Follow up of patients with history of cervical artery dissection. Cerebrovasc Dis 1995; 5: 43–9 Bassetti C, Carruzzo A, Sturzenegger M, Tuncdogan E. Recurrence of cervical artery dissection. A prospective study of 81 patients. Stroke 1996; 27: 1804–7 Schievink WI, Mokri B, Whisnant JP. Internal carotid artery dissection in a community: Rochester, Minesota, 1987–1992. Stroke 1993; 24: 1678–80 Fisher CM, Ojemann RG, Roberson GH. Spontaneous dissection of cervico-cerebral arteries. Can J Neurol Sci 1978; 5: 9–19 Boström K, Liliequist B. Primary dissecting aneurysm of the extracranial part of the internal carotid and vertebral arteries: a case report of three cases. Neurology 1967; 17: 179–86 Barnett HJM, Taylor DW, Elisiw M et al. Benefit of carotid endarterectomy in patients with symptomatic moderate or severe stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med 1998; 339: 1415–25
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Neuroradiological anatomy MH Wholey and WS Wu
Introduction The field of neuroanatomy is a prerequisite for all interventionalists who perform carotid artery stent placement. It is important not only to know the arterial anatomy but also have an understanding of the functional anatomy. Such a knowledge process is important in evaluating patients and working their disease in an efficient manner as well as to know which equipment and devices to utilize in intervening. Anatomical understanding and its variants are also important in the execution of the stent process and management of any unforeseen neurocomplications that should develop.
Neuroradiological arterial anatomy Aortic arch anatomy The standard angiographic technique for the aortic arch includes a 5–6-French pigtail catheter placed in the ascending aorta with an injection rate of 20–25 cm3/second for a total of 30–40 cm3 contrast depending upon the equipment. Digital subtraction angiography is useful for better detail, as it becomes essential when looking at neurovasculature. We will start with a left anterior oblique (LAO) projection of 25–35° to open the arch (refer to Figure 26.1).
rt vert
Variations of aortic arch anatomy More than 65% of most patients have classical aortic arch anatomy in which the left subclavian, left common carotid, and innominate or brachiocephalic arteries originate from the aortic arch.1 Common variations (27%) include the bovine arch anatomy with the take-off of the left common carotid artery from the shared innominate artery (refer to Figure 26.2).1 Another common variation (3%) is the take-off of the left vertebral artery from the aortic arch (refer to Figure 26.3).1 Less common is the anomalous take-off of the right subclavian off the aortic arch which then courses posterior to the esophagus and anterior to the spine (refer to Figure 26.4). Common carotid artery The right common carotid normally arises off the innominate artery and the left common arises off the aortic arch. The common carotid bifurcates at the bulb into the external and internal carotid arteries. The external branches off into the superior thyroid, lingual, and facial arteries. The ascending
It common carotid
rt common carotid lt vert
subclavian subclavian
It common carotid innominate
rt internal mammory
desending arch
ascending arch
Figure 26.1 The classic aortic arch is shown with the take-off of the innominant (also known as the brachiocepahlic), left common carotid, and left subclavian arteries.
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Figure 26.2 Common variation of aortic arch anatomy is the bovine arch with the take-off of the left common carotid artery from the shared innominate artery.
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Neuroradiological anatomy Sup. temporal
193
Ascend pharyngeal Post auricular
Internal maxillary
Occipital Facial
Internal carotid Lingual External carotid
Figure 26.3 CTA 64-slice scan showing an anatomical variation with the take-off of the left vertebral artery off the aortic arch.
pharyngeal arises normally near the bifurcation. Usually, hand injection of 6–8 cm3 in a lateral or steep oblique view will open the bifurcation (refer to Figure 26.5) The internal carotid artery is divided into the following segments: C1 (cervical), C2 (petrous), C3 (lacerum), C4 (cavernous), C5 (clinoid), C6 (ophthalmic), and C7 (communicating segment) (refer to Figures 26.6 and 26.7).2 Anterior cerebral circulation As the internal carotid exits into the supraclinoid it forms the circle of Willis. The internal carotid provides flow to the middle cerebral artery (MCA) along with the anterior cerebral
Carotid bulb Common carotid
Superficial thyroid
Figure 26.5 Common carotid injection showing the internal carotid and external carotid arteries with the various branches off the external carotid.
artery (ACA) (refer to Figures 26.8–26.10). The left and right ACA are communicated with the anterior communicating artery (ACOM). The left and right vertebral arteries form the basilar artery which then provides flow to the left and right posterior cerebral arteries (PCA). The PCA is then connected to the internal carotid artery with the posterior communicating artery (PCOM).
C6 C5
C7 C4 3
C1:Cervical C2: Petrous C3: Lacerum
C3
C4: Cavernous C5: Clinoid
C2 2 1 C1
C6: Opthalmic C7: Communicating Segment
Figure 26.4 Anatomical variation with the take-off of the anomalous right subclavian artery off the aorta.
Figure 26.6 Lateral projection of the distal internal carotid artery showing the following segments: C1: cervical; C2: petrous; C3: lacerum; C4: cavernous; C5: clinoid; C6: ophthalmic; and C7: communicating segment.
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MCA
Post communicating art (PCOM)
Ant communicating art (ACOM) R
Figure 26.7 Oblique view from a 64-slice CTA shows the distal internal carotid as it enters the carotid canal, exiting the petrous segment and entering the cavernous sinus. This is a frequent site of atherosclerotic disease.
The anterior view of the cerebrum shows the major branches of the internal carotid artery. These include the anterior cerebral artery (ACA) and the middle cerebral artery (MCA) (refer to Figures 26.8–26.10). Circle of Willis The circle of Willis is the communication of the anterior and posterior cerebral arterial circulations (refer to Figures 26.8–26.11). It is composed of the two distal internal carotid arteries (ICA) which, upon exiting the cavernous sinus, form the anterior cerebral and middle cerebral arteries. The anterior cerebral artery is composed of two segments called A1 and A2. The A1 or proximal segment frequently joins together by an anterior communicating artery (ACOM) before the A2 segment of the ACA continues on its course. The basilar artery formed by the two vertebral arteries arises and forms the two posterior cerebral arteries (PCA). The PCAs are connected with the junction of the distal ICA and MCA by a posterior communicating artery (PCOM).
ACA A2
ACOM
ACA A1 MCA
Post cerebral art. (PCA)3
cm
Figure 26.9 CTA 64-slice multiplanar reconstruction axial image showing the complete circle of Willis.
There are numerous variations in the circle of Willis, the most common being an absence of one or several of the communicating branches (ACOM, PCOM). Another common variation is the formation of a primitive posterior cerebral artery off the distal internal carotid artery (refer to Figures 26.11 and 26.13). This can best be seen on the AP projections. Branches of the cerebral ICA and the related effects of stroke The anterior cerebral artery (ACA) extends upward and forward from the internal carotid artery. The ACA supplies most of the medial surface of the cerebral cortex (anterior threefourths), frontal pole (via cortical branches), and anterior portions of the corpus callosum. Perforating branches (including the recurrent artery of Heubner and medial lenticulostriate arteries) supply the anterior limb of the internal capsule, the inferior portions of the head of the caudate, and anterior globus pallidus (refer to Figures 26.11 and 26.12) Since the ACA supplies the frontal lobes, the parts of the brain that control logical thought, personality, and voluntary movement (especially the legs), strokes in the ACA results in opposite leg weakness.3,4 If both anterior cerebral territories are affected, profound mental symptoms may result (akinetic mutism).3,4 The MCA branches include the following arteries: the anterior temporal, operculofrontal or “candelabra,” precentral,
PCOM PCA
M3 ACA A2
Basilar
ACA A1
M2
Rt MCA M1 Segment Right ICA
Figure 26.8 CTA 64-slice three-dimensional reconstruction showing the complete circle of Willis. Note the small aneurysm at the tip of the basilar artery.
Lt MCA M1 Left ICA
Figure 26.10 CTA 64-slice multiplanar reconstruction coronal image shows the anterior cerebral arterial anatomy.
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Neuroradiological anatomy ACA branches:
Cortical branches
MCA branches Precentral Central sulcus
Collosalamarginal Pericollosal
Pericollosal Lateral lenticulostriates
M3 MCA
Posterior cerebral A2 ACA
(Rolandic group)
Ant parietal
Collosalmarginal
M4 MCA
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Post. pariental
A2 ACA
Frontopolar Orbitofrontal Opthalmic
2 1
Angular art & branches Post temporal
A1 ACA
M2 MCA Genu MCA
Primitive PCA
1.Anterior temporal artery 2. Operculofrontal artery
M1 MCA
Figure 26.11 AP projection of the cerebral circulation revealing the anterior cerebral and middle cerebral arteries and their major branches. Lateral lenticulostriate arteries arise from the M1 segment of the MCA. These arteries supply the basal ganglia and other deep structures in the brain.
central sulcus (Rolandic group), anterior parietal, posterior parietal, angular artery and branches, and the posterior temporal arteries (refer to Figure 26.13).2 The MCA is the largest branch of the internal carotid. The artery supplies a portion of the frontal lobe and the lateral surface of the temporal and parietal lobes, including the primary motor and sensory areas of the face, throat, hand, and arm, and in the dominant hemisphere, the areas for speech.3,4 The MCA is the artery most often occluded in stroke. It is important to run the x-rays long enough to obtain good capillary and venous images to assess
Figure 26.13
Major branches of the ACA, PCA, and MCA.
for any areas of mass effect, delayed emptying, or stagnant vessels indicative of possible embolic events.3,4 (Please refer to Figures 26.14 and 26.15 for review of cerebral veins.) The MCA is divided into four segments (refer to Figures 26.10–26.12). The first is the horizontal segment of M1. Arising off the M1 segment are the lateral lenticulostriate branches which provide flow to basal ganglia structures: part of head and body of caudate, globus pallidus, putamen, and the posterior limb of the internal capsule.2 Damage to the internal capsule can result in contralateral hemiparesis and
Apex of Sylvian fissure
M4 MCA
M4
A2 ACA M3 MCA M2 MCA MCA Genu
Recurrent art of huebner Medial lenticulostriates
A1 ACA
Figure 26.12 Slight oblique view of the ACA and its branches. In order to open up the ACA, it is useful to align the image intensifier with a vector through the orbit.
Figure 26.14 Venous phase of the carotid artery injection in AP projection.
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superior sagittal sinus -posterior -anterior
transverse sinus
sigmoid sinus
internal jugular
Figure 26.15 Venous phase of the carotid artery injection in lateral projection.
sensory deficit. Speech may be affected (medial temporal lobe) as well as visual function (where Meyer’s loop optic radiations are affected).3,4 The Sylvian or M2 segment divides into superior and inferior divisions which can be a site for an embolus to lodge. Branches supply temporal lobe and insular cortex (sensory language area of Wernicke), parietal lobe (sensory cortical areas) and inferolateral frontal lobe.3,4 Superior division infarction
Intradural V4 Extraspinal V3
Foraminal V2 segment Extraosseous V1 segment
results in “brachiofacial paralysis” where sensorimotor deficit involving the face and arm, and the leg to a lesser extent, occurs.3,4 The foot is spared; there is ipsilateral deviation of the head and eyes; and no impairment of alertness is noted. If the inferior division is infracted, then patients may develop superior quadrantanopia/homonymous hemianopia, Wernicke aphasia (deficit in comprehension of spoken/written language), or left-sided visual neglect if on the left or right side, respectively.3,4 M3 and M4 segments provide distal branches of the MCA which course laterally to the insular cortex, loop around the operculum, and run along the cortex of the brain. On the lateral angiogram, they form a “Candelabra” effect. Embolization of individual cortical branches can produce highly circumscribed infarctions accompanied by specific neurologic deficits.3,4 Posterior cerebral circulation The posterior cerebral circulation is composed of the vertebrobasilar circulation with contribution of the circle of Willis from the posterior communicating arteries (PCOM) if they are present. The vertebral arteries arise off the bilateral subclavian arteries and are divided into four segments (refer to Figure 26.16). The vertebral artery takes off from the subclavian artery to the transverse foramina of the cervical vertebral body C5 or C6 (segment I). Segment II runs entirely within the transverse foramina of C5/6 to C2. Segment III is a tortuous interval beginning at the transverse C2 level and courses posteriorly to loop around the posterior arch of C1 and passes between the atlas and the occiput. The final segment IV is the intracranial segment which pierces the dura at the foramen magnum and continues until the junction of the pons and medulla where it merges with the other vertebral artery to form the basilar trunk. Important branches off the vertebral artery include the posterior inferior cerebellar artery (PICA) which provides flow to the inferior border of the cerebellum and brainstem. The vertebrals form the basilar artery which then has crucial brainstem branches followed by bilateral anterior inferior cerebellar arteries (AICA), the superior cerebellar arteries, and the posterior cerebral arteries (PCA) (refer to Figures 26.17–26.19).
Superior vermian arteries Post cerebral (PCA) Superior cerebellar Ant. inf. cerebellar (AICA) Basilar artery Post. inf. cerebellar (PICA) Vertebral artery
Figure 26.16 Bilateral vertebral arteries from an aortic arch injection and the major branches.
Figure 26.17 arteries.
Lateral projection of the vertebral and basilar
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Superior vermian arteries
Lt. post cerebral (PCA) Rt. sup. cerebellar Rt. ant. inf. cerebellar (AICA) Basilar artery Lt. post. inf. cerebellar (PICA) Lt. verterbal
Figure 26.18
AP projection of the posterior circulation.
Variations in posterior cerebral anatomy There are numerous variations in the posterior cerebral circulation. One vertebral artery is usually more dominant (larger caliber) than the other. Likewise, many of the branches off the basilar artery (PICA, AICA, and posterior cerebellar) can be incomplete (refer to Figure 26.20).
Figure 26.20 64-slice multislice CT multiplanar oblique image of the vertebrobasilar circulation with severe disease of the distal vertebral arteries bilaterally and variation in the PICA anatomy.
Also, we are looking at carotid lesions in conjunction with ultrasound velocity measurements. Stenoses must be looked at in several projections including lateral and oblique images but axially as well. With CT, one has the ability to look at 360°, which can result in a different perspective of a lesion (refer to Figure 26.22). Also, the length and size of stenoses
Role of CT and CTA The advent of multislice CT scanning, particularly the 64-slice equipment, is quickly altering the diagnosis and management of atherosclerotic occlusive disease of the carotid and vertebrobasilar circulation. CTA scans offer advantages of ease of use, relatively low risk, and speed of this new image modality. Drawbacks include radiation exposure, contrast doses, and difficulty in providing exact NASET-criteria degree of stenosis (refer to Figure 26.21). The basic diagnostic criteria of carotid bifurcation disease are changing. We are able to characterize plaque formations as calcified, soft tissue plaque, and fibrous (refer to Figure 26.21).
Post. cerebral artery Basilar artery Posterior inferior cerebellar artery (PICA)
Ant inferior cerebellar artery (AICA)
Severe stenosis
Moderate stenosis
Left vertebral artery
Figure 26.19 64-slice multislice CT multiplanar oblique image of the vertebrobasilar circulation.
Figure 26.21 64-slice multislice CT multiplanar oblique image of the carotid bifurcation revealing the plaque. Heavily calcified lesions make it difficult to assess the exact degree of stenosis.
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Soft tissue plaque
Conclusion For any interventionalist who embarks on carotid angiography, angioplasty, or stenting, it is essential to understand the fundamentals in neuroradiology. This brief chapter provided a glimpse of the anatomy involved. It is equally important to become proficient in understanding CT scans and MRI/MRA.
Calcium
Figure 26.22 The importance of rotating a mixed calcified and soft tissue plaque of the cervical carotid. It can vary from moderate to severe depending upon the angle. The most accurate is to look axially or “down the barrel” of the lesion which would provide an area stenosis; however, we do not know how to interpret this area stenosis yet.
REFERENCES 1. 2.
Haughton VM, Rosenbaum AE. The normal and anomalous aortic arch and brachiocephalic arteries. In Newton TH, Potts RG, eds. Radiology and the Skull and Brain, Vol 2. St Louis: Mosby, 1974: 1202–43 Osborne AG, Jacobs JM. Diagnostic Cerebral Angiography, second edition. New York: Lippincott-Rave, 1998: 98–150
3. 4.
Neafsey EJ, Castro A. Medical Neuroscience Lab Manual. <www.meddean.luc.edu/lumen/meded/Neuro/index.htm> Castro AJ, Neafsey EJ, Wurster RD, Merchut MP. Neuroscience: An Outline Approach. Elsevier, 2006: 30–100
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Doppler ultrasound and carotid angioplasty: carotid ultrasonography and transcranial Doppler S Kownator and F Luizy
Introduction Ultrasound imaging is recognized as an accurate method for the diagnosis and quantification of carotid artery stenosis.1–4 Duplex scan and color flow Doppler methods provide information concerning not only the degree of stenosis, but also the features and structure of the plaque.5–7 Subsequent studies comparing conventional angiography with Duplex scanning in the evaluation of carotid plaque morphology have confirmed the superiority of echography in this area.8,9 Therefore, ultrasonography may potentially be used in the evaluation of carotid stenosis, the analysis of the plaque structure before carotid stenting, and during follow-up. Transcranial Doppler provides useful data on cerebral hemodynamics and can detect high-intensity transient signals (HITS) as a marker of cerebral embolization. These data are particularly important before and during angioplasty and stenting.
Quantification of carotid stenosis Degree of stenosis Duplex quantification Hemodynamic assessment usually relies on the maximal peak systolic velocity (PSV) and the end-diastolic velocity (EDV) for the assessment of the degree of stenosis.10–15 These data are in accordance with the angiographic criteria as described in the North American Symptomatic Carotid Endarterectomy Trial (NASCET)16 (Figure 27.1). ●
●
●
For 70–99% carotid stenosis, a PSV of 240 cm/second and an EDV greater than 100 cm/second provide a sensitivity of 91%, specificity of 98%, positive predictive value of 90%, negative predictive value of 96%, and an overall accuracy of 95%. For 50–69% carotid stenosis, a PSV of more than 130 cm/second and an EDV of 100 cm/second provide the best combination, with a sensitivity of 92%, specificity of 97%, positive predictive value of 93%, negative predictive value of 99%, and an overall accuracy of 97%. For 30–49% carotid stenosis, criteria are less well defined, but a PSV of around 100 cm/second may be applicable.
Peak systolic velocity ratio The ratio of the PSV in the internal carotid artery (ICA) at the level of stenosis to the PSV in the ipsilateral common carotid artery (CCA) can accurately identify patients with high-grade carotid stenosis.17 An ICA/CCA systolic velocity ratio of 4 accurately predicts a greater than 70–99% ICA stenosis, with a sensitivity of 91%, specificity of 90%, predictive positive value of 87%, negative predictive value of 94%, and an overall accuracy of 91%. These methods can be used in the accurate selection of patients for endarterectomy or angioplasty. Anatomical quantification Although color flow duplex scanning is widely recognized for non-invasive assessment, there are generally no accepted criteria to quantify stenosis with color flow Doppler alone. However, the recent development of power Doppler allows a fine delineation to be made between the surface of the lesion and the lumen, so that the diameter or area of the stenosis can be measured (Figure 27.2).18 Diameter reduction The diameter is measured on a long-axis power Doppler view at the level of the stenosis and compared with the diameter of the normal distal ICA (NASCET method) or the diameter of
Figure 27.1 Tight internal carotid stenosis: pulse Doppler. (See Color plates.)
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Figure 27.2 Tight internal carotid stenosis: color Doppler. (See Color plates.)
the bulb (European Carotid Surgery Trial (ECST) method). Power Doppler is an improvement on color Doppler (Figure 27.3).19 Area reduction On the transverse power color flow view, the area of the residual lumen at the tight level of the stenosis is measured and compared with the surface of the distal carotid (NASCET) or the surface of the bulb (ECST). These measurements require accurate adjustment of the presets in power Doppler or color Doppler (Figure 27.4). Morphological approach Many publications have emphasized the relationship between plaque morphology and cerebral events: plaque structure appears to be an important factor in the onset of embolic events.19 The characterization of the structure of the plaques has been made possible with the development of high-resolution B-mode ultrasound. New modalities such as sonoCT provide a high-quality B-mode image which enables accurate analysis of the plaque structure.
Figure 27.4 Internal carotid stenosis: power Doppler and short axis: area reduction = 95%. (See Color plates.)
Ultrasound B-mode imaging This technique may be used to show the make-up of carotid plaque. Fibrous or calcified material is more echogenic than material such as lipid or intraplaque hemorrhage, which is more echolucent. Lipid-laden or hemorrhagic plaques have the potential to ulcerate and to embolize. Plaque fracture over the site of a hemorrhage may lead to luminal thrombus formation. Role of plaque morphology as an independent risk of cerebral events Various classifications have been proposed to characterize carotid plaques using ultrasonography, 20 for example homogeneous and heterogeneous plaques, or soft, dense, and calcified plaques. The classification of Geroulakos et al.21 seems to be the most suitable to classify the echogenic structure. This classification differentiates five types: ●
●
●
● ●
type I: uniformly echolucent plaques with or without a thin echogenic cap; type II: predominantly echolucent plaques with < 50% echogenic areas; type III: predominantly echogenic plaques with < 50% echolucent areas; type IV: uniformly echogenic plaques; type V: plaques that cannot be classified owing to heavy calcifications producing acoustic shadows.
Color flow Doppler or power Doppler is mandatory to quantify types I, II and III.
Figure 27.3 Internal carotid stenosis: power Doppler and long axis: diameter reduction = 60% according to the NASCET methodology. (See Color plates.)
Ulcerated plaque (Figure 27.5) Ultrasonographic assessment of an ulcerated plaque depends on the presence of:22,23
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of the circle of Willis to be evaluated. The following four situations may be discovered. ●
●
Figure 27.5 Internal carotid artery: ulcerated atheromatous plaque. (See Color plates.)
●
●
an eccentric defect of the surface of the plaque larger and deeper than 2 mm; a flow inside the ulceration in color Doppler mode.
Standardization of carotid plaque characterization Greyscale adjustment is a limiting factor in plaque characterization. Several methods have been introduced to avoid this problem and to improve the reproducibility of plaque evaluation by ultrasound. The easiest method differentiates among three types of plaque: echolucent (echogenicity of the blood in the vessel lumen), echogenic (echogenicity of the sternomastoid muscle), and hyperechogenic (echogenicity of the vertebra). Nicolaïdes’ group has published an elegant computerassisted method,24 which enables objective measurement of the echogenicity by estimating the greyscale median density value of the plaque. This median density value is evaluated after resampling the greyscale of the image using software. Lower values of grey median density are found in echolucent plaques and higher values in more echogenic lesions. Plaques with a median density value lower than 32 are associated with a higher rate of cerebral infarction as detected on computed tomographic (CT) scans.25 To summarize the relationship between plaque morphology and neurological events, echolucent plaques with an ulcerated surface are associated with a higher risk of embolism and therefore with an increased rate of clinical events.26,27 Transcranial Doppler The incidence of the stenosis depends not only on the degree of stenosis, but also on the capacity of supply by the circle of Willis. Transcranial Doppler28–30 provides a direct approach to the investigation of the hemodynamic repercussions of cervical stenosis.31,32 During recording of the middle cerebral artery (MCA), a short compression of the CCA (two or three cardiac cycles) is performed to stop the flow to the ICA. This compression must be done upstream of the stenosis. The variation in flow at the level of the MCA during the compression allows the patency
●
●
The MCA flow is not spontaneously altered, and compression of the CCA induces a moderate reduction in the flow with a mean velocity of 30 cm/second. The ICA stenosis has good hemodynamic compensation. The MCA flow is not spontaneously altered, and compression of the CCA does not change the MCA flow. There is a very high-grade stenosis of the cervical carotid, and a large anterior communicating artery to supply. There may also be a hypoplasia or an occlusion of the intracranial carotid artery, the ophthalmic artery downstream and the anterior cerebral artery upstream. The MCA flow is spontaneously altered, and there is an important reduction in the flow during the compression of the CCA, with a residual flow of 20 cm/second. The ICA stenosis is hemodynamically significant and there is no supply from the circle of Willis. The MCA flow is very reduced at baseline, and compression of the CCA stops the flow of the MCA. The ICA stenosis is hemodynamically significant and supply from the circle of Willis is inefficient.
Ultrasound and carotid stenting Duplex and color flow or power Doppler allows patients to be selected for either surgery or angioplasty. Previously, there were no specific ultrasound criteria for choosing angioplasty rather than surgery. However, evaluation by ultrasound can be helpful at the different stages of carotid stenting.
Before the procedure (Figures 27.6 and 27.7) Duplex provides an accurate evaluation of degree of stenosis. This technique also specifies the precise site of stenosis between the CCA, ICA, and external carotid artery (ECA) with precision regarding the association of multilevel stenosis. This information is particularly important in accurately choosing the correct stent. This choice also depends on the size of the vessel. At this stage, echography and better color or power Doppler enable several diameters to be measured accurately: ●
●
ICA: position and diameter of the residual lumen, and diameters of the bulb and distal carotid to choose the size of the balloon; diameter of the CCA, 2 cm before the bifurcation, to choose the size of the stent.33
Regarding the structure of the plaque, Okhi et al.34 showed, ex vivo, that hypoechogenicity of the plaque, as well as the degree of stenosis, is an independent risk factor for embolism during carotid angioplasty. The importance of embolism during carotid angioplasty and its relationship with plaque structure was studied in vivo in 20 patients undergoing carotid stenting.35,36 An ultrasound scan was performed before the procedure and the structure of
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Figure 27.7 Internal carotid stenosis: long axis, power Doppler. (See Color plates.)
Figure 27.6
Internal carotid stenosis: long axis, B mode.
the plaque was then analyzed. A histogram of brightness was produced using the HDI lab workstation, a research device developed by Philips Ultrasound (Bothell, WA). Angioplasty was performed with cerebral protection using the PercuSurge system. Debris was aspirated before deflation of the protection balloon. Filtration was performed on site. The debris was fixed with glutaraldehyde (2.5%) and observed first on an optical bench and then in an electron microscope. The amount of debris and the different types of particle were analyzed (Figures 27.8 and 27.9). A relationship was
160 140 120
ρ = −0.72
observed between plaque structure and the amount of debris. The more echogenic plaques and particularly those with calcification produced less debris but with a larger mean particle size. The more echolucent plaques produced more particles but of a smaller mean size. No relationship was seen between the degree of stenosis and amount of debris. Owing to characterization of the plaque using brightness of the plaque, ultrasound can be considered a good method for predicting the importance of embolism during carotid angioplasty. No plaques were found that were safe from embolism, which argues in favor of cerebral protection. Transcranial Doppler can detect intracranial stenosis either of the ICA or, more accurately, of the MCA. It may also provide information on the patency of the circle of Willis. This information could be particularly helpful if cerebral protection is considered to avoid cerebral events (Figure 27.10).
Median Number Log (number) Log (median)
100 80 60 40 20 0 −20
Figure 27.8 Relationship between median density value and number of particles. Hypoechoic plaques are related to a high number of particles.
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450 400 300
Median Mean size (µm) Log (mean size (µm)) Log (median)
250 200 150 100 50
ρ = −0.74
0 −50
Figure 27.9 Relationship between median density value and mean size of the debris. The size of the particles increases with median value: hypoechoic plaques produce larger particles of debris.
During the procedure Transcranial Doppler monitoring can account for HITS, according to the plaque components (Figure 27.11).37 Markus et al.38 showed that during angioplasty multiple embolic signals are detected immediately after balloon inflation, with a low rate of neurological events (one in nine had a minor stroke). Embolic signals were common immediately after the procedure but thereafter became less frequent. They concluded that embolization at the time of carotid angioplasty is very common, but usually asymptomatic monitoring by Doppler ultrasound allows the effectiveness of measures to reduce this embolization to be studied.
Al-Mubarak et al.,39 using transcranial Doppler, compared the frequency of HITS during carotid stenting in two groups: 39 patients without distal protection and 37 who used a distal balloon protection system (GuardWire). Three phases with increased HITS counts were identified during unprotected stenting: stent deployment, predilation and post-dilation. The distal balloon protection significantly reduced the frequency of HITS during the procedure, particularly during these three phases. HITS in the protection group were detected predominantly during sheath placement, guidewire manipulation, and distal balloon deflation. They concluded that distal balloon protection is effective in avoiding cerebral embolism.
After the procedure (Figures 27.12 and 27.13) Ultrasound provides an immediate, non-invasive picture after the procedure. PSV is recorded at different levels: CCA,
Figure 27.10 plates.)
TCD: Patency of circle of Willis. (See Color Figure 27.11
TCD: Detection of HITS. (See Color plates.)
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Textbook of peripheral vascular interventions ultrasound can also be used to assess the permeability of the ECA through the network of the stent, if the stent covers the bifurcation. This follow-up is necessary for the detection of complications such as intrastent restenosis, which may occur as a consequence of intrastent proliferation or stent collapse with loss of the cylindrical pattern, either involving all of the stent or in a localized region. Immediate data are important in the follow-up and in the evaluation of the long-term outcome.
Follow-up
Figure 27.12 plates.)
Post-angioplasty ultrasound imaging. (See Color
The intermediate and long-term evaluation of the carotid angioplasty and stenting requires hemodynamic and morphological follow-up. Ultrasound is particularly suited to this application.40 The evaluation of the PSV and the stent diameters are compared with measurements taken immediately after the procedure. ●
proximal, medial, and distal parts of the stent. The flow is also recorded above the stent in the ICA. The diameters at the same levels are measured. The technique allows modification of the artery shape induced by stenting and its hemodynamic consequences (i.e. an increasing flow velocity at the distal edge of the stent). Ultrasound allows the permeability of the ECA to be assessed through the network of the stent if the ostium is covered. These immediate data are important in the follow-up to the procedure and the evaluation of long-term results. Intrastent flow velocity differs with the type of stent used. PSV is generally higher in balloon-expandable stents (Palmaz Stent) than in self-expandable stents (Wallstent). The effect of these differences will be assessed through long-term follow-up. The long-term evaluation of carotid angioplasty requires both hemodynamic and morphological follow-up. Color duplex
Figure 27.13
Post-angioplasty ultrasound imaging.
●
●
●
Stent removal: the stent may become detached from the vessel wall, and a progressive thrombosis of the gap between the stent and the arterial wall has been observed. Restenosis: a PSV of 150 cm/second and/or a PSV ratio greater than 3 are highly predictive of restenosis (60%). Color or power Doppler imaging can be used to evaluate the variation in the diameter of the stenosed channel (Figures 27.14–27.16). Stent deformation: stent collapse is defined as a loss of apposition of part or all of the whole stent to the vessel wall, with alteration of the previous cylindrical configuration and reduction in the lumen diameter. Occlusion: even if stent occlusion is not a current complication, ultrasound can be very sensitive in its detection. Robbin et al. reported two cases in which occlusion was detected with ultrasound among 170 procedures.40 Griewing et al. reported one asymptomatic case among 20 stenting procedures in high-risk patients.41
Figure 27.14
Post-angioplasty ultrasound imaging.
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Figure 27.15 Post-angioplasty ultrasound imaging: in-stent restenosis. (See Color plates.) Figure 27.16 Post-angioplasty ultrasound imaging: in-stent restenosis. (See Color plates.)
Conclusion The most important advantage of carotid stenting compared with carotid endarterectomy is probably the increased comfort to the patient. Many studies have shown the results of both techniques to be similar with regard to their safety.
Ultrasound appears to be an excellent method at each stage of carotid stenting. Further studies are needed to refine ultrasound criteria in order to select patients for angioplasty rather than for surgery, and to refine the specific criteria for restenosis.
REFERENCES 1. 2. 3. 4.
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Spencer M, Reid J, Paulson P. Cervical carotid imaging with a continuous wave Doppler flow meter. Stroke 1974; 5: 145 Polak JF, Dobkin GR, O’Leary DH et al. Internal carotid artery stenosis: accuracy and reproducibility of color-Doppler-assisted duplex imaging. Radiology 1989; 173: 793–8 Strandness DE Jr. Extracranial arterial disease. In: Standness DE Jr, ed. Duplex Scanning in Vascular Disorders. New York: Raven Press, 1993: 113–57 Howard G, Baker WH, Chambless LE et al. An approach for the use of Doppler ultrasound as a screening tool for hemodynamically significant stenosis (despite heterogeneity of Doppler performance). A multicenter experience. Asymptomatic Carotid Atherosclerosis Study Investigators. Stroke 1996; 27: 1951–7 Reilly LM, Lubsky RJ, Hughes L et al. Carotid plaque histology using real time ultrasonography. Am J Surg 1983; 146: 188–93 Johnson JM, Kennelly MM, Decesare D et al. Natural history of asymptomatic carotid plaques. Arch Surg 1985; 120: 1010–12 Bluth E, Kay D, Merritt C et al. Sonographic characterisation of carotid plaque: detection of haemorrhage. AJR Am J Roentgenol 1986; 146: 1061–5 Rubin JR, Bondi JA, Rhodes RS. Duplex scanning versus conventional arteriography for the evaluation of carotid artery plaque morphology. Surgery 1987; 102: 749–55 Srinivasan J, Mayberg MR, Weiss DG, Eskridge J. Duplex accuracy compared with angiography in the Veterans Affairs Cooperative Studies Trial for Symptomatic Carotid Stenosis. Neurosurgery 1995; 36: 648–53; Discussion 653–5 De Bray JM, Glatt B. Quantification of atheromatous stenosis in the extra cranial carotid artery. Cerebrovasc Dis 1995; 5: 414–26 Alexandrov AV, Brodie DS, McLean A et al. Correlation of peak systolic velocity and angiographic measurement of carotid stenosis revisited. Stroke 1997; 28: 339–42 Soulez G, Therasse E, Robillard P et al. The value of internal carotid systolic velocity ratio for assessing carotid artery stenosis with Doppler sonography. AJR Am J Roentgenol 1999; 172: 207–12 Moneta GL, Edwards JM, Papanicolaou G et al. Screening for asymptomatic internal carotid artery stenosis: duplex criteria for discriminating 60% to 99% stenosis. J Vasc Surg 1995; 21: 989–94
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Carpenter JP, Lexa FJ, Davis JT. Determination of duplex Doppler ultrasound criteria appropriate to the North American Symptomatic Carotid Endarterectomy Trial. Stroke 1996; 27: 695–9 Winkelaar GB, Chen JC, Salvian AJ et al. New duplex ultrasound scan criteria for managing symptomatic 50% or greater carotid stenosis. J Vasc Surg 1999; 29: 986–94 North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high grade carotid stenosis. N Engl J Med 1991; 325: 445–53 Geroulakos G, Domjan J, Nicolaïdes A et al. Ultrasonic carotid artery plaque structure and the risk of cerebral infarction on computed tomography. J Vasc Surg 1994; 20: 263–6 Griewing B, Morgenstern C, Driesner F, Kessler C. Cerebrovascular disease assessed by color flow and power Doppler: comparison with digital substraction angiography in internal carotid artery stenosis. Stroke 1996; 27: 95–100 Steinke W, Ries S, Artemis N et al. Power Doppler imaging of carotid artery stenosis. Comparison with color Doppler flow imaging and angiography. Stroke 1997; 28: 1981–7 Gray-Weale AC, Graham JC, Burnett JR et al. Carotid artery atheroma: comparison of preoperative B-mode ultrasound appearance with carotid endarterectomy specimen pathology. J Cardiovasc Surg 1988; 29: 676–81 Geroulakos G, Ramaswami G, Nicolaïdes A. Characterization of symptomatic and asymptomatic carotid plaques using high resolution real time ultrasonography. Br J Surg 1993; 80: 1274–7 Hobson RW, Weiss DG, Fields WS et al. for the Veterans Affairs Cooperatives Study Group. Efficacy of carotid endarterectomy for asymptomatic carotid stenosis. N Engl J Med 1993; 328: 221–7 Johnson JM, Ansel AL, Morgan S, Decesare D. Ultrasonic screening for evaluation and follow up of carotid ulceration. Am J Surg 1982; 144: 614–17 El-Barghouty N, Geroulakos G, Nicolaïdes A et al. Computerassisted carotid plaque characterisation. Eur J Vasc Endovasc Surg 1995; 9: 389–93
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Textbook of peripheral vascular interventions El-Barghouty, Levine N, Flanagan A, Nicolaïdes A. Histological verification of computerised carotid plaque characterisation. Eur J Vasc Endovasc Surg 1996; 11: 414–16 deBray JM, Baud JM, Dauzat M. Consensus concerning the morphology and the risk of carotid plaques. Cerebrovasc Dis 1997; 7: 289–96 Polak JF, Shemanski L, O’Leary DH et al. Hypoechoic plaque at ultrasound of the carotid artery: an independent risk factor in adults aged 65 years or older. Radiology 1998; 208: 649–54 Aaslid R. Transcranial Doppler Sonography. New York: Springer, 1986 Babikian V, Sloan MA, Tegeler CH et al. Transcranial Doppler validation pilot study. J Neuroimaging 1993; 3: 242–9 Hennerici M, Rautenberg W, Sitzer G, Schwartz A. Transcranial Doppler ultrasound for the assessment of intracranial arterial flow velocity. Evaluation of intracranial arterial disease. Surg Neurol 1987; 27: 523–32 Kelley RE, Namon RA, Mantelle LL, Chang JY. Sensitivity and specificity of transcranial Doppler ultrasonography in the detection of high-grade carotid stenosis. Neurology 1993; 43: 1187–91 Schweizer J, Kaulen R, Altmann E: Applications of transcranial Doppler ultrasound and color-coded intracranial duplex ultrasound in patients with stenoses of the extracranial brain arteries. Vasa 1994; 23: 214–16 Henry M, Amor M, Henry I et al. Endovascular treatment of atherosclerotic stenosis of the internal carotid. J Am Coll Cardiol 1997; 29: 221A
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Ohki T, Marin ML, Lyon RT et al. Ex vivo human carotid artery bifurcation stenting: correlation of lesion characteristics with embolic potential. J Vasc Surg 1998; 27: 463–71 Henry M, Amor M, Henry I et al. Carotid stenting with cerebral protection: first clinical experience using the PercuSurge GuardWire system. J Endovasc Surg 1999; 6: 321–31 Henry M, Henry I, Klonaris C et al. Benefits of cerebral protection during carotid stenting with the PercuSurge GuardWire system: midterm results. J Endovasc Ther 2002; 9: 1–13 Benichou H, Bergeron P. Carotid angioplasty and stenting: will periprocedural transcranial Doppler monitoring be important? J Endovasc Surg 1996; 3: 217–23 Markus HS, Clifton A, Buckenham T, Brown MM. Carotid angioplasty. Detection of embolic signals during and after the procedure. Stroke 1994; 25: 2403–6 Al-Mubarak N, Roubin GS, Vitek JJ et al. Effect of the distal balloon protection system on microembolization during carotid stenting. Circulation 2001; 104: 1999–2002 Robbin ML, Lockhart ME, Weber TM et al. Carotid artery stents: early and intermediate follow-up with Doppler US. Radiology 1997; 205: 749–56 Griewing B, Brassel F, von Smekal U et al. Carotid artery stenting in patients at surgical high risk: clinical and ultrasound findings. Cerebrovasc Dis 2000; 10: 44–8
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The value of transcranial Doppler ultrasonography before, during, and after surgery for carotid occlusive disease NM Bornstein and AY Gur
Introduction The first carotid reconstruction for internal carotid artery (ICA) stenosis was reported in 1954 by Eastcott.1 Since then, carotid endarterectomy (CEA) has become widely accepted and is one of the most frequently performed procedures in many vascular surgical departments.2 The results of recently performed major randomized trials, such as the North American Symptomatic Carotid Endarterectomy Trial (NASCET), the European Carotid Surgery Trial (ECST) and the Asymptomatic Carotid Atherosclerosis Study (ACAS), can be expected to increase significantly the performance of CEA in the coming years.3 The role of additional tools for selecting patients for CEA, for predicting and preventing peri-operative complications, and for evaluating the results of carotid surgery will inevitably expand. In 1982, 24 years after the first CEA, Aaslid et al.4 introduced a pulsed transcranial Doppler (TCD) system using a low-frequency (2 MHz) transducer that enabled recordings of the blood-flow velocities (BFVs) from intracranial arteries through selected cranial foramina and thin regions of the skull (ultrasonic windows). TCD, like extracranial Doppler, is based on the principle that ultrasonic signals reflected off moving objects (erythrocytes) demonstrate a change in frequency that is shifted in direct proportion to the velocity of the moving object.5 It is a reliable, non-invasive technique for measuring BFV in the major arteries at the base of the brain, using portable, relatively inexpensive equipment. TCD has now become one of the most important tools for the evaluation of the cerebral vasculature, and has important clinical applications in CEA. This chapter will discuss the use of TCD in carotid surgery. For the sake of greater clarity, TCD applications in carotid surgery can be divided into preoperative, intraoperative and post-operative periods. They can be further divided between TCD studies, TCD combined with vasodilatory tests (carbon dioxide (CO2) inhalation, breath-holding test, Diamox test, L-arginine test) and TCD with microembolic detection. A TCD study can be used to record BFV and the pulsatility index (PI) for quantifying Doppler waveforms. The PI is the amplitude of the BFV waveform, or spectrum outline, divided by its time-mean value.6 PI = (Vs– Vd)/V
where Vs, Vd and V represent the systolic, diastolic, and timemean values of the Doppler velocity spectrum outline, respectively. TCD in combination with vasodilatory tests are used to assess cerebral vasomotor reactivity (VMR), which provides information on cerebral autoregulation and the collateral circulation.7 VMR can be assessed with TCD by measuring cerebral BFV before and after administration of a potent vasodilatory stimulus, all of which are based on known dilatory responses of the cerebral blood flow (CBF) to hypercapnia. This effect is a result of the ability of CO2 primarily to increase CBF to a significant degree and subsequently to form hydrogen ions, after which vasodilatation of the cerebral vessels occurs.8 The vasodilatory response can be calculated as: BFVafter − BFVbefore × 100 = VMR% BFVbefore where BFVafter refers to BFV after the administration of a vasodilatory agent and BFVbefore refers to BFV before the administration of a vasodilatory agent. Diamox (acetazolamide), a potent, reversible inhibitor of carbonic anhydrase, is widely used as a vasodilatory stimulus for evaluating VMR.9 Although the exact mechanism by which Diamox acts as a vasodilatory agent and increases the CBF remain controversial, it is most probable that these effects are stimulated by metabolic acidosis following intravenous administration of 1000 mg acetazolamide.10 In 1999, Micieli et al. used L-arginine as a vasodilatory agent for presurgical and post-surgical evaluations of VMR in patients with severe carotid stenosis undergoing CEA.11 L-arginine induces the vasodilatation of resistance vessels, which is mediated by nitric oxide (NO) at the endothelial level.12 Intravenous infusion of L-arginine at a dose of 500 mg/kg/30 minutes significantly increases BFV as measured by TCD. The detection of embolisms has emerged as another important area for applying TCD. High-intensity transient signals were first observed during TCD ultrasound testing by Padayachee et al. in the mid- to late-1980s.13 These signals correspond to microembolic particles composed of platelets, fibrinogen, cholesterol, or gaseous material, and they have been detected in patients with various cerebrovascular disorders as well as during surgical procedures. 207
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Applications of transcranial Doppler before carotid endarterectomy An increased stroke risk as predicted by a compromised VMR was first determined in xenon/computerized tomography (Xe/CT) CBF studies with Diamox.14 Chimovitz et al. used TCD and the Diamox test in the assessment of cerebral perfusion reserve in patients with carotid stenosis and transient ischemic attacks (TIAs).15 The association of impaired cerebral perfusion reserve and TIAs suggested that TCD and the Diamox test may enable the identification of a subgroup of patients with carotid occlusive disease who are at higher risk for stroke. TCD and the Diamox test were used in a pilot study to evaluate the role of impaired VMR as a predictive factor of stroke in asymptomatic patients with severe (> 70%) ICA stenosis.16 There was a statistically significant correlation between cerebral ischemic events and impaired VMR. These findings suggested that preventive carotid surgery should be considered in a high-risk subgroup of asymptomatic patients with severe carotid stenosis and impaired VMR. Later, larger series in which VMR was determined by TCD and CO2 inhalation confirmed the important role of impaired VMR in predicting ischemic stroke in patients with carotid stenosis.17,18 These data support the value of TCD with vasodilatory tests in identifying high-risk subgroups of patients for whom surgery might be considered. Indeed, the identification of high-risk groups is the main goal of the Asymptomatic Carotid Stenosis and Risk of Stroke Study (ACSRS), in which special attention will be paid to parameters such as VMR using TCD with vasodilatory tests.19 TCD and the Diamox test were also used to investigate the VMR of 44 patients with bilateral severe carotid disease. A more significantly preserved VMR was found in the asymptomatic than in the symptomatic patients.20 These findings were supported by Matteis et al.21 and the results suggest that TCD with vasodilatory tests can contribute to the selection of CEA within the different groups of patients with carotid stenosis based on their individual hemodynamic features. In contrast to the important selective role played by TCD combined with vasodilatory tests in association with carotid surgery, attempts to use TCD before CEA to prevent complications during surgery or to assist presurgical planning (e.g. performing CEA with or without shunt) have been less successful. Lucertini et al. evaluated VMR using TCD and the Diamox test as a preoperative tool in predicting cerebral tolerance to carotid clamping in a consecutive series of 115 CEAs.22 There was no significant difference in VMR between the shunted and non-shunted subgroups. Although Visser et al. have suggested preoperative application of TCD to identify patients who will not require a shunt during CEA, they found only a 60% probability for TCD to predict the need for a shunt.23 Positive results of the prediction of cerebral ischemia during CEA and the indications for clamping were obtained only in one preoperative TCD and CO2-reactivity study.24
Applications of transcranial Doppler during carotid endarterectomy Although intraoperative TCD monitoring has become a recognized tool in carotid surgery in recent years, its usefulness
during CEA remains controversial. A 5-year experience with TCD monitoring of CEAs was summarized by Brozman et al.25 On the basis of intraoperative TCD data (70 consecutive CEAs), they recommended the use of intraluminal carotid shunt only in cases in which there was a reduction in the mean BFV in the middle carotid artery (MCA) of more than 50% relative to the initial value at the start of the operation. Totaro et al. also support TCD as a useful method to evaluate the risk of cerebral ischemia during carotid surgery and to identify those patients in whom shunt insertion is mandatory.26 A large study by Ackerstaff et al. included 1058 patients who underwent CEA.27 TCD monitoring was combined with BFV measurements in the MCAs as well as being used in the detection of cerebral microembolisms. TCDdetected microemboli during dissection and wound closure, a 90% MCA velocity decrease at cross-clamping, and 100% increase in PI at clamp release, were associated with intraoperative stroke. The results of most other studies that were carried out to evaluate the role of TCD monitoring in predicting cerebral ischemia during CEA were negative. The MCA velocities were measured by TCD during 50 consecutive CEAs before, during, and after clamping.28 The changes in velocity were similar among patients who developed complications and those who did not. These results do not support the view that TCD monitoring is helpful in deciding whether to use a shunt during carotid surgery. Similar conclusions were reached in subsequently performed studies where the attempts to use TCD for predicting cerebral ischemia and the need for shunting were also unsuccessful.29,30 As mentioned above, TCD monitoring during carotid surgery also includes TCD microembolic detection. Embolic signal detection by means of TCD is a very promising tool, both for clinical application and for research purposes. Since the initial detection of circulating solid microemboli in patients with carotid artery disease using TCD, some studies have used this technique to investigate patients during carotid surgery.31–33 In a prospective study on 100 consecutive patients undergoing CEA, 92% of the emboli were successfully detected during TCD monitoring.34 Most of these emboli were characteristically composed of air microbubbles and were not associated with the development of adverse clinical events such as strokes or TIAs. However, emboli that were characterized by particulate material were associated with the development of both neurological and cognitive deficits. Another study showed a statistically significant relationship between the presence of multiple microemboli (n = 10) during the dissection phase of CEA procedure and peri-operative cerebral complications with new ischemic brain lesions on magnetic resonance images.35 Microembolism during shunting was also shown to be related to intraoperative complications. Nevertheless, the limitations of TCD for microembolic detection are still substantial. They include both technical and methodological aspects as well as problems with analysis and interpretation of the obtained results.36 Therefore, with the improvement in TCD techniques and clearer interpretations of microembolic recording, it seems probable that embolic detection by TCD will one day be an indispensable tool of intraoperative monitoring during carotid surgery.
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Applications of transcranial Doppler after carotid endarterectomy Although the benefit of CEA has been firmly established, mostly in symptomatic patients with carotid stenosis, its effects on CBF and cerebral hemodynamics have not been fully clarified.37 Russel et al. assessed VMR and CBF before and 3 months after CEA using xenon-133 inhalation with single-photon emission computed tomography and the acetazolamide test.38 They found a significant improvement in VMR after carotid surgery in symptomatic patients with severe carotid stenosis and compromised perfusion reserve before CEA. The same results were achieved by Hartl et al., who used TCD and CO2 inhalation, but these investigators did not differentiate between symptomatic and asymptomatic patients.39 Barzo et al.40 used TCD and the Diamox test to demonstrate changes in VMR following CEA, and demonstrated normalized VMR even in the early postoperative period as well as in both the symptomatic and asymptomatic patient groups. A bilateral increase in VMR using TCD and CO2 inhalation was obtained after unilateral CEA in symptomatic and asymptomatic patients41 and in patients with contralateral occlusion.42 Changes in cerebral hemodynamics after CEA were evaluated in symptomatic and asymptomatic patients with severe carotid stenosis and impaired VMR before carotid surgery.43 VMR was assessed using TCD and the Diamox test. The 21 symptomatic and 21 asymptomatic study patients were evaluated before and after carotid surgery, and a significant improvement in VMR in asymptomatic patients was found 3 months after CEA compared with symptomatic patients. These data strongly
209
suggested that CEA improves cerebral hemodynamics, mainly in asymptomatic patients. Thus, performing TCD together with vasodilatory tests may be useful in identifying asymptomatic patients with impaired VMR and indicate their candidacy for carotid surgery. TCD with the Diamox test can identify subjects with a totally occluded ICA and reduced VMR who may improve hemodynamically with an extracranial– intracranial bypass.44 These findings were also obtained by the post-operative TCD combined with vasodilatory tests. In more recently published studies, post-CEA TCD assessment of BFVs and PIs in the MCAs was useful in identifying patients at risk of developing a hyperperfusion syndrome.45,46
Conclusion The TCD plays an important role and has special applications in the evaluation of patients with carotid stenosis who are potential candidates for carotid surgery. In the presurgery period, TCD combined with vasodilatory tests has clinical application, especially when there is some uncertainty, such as in asymptomatic patients, or patients with symptomatic moderate carotid stenosis, in order to select for carotid surgery a different high-risk subgroup of patients for whom surgery might be justified. For intrasurgical monitoring, TCD will play a greater role in microembolic detection and will focus on the prevention of peri-operative complications (e.g. strokes or hyperperfusion syndromes). Finally, TCD or TCD combined with vasodilatory tests has clear scientific applications in the post-surgery period for the evaluation of the effects of CEA on cerebral hemodynamics.
REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9.
10.
Eastcott HHG. The beginning of carotid surgery. In: Bernstein EF, Callow AD, Nicolaides AN, Shifrin EG, eds. Cerebral Revascularisation. Nicosia: Med-Orion, 1993: 263–73 Raithel D. Current surgical techniques of carotid endarterectomy. In: Bernstein EF, Callow AD, Nicolaides AN, Shifrin ED, eds. Cerebral Revascularisation. Nicosia: Med-Orion, 1993: 301–7 Sacco RL. Extracranial carotid stenosis. N Engl J Med 2001; 345: 15: 1113–8 Aaslid A, Markwalder T, Nornes H. Noninvasive transcranial Doppler ultrasound recording of flow velocities in basal cerebral arteries. J Neurosurg 1982; 57: 769–74 Bornstein NM. Transcranial Doppler. In: Bernstein EF, Callow AD, Nicolaides AN, Shifrin ED, eds. Cerebral Revascularisation. Nicosia: Med-Orion, 1993: 85–91 Lindegaard K-F, Bakke SJ, Grolimund P et al. Assessment of intracranial hemodynamics in carotid artery disease by transcranial Doppler ultrasound. J Neurosurg 1985; 63: 890–8 Dahl A, Lindegaard K-F, Russel D et al. A comparison of transcranial Doppler and cerebral blood flow studies to assess cerebral vasoreactivity. Stroke 1992; 23: 15–9 Severinghaus JW, Cotev S. Carbonic acidosis and cerebral vasodilatation after Diamox. Scand J Clin Lab Invest 1968; 1 (Suppl 102): E Bornstein NM, Gur AY, Shifrin EG, Morag BA. The value of a combined transcranial Doppler and Diamox test in assessing intracerebral hemodynamics. In: Caplan LR, Shifrin EG, Nicolaides AN, Moore WS, eds. Cerebrovascular Ischemia. Investigation and Management. Nicosia: Med-Orion, 1996: 143–8 Heuser D, Astrup G, Lassen NA, Betz E. Brain carbonic acid acidosis after acetazolamide. Acta Physiol Scand 1975; 93: 385–90
11.
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Micieli G, Bosone D, Zappoli F et al. Vasomotor response to CO2 and L-arginine in patients with severe internal carotid artery stenosis; pre- and post-surgical evaluation with transcranial Doppler. J Neurol Sci 1999; 163: 153–8 Moncada, S, Palmer RMJ, Higgs EA. Biosynthesis of nitric oxide from L-arginine: a pathway for the regulation of cell function and communication. Biochem Pharmacol 1989; 38: 1709–15 Padayaachee TS, Gosling RG, Bishop CC et al. Monitoring middle cerebral artery blood velocity during carotid endarterectomy. Br J Surg 1986; 73: 98–100 Yonas H, Smith HA, Durham SR et al. Increased stroke risk predicted by compromised cerebral blood flow reactivity. J Neurosurg 1993; 79: 483–9 Chimowitz MB, Furlan AJ, Jones SC et al. Transcranial Doppler assessment of cerebral perfusion reserve in patients with carotid occlusive disease and no evidence of cerebral infarction. Neurology 1993; 43: 353–7 Gur AY, Bova I, Bornstein NM. Is impaired cerebral vasomotor reactivity a predictive factor of stroke in asymptomatic patients? Stroke 1996; 27: 2188–90 Silvestrini M, Vernieri F, Pasqualetti P. Impaired cerebral vasoreactivity and risk of stroke in patients with asymptomatic carotid artery stenosis. JAMA 2000; 283: 2122–7 Marcus H, Cullinane M. Severely impaired cerebrovascular reactivity predicts stroke and TIA risk in patients with carotid artery stenosis and occlusion. Brain 2001; 124: 457–67 Nicolaides AN. Asymptomatic carotid stenosis and the risk of stroke (the ACSRS Study): identification of a high risk group. In: Caplan LR, Shifrin EG, Nicolaides AN, Moore WS, eds. Cerebrovascular Ischemia. Investigation and Management. Nicosia: Med-Orion, 1996: 435–41
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Textbook of peripheral vascular interventions Gur AY, Bornstein NM. Bilateral severe carotid stenosis: is stroke unavoidable? (Abstract). Proceedings of the International Symposium on Cerebral Hemodynamics: Transcranial Doppler, Cerebral Blood Flow, and Other Modalities, Institute of Applied Physiology and Medicine, Seattle, 1996: 53 Matteis M, Vernieri F, Caltagirone C et al. Patterns of cerebrovascular reactivity in patients with carotid artery occlusion and severe contralateral stenosis. J Neurol Sci 1999; 168: 47–51 Lucertini G, Cariati P, Ermirio D et al. Can cerebral vasoreactivity predict cerebral tolerance to carotid clamping during carotid endarterectomy? Cardiovasc Surg 2002; 10: 123–7 Visser GH, Wieneke GH, van Huffelen AC, Eikelboom BC. The use of preoperative transcranial Doppler variables to predict which patients do not need a shunt during carotid endarterectomy. Eur J Vasc Endovasc Surg 2000; 19: 226–32 Lam JM, Smielewski P, al-Trawi P et al. Prediction of cerebral ischaemia during carotid endarterectomy with preoperative CO2reactivity studies and angiography. Br J Neurosurg 2000; 14: 441–8 Brozman M, Bafrnec L, Raisova M et al. Five-year experience with TCD monitoring of carotid endarterectomies. In: Klingelhöfer J, Bartels E, Ringelstein EB, eds. New Trends in Cerebral Hemodynamics and Neurosonology. Amsterdam: Elsevier, 1997L 765–75 Totaro R, Varroni A, Gizzi E et al. Transcranial Doppler sonography in the pre-, intra- and postoperative evaluation of 85 patients undergoing carotid endarterectomy. Clin Ther 1998; 149: 267–70 Ackerstaff RG, Moons KG, van de Vlasakker CJ et al. Association of intraoperative transcranial doppler monitoring variables with stroke from carotid endarterectomy. Stroke 2000; 31: 1817–23 Bornstein NM, Rossi GB, Trevers TA, Shifrin EG. Is transcranial Doppler effective in avoiding the hazards of carotid surgery? Cardiovasc Surg 1996; 4: 335–7 Grubhofer G, Lassnigg A, Pernerstofer T et al. Systemic blood pressure and cerebral blood flow velocity during carotid surgery. Thorac Cardiovasc Surg 1999; 47: 381–5 McCarthy RJ, McCabe AE, Walker R, Horrocks M. The value of transcranial Doppler in predicting cerebral ischaemia during carotid endarterectomy. Eur J Vasc Endovasc Surg 2001; 21: 408–12 Spencer MP, Thomas GI, Nicholls SC, Sauvage LR. Detection of middle cerebral artery emboli during carotid endarterectomy using transcranial Doppler ultrasonography. Stroke 1990; 21: 415–23 Marcus HS, Harrison MJ. Microembolic signal detection using ultrasound. Stroke 1995; 26: 1517–9
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Babikian VL, Cantelmo NL. Clinical applications of microemboli detection in cerebrovascular disease. In: Klingelhöfer J, Bartels E, Ringelstein EB, eds. New Trends in Cerebral Hemodynamics and Neurosonology. Amsterdam: Elsevier, 1997: 385–92 Gaunt ME. Transcranial Doppler: preventing stroke during carotid endarterectomy. Ann R Coll Surg Engl 1998; 80: 377–87 Ackerstaff RG, Jansen C, Moll FL. Carotid endarterectomy and intraoperative emboli detection: correlation of clinical, transcranial Doppler, and magnetic resonance findings. Echocardiography 1996; 13: 543–50 Marcus H. Methodological aspects of microembolic signal detection. In: Klingelhvfer J, Bartels E, Ringelstein EB, eds. New Trends in Cerebral Hemodynamics and Neurosonology. Amsterdam: Elsevier, 1997: 347–54 Engell HC, Boysen G, Ladegaard-Pedersen JH, Henriksen H. Cerebral blood flow before and after carotid endarterectomy. Vasc Surg 1972; 6: 14–19 Russel D, Dybevold S, Kjartansson O et al. Cerebral vasoreactivity and blood flow before and 3 months after carotid endarterectomy. Stroke 1990; 21: 1029–32 Hartl WH, Janssen I, Fürst H. Effect of carotid endarterectomy on patterns of cerebrovascular reactivity in patients with unilateral carotid artery stenosis. Stroke 1994; 25: 1952–7 Barzo P, Vörös E, Bodosi M. Use of transcranial Doppler sonography and acetazolamide test to demonstrate changes in cerebrovascular reserve capacity following carotid endarterectomy. Eur J Vasc Endovasc Surg 1996; 11: 83–9 Visser GH, van Huffelen AC, Wieneke GH, Eikelboom BC. Bilateral increase in CO2 reactivity after unilateral carotid endarterectomy. Stroke 1997; 28: 899–905 Vriens EM, Wieneke GH, Hillen B et al. Flow redistribution in the major cerebral arteries after carotid endarterectomy: a study with transcranial Doppler scan. J Vasc Surg 2001; 33: 139–47 Bornstein NM, Gur AY, Shifrin EG, Morag BA. Does carotid endarterectomy modify cerebral vasomotor reactivity? Cerebrovasc Dis 1997; 7: 201–4 Karnik R, Valentin A, Ammerer H-P et al. Elevation of vasomotor reactivity by transcranial Doppler and acetazolamide test before and after extracranial–intracranial bypass in patients with internal carotid artery occlusion. Stroke 1992; 23: 812–17 Blohme L, Pagani M, Parra-Hoyos H et al. Changes in middle cerebral artery flow velocity and pulsatility index after carotid endarterectomy. Eur J Vasc Surg 1991; 5: 659–63 Muller M, Behnke S, Walter P Cerebrovascular resistance and blood flow velocity changes after carotid endarterectomy. Vasa 1999; 28: 279–82
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Carotid plaque characterization using ultrasound AN Nicolaides, M Griffin, S Kakkos, G Geroulakos, E Kyriacou, and N Georgiou
Introduction The multidisciplinary approach combining angiography, high-resolution ultrasound, thrombolytic therapy, plaque pathology, histochemistry, coagulation studies, and more recently molecular biology, have lead to the realization that carotid plaque rupture is a key mechanism underlying the development of cerebrovascular events.1–3 Plaques with a large extracellular lipid-rich core, thin fibrous cap, reduced smooth muscle density, and increased numbers of activated macrophages and mast cells appear to be most vulnerable to rupture.3,4 Fibrous caps may rupture because of reduced collagen synthesis as well as increased matrix degradation or in response to extrinsic mechanical or hemodynamic stresses.5 Plaques at the carotid bifurcation coincide with points at which stresses produced by biomechanical and hemodynamic forces are maximal.6 Histological studies on the vascular biology of symptomatic and asymptomatic carotid plaques have been reviewed by Golledge et al.7 They showed that the features of unstable plaques removed from symptomatic patients were surface ulceration and plaque rupture (48% of symptomatic versus 31% of asymptomatic, p < 0.001), thinning of the fibrous cap and infiltration of the cap by a greater number of macrophages and T-lymphocytes. The identification of unstable plaques in vivo and subsequent plaque stabilization may prove to be an important modality for a reduction in the lethal consequences of atherosclerosis.8,9 This putative concept of plaque stabilization, although attractive, has not yet been rigorously validated in humans. Indirect data from clinical trials involving lipid lowering/modification and lifestyle/risk factor modification provide strong support for this new approach.10 Ultrasonic characteristics of unstable (vulnerable) plaques have been determined11–13 and populations or individuals at increased risk for cardiovascular events can now be identified.14 In addition, high-resolution ultrasound has enabled us to identify the different ultrasonic characteristics of unstable carotid plaques associated with amaurosis fugax, transient ischemic attacks TIAs, stroke and different patterns of CT brain infarction.12,13 This information has provided new insight into the pathophysiology of the different clinical manifestations of extracranial atherosclerotic cerebrovascular disease using non-invasive methods. The aim of this chapter
is to highlight the advances in ultrasonic plaque characterization and their potential applications in clinical practice.
Ultrasonic plaque classification High-resolution ultrasound provides information not only on the degree of carotid artery stenosis but also on the characteristics of the arterial wall including the size and consistency of atherosclerotic plaques. Several studies have indicated that “complicated” carotid plaques are often associated with ipsilateral neurological symptoms and share common ultrasonic characteristics, being more echolucent (weak reflection of ultrasound and therefore containing echo-poor structures) and heterogeneous (having both echolucent and echogenic areas). In contrast, “uncomplicated” plaques, which are often asymptomatic, tend to be of uniform consistency (uniformly hypoechoic or uniformly hyperechoic) without evidence of ulceration.11,15,16 Different classifications of plaque ultrasonic appearance have been proposed. Reilly classified carotid plaques as homogeneous and heterogeneous,15 defining as homogeneous plaques those with “uniformly bright echoes” that are now known as uniformly hyperechoic (type 4). Johnson classified plaques as dense and soft;17,18 Widder as echolucent and echogenic, based on their overall level of echo patterns;19 while Gray-Weale described four types: type 1: predominantly echolucent lesions; type 2: echogenic lesions with substantial (> 75%) components of echolucency; type 3: predominately echogenic with small area(s) of echolucency occupying less than a quarter of the plaque; and type 4: uniformly dense echogenic lesions.20 Geroulakos subsequently modified the Gray-Weale classification by using a 50% area cut-off point instead of 75% and by adding a fifth type, which as a result of heavy calcification on its surface cannot be correctly classified.11 In an effort to improve the reproducibility of visual (subjective) classification, a consensus conference has suggested that echodensity should reflect the overall brightness of the plaque with the term hyperechoic referring to echogenic (white) and the term hypoechoic referring to echolucent (black) plaques.21 The reference structure to which plaque echodensity should be compared with, should be blood for hypoechoic, the sternomastoid muscle for isoechoic, and bone 211
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for hyperechoic plaques. More recently, a similar method has been used by Polak.22 In the past a number of workers had confused echogenicity with homogeneity.15 It is now known that measurements of texture are different from measurements of echogenicity. The observation that two different atherosclerotic plaques may have the same overall echogenicity but frequently have variations of texture within different regions of the plaque was made as early as 1983.23 The term “homogeneous” should therefore refer to plaques of uniform consistency irrespective of whether they are predominantly hypoechoic or hyperechoic. The term “heterogeneous” should be used for plaques of non-uniform consistency – that is, having both hypoechoic and hyperechoic components (Gray-Weale20 types 2 and 3). Although O’Donnell had proposed this otherwise simple classification in 198516 and Aldoori in 1987,24 there has been considerable diversity in terminology used by others, as shown in Table 29.1. 18,22,25–32 Because of this confusion, plaques having intermediate echogenicity, or complexity, are frequently inadequately described. For example, echolucent plaques have been considered as heterogeneous.26 A reflection of this confusion is a report from the Committee on Standards for Noninvasive Vascular Testing of the Joint Council of the Society for Vascular Surgery and the North American Chapter of the International Society for Cardiovascular Surgery proposing that carotid plaques should be classified as homogeneous or heterogeneous.33 Regarding the clinical significance of carotid plaque heterogeneity, it seems that the heterogeneous plaques described in the three studies published in the 1980s (Table 29.1), include hypoechoic plaques. Also, heterogeneous plaques in all studies listed in Table 29.1 contain hypoechoic areas (large or small) and appear to be the plaques which are associated with symptoms or, if found in asymptomatic individuals, they are the plaques that subsequently tend to become symptomatic.
Table 29.1
Correlation with histology Reilly has shown for the first time that carotid plaque characteristics on B-mode ultrasound performed before operation correlate with carotid plaque histology.15 As indicated above, by evaluating visually the sonographic characteristics of carotid plaques, two patterns were identified: a homogeneous pattern containing uniform hyperechoic echoes corresponding to dense fibrous tissue and a heterogeneous pattern containing a mixture of hyperechoic areas representing fibrous tissue and anechoic areas that represent intraplaque hemorrhage or lipid.33 Thus, it was realized early on that ultrasound could not distinguish between hemorrhage and lipid. Because most heterogeneous lesions contained intraplaque hemorrhage and ulcerated lesions, it was thought at the time that the presence of a plaque hemorrhage reflected the potential for plaque rupture and development of symptoms. However, it was subsequently realized that plaque hemorrhage was very common and was found in equal frequency in both symptomatic and asymptomatic plaques34 and that ultrasound was highly sensitive in demonstrating plaque hemorrhage (27/29, 93%), as well as specific (84%).16,31,35 It was both sensitive and specific in demonstrating calcification in carotid endarterectomy specimens.36 Aldoori reported that plaque hemorrhage was seen histologically in 21 patients, 19 (78%) of whom were diagnosed preoperatively as having echolucent heterogeneous plaques on ultrasound imaging.24 Gray-Weale20 also validated his plaque classification by demonstrating a statistically significant relationship (p < 0.001) between ultrasound appearance of type-1 and type-2 plaques (echolucent appearance) and the presence of either intraplaque hemorrhage or ulceration in the endarterectomy specimen. It is now apparent from those ultrasound–histology correlations that Reilly’s heterogeneous plaques correspond closely to Gray-Weale’s echolucent (type 1 and 2) plaques.
Design of published studies on carotid plaque characterization in relation to risk for neurologic events
Authors Year (ref) O’Holleran et al. 198718 Sterpetti et al. 198825 Langsfeld et al. 198926 Bock et al. 199327 Polak et al. 199822 Mathiesen et al. 200128 Grønholdt et al. 200129 Liapis et al. 200130 AbuRahma et al. 199831 Carra et al. 200332
Carotid bifurcations n
Follow-up in years
Type of patients A=asymptomatic S=symptomatic
Plaque characteristics studied
296
3.8
A
Calcified, dense, soft
238
2.8
A and S
Homogenous, heterogenous
419
1.8
A
Plaque types 1 to 4
242
2.3
A
Echolucent, echogenic
270
3.3
A
Hypo-, iso-, hyperechoic
223 111 135
3.0 4.4 4.4
A A S
Plaque types 1 to 4 Gray scale median Gray scale median
442
3.7
A and S
Plaque types 1 to 4
391
3.1
A
Homogenous, heterogenous
291
2.7
A
Homogenous, heterogenous
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Carotid plaque characterization using ultrasound The above findings were confirmed by studies performed in the 1990s using a new generation of ultrasound scanners with improved resolution. Van Damme37 reported that fibrous plaques (dense homogeneous hyperechoic lesions) were detected with a specificity of 87% and a sensitivity of 56%. Recent intraplaque hemorrhage was echographically apparent as a hypoechoic area in 88% of cases, corresponding to a specificity of 79% and a sensitivity of 75%. Kardoulas,38 in another study, confirmed Van Damme’s results on fibrous plaques, with fibrous tissue being significantly greater (73%) in plaques with an echogenic character compared with those with an echolucent morphology (63%; p = 0.04). The European carotid plaque study group that performed a multicenter study, confirmed that plaque echogenicity was inversely related to hemorrhage and lipid, (p = 0.005) and directly related to collagen content and calcification (p < 0.0001).39 Plaque shape (mural versus nodular) on ultrasound has been shown to be associated with histology features characteristic of unstable plaques. Weinberger40 demonstrated that mural plaques propagating along the carotid wall had a 72% frequency of recent organizing hemorrhage. In contrast, nodular plaques causing local narrowing of the vessel had only a 23% incidence of organizing hemorrhage (p < 0.01). We now know that stable atherosclerotic plaques have, on histological examination, a thick fibrous cap, a small lipid core, and are rich in smooth muscle cells (SMCs) which produce collagen and have a poor macrophage content. In contrast, unstable plaques that are prone to rupture and development of symptoms have a thin fibrous cap, a large lipid core, few SMCs and are rich in macrophages.3 Macrophages are responsible for the production of enzymes such as matrix metalloproteinases (stromelysins, gelatinases, collagenases) that play an important role in remodeling the plaque matrix and erosion of the fibrous cap.41 Recently, Lammie42 reported a highly significant association between a thin fibrous cap and a large necrotic core (p < 0.002) in carotid endarterectomy specimens and a good agreement between ultrasound and pathological measurements of fibrous cap thickness (thick vs. thin fibrous cap, κ = 0.53).
Table 29.2
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There is considerable debate on the question of whether thrombosis on the surface of the plaque, being an otherwise significant feature of complicated plaques, can discriminate between symptomatic and asymptomatic plaques. Acute thrombosis on ultrasound appears as a completely echolucent defect adjacent to the lumen43 and it is almost certain that by the time the operation is performed (usually several weeks after the event), that the thrombus has undergone remodeling. Natural history studies (Table 29.2) Johnson did the first study to show the value of ultrasonic characterization of carotid bifurcation plaques in asymptomatic patients in the early 1980s.17,18 In that study, hypoechoic carotid plaques in comparison to hyperechoic or calcified ones increased the risk of stroke during a follow-up period of 3 years; this effect was prominent in patients with carotid stenosis of more than 75% (as estimated by cross-sectional area calculations and spectral analysis), as stroke occurred in 19% of them. None of the patients with calcified plaques developed a stroke. A second study performed in the 1980s by Sterpetti25 has shown that the severity of stenosis (lumen diameter reduction greater than 50%) and the presence of a heterogeneous plaque were both independent risk factors for the development of new neurological deficits (TIA and stroke). Twenty seven percent of the patients with heterogeneous plaques and hemodynamically significant stenosis developed new symptoms. Unfortunately, their study had mixed cases as 37% of the patients had a history of previous neurological symptoms, mainly hemispheric ones. History of these neurological symptoms was a risk factor for the development of new neurological symptoms during the follow-up period, although this was found only in the univariate analysis. Because no subgroup analysis was performed, no conclusion can be drawn regarding asymptomatic or symptomatic patients. In a similar study of patients with asymptomatic carotid stenosis AbuRahma31 reported that the incidence of ipsilateral strokes during follow-up was significantly higher in patients
Results of prospective studies of plaque characterization in relation to risk for neurologic events
Authors year (ref)
Endpoint
Stenosis
Findings
O’Holleran et al. 198718
Stroke, TIA
>75%
Sterpetti et al. 198825
Stroke, TIA
>50%
Langsfeld et al. 198926
>75%
Bock et al. 199327
Neurological symptoms Stroke, TIA
–
Polak et al. 199822 Mathiesen et al. 200128
Stroke Neurological
>50% >35%
Grønholdt et al. 200129
Ipsilat. Stroke
>80%
Liapis et al. 200130 AbuRahma et al. 199831
Stroke, TIA Stroke, TIA
>70% –
Carra et al. 200332
Stroke, TIA
>70%
Cumulative 5 year stroke risk was: 80% for soft (echolucent plaques) 10% for dense (echogenic and calcified plaques) Events: 27% for heterogenous plaques 9% for homogenous plaques Events: 15% for echolucent plaques 9% for echogenic plaques Annual event rate: 5.7% for echolucent plaques 2.4% for echogenic plaques RR for ipsilateral stroke was 2.78 in hypoechoic plaques RR for cerebrovascular events was 4.6 in subjects with echolucent plaques RR for ischemic stroke was 7.9 in subjects with echolucent plaques RR was 2.96 for stroke and 2.02 for TIA in echolucent plaques Ipsilateral stroke occurred in: 13.6% of heterogenous plaques 3.1% of homogenous plaques Ipsilateral event occurred in: 5% of heterogenous plaques 1.3% of homogenous plaques
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having heterogeneous plaques than in those having homogeneous ones: 13.6 vs. 3.1% (p = 0.0001; odds ratio: 5.0). Similarly, the incidence rate of all neurological events (stroke or TIA) was higher in patients with heterogeneous than in those with homogeneous plaques: 27.8 vs. 6.6% (p = 0.001; odds ratio: 5.5). Heterogeneous plaques were defined as those composed of a mixture of hypoechoic, isoechoic, and hyperechoic lesions; and homogeneous plaques those which consisted of only one of the three components. Similar results indicating an increased risk in patients with heterogeneous plaques were reported by Carra (Table 29.2).32 A study published in the 1980s by Langsfeld26 confirmed that patients with hypoechoic plaques (type 1: predominantly echolucent raised lesion, with thin “egg shell” cap of echogenicity; and type 2: echogenic lesions with substantial areas of echolucency) had a twofold risk of stroke: 15% in comparison to 7% in those having hyperechoic plaques (type 3: predominately echogenic with small area(s) of echolucency deeply localized and occupying less than a quarter of the plaque; and type 4: uniformly dense echogenic lesions). A confounding factor was that patients with greater than 75% stenosis were also at increased risk. However, the overall incidence of new symptoms was low, in contrast with previous studies, perhaps because only asymptomatic patients were included in that study. Based on their results, the authors proposed an aggressive approach in those patients with greater than 75% stenosis and heterogeneous plaques. There is some confusion regarding the interchangeable use of the terms heterogeneous and hypoechoic in that article. The authors raised the point that it is important for each laboratory to verify its ability to classify plaque types. The same group in another study published 4 years later reported a 5.7% annual vessel event rate (TIA and stroke) for echolucent carotid plaques versus 2.4% for the echogenic ones (p = 0.03).27 Given the fair interobserver reproducibility for type-1 plaques, the use of reference points was proposed: anechogenicity to be standardized against circulating blood, isoechogenicity against sternomastoid muscle, and hyperechogenicity against bone (cervical vertebrae). This method was used in the late 1990s by Polak22 who investigated the association between stroke and internal carotid artery plaque echodensity in 4886 asymptomatic individuals aged 65 years or older, who were followed up prospectively for 48 months. Some 68% of those had carotid artery stenosis, which exceeded 50% in 270 patients. In this study plaques were subjectively characterized as hypoechoic, isoechoic, or hyperechoic in relation to the surrounding soft tissues. Hypoechoic plaques causing stenoses of 50–100% were associated with a significantly higher incidence of ipsilateral, non-fatal stroke than iso- or hyperechoic plaques of the same degree of stenosis (relative risk 2.78 and 3.08, respectively). The authors of this study suggested that quantitative methods of grading carotid plaque echomorphology such as computer-assisted plaque characterization might be more precise in determining the association between hypoechoic (echolucent) plaques and the incidence of stroke. Subsequent studies28–30 have supported the finding that hypoechoic plaques are associated with an increased risk when compared with hyperechoic plaques (see below). We now know that echolucent and heterogeneous plaques are not mutually exclusive and the risk is increased in both. Type-2 plaques, which are associated with the highest incidence of neurological events, are by definition
included in both echolucent and heterogeneous groups (see later section on plaque types). B-mode image normalization Ultrasound examination and plaque characterization have been until now highly subjective. When the examination is performed in a dimly lit room the gain is usually reduced by the operator; when it is performed in a brightly lit room the gain is increased. Although the human eye can adjust to image brightness to a certain extent, reproducible measurements of echodensity are not possible. Ultrasonic image normalization, which was introduced in the late 1990s, has enabled us to overcome this problem. Computer-assisted plaque measurements of echodensity were initially made from digitized B-mode images of plaques taken from a duplex scanner with fixed instrument settings including gain and time control. The median of the frequency distribution of gray values of the pixels within the plaque (grayscale median (GSM); scale 0–255; 0 = black, 255 = white) was used as the measurement of echodensity. Early work had demonstrated that plaques with a GSM of less than 32; that is, echolucent plaques, had a five-fold increase in the prevalence of silent brain infarcts on CT brain scans.44 Other teams found similar results but the cut-off point was different from 32.45 Soon it became apparent that ultrasonic image normalization was necessary, so that images captured under different instrument settings, from different scanners, by different operators and through different peripherals such as video or magnetooptical disk, could be comparable. As a result a method has been developed to normalize images by means of digital image processing using blood and adventitia as the two reference points.46 With the use of commercially available software (Adobe Photoshop version 3.0) and the “histogram” facility, the GSM of the two reference points (blood and adventitia) in the original B-mode image was determined. Algebraic (linear) scaling of the image was performed with the “curves” option of the software so that in the resultant image the GSM of blood was equal to 0 and that of the adventitia to 190. Thus brightness of all pixels in the image including those of the plaque became adjusted according to the two reference points. This resulted in a significant improvement in the comparability of the ultrasonic tissue characteristics. Appropriate areas of blood and adventitia for image normalization and the avoidance of areas of acoustic shadow in the selection of the plaque area are imperative. The duplex settings recommended are as follows: maximum dynamic range, low persistence, and high frame rate. A high-frequency linear array transducer, ideally 7–10 MHz, should be used. A high dynamic range ensures a greater range of grayscale values. High frame rate ensures good temporal resolution. In addition to these pre-sets the time gain compensation curve should be positioned vertically through the lumen of the vessel, as there is little attenuation of the beam at this point. This ensures that the adventitia of the anterior wall has the same brightness as the adventitia of the posterior wall. The overall gain should be adjusted to give optimum image quality (bright echoes with minimum noise in the blood). A linear post-processing curve should also be used and finally where possible the ultrasound beam should be at 90°, to the arterial wall (Figure 29.1).
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Figure 29.1 Image obtained for plaque analysis. The ultrasound beam is at right angles to the adventitia; the time gain compensation curve (TGC) is vertical through the vessel lumen; a bright segment of adventitia is visible adjacent to the plaque.
The previously discussed guidelines should result in the following: an area of noiseless blood, an echodense piece of adventitia in the vicinity of the plaque, and visualization of the extent and borders of the plaque. It is here that color images can provide further information about plaque outline. Two major reproducibility studies have been performed in order to establish the validity of the method of image
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normalization and the value of GSM measurements.47,48 These studies have demonstrated that GSM after image normalization is a highly reproducible measurement that could be used in natural history studies of asymptomatic carotid atherosclerotic disease, aiming to identify patients at higher risk of stroke. A key issue for the successful reproducibility of normalized images is that only the inner two-fourths of the brightest section of adventitia should be sampled for normalization. Adequate training is essential if the level of reproducibility reported above is to be achieved. It is necessary not only in the use of the software but also in the appropriate scanning technique. The authors have developed a research software package, now commercially available, that can be used to analyze ultrasonic images of plaques. This package has five main modules. The first provides a user-friendly way to normalize images (Figure 29.2). A zooming facility allows enlargement of the image so that the middle two-fourths of the adventitia can be selected accurately. The second provides a means of calibration and of making measurements of distance or area in mm and mm2 respectively. The third provides a method of normalizing images to a standard resolution (20 pixels per mm). This is because a number of texture features are resolution dependent and various degrees of image magnification even on the same scanner do alter the resolution (see section on “Texture features”). The fourth provides the user with a means of selecting the area of interest (plaque) and saving it as a separate file (Figure 29.3). An image enhancement facility allows
(a)
(b) Figure 29.2 A user-friendly method of image normalization. Original image is on the left. By sampling pixels representing blood and pixels of center of adventitia after magnification, the normalized image is produced on the right. This image can be saved in a database. For reproducibility of GSM and other texture features the middle two-fourths of the adventitia are sampled after zooming.
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Figure 29.3 This module provides the facility for outlining the plaque and saving it as a separate file in the database. The color image on the right provides some indication of the extent of hypoechoic areas near the lumen. (See Color plates.)
clearer visualization of the edges of the plaque. The fifth classifies plaques according to the Geroulakos classification11 and extracts a number of texture features and saves them on a file for subsequent statistical analysis. In addition, images are color-contoured. Pixels with a grayscale value in the range 0–25 are colored black. Pixels with values 26–50, 51–75, 76–100, 101–125, and values greater than 125 are colored blue, green, yellow, orange, and red, respectively (Figure 29.4). In addition this module allows printing of the plaque images and selected features or saving the latter in a file (Figure 29.5). For the purpose of automatic classification by computer, the Geroulakos classification has been redefined in terms of pixels and gray levels. Examples of plaque types 1–4 are shown in Figure 29.6. For type-5 plaques only, the calcified or visible bright areas of the plaque are selected ignoring the areas of acoustic shadows where information on plaque texture is lacking.
Type 1. Uniformly echolucent (black): Less than 15% of the plaque area is occupied by colored areas i.e. with pixels having a grayscale value greater than 25. If the fibrous cap is not visible, the plaque can be detected as a black filling defect only by using color flow or power Doppler. ● Type 4 and 5. Uniformly echogenic: colored areas occupy more than 85% of the plaque area. A reproducibility study between visual classification and computer classification has demonstrated a κ statistic of 0.61 (Table 29.3). It should be noted that the computer cannot distinguish between plaque types 4 and 5. This is because the operator selects only the calcified area of plaque type 5. However, this is not a major drawback since both plaque types 4 and 5 are associated with low risk. The high event rate associated with plaque types 1–3 and low event rate with plaques 4 and 5 found after image normalization and visual classification is also found after image normalization and typing by ●
Figure 29.4 This module extracts a large number of well-established standard first-order and second-order statistical features used in image analysis. The program determines the type of plaque automatically and allows input from the operator about the presence of a dark area adjacent to the lumen, presenting symptoms and percent carotid stenosis. (See Color plates.)
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Figure 29.5 Print out of normalized grayscale image of plaque and color-contoured image with selected plaque characterization features. (See Color plates.)
computer (Table 29.4). In fact, after image normalization and computer classification the group of patients with plaque types 1–3 contains 99 of all 106 (93.5%) neurological events. When compared with type-4 and type-5 plaques the relative risk is 3.3 (95% CI 1.56–7.00). Also, after image normalization and computer classification plaque types 1–3 contain 44 (93.6%) of all 46 strokes (RR 3.4 with 95% CI 1.07–10.9).
Carotid plaque echodensity and structure in normalized images The clinical importance of ultrasonic plaque characterization following image normalization has been focused on two main areas: first, cross-sectional studies aiming at better understanding of the pathophysiology of carotid disease; and second, natural history studies seeking to identify high- and low-risk groups for stroke in order to refine the indications on selection of symptomatic or asymptomatic patients not only for carotid endarterectomy but also for stenting. Cross-sectional studies The use of image normalization and computer analysis has resulted in the identification of differences in carotid plaque structure – in terms of echodensity and degree of stenosis – not only between symptomatic and asymptomatic plaques in general but also between plaques associated with retinal or hemispheric symptoms.49 In asymptomatic and symptomatic
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patients presenting with amaurosis fugax, TIAs, and stroke with good recovery having 50–99% stenosis on carotid duplex scan, plaques associated with symptoms were significantly more hypoechoic, with higher degrees of stenosis than those not associated with symptoms (mean GSM = 13.3 vs. 30.5, and mean degree of stenosis = 80.5% vs. 72.2%). Furthermore, plaques associated with amaurosis fugax were hypoechoic (mean GSM = 7.4) and severely stenotic (mean stenosis = 85.6%). Plaques associated with TIAs and stroke had a similar echodensity and a similar degree of stenosis (mean GSM = 14.9 vs. 15.8, and degree of stenosis = 79.3% vs. 78.1%).50 These findings confirm previous reports, which have shown that hypoechoic plaques are more likely to be associated with symptoms. In addition they support the hypothesis that amaurosis fugax has a different pathophysiological mechanism to that of TIAs and stroke. Our group has found that GSM separates echomorphologically the carotid plaques associated with silent non-lacunar CT-demonstrated brain infarcts from plaques that are not so associated. The median GSM of plaques associated with ipsilateral non-lacunar silent CT-demonstrated brain infarcts was 14, and that of plaques that were not so associated was 30 (p = 0.003).48 Additionally, emboli counted on transcranial Doppler (TCD) in the ipsilateral middle cerebral artery were more frequent in the presence of low-plaque echodensity (low GSM), but not in the presence of a high degree of stenosis. These data support the embolic nature of cerebrovascular symptomatology.49 There are several biologic findings that can explain the association of hypoechoic plaques with symptoms. Our group has found that hypoechoic plaques with a low GSM have a large necrotic core volume.51 In addition, hypoechoic plaques have increased macrophage infiltration on histological examination of the specimen after endarterectomy.52 The role of biomechanical forces in the induction of plaque fatigue and rupture has been emphasised.53–55 In our group of patients, carotid plaques associated with amaurosis fugax were hypoechoic and were associated with very high-grade stenoses. It may well be that the plaques that are hypoechoic and homogeneous undergo low internal stresses and therefore do not rupture but progress to tighter stenosis with poststenotic dilatation, turbulence, and platelet adhesion in the post-stenotic area resulting in the eventual production of showers of small platelet emboli. Such small platelet emboli may be too small to produce hemispheric symptoms but are detected by the retina. In contrast, plaques associated with TIAs and stroke were less hypoechoic and less stenotic than those associated with amaurosis fugax. These plaques are hypoechoic but more heterogeneous and may undergo stronger internal stresses. Therefore, they may tend to rupture at an earlier stage (lower degrees of stenosis), producing larger particle debris (plaque constituents or thrombi) that deprives large areas of the brain of adequate perfusion. Prospective studies The Tromsø study, conducted in Norway in 223 subjects with carotid stenosis > 35%, has found that subjects with echolucent atherosclerotic plaques have increased risk of ischemic cerebrovascular events independent of degree of stenosis.28 The authors give no details on patient’s neurological history.
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Figure 29.6
(a)
(b)
(c)
(d)
Examples of plaque types: (a) type 1; (b) type 2; (c) type 3; and (d) type 4. (See Color plates.)
The adjusted relative risk for all cerebrovascular events in subjects with echolucent plaques was 4.6 (95% CI 1.1–18.9), and there was a significant linear trend (p = 0.015) for higher risk with increasing plaque echolucency. Ipsilateral neurological events were also more frequent in patients with echolucent or predominantly echolucent plaques (17.4 and 14.7%, respectively). The authors concluded that evaluation of plaque morphology in addition to the grade of stenosis might improve clinical decision-making and differentiate treatment for
individual patients and that computer-quantified plaque morphology assessment, being a more objective method of ultrasonic plaque characterization, may further improve this. This method has been recently used by Grønholdt,29 who found that echolucent plaques causing > 50% diameter stenosis were associated with increased risk of future stroke in symptomatic (n = 135) but not asymptomatic (n = 111) individuals. Echogenicity of carotid plaques was evaluated with high-resolution B-mode ultrasound and computer-assisted
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Table 29.3 The relationship between plaque visual classification after image normalization and plaque classification by computer (κ = 0.61). Because of the low event rate in plaque types 4 and 5 and because the computer cannot distinguish between them, these plaques have been grouped together Plaque type classification by computer after image normalization Plaque type: visual classification after image normalisation 1 2 3 4/5 Total
1
2
57 (51%) 6 (1.6%) 0 0 63 (6%)
53 251 9 0 313
(47%) (68%) (3%) (29%)
image processing. The mean of the standardized median grayscale values of the plaque was used to divide plaques into echolucent and echorich. Relative to symptomatic patients with echorich 50–79% stenotic plaques, those with echorich 80–99% stenotic plaques, echolucent 50–79% stenotic plaques, and echolucent 80–99% stenotic plaques had relative risks of ipsilateral ischemic stroke of 3.1 (95% CI 0.7–14), 4.2 (95% CI 1.2–15), and 7.9 (95% CI 2.1–30), equivalent to absolute risk increase of 11, 18, and 28%, respectively. The authors suggested that measurement of echolucency, together with the degree of stenosis, might improve selection of patients for carotid endarterectomy. The relatively small number of asymptomatic individuals was probably the reason why plaque characterization was not helpful in predicting risk in the asymptomatic group.
3
4/5
Total
2(1.8%) 110 (30%) 281 (91%) 92 (34%) 486 (46%)
0 3 (0.8%) 20 (6.5%) 178 (66%) 201(19%)
112 370 310 270 1062
(100%) (100%) (100%) (100%) (100%)
Two studies have investigated plaque surface characteristics and the type of plaque in relation to symptoms. The first one was a retrospective analysis of 578 symptomatic patients (242 with stroke and 336 with TIAs) recruited for the B-scan Ultrasound Imaging Assessment Program. A matched casecontrol study design was used to compare brain hemispheres with ischemic lesions to unaffected contralateral hemispheres with regard to the presence and characteristics of carotid artery plaques. Plaques were classified as smooth when the surface had a continuous boundary, irregular when there was an uneven or pitted boundary, and pocketed when there was a crater-like defect with sharp margins. The results demonstrated an odds ratio of 2.1 for the presence of an irregular surface and of 3.0 for hypoechoic plaques in carotids associated with TIAs and stroke.68 The second study included 258 symptomatic and 65 asymptomatic patients. Carotid plaque morphology was classified according to Gray-Weale,20 and plaque surface features were assessed. The results demonstrated that plaque types 1 and 2 were more common in symptomatic patients. The incidence of ulceration was 23% in the symptomatic and 14% in the asymptomatic group (p = 0.04).69 In the absence of any prospective natural history studies in which ultrasound has been used for identifying plaque ulceration, the finding of plaque ulceration cannot be used for making clinical decisions.
Ultrasonic plaque ulceration Several studies have indicated a strong association between macroscopic plaque ulceration and the development of embolic symptoms (amaurosis fugax, TIAs, stroke) and signs such as silent infarcts on CT brain scans.56–60 However, the ability of ultrasound to identify plaque ulceration is poor.15,19,61–67 The sensitivity is low (41%) when the stenosis is greater than 50% and moderately high (77%) when the stenosis is less than 50%. This is because ulceration is much easier to detect in the presence of mild stenosis, when the residual lumen and plaque surface are more easily seen, than with severe stenosis, when the residual lumen and the surface of the plaque are not easily defined because they are not always in the plane of the ultrasound beam.
Stenosis: a confounding factor Natural history studies have demonstrated that the risk of developing ipsilateral symptoms including stroke increases with
Table 29.4 The ipsilateral AF, TIAs, and strokes that occurred during follow-up in patients with different types of plaque after image normalization and classification by computer Plaque type Classified by computer
Events absent
AF
1 2 3 4/5 Total
56 271 435 194 956
2 6 10 0 18
(88.9%) (86.6%) (89.7%) (97.1%) (90.0%)
(3.2%) (1.9%) (2.1%) (1.7%)
TIAs
Stroke
All Events
Total
1 17 19 5 42
4 19 21 2 46
7 42 50 7 106
63 (100%) 313 (100%) 485 (100%) 201(100%) 1062 (100%)
(1.6%) (5.4%) (3.9%) (2.5%) (3.8%)
(6.3%) (6.1%) (4.3%) (1.5%) (4.4%)
(11.1%) (13.4%) (10.3%) (3.5%) (10.0%)
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increasing severity of internal carotid artery stenosis (Table 29.5). In addition, a number of important messages have emerged recently. One is that the different methods used on either side of the Atlantic to express the degree of stenosis have a different relationship to risk. Another is the realization that a considerable number of events occur in patients with low-grade asymptomatic carotid stenosis. Also, the relationship between risk and degree of internal carotid stenosis depends on the methodology used. Finally, both the severity of internal carotid stenosis and plaque characterization texture features are independent predictors of risk and can complement each other. Thus, one cannot consider plaque characterization independent of stenosis. Two main methods are currently used to express percent diameter stenosis. The first one defines the residual lumen as a percentage of the normal distal ICA. It has been used in North America since the late 1960s and more recently the North American Symptomatic Carotid Endarterectomy Trial (NASCET)70 and the Asymptomatic Carotid Atherosclerosis Study (ACAS).71 It has become known as the North American, “NASCET” or “N” method.72 The second method expresses the residual lumen as a percentage of the diameter of the carotid bulb and has been used in the European Carotid Surgery Trial (ECST)73 to become known as the European or “ECST” or “E” method.74 The relationship between both methods is shown in Figure 29.7. Several natural history studies17,27,75–82 indicate that the risk of stroke in asymptomatic patients is low (0.1–1.6% per year) for NASCET stenosis less than 75–80% and higher (2.0–3.3% per year) with greater degrees of stenosis (Table 29.5). Different cut-off points, ranges, and methods of grading stenosis have been used in these natural history studies17,27,75–82 and randomized controlled trials.70,71,73,83 Universal agreement as to the best method for grading ICA stenosis and optimum cut-off points in relation to risk have not yet been established. The NASCET randomized controlled study has used angiography and a cut-off point of 70% stenosis in relation to the distal internal carotid which is equivalent to 83% stenosis in relation to the bulb (Figure 29.7). The ECST randomized controlled study has used angiography also, but used a cut-off point of 70% stenosis in relation to the bulb which is equivalent to 47% stenosis in relation to the distal internal carotid artery. Many vascular surgeons are under the impression that these cut-off points are similar! The only similarity is the value of 70%. In reality the difference in terms of plaque size or residual lumen is considerable. However, with increasing degrees of stenosis the values of the two methods converge and the discrepancy decreases (Figure 29.7). The results of the Asymptomatic Carotid Stenosis and Risk of Stroke (ACSRS) prospective natural history study have demonstrated that the risk of ipsilateral ischemic hemispheric events have a linear relationship with ECST stenosis (Figure 29.8) but not with NASCET stenosis (Figure 29.9).84 Natural history studies including the ACSRS that have included patients with asymptomatic carotid stenosis up to 99% (Table 29.5) have demonstrated that a considerable number of events occur at low grades of stenosis. In fact in the ACSRS study 37 (34%) of 108 ipsilateral ischemic hemispheric events including 16 (35%) of the 46 strokes (Table 29.6) occurred in patients with stenosis less than 60% NASCET (< 77% ECST), the selection criterion for carotid endarterectomy in asymptomatic patients as indicated from the findings
of the ACAS trial. Only ten (9%) of the events including three (3%) strokes occurred in patients with stenosis less than 70% ECST equivalent to approximately 50% NASCET. The question that has been posed is whether plaque characterization can improve the selection of patients at increased risk in the range of 50–70% NASCET (equivalent to 72–83% ECST).
Plaque type and risk As pointed out above, most natural history studies performed in the past have used different methods of plaque classification without prior image normalization. It is now realized that image normalization results in a marked change in the appearance of plaques with reclassification of a large number. The relationship between plaque classification before image normalization and after image normalization in patients admitted to the ACSRS study is shown in Table 29.7.85 Before image normalization 131 plaques were classified as type 1, 288 as type 2, 319 as type 3, 166 as type 4, and 188 as type 5. It can be seen that after image normalization 66% of type 1, 49% of type 2, 46% of type 3, 66% of type 4, and 82% of type 5 were reclassified as a different plaque type (κ statistic 0.22) demonstrating that there was a poor agreement between plaque classification before and after image normalization. After image normalization 652 (60%) of the plaques changed category. This marked change in plaque category is found in all plaque types including type 5. Before image normalization plaques with a calcified cap that had more than 15% of the plaque obscured by an acoustic shadow were classified as type 5. After image normalization the area of plaque adjacent to the calcification and acoustic shadow could be seen and outlined more easily in relation to blood. This area changed considerably in many plaques and explains why a large number of plaques initially classified as type 5 changed to type 4, 3, and even 2 after image normalization (Table 29.7). The ipsilateral neurological events (AF, TIAs, and stroke) that occurred in the ACSRS study during follow-up in patients with different types of plaque before and after image normalization are shown in Tables 29.8 and 29.9 respectively. It can be seen that after image normalization the incidence of events in relation to different plaque types has changed. After image normalization there was a decreased incidence in patients with plaque types 4 and 5 with the vast majority of events occurring in plaque types 1, 2, and 3. Before image normalization only 82 (71%) of the 116 neurological events occurred in plaque types 1–3, but after image normalization the number increased to 109 (94%). When plaque types 1–3 are compared with plaque types 4 and 5 before image normalization the relative risk of having an event is 1.12 (95% CI 0.76–1.66) (Chi sq. p = 0.45). Also, 37 (73%) of the 51 ischemic strokes have occurred in patients with plaque types 1–3 (Table 29.8). When plaque types 1–3 are compared with plaque types 4 and 5 after image normalization the relative risk of having an event is 4.8 (95% CI 2.27–10.28) (Chi sq. p = 0.0001). Also, 49 (96%) of the 51 ischemic strokes have occurred in patients with plaque types 1–3 (Table 29.9). When echolucent plaques (type 1 and 2) are compared with echogenic (type 3 and 4) the incidence of ipsilateral neurological events is 61 (14.9%) out of 409 in the former and 53 (8.3%) out of 635 in the latter (Table 29.9) (RR 1.6 95% CI 1.16–2.32) (Chi sq. p = 0.003).
, accessed April 28, 2006 Hartmann M, Bose A, Henkes H et al., for the Wingspan Investigators. One year stroke risks in high grade, symptomatic, medically refractory intracranial atherosclerosis after angioplasty and stenting: The Wingspan Trial. Presented at the International Stroke Conference, Kissimmee, Florida, February 18, 2006 Jiang WJ, Xu XT, Du B et al. Comparison of elective stenting of severe versus moderate intracranial atherosclerotic stenosis. Neurology 2007; 68: 420–6 Jiang WJ, Du B, Xu XT et al. Elective stenting of symptomatic intracranial atherosclerosis: long-term outcome and predictors. Presented at the International Stroke Conference, San Francisco, California, February 8, 2007 Cruz-Flores S, Diamond AL. Angioplasty for intracranial artery stenosis (Cochrane Review). In: The Cochrane Library, Issue 3, July 19, 2006 Derdeyn CP, Grubb RL Jr, Powers WJ. Cerebral hemodynamic impairment: Methods of measurement and association with stroke risk. Neurology 1999; 53: 251–9 Naritomi H, Sawada T, Kuriyama Y et al. Effect of chronic middle cerebral artery stenosis on the local cerebral hemodynamics. Stroke 1985; 16: 214–9 Grubb RL Jr, Derdeyn CP, Fritsch SM et al. Importance of hemodynamic factors in the prognosis of symptomatic carotid occlusion. JAMA 1998; 280: 1055–60 Constantinides P. Pathogenesis of cerebral artery thrombosis in man. Arch Pathol 1967; 83: 422–8 Caplan LR. Intracranial branch atheromatous disease: A neglected, understudied, and underused concept. Neurology 1989; 39: 1246–50 Derdeyn CP, Videen TO, Yundt KD et al. Variability of cerebral blood volume and oxygen extraction: stages of cerebral haemodynamic impairment revisited. Brain 2002; 125: 595–607 Schumacher HC, Khaw AV, Meyers PM et al. Intracranial angioplasty and stent placement for cerebral atherosclerosis. J Vasc Interv Radiol 2004; 15: S123–S132 Sauvageau E, Ecker RD, Levy EI et al. Recent advances in endoluminal revascularization for intracranial atherosclerotic disease. Neurological Research 2005; 27: S89–94
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56. 57. 58. 59.
Furlan A, Higashida R, Wechsler L et al. Intra-arterial pro-urokinase for acute ischemic stroke: the PROACT II study: a randomized controlled trial. JAMA 1999; 282: 2003–11 Churchill Livingstone is an imprint of Elsevier Inc. The place of publication is Philadelphia. Abou-Chebl A, Yadav JS, Reginelli JP et al. Intracranial hemorrhage and hyperperfusion after carotid artery stenting. J Am Coll Cardiol 2004; 43: 1596–601 Jiang WJ, Xu XT, Du B et al. Long-term outcome of elective stenting for symptomatic intracranial vertebrobasilar stenosis. Neurology 2007; 68: 856–8
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Intracranial stenting for cerebrovascular pathology El Levy, AS Boulos, BR Bendok, SH Kim, AI Qureshi, LR Guterman, and LN Hopkins
Introduction Only within the past few years have technological advances provided clinicians with stents capable of negotiating the tortuosity of the intracranial circulation, The recent development of smaller, more pliable stents and delivery devices has greatly broadened the application of intracranial stenting for various clinicopathological disease processes. This chapter discusses the utility of stent implantation for the following cerebrovascular diseases: intracranial atherosclerosis and stenosis, arterial dissection, fusiform and wide-necked aneurysms, venous occlusive disease, and acute vessel thrombosis. In addition some of the basic technical aspects of intracranial stent insertion are described, along with the peri-procedural medical management of the patients.
Historical background Although intracranial applications for stent technology are only a few years old, these intravascular devices have been in existence since the 1960s. In a review of neurovascular stenting by Horowitz and Purdy,1 pioneering work by several groups is described. Dotter and Judkins2 first proposed the concept of intravascular stenting in 1964. Shortly afterwards, animal work performed by Dotter in 19693 demonstrated long-term patency in the dog popliteal artery following intravascular placement of a coilspring tube graft. More than a decade later, a second report by Dotter et al.4 described the use of nitinol stents in the canine vasculature. Throughout the early 1980s, several investigators tested stents in various animal models. In 1987, Rousseau et al.5 described the first case of stent placement in a human coronary artery. The origins of the word “stent” remain unclear. Horowitz and Purdy1 referenced a stent as the prosthesis developed by British dentist Charles Thomas Stent in the mid-1800s. They also mention that “stent” may be an alteration of the word “stint.” More recently Palmaz6 defined stents as expandable coil or mesh tube prostheses that can be introduced into the body through a catheter. As technological advances continue This chapter is reproduced from Levy El, Boulos AS, Bendok BR et al. Intracranial stenting for cerebrovascular pathology. Contemporary Neurosurgery 2000; 23(25): 1–9 with kind permission of Lippincott, Williams & Wilkins.
to supply clinicians with transcatheter intra-arterial devices, novel applications may provide alternative therapies for various clinicopathological entities.
Atherosclerotic disease: stent-assisted angioplasty Before the availability of intracranial stents, symptomatic, medically refractory atherosclerosis of the intracranial vasculature was primarily treated with balloon angioplasty. Although balloon angioplasty has demonstrated efficacy in the coronary vasculature, cerebral vessels have less adventitia and are surrounded by cerebrospinal fluid and, therefore, may be at greater risk for dissection and abrupt closure, Subsequent to the initial report by Sundt et al.7 in 1980, several advances in both technique and devices have increased the efficacy of intracranial balloon angioplasty. Nearly a decade would pass before Ahuja et al. and other clinicians reported multiple cases with more widespread application of intracranial angioplasty. In a recent report by Connors and Wojak,8 a cohort of 50 patients received angioplasty in which the balloons were undersized and inflated slowly and deliberately. Even though 16% of this group had residual stenosis of more than 50% of the luminal diameter, none had strokes or suffered acute occlusion. These authors admitted that the slow inflation technique and undersizing may yield suboptimal angiographic results, but felt that it greatly decreased the likelihood of intimal damage and acute thrombosis. Although postangioplasty results may appear suboptimal in many cases (because of recoil and residual stenosis), Derdeyn et al.9 described the restoration of normal cerebral blood flow and oxygen extraction despite residual stenosis of 40% in the setting of supraclinoid internal carotid artery stenosis that caused misery perfusion (inadequate perfusion relative to the metabolic demands of the parenchyma ipsilateral to the stenosis). Similar improvements in cerebral blood flow and oxygen extraction have been reported after basilar artery angioplasty. As suggested by Mori et al.,10 lesion morphology often determines the suitability of balloon angioplasty, Lesions that are tortuous, angulated or greater than 10 mm in length (type C) have a restenosis rate of 100% at 1 year and a stroke risk of 87% at 1 year, with only a 33% likelihood for immediate success. Lesions less than 5 mm in length with a concentric 247
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configuration (type A) are well suited for angioplasty, with a 92% immediate success rate and no restenosis at 1 year. Type B lesions are 5–10 mm in length and eccentric, and may or may not be best suited for angioplasty, as evidenced by a 33% rate of recurrent stenosis at 1 year. To date, several small retrospective series have examined the angiographic and clinical outcomes in patients with intracranial atherosclerotic disease treated by the use of intracranial stents, In a series reported by Gomez et al.,11 12 basilar artery stenoses were treated with stents. There were no permanent significant complications such as vessel occlusion, stent thrombosis, or vessel rupture. The mean residual stenosis was 10% (before stenting, the mean stenosis was 71%). Although the results of this series suggest that intracranial stenting is feasible with low morbidity, significant mortality and morbidity rates following stenting of the intracranial posterior circulation have been reported by other clinicians. In a series of 11 patients treated with stent-assisted vertebrobasilar angioplasty, Levy et al.12 reported three periprocedural deaths and one delayed death from procedure-related brainstem infarction. Among the survivors, follow-up angiography revealed in-stent hyperplasia in one patient, a new stenosis proximal to the stented lesion in a second patient, and in-stent aneurysm formation in a third patient. Some atherosclerotic lesions in the intracranial circulation may be less amenable to balloon angioplasty alone because of the bony confinements of the cerebral vasculature, The petrous portion of the carotid artery is especially refractory to balloon dilatation. In a report by Fessler et al.,13 angioplasty of a flow-limiting stenotic lesion of the petrous carotid artery resulted in minimal improvement in the diameter of the vessel lumen. This suboptimal result was probably due to the limited capability for vessel expansion in the carotid canal. In such cases, stenting may improve the post-angioplasty vessel lumen diameter. Stenting for atherosclerotic stenosis may also be especially useful for stenotic lesions that recur after angioplasty or following minimally responsive luminal dilatation to angioplasty alone. Following angioplasty, restenosis results from intimal injury-induced fibrosis. Stenting of these lesions carries a lower risk of embolic shower compared with stenotic lesions resulting from atheromatous plaques. In addition, these fibrous lesions tend to have better post-stent angiographic results. Technical performance of intracranial stenting involves the following key stent parameters: sizing of the stent to the vessel lumen, “trackability” (the ease of negotiating the tortuosity of the intracranial vessels), thickness, porosity, flexibility, balloon overhang (length of stent relative to balloon), adherence, rate of balloon inflation and outward radial force exerted by the stent. Several patient-dependent anatomical considerations often dictate the stents that will be used. These factors include vessel tortuosity and flexibility, lumen diameter, and the distortability of the vasculature and its inherent curvature (which is extremely low for vessels surrounded by a bony canal). Aortic arches with bovine configurations or severely angulated vessels off the aortic arch present even more complexity. All of these anatomical factors must be appreciated when choosing the optimal stent design for the procedure. Stent selection should be based on the aforementioned parameters as they relate to the patient’s anatomy.
For atherosclerotic lesions of the intracranial circulation, it may not be necessary to achieve a vessel diameter equivalent to that of the parent vessel, However, a poor technical result may increase the possibility of subacute stent thrombosis or restenosis, or both (Figure 32.1). These lesions develop slowly, often allowing the brain to obtain supply from the collateral circulation as a compensatory mechanism for augmenting flow to hypoperfused regions. Thus, moderate improvements in luminal diameter may provide sufficient restoration of flow. As observed in conjunction with carotid endarterectomy procedures, recanalization of a clinically significant, high-grade intracranial stenosis may cause reperfusion hemorrhage. Oversizing stents in an attempt to achieve minimal residual stenosis also increases the risk of vessel rupture and dissection.
(a)
(b) Figure 32.1 (a) Digital subtraction angiogram of a right vertebral artery injection demonstrating bilateral vertebrobasilar junction highgrade stenosis with reflux of contrast down the left vertebral artery; (b) angiogram following stent placement in the distal right vertebral artery demonstrating excellent resolution of the stenotic segment. There is no longer reflux of contrast into the left vertebral artery.
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Intracranial stenting for cerebrovascular pathology In addition, stents that are deployed rapidly and with high outward radial force increase the risk of dissection. Finally, stents differ in trackability. It is important that the stent chosen for stent-assisted angioplasty can be navigated through turns without significant resistance, to increase the likelihood of placement and reduce the risk of vessel injury. Recently, the group has begun to treat patients with high-grade stenosis with a staged approach.14 This approach consists of submaximal angioplasty and then repeat angioplasty ≥ 1 month later. Stenting of the lesion is performed at that time. With this staged approach, no permanent neurological morbidity has been observed.
Stent-assisted aneurysm management Future endovascular techniques will eventually replace surgery for intracranial aneurysms. Current techniques result in a significant rate of regrowth because of coil compaction and incomplete obliteration. Hemodynamic studies suggest that endosaccular occlusion with current coil technology are unlikely to cure aneurysms without complete elimination of neck remnants, especially at the inflow zone. Stents represent a method of neck remodeling with significant diversion of flow from the aneurysm inflow zone. Stenting of fusiform aneurysms, described by Higashida et al.15 and by the present group,16 may obviate the need for these technically challenging and risky procedures. Initially, both Guglielmi detachable coils (Boston Scientific Target, Fremont, CA) and a stent were used for the endovascular management of such cases, At present, however, this group and other investigators are advocating the use of low-porosity stents (i.e. without coils) as the primary treatment for vertebrobasilar fusiform aneurysms. Using in vitro side-wall aneurysm modelling, Lieber et al.17 demonstrated that aneurysm flow from the parent vessel lumen and into the aneurysm could be controlled with low-porosity stents. It seems logical, with sufficiently low porosity, that stents can recreate normal intraluminal laminar flow within the parent vessel with concomitant aneurysm thrombosis. Using laserbased imaging technology, investigators have demonstrated reduced flow vortices into aneurysms, with resultant stagnation and eventual thrombosis following stent placement. In addition to fusiform vertebrobasilar aneurysms, intimal dissections (which may develop into pseudoaneurysms) can be effectively treated with stents. As detailed by Lylyk et al.,18 dissecting aneurysms can be treated with stent-assisted coiling. In another report, Mericle et al.19 described stenting of a pseudoaneurysm arising from a dissection of the horizontal petrous internal carotid artery, Stenting of this lesion prevented coil herniation into the parent vessel and obviated the need for tight coil packing into a friable pseudoaneurysm dome. Malek et al.20 reported on an iatrogenic dissection of the basilar artery following angioplasty and stenting of a stenotic segment. This dissection was managed by deploying a tandem stent that covered the intimal flap, thereby restoring flow through the basilar artery. In the authors’ experience, lowporosity Magic Wallstents (Boston Scientific, Natick, MA) may be sufficient to treat these fusiform pseudoaneurysms and dissections without the additional need for coils.
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Before the development of remodelling techniques and intracranial stents, wide-necked aneurysms posed great challenges to endovascular surgeons. Coil herniation into parent vessels is more likely to occur in aneurysms with fundus-toneck ratios of < 2. Tight packing of these aneurysms is also more difficult, with follow-up angiography demonstrating coil compaction over time. Stent-assisted coiling of these aneurysms provides a buttress to protect the parent vessel from coil herniation, diverts flow from the aneurysm inflow zone, and allows for tighter coil packing (Figure 32.2). Case reports from Sekhon et al.,21 Lavine et al.22 and others23,24 have demonstrated optimal angiographic results following stentassisted coiling of wide-necked aneurysms. In a series of ten patients reported on by Lanzino et al.,24 aneurysms were treated with either stent-assisted coiling or stenting alone. No permanent complications occurred, and good angiographic results (> 90% occlusion) were achieved in patients treated initially with stent-assisted coiling. In a widenecked aneurysm model created by Imbesi and Kerber,25 the placement of a stent across the aneurysm neck was sufficient to disturb the slipstreams entering the aneurysm. Additional coil deposition caused even further disruptions of the slipstreams into the aneurysm. Such hemodynamic alteration may result in aneurysm thrombosis. New liquid embolic agents show promise in the stentassisted management of wide-necked aneurysms, The advantage of these agents over coils is that they can assume the configuration of the aneurysm sac without leaving residual dead space. Ideal coil packing of an aneurysm results in only 30–40% occlusion of the fundus volume. Although higher rates of complete endosaccular occlusion might be achieved with the use of liquid embolics, parent vessel protection is often required to prevent extrusion of the agent into the vessel. Parent vessel protection can be achieved by means of balloon occlusion and/or stent placement. Animal studies by Murayama et al.26 have demonstrated excellent results with a combination of liquid embolic agent and stent placement (with and without concomitant deposition of coils) for the treatment of wide-necked aneurysms. Although some fear that jailing of vessels by stent struts may lead to small branch vessel occlusion, the strut diameter that is currently used intracranially is insufficient to occlude these vessels, As demonstrated by Wakhloo et al.27 in animal and in vitro studies, the pressure differential between parent arteries and their side-branches maintains vessel patency across stent struts that do not cover more than 50% of the branch vessel orifice. Risks of aneurysm treatment with liquid embolics include leakage of the agent into the parent vessel, resulting in ischemia and possible vessel thrombosis.
Arteriovenous fistulae and venous occlusions Dural sinus thrombosis resulting in intracranial hypertension may cause symptoms ranging from headaches to blindness and even brain death. In many cases, dural sinus thromboses can be treated using pharmacological thrombolysis, mechanical clot evacuation and/or anticoagulation therapy. Complex, symptomatic arteriovenous fistulae may require a combination of these interventions. Murphy et al.28 describe a case of a type IV transverse sinus arteriovenous fistula with a transverse
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(a)
(b)
(c) Figure 32.2 (a) Anteroposterior (left) and lateral (right) angiographic views demonstrating a large basilar trunk aneurysm; (b) unsubtracted angiogram demonstrating the stent acting as a buttress against the coil mass; (c) angiogram of the basilar artery following successful stem-assisted coiling of the aneurysm with preservation of the anterior inferior cerebellar arteries.
sinus thrombosis in which the patient was treated with mechanical thrombolysis followed by the insertion of multiple stents. Stents were placed from the transverse sinus to the internal jugular vein. This procedure re-established normal drainage and simultaneously obliterated the dural arteriovenous fistulae, Malek et al.29 describe the case of a 13-year-old
boy with aphasia and right hemiparesis secondary to multiple dural arteriovenous fistulae and posterior sagittal, bilateral transverse and occipital sinus occlusions. After failure of medical therapy, angioplasty of the left transverse sinus and occipital sinus was performed. Over the next few days, the occlusions recurred. Repeat angioplasty followed by stenting
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(b)
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(e) Figure 32.3 An elderly man presented with sudden onset of left-sided weakness and a depressed level of consciousness. (a) Intracranial angiogram demonstrating right carotid occlusion in the supraclinoid region without crossover filling of the right hemisphere through the anterior communicating artery or significant meningeal collateralization; (b) angiogram demonstrating a right internal carotid artery (ICA) occlusion at the level of the posterior communicating and ophthalmic arteries; (c) anteroposterior view demonstrating the 2 5 × 8.0 mm stent in the proximal portion of the middle cerebral artery (MCA); (d) lateral view demonstrating the 2.5 × 8.0 mm stent in the proximal portion of the MCA; (e) right ICA injection demonstrating filling of the MCA and the distal branches with persistent occlusion of the anterior cerebral artery circulation.
of the occipital sinus was performed. At 3 months’ follow-up, the occipital sinus was patent and was the significant conduit for drainage of venous outflow. The patient was asymptomatic at the 12-month follow-up evaluation. Stenting of occluded venous sinuses should not be considered first-line therapy but, rather, as one option for failed medical therapy and/or failed thrombolysis (medical and mechanical), The choice of a low-porosity stent in this setting seems preferable as the stent may function both to maintain vessel patency and to seal arteriovenous fistulae sites.
Stent placement for acute stroke Despite many novel devices and pharmacotherapies, acute stroke remains a leading cause of morbidity and mortality in the US. In 2001, there were an estimated 800,000 new strokes. Although intra-arterial thrombolytic agents have enabled clinicians to recanalize vessels, maintaining lumen patency, especially in the face of underlying focal stenosis, can be more difficult. Following failed thrombolysis with intra-arterially administered therapeutic agents such as reteplase or abciximab, balloon angioplasty or microsnares are sometimes used to morselize clot. Should the clot be effectively lysed, the presence of residual stenosis or dissection can present a
dilemma. The stenosis can be managed by subsequent stent insertion. In this setting, this group has occasionally used stents intracranially to treat significant residual stenosis. The rationale behind such an intervention is that residual narrowing may induce sluggish flow through diseased portions of the vessel, resulting in recurrent acute thrombosis. Recently, stents have been inserted in vessels that continue to occlude acutely despite maximal pharmacotherapeutic thrombolysis (LN Hopkins, unpublished data). In this setting, stent insertion has been used as a last resort following hours of failed mechanical and pharmacological thrombolysis. Perhaps stents should be considered sooner for occlusions that seem resilient to conventional intra-arterial thrombolysis. In the authors’ experience, excellent angiographic results were achieved, but clinical outcome was poor owing to prolonged ischemic time from large vessel occlusion (Figure 32.3).
Periprocedural medical management Catheters, wires, balloons, and stents all have the potential to cause intimal injury and subsequent thrombosis, embolus, and vessel occlusion. In addition, all devices are thrombogenic. When blood encounters foreign substances, a monolayer of platelets and fibrin becomes adherent, depending on
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the surface charge, chemical properties, and surface irregularities of the foreign body. Therefore, proper anticoagulation and antiplatelet premedication is essential before these devices are introduced within the intracranial circulation. Clinicians must also be careful when using and dosing a variety of anticoagulants in settings of acute stroke or critical stenosis, as intracerebral hemorrhage can occur. For most intracranial stent procedures, an intra-arterial or intravenous bolus of 70 U/kg of heparin is administered following catheterization of the common carotid artery In addition, all saline flush bags are primed with heparin (1 U/ml). The activated coagulation time should be kept between 250 and 300 seconds. If possible, patients should be placed on aspirin and clopidogrel for 2–3 days before the procedure or given a loading dose of 300 mg earlier that day. Aspirin is the most widely used antiplatelet medication. The mechanism of action is by inhibition of cyclooxygenase-1. Therefore, thrombin and cellular proliferation from plateletactivated mitogenic activity are uninhibited with aspirin treatment alone. Clopidogrel is often used synergistically with aspirin. Clopidogrel is a thienopyridine derivative that inhibits the binding of ADP to its platelet receptor and prevents platelet aggregation. The antiplatelet action is irreversible and lasts for 7–10 days. Evidence in the cardiac literature supports the use of combination antiplatelet regimens. In the Stent Anticoagulation Restenosis study,30 the rate of complications such as myocardial infarction, death, repeat angioplasty, or requirement for coronary bypass at 1 month was reduced by 80% for the aspirin and ticlopidine group compared with the aspirin-only group. The advantage of a combination antiplatelet regimen is supported in animal models, as demonstrated by a marked reduction in the deposition of platelets and fibrinogen on stents placed in baboons treated with a combination of aspirin and clopidogrel versus those treated with aspirin alone. Some clinicians use glycoprotein IIb/IIIa inhibitors along with aspirin and either lower-dose heparin (40 U/kg) or no heparin, with low rates of intraprocedural complications. A platelet glycoprotein IIb/IIIa receptor-specific antibody, abciximab, prevents the binding of fibrinogen to these platelet receptors, thus inhibiting platelet aggregation. When administered intravenously, abciximab has a half-life of 10 minutes, but its pharmacological action lasts for 48 hours (although it is easily reversed with platelet transfusion). Eptifibatide, a cyclic peptide that may be a more specific inhibitor of glycoprotein IIb/IIIa receptors, is shorter acting and may be less likely to result in hemorrhagic complications. Platelet inhibition lasts for 2–4 hours following the administration of eptifibatide. The coronary literature supports such anticoagulation regimens; however, a paucity of documentation exists in the neurosurgical literature. Heparin can be reversed with protamine, whereas platelet transfusions are needed to reverse the effects of abciximab. Several studies in the cardiac literature suggest safety and trends towards benefits with these agents: however, few reports in the neurosurgical literature have examined the use of these agents during and after intracranial endovascular therapy. Preliminary data from this group suggest that hemorrhage of a chronically ischemic brain is more likely to occur
with glycoprotein IIb/IIIa inhibitors, so these agents are not administered in patients with atherosclerotic disease causing high-grade stenosis or chronic hypoperfusion seen on singlephoton emission computed tomographic studies. In patients without ischemic changes on preoperative magnetic resonance imaging, some clinicians administer a combination of intraprocedural heparin (one-time intravenous bolus of 70 U/kg for a target activated coagulation time of 200 seconds) and a 0.25 mg/kg intravenous bolus of abciximab over 10–60 minutes before the procedure. Following the procedure, abciximab is intravenously infused for 12 hours at a rate of 10 µg/minute. In place of abciximab, eptifibatide may be administered with a loading dose of 135 µg /kg followed by a 20–24 hour infusion of 0.5 µg/kg. Immediately after stenting, patients who may be considered for short-term therapy with glycoprotein IIb/IIIA inhibitors must undergo a computed tomographic scan to exclude post-procedural intracranial hemorrhage, which would preclude the use of these agents. Following routine stent placement, heparin therapy is discontinued but not actively reversed. Patients are typically maintained on clopidogrel (75 mg/day) for 1 month and aspirin indefinitely. Modifications of anticoagulation regimens depend on the indication for stenting (for acute stroke, some interventionists would not discontinue heparin immediately after the procedure) and any complication that may have resulted.
Technique of stent placement The technique of stent placement varies slightly from institution to institution. The following is a general outline of the steps followed by this group to place stents in the intracranial circulation for stenting for most indications. The procedure is performed in a suite with biplane digital subtraction angiography and fluoroscopic imaging capabilities. Following femoral artery puncture, a 6-French sheath is inserted. A 5-French catheter is advanced over a 0.035-inch hydrophilic wire into the aortic arch, and the artery of interest is catheterized. A roadmapping technique is used. The sheath and catheter are removed with the wire left in place, and a 6-French guide catheter is then placed into the vessel, Routine transfemoral angiography is performed, and a 3-French catheter is advanced coaxially over a 0.014-inch microwire into the intracranial vessel. The wire is removed, and a stiffer 300-cm 0.014-inch exchange wire is then placed through the microcatheter. This system is then manipulated across the lesion. The microcatheter is withdrawn and a balloonmounted, over-the-wire stent is navigated across the area of interest, where it is deployed at 6–8 atmospheres of pressure. Angiograms are obtained following balloon deflation. As previously mentioned, this group performs angioplasty followed by delayed (≥ 1 month) repeated angioplasty and stent placement for severely stenotic lesions.14
Future directions Novel modifications of stent surfaces using biomaterials science and surface-coating techniques have opened a new area in stent research. Investigators have demonstrated some
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Intracranial stenting for cerebrovascular pathology promising results in both human and animal studies with the use of heparin-coated stents. Although rates of subacute thrombosis with hepar in-coated stents are lower in some series, consistently significant reductions in restenosis rates have not been demonstrated. Stents that have shown promise in the cardiac literature are those coated with phosphorylcholine, paclitaxel (taxol), nitric oxide and rapamycin (sirolimus).31–34 Of the many drug-coated stents under clinical investigation, rapamycin-coated stents seem exceptionally promising. Zohlnhöfer et al.34 showed that gene-expression patterns of human neointima demonstrate the upregulation of FKBP12 at the messenger RNA and protein level of human neointima. FKBP12 is involved in controlling transforming growth factorβ (TGF-β) receptor I signaling. Rapamycin, which acts at the FKBP12 receptor site, has been shown to reduce neointimal formation in animal models. The arrest of neointimal formation and resultant in-stent restenosis may be due to rapamycin’s effects in blocking protein synthesis and the concomitant induction of cell-cycle arrest. Recent human trials suggest that rapamycin-coated stents reduce restenosis rates. In one of the first human trials of sirolimus-coated stents, reported by Sousa et al.,33 none of the patients treated with the coated stents demonstrated restenosis at the 4–6 month follow-up evaluation. The results from the Rapamycin-Eluting Versus Plain Polymer Stents (RAVEL) study of 220 European patients were recently disclosed.35 RAVEL was a randomized, multicenter, double-blinded study of sirolimus-coated, balloon-expandable stents in patients with single lesions in the coronary vasculature. According to the results of this study, no restenosis was found at 6 months in patients treated with the coated stents, and neointimal volume was 2 vs. 37% in those treated with noncoated stents. Although these data come from findings following stenting of cardiac vessels, the same response may be demonstrated in the intracranial vasculature. A second drug-coated stent that has recently shown clinical promise for inhibiting in-stent restenosis is the paclitaxelcoated stent. Paclitaxel inhibits restenosis by altering the stability of mictrotubules. This alteration leads to the inhibition of cell replication and intracellular signaling. In animal models, reductions in neointimal proliferation at blood concentrations
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100 times lower than antineoplastic levels have been shown.36 In a recent pilot clinical trial, none of the 21 patients demonstrated restenosis of stented coronary lesions. The ASian Paclitaxel-Eluting stent Clinical Trial (ASPECT) trial32,37 compared the safety and efficacy of high-dose and low-dose paclitaxel-coated stents versus uncoated stents in patients with single lesions in coronary arteries. At 6 months, restenosis rates had dropped from 27% in the control group to 4% in the highdose paclitaxel group. These findings are attributed to reductions in the volume of neointimal hyperplasia. It will be interesting to see how the rapamycin- and paclitaxel-coated stents will be applied in the future for stenting of intracranial stenotic lesions. Radioactive stents have generated much interest; however, the results have been variable and seem to be dependent on the animal model, the time to sacrifice and the radioactivity of the stents. It is hoped that development and further research of coated stents will provide clinicians with prosthetic devices that locally inhibit platelet-fibrin deposition, mitigate clot formation and restenosis, and promote local endothelialization.
Caveats Intracranial stenting is a novel technique, still in its early developmental stages. Although intracranial stents are being used with increasing frequency, it is important to remember that there are no long-term data regarding rates of patency, restenosis, or vessel injury. In addition, the effects of stentinduced intimal hyperplasia are not known in the cerebral vasculature, and the treatment for in-stent stenosis may be problematic. Stenting of intracranial vascular pathology may provide clinicians with therapeutic interventions where none existed previously. The subset of patients who are not surgical candidates, for reasons such as severe cardiopulmonary problems, now has alternative non-surgical options for intracranial revascularization for severe stenoses or aneurysm occlusion. Clearly, long-term, prospective data are needed to understand and define the efficacy of intracranial stenting for diverse cerebrovascular disease processes.
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Horowitz MB, Purdy PD. The use of stents in the management of neurovascular disease: a review of historical and present status. Neurosurgery 2000; 46: 1335–43 Dotter CT, Judkins M. Transluminal treatment of arteriosclerotic obstruction. Description of a new technique and a preliminary report of its application. Radiology 1964; 172: 904–20 Dotter CT. Transluminally-placed coilspring endarterial tube grafts. Long-term patency in canine popliteal artery. Invest Radiol 1969; 4: 329–32 Dotter CT, Buschmann RW, McKinney MK, Rosch J. Transluminal expandable Nitinol coil stent grafting: preliminary report. Radiology 1983; 147: 259–60 Rousseau H, Joffre J, Puel J et al. Percutaneous vascular stent: experimental studies and preliminary clinical results in peripheral arterial diseases. Int Angiol 1987; 6: 153–61 Palmaz JC. Intravascular stenting: from basic research to clinical application. Cardiovasc Interv Radiol 1992; 15: 279–84 Sundt TM Jr, Smith HC, Campbell JK et al. Transluminal angioplasty for basilar artery stenosis. Mayo Clin Proc 1980; 55: 673–80
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Connors JJ III, Wojak JC. Percutaneous Transluminal angioplasty for intracranial atherosclerotic lesions: evolution of technique and short-term results. J Neurosurg 1999; 91: 415–23 Derdeyn CP, Cross DT III, Moran CJ, Dacey RG Jr. Reversal of focal misery perfusion after intracranial angioplasty: case report. Neurosurgery 2001; 48: 436–40 Mori T, Kazita K, Chokyu K et al. Short-term arteriographic and clinical outcome after cerebral angioplasty and stenting for intracranial vertebrobasilar and carotid atherosclerotic occlusive disease. AJNR Am J Neuroradiol 2000; 21: 249–54 Gomez CR, Misra VK, Campbell MS, Soto RD. Elective stenting of symptomatic middle cerebral artery stenosis. AJNR Am J Neuroradiol 2000; 21: 971–5 Levy El, Horowitz MB, Koebbe CJ et al. Transluminal stentassisted angioplasty of the intracranial vertebrobasilar system for medically refractory, posterior circulation ischemia: early results. Neurosurgery 2001; 48: 1215–23 Fessier RD, Lanzino G, Guterman LR et al. Improved cerebral perfusion after stenting of a petrous carotid stenosis: technical case report. Neurosurgery 1999; 45: 638–42
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Murayama Y. Vinuela F. Tateshima S et al. Endovascular treatment of experimental aneurysms by use of a combination of liquid embolic agents and protective devices. AJNR Am J Neuroradiol 2000; 21:1726–35 Wakhloo AK, Tio FO, Lieber BB et al. SeIf-expanding Nitinol stents in canine vertebral arteries: hemodynamics and tissue response. AJNR Am J Neuroradiol 1995; 16: 1043–51 Murphy KJ, Gailloud P, Venbrux A et al. Endovascuiar treatment of a grade IV transverse sinus dural arteriovenous fistula by sinus recanalization, angioplasty, and stent placement: technical case report. Neurosurgery 2000: 46: 497–501 Malek AM, Higashida RT Balousek PA et al. Endovascuiar recanalization with balloon angioplasty and stenting of an occluded occipital sinus for treatment of intracranial venous hypertension: technical case report. Neurosurgery 1999; 44: 896–901 Leon MB, Baim DS, Popma JJ et al. A clinical trial comparing three antithrombotic-drug regimens after coronary-artery stenting. Stent Anticoagulation Restenosis Study Investigators, N Engl J Med 1998; 339: 1665–71 Buergler JM, Tio FO, Schulz DG et al. Use of nitric-oxide-elut-ing polymer-coated coronary stents for prevention of restenosis in pigs. Coron Artery Dis 2000; 11: 351–7 Park S-J. The clinical effectiveness of Paclitaxel-coated coronary stents for the reduction of stenosis in the ASPECT Trial. American Heart Association Scientific Session, Anaheim, CA, 2001 Sousa JE, Costa MA, Abizaid A et al. Lack of neointimal proliferation after implantation of Sirolimus-coated stents in human coronary arteries: a quantitative coronary angiography and three-dimensional intravascular ultrasound study. Circulation 2001; 103: 192–5 Zohlnhöfer D, Klein CA, Richter T et al. Gene expression profiling of human stent-induced neointima by cDNA array analysis of microscopic specimens retrieved by helix cutter atherectomy: detection of FK506-binding protein 12 upregulation 2001; 103: 1396–402 Morice M, Serruys P, Sousa 1 et al. The Ravel Trial: Transcatheter Therapeutics, 2001 <www.tctmd.com/expertpresentations> Heldman AW, Cheng L, Jenkins GM et al. Paclitaxel stent coating inhibits neointimal hyperplasia at 4 weeks in a porcine model of coronary restenosis. Circulation 2001; 103: 2289–95 Anonymous: Transcatheter Therapeutics, 2001 <www. tctmd.com/ expert-presentations>
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The stroke unit P Lylyk and JF Vila
Introduction Stroke is the most common admission diagnosis in patients with acute neurological disorders. In 1999, stroke killed 167, 366 people, every 53 seconds someone suffers a stroke, and it causes one out of every 14.3 deaths in the US. About 4,600,000 stroke survivors are alive today, but there is a high degree of recurrence and long-term disability in 30% of cases. The chance of having a stroke before the age of 70 years is 1 in 20 for both genders. The annual incidence rate has declined for total stroke.1 The development of units specialized in stroke patient management modified its natural history,1–5 starting in the 1960s when stroke patients were assisted in neurological wards incorporating early and intensive rehabilitation. The ischemic tissue at risk owing to infarction led to the concept of tissue in penumbra, defined as a region of restricted blood supply in which energy metabolism is preserved.6 The influence of the time elapsing from the onset of ischemia to the initiation of treatment has introduced the concept of the therapeutic window. This temporal concept generated the need to make available promptly diagnostic and therapeutic procedures performed and interpreted by experienced physicians, a decisive demand in developing stroke teams.7 However, it was effective stroke treatment with intravenous thrombolytics that became the determining factor for the American Heart Association Council to recommend the admission of stroke patients to specialized centres where strategies were developed to minimize delays.3,4,8 Transfer time was reduced with more centres providing the basic requirements for intravenous treatment with tissue plasminogen activator (tPA), while consultation times were lowered through social communication strategies and in-hospital times reduced with stroke teams.9 Stroke units and stroke teams are the best approach to improving the time liness of caring for stroke. Several studies have shown that stroke units are associated with reductions in morbidity, mortality, hospital stay, and cost.4,8,10 Estimated cost per stroke in the US varies according to whether indirect cost derived from disability and mortality is taken into account. In 1993 the annual cost reached $30 billion. Hospital, equipment, rehabilitation, and medical costs accounted for US$17 billion and the remainder, US$13 billion, was due to indirect costs such as post-stroke productivity reduction. Hospital costs during the acute period comprise approximately 20% of the total figure. In the first 90 days after onset of stroke, costs amounted to US$6 billion; that is, US$15,000 per patient.11
The life cost of stroke varies widely by type of stroke and entails considerable costs beyond the first years after a stroke.12,13 In Europe the estimated global cost of stroke increased to US$43.3 billion in 1998.14 Given the marked economic significance of stroke, care should be of high priority for hospitals.15 The major predictors of acute hospital costs of stroke in this environment are length of stay, stroke severity, heart disease, male gender, and use of heparin.16 Information about the distribution of costs during the first hours of stroke, the time of greatest expenses and greatest therapeutic benefit, is not available. Treating ischemic stroke with tPA within 3 hours of symptom onset results in a net cost saving to the health-care system.17 The stroke unit is a geographical area specifically devoted to stroke cases, although available systems such as intensive care units (ICUs) may be used. Stroke teams are staffed by health-care professionals including clerks, paramedical assistants, emergentologists, neurologists, interventional neuroradiologists, social workers, and rehabilitation teams. This staff is trained to recognize patients with stroke, with or without risk to life, the exact time of stroke onset, the therapeutic window, and the therapeutic complexity required in each case. The success of this type of organization depends on each member’s responsibility. A mistake made by any one of them will have the same consequence: delay in the patient’s assistance, less therapeutic efficacy, and major complications. The clerk who receives the call for stroke co-ordinates to send the patient to a stroke unit selected according to geographical position and needs. The clerk confirms acceptance and informs the meeting point to the stroke teams using beepers. If the patient’s life is at risk or if the information is inaccurate, the meeting point is the emergency department when available; otherwise, the meeting point is the computed tomography (CT) room. The purpose of this organization is to provide a rapid response service for stroke patients, improve diagnosis, and rapidly implement stroke therapies. The stroke team concept may improve the efficiency of stroke care in small communities and academic hospitals. Stroke units may be classified according to their diagnostic and therapeutic resources. Regardless of their level of technological complexity, these organizations share basic requirements such as mobile beds, air mattresses, central oxygen and delivery device, electrocardiographic and electroencephalographic monitors, endotracheal intubation, infusion pump, pulse oximetry, pneumatic boots, defibrillator, set of needles, intubation equipment, portable chest x-ray, and other usual devices. 255
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The low-level complexity stroke unit requires an aroundthe-clock CT team as well as a stroke team. These conditions are mandatory for the use of intravenous thrombolytics in ischemic stroke and for hemorrhagic stroke management.18,19 Major technological resources and immediate availability enhance the therapeutic options in the stroke unit (Table 33.1). Treatment starting after the first 3 hours of evolution requires the differentiation of necrotic from penumbra areas in the ischemic area. Even though the difference has not been definitively established, studies with magnetic resonance imaging (MRI) allow a greater approximation than those performed with CT.20,21 Equipment with ultrasound contributes to the efficiency of the stroke unit; however, its peak complexity is reached when high-resolution digital subtraction angiography (DSA) equipment is available, managed by specialists in the field of endovascular diagnosis and treatment. Patients must be assisted in a stroke unit according to therapeutic requirements. The basic level of complexity is limited to the use of intravenous thrombolytics in the first 3 hours. Ischemic stroke cases should not be accepted because the transportation, evolution, and in-hospital time exceed the patient’s therapeutic window. Economic limitations for the development of highcomplexity centres should be a stimulus for comprehensive network linking.22 The increase in complexity calls for greater investment, which only makes sense if a sustained demand exists. Educational efforts to improve public awareness about stroke decrease the delays in calling for assistance. Medical education can be successful in reducing the utilization of associated charges for specific diagnostic tests, necessary to achieve significant cost savings. Community education programmes and keeping the population informed are required for several reasons. Members of the community believe in progress and are anxious for news and information that will enable them to shape their future. Civic information increases social demand stimulating the development of stroke units, but the information to be released should be analyzed carefully. Before announcing the advantages of stroke units, it is crucial to set them up, prepare stroke teams, define their complexity, and try out how they work. At this stage, companies specialized in social communication and ethical advertising should be consulted, and an awareness programme designed in accordance with local idiosyncrasy. Once assistance has been organized, the community may be informed about the advantages of the centers specialized
Table 33.1
in stroke assistance. Assistance work is organized by protocol and the information stored in a data bank. Its analysis allows the monitoring of therapeutic results, secondary prevention, control of vascular risk factors and optimized hospitalization, as well as their costs. This information is also used for ongoing medical education of the stroke team, paramedical assistants, technicians, resident physicians, students, and patients and their families. The stroke unit is the appropriate place for research on cerebral vascular pathology and is a major contributor to efficacy trials.
Stroke Stroke may be defined as an acute neurological syndrome secondary to a focal circulatory fault due to ischemia or hemorrhage,23 avoiding its use to qualify subacute and chronic defects.24 Sound knowledge of bimolecular changes in neural tissue brought on by focal ischemia is the basis for rational therapy. Knisely wrote that “Living things live in four dimensions, three of space and one of time. The living histology of each tissue provides the architecture and the physiology provides items which change along the time dimension.” 25 Stroke is a polygenic disorder. In acute ischemia the biomolecular changes are temporary and in chronic ischemia the structural changes are prominent. Specific changes in gene expression may be used to infer injury or recovery. The expression “change” in molecular terms varies when the blood flow decreases. A decrease in protein synthesis occurs when the blood flow decreases by 50% through the inactivation of
Hypoxia area (HIF) Cell function stopped (alive) Denatured protein (HSP-70) > Ions ≥ Flow Cell stops protein production > VEGF ≥ Permeability < Glycolysis ≤ Metabolism Selective cell death Necrosed cells DNA: Repaired or Damaged (Apoptosis)
ml/100 g/min (cb flow)
Assistance levels in the stroke unit
A: Basic
B: Medium
C: High
Stroke team CT scan
Stroke team CT scan MRI TCD
Stroke team CT scan MRI TCD Interventional neuroradiology
CT: computed tomography; MRI: magnetic resonance imaging; TCD: transcranial Doppler
Cell depolarization (Spreading Depression)
Figure 33.1 Predominant molecular expressions in areas with dissimilar levels of focal cerebral blood flow. Physiopathological changes in cells depend on their localization within the penumbra zone. HSP-70: heat shock proteins; HIF: hypoxic inducible factor (regulation of genes by HIF receptors). (Modified from Sharp et al.26)
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The stroke unit Flow Direction Venous end
Capillary O2 30 µm O2
Brain Tissue
Normoxia
Interface
Tissue Ratio
0
0
(a) Capillary
Venous end
0
Hypoxia (Watershed Capillary)
30 µm
Brain Tissue
Interface
Tissue Ratio
O2
O2
0
(b) Figure 33.2 The rate of diffusion of oxygen molecules is directly proportional to the driving force, which is the slope of the pressure versus distance curve. The oxygen dissociation curve is continuous at the tissue interface: (a) distance between capillaries, tissue interface status and all other conditions are normal (erythrocyte concentrations, oxygen partial pressure and flow rate); (b) distance between capillaries is doubled (brain edema) with all other conditions normal. A large hypoxic and anoxic area develops in the brain tissue interface between capillaries. (Modified from Knisely et al.25).
several elongation factors. Adenosine triphosphate (ATP) is decreased or blocked when the blood flow falls to 20% of its normal level. Protein synthesis continues in cells that survive an infarct, provided blood vessels are spared, playing a role in inflammatory cell invasion. Adjacent to infarcts there is a rim representing selective neuronal change that defines infarct margins (tunnel stained), the cells of which may have damaged DNA. However, DNA repair genes may contribute either to cell death or to survival. Responding to cell injury, the major specifically induced protein is heat shock protein-70 (HSP-70) Overall, this area has been defined as a molecular penumbra of protein denaturation.26 The zone of expression extends beyond the tunnel stained rim adjacent to the infarct. Hypoxic inducible factor (HIF) is induced by changes in molecular oxygen levels in tissue outside the infarction. The genes induced by HIF tend to increase blood flow, glucose delivery, and maintenance of energy after chronic hypoxia. Vascular endothelial growth factor (VEGF) is an HIF target gene induced by focal ischemia. VEGF is
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believed to influence the permeability of existing vessels and contribute to edema.27 In the brain, open capillaries are distributed with striking regularity related to oxygen supply.28,29 Oxygen is not stored in the brain. Each capillary supplies a geometrically limited short radius cylinder of brain tissue, so that the maximal possible effective oxygen diffusion distance is short. When the distance between the capillary increases as a result of edema, the tissue in the interface becomes hypoxic. In this area the rate of oxygen restriction varies between the region receiving oxygen and that which is deprived.25 The present authors coined the term watershed capillary hypoxia to denote the hypoxia at the tissue interface that explains the physiopathological mechanism of the neurological defects in acute and chronic edema. Ischemia with hypoxia and hypoxia without ischemia produce remarkably different physiological responses in the brain. Ischemia is associated with raised extracellular glutamate concentrations and induces the expression of stress protein (HSP). Hypoxia without ischemia is not associated with glutamate elevation and doe not induce any gene product. The relative benignity of hypoxia without ischemia has also been demonstrated. More uncommonly, hypoxia may produce neuronal changes in the thalamus, pontine nuclei and arterial border zones alone, but no laminar necrosis typical of hypoxia-ischemia.30 After focal ischemia, several immediate-early genes are induced throughout the hemisphere, most likely by spreading depression or repeated ischemic depolarization.31 Bilateral changes in the cortex after focal ischemia play a role in plastic changes.32 After focal ischemia, there are multiple molecular penumbrae changing throughout time.26
Prehospital management The objective of adequate prehospital management is the preservation of life, by recognizing a stroke and organizing patient transfer. Life preservation is the first assistance objective, where each risk condition is managed according to standard assistance control for each vital parameter. Immediately after the patient has been stabilized, stroke diagnosis must be confirmed (Table 33.2). The exact time of onset of the neurological defect should be known, as inaccuracy in onset time is the most frequent
Table 33.2
Differential diagnosis of stroke
Seizure Migraine Hypoglycemia Tumor Syncope Hysteria Multiple sclerosis Infection Drug overdose Head injury Hypertensive crisis Subdural or epidural hematoma
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cause of hemorrhagic transformation due to thrombolytics. Onset time is known accurately in approximately half of the patients admitted, of whom about half are admitted within 6 hours of the stroke. Once the stroke is recognized, the nearest stroke unit is called to coordinate patient transport and admission. Clerical delays will be cause for malpractice suits in the near future. It is useful to draw up a list of procedures for prehospital recognition of stroke patients, after consulting guidelines validated by the University of California Stroke Unit.33 The objective of safe and quick transportation is to shorten treatment administration time. If the person who calls recognizes that the patient is suffering from a stroke, the patient should be transferred immediately, unless the ambulance arrives within minutes. Many patients wait for half an hour or more before being taken to assistance centres that are only minutes away. Patients who require special care owing to their clinical condition or have lost consciousness must be transported according to standard recommendations.
In-hospital management The objective of in-hospital management is life preservation, to achieve a precise diagnosis and quick commencement of treatment. If the patient’s life is at risk the meeting point is the emergency department. If breathing is abnormal, an airway is opened and breathing is checked for adequate ventilation. Respiratory frequency, respiratory pattern, and respiratory efficiency, by monitoring oxygen saturation with pulse oximetry, are recorded, aiming at a target exceeding 95% saturation. A blood sample is sent to the laboratory to determine blood gases and the team proceeds to respiration management according to standard therapeutic guidelines. Mechanical ventilation is most often required after the first day, with the onset of cerebral edema or hematoma formation, and may also occur in brainstem compression or when sedation is necessary.34 Both high blood pressure and low blood pressure have been regarded as independent prognostic factors for poor outcome, relationships that appear to be mediated in part by increased rates of early recurrence and death resulting from presumed cerebral edema in patients with high blood pressure, and increased coronary heart disease events in those with low blood pressure.35 Arterial hypotension must be corrected immediately according to its cause, but high arterial pressure figures require consideration. The increase in blood pressure in stroke is a uniform response to the ischemic event per se, but is unrelated to stroke severity.36 Blood pressure increase contributes to improved cerebral perfusion and the neurological defects caused by ischemia in patients with vasospasm due to subarachnoid hemorrhage, but in ischemic stroke this has not been proven.37 Dynamic cerebral autoregulation is globally impaired after ischemic stroke, when blood pressure figures, which are high at the beginning, spontaneously decrease within the first few days.38 The pharmacological decrease implies a risk for patients with ischemic stroke. The relative risk to early progression increases for every 20 mmHg of pharmacological basal pressure drop. Initial arterial pressure figures in a stroke patient receiving thrombolytics predict a hemorrhagic transformation, more accurately than images by CT scan.39 It has been established
that initial arterial pressure is related neither to stroke severity nor to its forecast at 3 months.40 In a moderate stroke, pressure figures for the first 24 hours predict arterial pressure 3 months in advance, thus enabling an early diagnosis of arterial hypertension.41 Isolated evidence suggests that the increase in arterial pressure can improve the neurological defects of ischemic stroke in certain cases. Some clinical conditions call for a decrease in arterial pressure figures in stroke patients.42 The authors’ drug of choice for this is nitroprusside, dissolving 50 mg in 250 ml of physiological solution and starting at 0.5 µg/kg per minute, then increasing by 0.5 µg/kg per minute every 5–10 minutes until the desired effect occurs. Arterial pressure is monitored every 10 minutes; basal figures should fall by no more than 15% in each control. Nitroprusside is preferred because of its cost–benefit ratio, availability and experience in this environment. Other drugs such as labetalol, nitrates, and enalapril are useful and recommended. Current guidelines for the management of stroke hypertension appear to have little influence on prescribing patterns, leading to considerable variations in practice.43 Systolic arterial pressure figures < 180 mmHg and diastolic arterial pressure figures < 105 mmHg are required in patients with stroke in the following conditions: during thrombolytic treatment, after subocclusive carotid stenosis treatment, arterial dissection, internal bleeding, recent surgery, acute myocardial infarction, hypertensive encephalopathy, intracranial hemorrhage, renal failure, subarachnoid hemorrhage with untreated aneurysm, abdominal aorta aneurysm, and hyperperfusion syndrome, among others. Having excluded the above cases, spontaneous blood pressure figures are respected when they remain within theoretical limits, i.e. systolic pressure < 220 mmHg and diastolic pressure < 120 mmHg, but they are corrected pharmacologically if there is evidence of alterations in cerebrovascular self-regulation. The decision to decrease arterial pressure must take into account particular clinical aspects, such as the presence of critical stenosis or carotid occlusion. In the authors’ experience, patients with those conditions have suffered seizures, loss of consciousness or stroke with the acute drop in pressure. An increase in main arterial blood pressure associated with bradycardia is a sign of increased intracranial pressure (ICP) due to edema, spontaneous hemorrhage or hemorrhagic transformation of an infarct. Hypoglycemia (< 70 mg/dl) may simulate an ischemic stroke. In patients with a history of diabetes or who take hypoglycemic drugs differentiated diagnosis is mandatory. If the appropriate test is not available and hypoglycemia is suspected, 20 cm3 of a 25% glucose solution should be given intravenously. The reversal of focal neurological defects due to hypoglycemia is immediate. Hyperglycemia in diabetic patients requires a sliding insulin scale to maintain a reasonable glucose level lower than 200 mg/dl and down to 60 mg/dl.34 In non-diabetic stroke patients it appears to be associated with poorer prognosis. Hyperthermia within 6 hours of acute stroke is associated with increased mortality. Fever should prompt investigation into the possibility of infection, and aggressive measures are justified because it may be harmful. A body temperature of > 38 ºC must be actively treated with antipyretics.44 The patient with hemorrhagic stroke may have hyperthermia
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The stroke unit when blood occupies the subarachnoid space or the ventricles. The onset of fever with an increase in focal neurological defect strongly suggests septic emboli as the origin of the stroke. Patients who fail the swallowing assessment should have a nasogastric tube inserted. Defects in sphincter control are treated in accordance with standard guidelines. Fluid management must be balanced with saline solutions as required.45 Electrolytes are monitored daily during the first few days, especially if blood occupies the ventricles or the subarachnoid space. Above all, fluid prescription should be reassessed at regular intervals in the light of laboratory values and the patient’s clinical status.12,46–50
Stroke classification The usual retrospective classification of ischemic stroke into transient ischemic attack, reversible ischemic neurological defect, minor and major is hardly useful in patients with actively coursing acute defects. The term stroke refers to clinical defects alone. The clinical classification used by this group derives from the magnitude of the neurological defect and the time elapsed, both weighty issues when deciding treatment and evaluating its risk (Table 33.3). The magnitude of the defect is measured by means of the National Institute of Health Stroke Scale (NIHSS).51 Currently, this group uses the modified NIHSSm classification, which avoids area of conflict present in the previous scale, such as level of consciousness, facial palsy, ataxia, and dysarthria (Table 33.4).52 These modifications achieve greater interobserver and intraobserver agreement and make its administration easier. All of these scales are complementary to the traditional neurological examination. Upon admission and on each examination, the neurological defect is quantified (according to NIHSS) at a given time (military time, 00.00), in such a way that at each evaluation the neurological evolution may be ascertained and thereby the functional anatomy condition of the affected cerebral territory inferred.53 Pathogenically, stroke is classified into ischemic or hemorrhagic. Ischemic stroke is more frequent, having a prevalence of 84%. The most common variety of ischemic stroke is
Table 33.3
Clinical classification of stroke∗
1. Progressive stroke 2. Regressive stroke
3. Stable stroke
The neurological defect increases with time, expressed by NIHSS score, related to prior evaluation The neurological defect decreases with time, expressed by NIHSS score, related to prior evaluation If the defect disappears within 24 hours, it is termed transient The neurological defect remains unchanged, expressed by NIHSS score, related to prior evaluation
∗JF Vila. If the pathogenesis is known, a qualification should be added, e.g. hemorrhagic progressive stroke NIHSS: National Institutes of Health Stroke Scale
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Table 33.4 Modified National Institutes of Health stroke scale Item no.
Item name
Scoring guide
1b
LOC questions
1c
LOC commands
2
Gaze
3
Visual fields
5a
Right arm motor
5b
Right leg motor
6a
Left arm motor
6b
Left leg motor
8
Sensory
9
Language
11
Neglect
0: 1: 2: 0: 1: 2: 0: 1: 2: 0: 1: 2: 3: 0: 1: 2: 3: 4: 0: 1: 2: 3: 4: 0: 1: 2: 3: 4: 0: 1: 2: 3: 4: 0: 1: 0: 1: 2: 3: 0: 1: 2:
answers both correctly answers one correctly answers neither correctly performs both tasks correctly performs one task correctly performs neither correctly normal partial gaze palsy total gaze palsy no visual loss partial hemianopsia complete hemianopsia bilateral hemianopsia no drift drift before 10 seconds falls before 10 seconds no effort against gravity no movement no drift drift before 10 seconds falls before 10 seconds no effort against gravity no movement no drift drift before 10 seconds falls before 10 seconds no effort against gravity no movement no drift drift before 10 seconds falls before 10 seconds no effort against gravity no movement normal abnormal normal mild aphasia severe aphasia mute or global aphasia normal mild severe
Score (out of 31): LOC: level of consciousness
atherothrombotic, followed by cerebral embolus, whereas only 38% of cases are classified as lacunar brain infarctions. Hemorrhagic stroke has a prevalence of 16%, in 10% of which blood is located in brain tissue and in the remaining 6% in the subarachnoid space.1 This pathogenic classification requires a neuroradiological study. A typical stroke subgroup classification54 is described in Table 33.5.
Neuroimaging Nineteen per cent of costs are associated with diagnostic tests used to evaluate the etiology of stroke: 91% of the patients undergo CT or MRI studies, 81% echocardiograms,
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Table 33.5 Stroke subgroup classification Ischemic stroke (TOAST-collapsed group) Atherosclerosis Cardioembolic Lacunar Others of determined aetiology Undetermined etiology Hemorrhagic stroke Primary Secondary TOAST: Trial of ORG 10172 in Acute Stroke Treatment.
48% non-invasive evaluation of the carotid arteries, 20% angiography and 6% electroencephalography. Rapid cranial CT is the most useful initial diagnostic test, crucial to approach the stroke.55 Diagnostic brain CT scan with 10 mm for each cut, without contrast, should be performed on an urgent basis to differentiate hemorrhagic from ischemic infarction. Findings must be interpreted in the light of the neurological symptoms. The possibility of subarachnoid hemorrhage (SAH), even without evidence of blood on the CT scan, warrants a lumbar puncture, but this is an exclusion criterion for thrombolytic therapy. Indirect signs of ischemia, which can be detected at a very early stage, include loss of insular ribbon, blurring of the interface between the grey matter or basal ganglia and
white matter, asymmetry of the cortical sulci or fissures and hyperdense vessel signs.47 Such signs, together with widespread marked hypodensity, increase the risk of intracranial hemorrhage after thrombolytics.56 CT affords valuable additional information, e.g. old infarct, small lacunar infarct, leucoaraiosis, and hydrocephalus. Studies using MRI suggest that ischemia produces a zone of potentially salvageable brain tissue. Diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) during MRI examination should allow more precise identification of early cerebral injury and characterization of regional blood flow. DWI can disclose focal ischemia within 2 hours after stroke onset. Ultra-early DWI is a predictor of early neurological deterioration after middle cerebral artery (MCA) occlusion.57,58 Perfusion MRI is performed by measuring the first cerebral pass of paramagnetic contrast agent, which provides maps of quantified flow changes in ischemic lesion. The lesion on PWI is larger than seen on DWI, a mismatch in size that may represent salvageable tissue following thrombolysis.59,60 The results of studies with apparent diffusion coefficient (ADC) volume to assess the areas at risk of hemorrhagic transformation and as a forecast of neurological evolution are controversial. MRI may also help in the immediate therapeutic decision and to assess the response to treatment.61–63 Clinicoradiological correlation needs further investigation including functional outcome scales.58 From the assistance provided by CT and the stroke team, the patient likely to benefit from thrombolysis may be readily selected.
1
(a)
(b)
(c)
Figure 33.3 Computed tomographic scans with cord sign (1). and predictive signs of hemorrhagic transformation: (a) hypodensity more than one-third of middle cerebral artery area: (b) disappearance of grey–white borders (observed in insular ribbon) and sulcus; (c) mass effects.
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(a)
(b)
(c)
(d)
261
Figure 33.4 Ischemic stroke of less than 3 hours: (a) abnormal signal in diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) in the left middle cerebral artery; (b) control after intravenous tissue plasminogen activator decreased the abnormal signal in DWI and PWI. (See Color plates.)
(a) Figure 33.5
(b) (a) Focal and; (b) multifocal stenoses in the posterior circulation, differentiated by digital subtraction angiography.
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Figure 33.6 Unstable right ischemic stroke. Digital subtraction angiography shows spontaneous and simultaneous dissection of all cervical vessels in a 45-year-old woman.
Ultrasound techniques are useful for assessment of the vessel wall and the lumen, blood-flow pattern and emboligenic focus. Pulsed-wave Doppler mode, B-mode echo tomography and transcranial Doppler (TCD) are used as a three-dimensional display duplex system. Diagnostic accuracy increases and provides a non-invasive technique for arterial assessment. With duplex carotid Doppler ultrasound and TCD, cerebral blood flow has been monitored during antihypertensive, vasospasm or thrombolytic treatment.64 A new approach has been to introduce bolus tracking, the measurement of the temporal pattern of echo-contrast bolus arrival in brain vessels by TCD, extracranial duplex or transcranial colour-code duplex sonography. Prolonged circulation time was found in patients with SAH, stroke, carotid stenosis, and hydrocephalus, while cerebral arteriovenous malformation (AVM) led to relevant cerebral circulation time shortening.65 However, sensitivity and specificity are lower than in digital angiography. Some authors consider that ultrasound may contribute to thrombus dissolution.66 Transesophageal echocardiography and Doppler ultrasonography have increased the rate of detection of cardiac,
aortic, and arterial causes of embolism. TCD, which to measure flow velocities in the basal arteries and routinely used to detect vasospasm, allows rising velocities to be interpreted as progressive vessel narrowing.37,67 Cerebral DSA is the gold standard for demonstrating vascular disease and is essential for diagnosis, hemodynamic status and endovascular treatment. By injecting contrast into the arch of the aorta, a procedure termed parenchymography, it is possible to obtain images of the microcirculation.68 This technique measures the change in basal cerebral perfusion before and after vasomotor stimuli, enabling focal perfusion defects and luxury perfusion to be detected in hypoxic ischemia. During clinical examination, blood samples are taken after predetermined arrangement with the appropriate laboratory. The analysis of blood samples and obtaining the required results by a telephone call usually take 30 minutes (Table 33.6). Partial thromboplastin time (PTT) is only needed before treatment if the patient receives heparin during the previous 48 hours and prothrombin time (PT) for possible use as anticoagulation therapy.
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263
Laboratory tests
Complete blood count Blood urea nitrogen Creatinine Platelet count Hematocrit Prothrombin time Activated partial thromboplastin time Glucose Electrolytes Pregnancy test
Figure 33.7 Ostial vertebral artery stenosis is a shadow point in ultrasound studies.
In summary, clinical classification discloses the magnitude and functional condition of the ischemic area, neuroradiological studies establish the pathogenesis and risk of treatment, and laboratory studies assess the feasibility of a given treatment.19,47,69–71 The following questions are therefore relevant to the therapeutic result. 1. Which is the pathogenesis of the stroke? 2. What is the severity of the neurological defect? 3. Are there functions to be recovered? 4. Is the condition stable? 5. Is the onset time known accurately? 6. Are there predisposing factors? 7. Was there a precipitating factor? 8. Which is the natural history of the lesion? 9. What level of feasibility does the selected treatment provide? 10. Is it a compassionate treatment? 11. Was it approved by the patient?
Ischemic stroke Among all therapeutic strategies into which studies are being conducted, for the treatment of ischemic stroke due to intracranial or cervical vessel occlusion, rapid dissolution of the thrombus–embolus is crucial for a satisfactory outcome. The treatment that has successfully undergone thorough trials is thrombolysis with intravenous drugs within 3 hours of onset.19 The thrombolytic technique varies according to the therapeutic window, the location of the thrombus–embolus and its size. It may be intravenous, intra-arterial, mechanical, or combined. Patients eligible for receiving thrombolytic therapy immediately after a diagnosis of ischemia are hospitalized in the stroke unit or ICU.
In 1996 the Food and Drugs Administration (FDA) approved tPA as an effective treatment for stroke when given within 3 hours after onset. In the National Institute of Neurological Disorders and Stroke (NINDS) Recombinant Tissue Plasminogen Activator Stroke study,72 intravenous tPA proved more effective than placebo, whereas the results of the European Cooperative Acute Stroke Study (ECASS I and II) and the Alteplase Thrombolysis for Acute Neuro-interventional Therapy in Ischemic Stroke (ATLANTIS) study were inconclusive.73–76 Intravenous thrombolysis with tPA is effective in carefully selected patients treated within 3 hours of symptom onset; it is the only proven therapy for ischemic stroke.17 In the NINDS study, the administration of tPA was associated with an additional 15% absolute risk reduction in death and disability. The risk of symptomatic intracerebral hemorrhage was 3.8%, and 86% of the patients treated over 3 hours after onset had negative results.56 Patients with baseline scores over 20 on the NIHSS or hypoattenuation on CT scanning that involved more than one-third of the territory of the MCA were associated with a higher risk of symptomatic intracerebral bleeding.72,77 However, in these subgroups the patients who received tPA were more likely to have near normal or normal scores on functional scales at 3 months. Neurological improvement was significantly more frequent in patients with hemorrhagic transformation after intravenous tPA than in those without.78 At any rate, such cases are still candidates for tPA.18 Patients with lacunar syndrome appeared to respond in their scores as other stroke subtypes. None of the patients in this subgroup older than 75 years turned out near normal on NIHSS score. In the Multicentre Acute Stroke Trial–Europe (MAST E) and the Multicentre Acute Stroke Trial–Italy (MAST I) study groups, streptokinase was no more effective than placebo.79,80 Biomolecular changes in time vary in response to treatment. The authors believe that times to recanalization testify to treatment efficacy better than times of starting thrombolytic administration. This is more likely to be a factor that explains the heterogeneous response to treatment in MCA model occlusion, such as starting thrombolytic drugs 3 hours after onset time. Intracerebral hemorrhage after thrombolytics increased to 10.7% in patients who had protocol deviations. Intravenous tPA may be administered relatively safely to menstruating women.81 It should be clearly explained to the patients and their families that there is a 12% chance of improved neurological
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(a)
(b) Figure 33.8 Ischemic stroke due to acute occlusion of the right internal carotid artery: (a) focal right hypoperfusion in parenchymography; (b) improved perfusion after endovascular treatment of the occluded carotid artery.
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The stroke unit outcome at 3 months against a 3% chance of early death from thrombolytic-induced intracerebral hemorrhage. The benefit is sustained for up to 1 year and CT scans disclose a mean 10 cm3 reduction in infarct volume at 3 months.
The first 03.00 hours after onset In selected patients with ischemic stroke, thrombolytic therapy should be started immediately, wherever they are.82 While the drug is being administered the patient is transferred to the stroke unit. With adequate organization, this group prefers to administer thrombolytics
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intravenously at first, followed later by the intra-arterial route, or intra-arterially directly.83 In basic stroke units tPA is administered intravenously with temporal limitations. It is a myth that only academic centres participated in the NINDS study. Vessel occlusion during endovascular procedures is a frequent complication calling for immediate treatment. The management of patients with stroke who may be eligible for intravenous tPA therapy is described in Table 33.7. It has been proposed that a lack of intravenous tPA could expose a subgroup of patients to a risk of hemorrhage (Table 33.8), in those with intracerebral hemorrhage predictors or in whom the artery has undergone spontaneous
STROKE Call to SU
Times* Calculate before transfer Onset, transport and in-hospital (Table 33.1) < 3 hours basal complexity SU > 3 hours basal complexity SU
Alert hospital* Alert stroke team Meeting point (Life at risk?)
No CT room Vital Blood samples Stroke? (Table 33.2) Baseline NIHSS score
Yes Emergency department ABCs Parameters Assess vital signs Provide oxygen
Blood samples (Table 33.6) Stroke? (Table 33.2) Baseline NIHSS score
Non-contrast scan Stroke classifications (Table 33.3) Photogenic (Table 33.5) Blood samples (Table 33.6) Read CT scans (Table 33.6)
Hemorrhagic
Ischemic
TREATMENT
Figure 33.9 Algorithm for the management of patients with suspected stroke. *Administrative decision; SU: stroke unit; ABC: airways, breathing, circulation; CT: computed tomography; NIHSS: National Institutes of Health Stroke Scale.
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recanalization and when neurological deficits are not due to stroke (Table 33.8). Another way to administer fibrinolytic drugs during this period is intravenously following intra-arterial routes alone; these have mainly been used successfully in recent research studies.83 Vessel recanalization may be performed by the extraction or mechanical rupture of the thromboembolus with a retriever or balloon device, with or without thrombolytic-associated drugs.84
Management 03.00–08.00 hours after onset Thrombolysis can be started with intravenous drugs within 3 hours after onset and subsequently intra-arterial drugs in patients in the borderline time zone. New developments continue to be made in the field of thrombolytic therapy.
Table 33.7 Management of patients with stroke who may be eligible for intravenous tissue plasminogen activator (tPA) therapy Inclusion criteria Ischemic stroke with a defined onset of < 3 hours from time tPA is to be started Neurological deficits in NIHSS < 21/42 CT scan shows no evidence of intracranial hemorrhage Exclusion criteria History Stroke or serious head trauma within past 3 months Major surgery or serious trauma within past 14 days Intracranial hemorrhage, AVM, or aneurysm Arterial puncture at a non-compressible site or lumbar puncture within previous 7 days Clinical Rapidly improving neurological signs or minor symptoms Systolic BP > 180 mmHg or diastolic BP > 110 mmHg Seizure at onset Symptoms suggestive of subarachnoid hemorrhage Recent myocardial infarction-induced pericarditis Gastrointestinal or urinary tract hemorrhage within previous 21 days Laboratory tests Taking anticoagulants or prothrombin time > 15 seconds or INR > 1.7 Received heparin within 48 hours preceding stroke onset and has raised partial thromboplastin time Platelets < 100,000/mm3 Glycemia < 50 mg/dl or > 400 mg /dl Positive pregnancy test In-hospital times Examination: 15 minutes CT scans and laboratory tests: 20 minutes Eligibility: 10 minutes Consent: 5 minutes Intravenous tPA < 180 minutes Treatment and management tPA 0.9 mg/kg total, maximum 90 mg Administer 10% of dose as an intravenous bolus in 1 minute Administer remaining 90% as a constant infusion over 1 hour Monitoring recanalization with TCD Do not give anticoagulant or antiplatelet agents for 24 hours from starting administration Admission to stroke unit Maintain systolic BP < 180 mmHg and diastolic BP < 115 mmHg Monitor BP for the first 24 hours after starting treatment, every 15 minutes for 2 hours after starting infusion, then every 30 minutes for 6 hours, then every hour for 18 hours Restrict central venous line placement or arterial puncture for 24 hours Do not insert indwelling bladder catheter for > 30 minutes after tPA Avoid insertion of nasogastric tube for 24 hours after tPA administration Patient weight is estimated for determination of drug dosages NIHSS: National Institutes of Health Stroke Scale; CT: computed tomography; AVM: arteriovenous malformation; BP: blood pressure; INR: International Normalized Ratio; TCD: transcranial Doppler.
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Intracerebral hemorrhage predictors
CT scans hypodensity > 1/3 MCA MRI ADCv < 500 ± 100 × 10−6mm/s2 NIHSS > 21/42 Time of onset > 180 minutes High blood pressure Blood glucose concentration > 120 mg/dl Concomitant antiaggregants CT: computed tomography; MCA: middle cerebral artery; MRI: magnetic resonance imaging; ADCv: apparent diffusion coefficient volume; NIHSS: National Institutes of Health Stroke Scale.
Interventional neuroradiology introduces new directions in the treatment of stroke, which are now being explored. Intra-arterial thrombolytic administration requiring neurointerventional specialist technique has the advantage of acting at the site of arterial occlusion. Drugs commonly used are urokinase, tPA, and prourokinase. Seventy per cent of patients who undergo this treatment achieve arterial recanalization, higher than those who undergo intravenous thrombolytic therapy. In the Prolyse in Acute Cerebral Thromboembolism (PROACT)85 trial, intra-arterial prourokinase was more effective than placebo. Intracerebral hemorrhage occurred in 10% and in 2% of those in the heparin group. PROACT II was shown to provide benefit in stroke by occlusion of the MCA starting more than 3 hours after onset.85–88 The authors use urokinase routinely owing to experience, availability and cost. The absolute volume of ischemic tissue on DWI with ADC values below a cut-off value < 500 ± 100 × 10-6 mm/s2 is a predictor of hemorrhagic transformation if rtPA is given over 3 hours after onset.89 Mechanical thrombolytic devices can replace thrombolytic drugs, and should be a critical option in large thrombi or in thrombi comprising material resistant to thrombolytic drugs.84 A further emergent therapy is ultrasonic thrombus
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disruption. The risk of hemorrhagic transformation is related to ischemic time, so that recanalization time is more critical than starting therapeutic time. Intra-arterial fibrinolysis demands the availability of high-definition radiological equipment, stocked material and experienced interventional neuroradiology. Patients with stroke may be eligible for intra-arterial tPA therapy (Tables 33.9 and 33.10). Recanalization due to the intravenous fibrinolytic is uncommon. Intra-arterial thrombolytic therapy could also be used in the early post-operative period; this appears efficacious but carries an increased risk of symptomatic intracranial hemorrhage.90–92 Laboratory controls before thrombolysis include hemography with platelet count, Quick, PTT, and fibrinogen; during thrombolysis every 100,000 U of urokinase, PTT and fibrinogen; and after thrombolysis, at 1, 6, and 24 hours, platelets, Quick, PTT, and fibrinogen. As radiological contrast is prothrombotic, vascular recanalization is monitored by TCD, and when flow appears angiography is carried out. In patients with stroke, there is suspicion of intracranial hemorrhage when there are symptoms such as neurological deterioration, bradycardia, acute hypertension, headache, nausea, and vomiting (Table 33.11).
Endovascular treatment Recent advances in technology have led to a renewed interest in treating cervical and intracranial lesions. Percutaneous transluminal angioplasty with stenting (PTAS) may be beneficial therapy in selected cases with atherosclerotic stenosis. An increased risk for stroke in patients with intracranial atherosclerosis has been observed, but the management of these high-risk patients is controversial.93,94 When anticoagulation and antiaggregation treatment has failed, PTAS should be considered. Elective stenting of symptomatic basilar artery atherosclerotic lesions refractory to medical therapy is feasible with a lower risk than the natural history.95,96 The natural history of
(b)
Figure 33.10 Digital subtraction angiography: anteroposterior view: (a) occlusion of right posterior cerebral artery; (b) control after treatment with 30,000 U of intra-arterial urokinase.
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intracranial internal carotid artery stenosis features more stable lesions than at other sites, and lesion regression may still occur in some patients.97 Recent data from the North American Symptomatic Carotid Endarterectomy Trial (NASCET) have demonstrated that early surgery for carotid stenosis may be safely performed in minor disabling stroke, whereas acute carotid thrombosis should be considered for thrombectomy. Patients with recently symptomatic high-grade carotid artery stenosis and ipsilateral hemodynamic alterations are at high risk for disabling stroke.98 PTAS is recommended in the course of diagnostic angiography. There have been several case reports of successful treatment of cervical stenosis.99–101 Carotid plaque is friable and stroke may occur despite meticulous technique. Protected carotid stenting has been successfully and safely performed with a cerebrovascular protection device; if carotid flow is required, filter protection devices are useful.102–104 Flow should
be monitored because the filter may become occluded with particles from the plaque. Even at an experienced centre, carotid surgical treatment incurs the risk of peri-operative arrhythmia, congestive heart failure, myocardial infarction, and death. During postoperative hemodynamic instability, clinical deficits, cardiac rhythms, blood pressure, and cervical and intracranial arterial velocities are monitored. The most frequent complications are blood pressure variations, bradycardia, vessel occlusions, femoral hematoma or pseudoaneurysms, urinary infections, stroke, hyperperfusion syndrome, and reperfusion injury. To prevent stent-induced thrombosis, the authors administer 100 mg aspirin plus 300 mg clopidogrel by the oral route before the procedure, continuing with 100 mg of aspirin plus 75 mg of clopidogrel daily by the oral route for 90 days.105 Statins are discontinued owing to their interaction with tienopyridines.106
Table 33.9 Management of patients with stroke who may be eligible for intra-arterial tissue plasminogen activator (tPA) therapy Inclusion criteria Ischemic stroke with a defined onset of < 6 hours from time tPA is to be started Neurological deficits in NIHSS < 21/42 CT scan shows no evidence of intracranial hemorrhage Exclusion criteria History Stroke or serious head trauma within past 3 months Major surgery or serious trauma within past 14 days Intracranial hemorrhage. AVM or aneurysm Arterial puncture at a non-compressible site or lumbar puncture within previous 7 days Clinical Rapidly improving neurological signs or minor symptoms Systolic BP > 180 mmHg or diastolic BP > 110 mmHg Seizure at onset Symptoms suggestive of subarachnoid hemorrhage Recent myocardial infarction-induced pericarditis Gastrointestinal or urinary tract hemorrhage within previous 21 days Laboratory tests Taking anticoagulants or prothrombin time > 15 seconds or INR > 1.7 Received heparin within 48 hours preceding stroke onset and has elevated partial thromboplastin time Platelets < 100 000/mm3 Glycemia < 50 mg/dl or > 400 mg/dl Positive pregnancy test Treatment and management tPA 1 mg/minute, maximum 20 mg Administer as a constant infusion over 1 hour Monitor recanalization with TCD Digital subtraction angiography when TCD shows recanalizations Do not give anticoagulant or antiplatelet agents for 24 hours from starting administration Admission to stroke unit Maintain systolic BP < 180 mmHg and diastolic BP < 115 mmHg Restrict central venous line placement or arterial puncture for 24 hours Do not insert indwelling bladder catheter for > 30 minutes after tPA Avoid insertion of nasogastric tube for 24 hours after tPA administration Withdraw introducer after partial thromboplastin time is normalized NIHSS: National Institutes of Health Stroke Scale; CT: computed tomography; AVM: arteriovenous malformation; BP: blood pressure; INR: International Normalized Ratio; TCD: transcranial Doppler
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Management of patients with stroke who may be eligible for intra-arterial urokinase therapy
Inclusion criteria Ischemic stroke with a defined onset of < 6 hours, or < 8 hours in posterior arterial territory Neurological deficits in NIHSS < 21/42 CT scan shows no evidence of intracranial hemorrhage Exclusion criteria History Stroke or serious head trauma within past 3 months Major surgery or serious trauma within past 14 days Intracranial hemorrhage. AVM or aneurysm Arterial puncture at a non-compressible site or lumbar puncture within previous 7 days Clinical Rapidly improving neurological signs or minor symptoms Systolic BP > 180 mmHg or diastolic BP > 110 mmHg Seizure at onset Symptoms suggestive of subarachnoid hemorrhage Recent myocardial infarction-induced pericarditis Gastrointestinal or urinary tract hemorrhage within previous 21 days Laboratory tests Taking anticoagulants or prothrombin time > 15 seconds or INR > 1.7 Received heparin within 48 hours preceding stroke onset and has elevated partial thromboplastin time Platelets < 100,000/mm3 Glycaemia < 50 mg /dl or > 400 mg /dl Positive pregnancy test Treatment and management Heparin 2000 IU i.v. Superselective spray injections with urokinase 1000 U each Monitor recanalization with TCD Digital subtraction angiography when TCD shows recanalizations Discontinue infusion when artery is recanalized or with fibrinogen < 80 mg /dl Withdraw the introducer after PTT is normalized and with fibrinogen > 100 mg /dl If patient remains anticoagulated, withdraw the introducer When the fibrinogen value is > 100 mg/dl, sodium heparin is administered by an infusion pump at 1000 U/hour. Target: PTT 1.5–2 times basal level At 24 hours start with aspirin 100 mg/day If chronic anticoagulation is required, maintain i.v. heparin for 3 days Coumadin 5 mg/day is administered with the heparin and on the third day this is discontinued with INR > 1.5, continuing with Coumadin according to INR NIHSS: National Institutes of Health Stroke Scale; CT: computed tomography; AVM: arteriovenous malformation; BP: blood pressure; INR: International Normalized Ratio; TCD: transcranial Doppler; PTT: partial thromboplastin time.
If a patient receives hydantoin or carbamazepine, the plasmatic level of homocysteinaemia is evaluated. If the latter is high, folic acid 2.5 mg, pyridoxine 25 mg and cyanocobalamin 400 µg daily by the oral route are indicated.107–109 The term hyperperfusion syndrome describes complications including headache, seizure, visual deficits, and high blood pressure due to occipital ischemic lesion. MRI shows hyper-intensities in T2-weighted signals, fluid attenuated invertion recovery (FLAIR) and ADC localized in the subcortical occipital area, ipsilateral to the treated vessel. Such hyperintensities are due to edema secondary to loss of focal cerebrovascular autoregulation. Immediate treatment of high blood pressure leads to syndrome and abnormal image reversal, as occurs in reversible posterior leucoencephalopathy due to hypertension.110,111 The term reperfusion injury syndrome describes complications including headache, focal seizure and neurological deficits due to intracranial bleeding. Such features have been attributed to raised ipsilateral cerebral blood flow without changes in the systemic
blood pressure. Symptoms usually develop 5–7 days postoperatively, their frequency after endarterectomy ranging from 0.3 to 1.2%.112 Some patients present increased velocities on Doppler evaluation of the ipsilateral carotid artery.113 Intracranial hemorrhage due to cerebral reperfusion is preferentially localized in the basal ganglia. Bleeding attributed
Table 33.11
Management of intracranial hemorrhage
Discontinue thrombolytic drugs Immediate CT scan or MRI Prothrombin time, partial thromboplastin time, platelet count and fibrinogen Without hemorrhage: end algorithm With hemorrhage: consult neurosurgeon and hematologist CT: computed tomography; MRI: magnetic resonance imaging
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Figure 33.11 Non-contrast computed tomographic scans after surgical treatment. Hemorrhagic transformation after intravenous tissue plasminogen activator for ischemic stroke on the right side with less than 3 hours since onset.
to a reperfusion-induced injury may cause more deleterious brain damage than the ischemia. Many factors have been implicated where an inflammatory reaction plays a major role.114–117 The relevant query is therefore: what are the interrelationships between the perforating vessel and the reperfusion injury? Some patients have neither symptoms, high blood pressure nor raised velocities on Doppler evaluation. In three cases treated in this centre, the hemorrhage occurred in the basal ganglia within the first 6 hours of endovascular surgery, and in two it proved mortal. Benign hemorrhages due to reperfusion insult have been observed after endarterectomies and angioplasty, with or without stenting.104 From the clinical, radiological, and physiopathological standpoint, reperfusion insult differs from damage due to hyperperfusion secondary to arterial hypertension. In the latter, there is loss of cerebrovascular autoregulation with edema localized in the posterior supratentorial territory, whereas intracranial hemorrhages occur in reperfusion insult. Cervical and intracranial PTAS is a feasible procedure, although pretreatment with antiaggregant agents to avoid complications should be studied further. Ischemic stroke in the spinal cord often results in partial transverse anterior lesion in the thoracic area and conus medullaris, with paraplegia, impaired sensory level, dysesthesias, pain and urinary dysfunction. Predisposing factors are aortic aneurysm or dissection, femoral catheterization,
abdominal surgical procedure, embolus from vertebral disc, syphilis, atherosclerosis and spinal vascular malformation. MRI shows signal abnormalities in the anterior horns with increased proton density in T2 relaxation time, with an owl’s eyes appearance. More diffuse signal abnormality indicates worse prognosis.118 Experimentally, hyperbaric oxygen therapy may be used under protocol evaluations.
Anticoagulation Anticoagulation with heparin is commonly used in cardioembolic or progressing ischemic stroke. In the International Stroke Trial (IST) study,119 the use of heparin was associated with increased brain hemorrhage to counterbalance the reduction in the absolute risk of recurrent ischemic stroke. The occurrence of hemorrhagic stroke and death increases with high-dose subcutaneous heparin. In the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) study the use of low molecular weight heparinoid (danaparoid) failed to alter the outcome at 3 months compared with placebo.120 Early anticoagulation may be useful in severe symptomatic stenosis, venous sinus thrombosis, arterial dissection, intraluminal clot syndrome, and hypercoagulable conditions.121 The heparin starting dose in continuous intravenous infusion to
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(a)
(b)
(c)
Figure 33.12 Stable ischemic stroke in the vertebrobasilar territory: (a) magnetic resonance image disclosing ischemic lesions due to clots in the left cerebellar hemisphere (posterior inferior cerebellar artery) and in both occipital lobes (posterior cerebral artery); (b) digital subtraction angiography: critical stenosis of the right vertebral artery; (c) immediate control following percutaneous transluminal angioplasty with stenting.
maintain PTT is 1.5–2.0 times the control value; PTT is checked 6 hours after dose initiation. Therefore, anticoagulation should not be used routinely in ischemic stroke, and low-dose subcutaneous heparin is recommended in immobile patients.122 A meta-analysis of data from trials of early treatment with anticoagulant drugs for patients with ischemic stroke suggests no clinical benefit.121,123,124
Antiaggregation In the IST119 and the Chinese Acute Stroke Trial125 study, oral administration of aspirin in the first 48 hours was shown
to provide limited benefit. Early death, recurrent stroke or late death may be prevented in one out of 100 patients by giving 160–300 mg/day within 48 hours of symptom onset.125,126 Abciximab appears to be safe when administered up to 24 hours after stroke onset, and may improve functional outcome. Abciximad (bolus dose of 0.25 mg/kg followed by continuous infusion of 0.125 µg/kg per minute for 12 hours) induces 80% blockade of glycoprotein llb/llla receptors, a reduction in ADP-induced platelet aggregation to < 15% basal level and prolongation of the bleeding time to > 30 minutes, for more than 6 hours.127 The use of monoclonal antibodies that bind to the glycoprotein receptor llb/llla of human platelets is recommended alone or as an adjuvant of platelet
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(a)
(b)
(c) Figure 33.13 Ischemic stroke in fast regression: digital subtraction angiography lateral view and three-dimensional reconstruction: (a) pretreatment subocclusive symptomatic stenosis in the left internal carotid artery; (b) percutaneous transluminal angioplasty with stenting under cerebral protection with balloon; and (c) immediate control after treatment.
(a)
(b)
Figure 33.14 Unstable ischemic stroke with fast regression (transient ischemic attack). Critical symptomatic stenosis of the right intracavernous internal carotid artery: (a) digital subtraction angiography before treatment with percutaneous transluminal angioplasty with stenting; (b) control after treatment.
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(a)
(b)
(c) Figure 33.15 Percutaneous transluminal angioplasty (PTA) vertebral: (a) vertebral ostium with severe stenosis and thrombus; (b) partially organized thrombus (H&E); (c) post-stenting control.
Ancrod decreases the plasma concentration of fibrinogen. In a trial with stroke patients within 3 hours after onset, ancrod increased the chance of total or near total recovery.47,129
flow and proportional oxygen transport.130 Hemodilution has failed to prove effective in the treatment of ischemic stroke in patients with normal hematocrit values,131 but is effective when the level exceeds 55%. In ischemia due to vasospasm, hemodilution may contribute to recovery from the neurological defect, but available evidence is insufficient for its recommendation. While the optimal level of hematocrit reduction and its type remain unknown, hemodilution should be neither underrated nor encouraged, except in cases of abnormally high hematocrit value.132
Hemodilution
Neuroprotection
As cerebral blood flow is inversely proportional to hematocrit value, an increase in hematocrit is considered a vascular risk factor. Reductions ranging from 30 to 40% increase cerebral
Pharmacological agents induce neuroprotective effects in animal models of stroke. However, success with neuroprotective agents in animal stroke models correlates poorly with
antiaggregation and of anticoagulation in patients with thrombosis, or during endovascular procedures in cases of high thrombotic risk. Its effectiveness in stroke is under study.128
Ancrod
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(a)
(b)
(c) Figure 33.16 Percutaneous transluminal angioplasty (PTA) basilar: (a) severe basilar stenosis; (b) magnetic resonance image disclosing ischemic lesions in the left cerebellar hemisphere; and (c) poststenting control.
clinical efficacy.56 Treatment with oral citicoline within the first 24 hours after onset in patients with moderate to severe stroke increased the probability of complete recovery at 3 months, and citicoline is the only putative neuroprotector to have shown partial positive results in all randomized, double-blind trials.133 New neuroprotective strategies include embolization with encapsulated drugs or cells to induce gene expression, hypothermia and hyperbaric oxygen therapy. Neurological defects due to dysfunction of cells located in hypoxic-ischemic penumbra areas may be reverted.134 The reversal of chronic neurological defects after surgical treatment of critical carotid stenosis and with hyperbaric oxygen therapy in frontal vascular leucoaraiosis supports such interpretation.135–137 Tissue interface hypoxia due to reversible interstitial edema further sustains these observations (Figure. 33.2). Currently, it is possible to increase cerebral flow without modifying arterial pressure, by means of abdominal aortic flow obstruction with balloons. The goal is to improve distal intracranial circulation by opening collaterals without significantly modifying arterial pressure. This provides a therapeutic alternative to manage cerebral perfusion in stroke and in
vasospasm without resorting to sympathicomimetic drugs. It is a safe technique, the effectiveness of which is under investigation.138,139 Since low temperature decreases cell metabolism, hypothermia has been proposed as neuroprotective ther-apy.40–142 Nowadays, specially designed devices quickly reduce cerebral temperature,143 but the drop in body temperature modifies the expression of the biological parameters habitually used as references for the early diagnosis of infection. Severe infections are usual complications in patients with hypothermia, as well as in those in a barbituric coma.144
Complications of stroke Medical complications Preliminary death rates for stroke reach 40%; half of the fatalities attributable to stroke are the result of medical complications and the other half of neurological complications (Table 33.12). The underlying stroke pathology influences mortality at 30 days. For infarction it is 15%, for SAH. 45%, and for intracerebral hemorrhage 48–82%. The causes
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(b)
(c) Figure 33.17 Symptomatic subocclusive stenosis in the right internal carotid artery: (a) digital subtraction angiography (DSA), lateral view; (b) DSA, AP view after percutaneous transluminal angioplasty with stenting; and (c) hemorrhagic stroke 6 hours after treatment; computed tomographic scan, axial images. Subarachnoid, intraventricular and basal ganglion bleeding by reperfusion.
of 6 month mortality include heart disease (35%), recurrent stroke (25%), pneumonia (15%), and pulmonary embolism (10%).145–147 Neurological complications Cerebral infarction with mass effect Cerebral edema due to ischemia increases through the first hours. Signs of cerebral edema and increased ICP reduce the level of consciousness and indicate the progression of neurological deficit. Development of these signs should prompt an urgent CT scan. In patients with suspected increased ICR invasive measurement may be needed to monitor treatment (Table 33.13a). Clinical management of increased ICP involves osmotherapy and hyperventilation. The target of hyperventilation is an arterial carbon dioxide tension of 25–30 mmHg, which provides a reduction in ICP by cerebral vasoconstriction. The most commonly used osmotherapy agent is mannitol 0.5–2 g/kg intravenously over 30 minutes,
repeated every 4 hours. Furosemide may be a supplement and hypertonic saline an alternative agent. The main side-effects are hypotension, hypokalemia, hemolysis and heart failure. If ICP persists or progresses, intubation and mechanical hyperventilation (target carbon dioxide tension 30 mmHg) can lower ICP (Table 33.13b). Intraventricular catheter placement may lower ICP by removing cerebrospinal fluid. Surgical decompression can prove life-saving for infarction patients (Table 33.13c).47,147 Depressive hemicraniectomy Hemicraniectomy with durotomy or duroplasty has been reported to improve outcome.148 A total of 129 treated patients presented an overall mortality rate of 23.2% and most had a Barthel index lower than 60. When performed before signs of anisocoria, temporal lobe amputation may be avoided.149 Temporal lesions have been observed in the absence of raised ICP, so a normal ICP may fail to refect the risk of
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(a)
(b)
(c)
(d) Figure 33.18 (a) aortic obstruction with inflated balloons above and below the renal arteries; (b) transcranial Doppler showing increased middle cerebral artery flow during the procedure, without significant changes in mean arterial pressure; and (c) pre- and post-treatment parenchymogram disclosing improvement in the focal perfusion defect of the left hemisphere. NIHSS score improved from 06 to 02 points.
uncal hernia appropriately Remarkable volume gain is achieved beyond 12 cm in diameter. Surgery with craniectomy is indicated for large cerebellar infarcts, early brainstem compression, hydrocephalus and large, non-dominant hemispheric infarctions. Inclusion criteria are: CT scan findings with hypodensity greater than two-thirds of MCA, with or without brainstem lesion (except for third nerve pair lesion with < 6 hours of onset). The therapeutic window is < 24 hours, but can be indicated later only when neurological defects attributable to mass effects are < 3 points on the global coma scale (GCS).150 The GCS is useful in supratentorial lesions, but remains controversial in infratentorial lesions.
Hemorrhagic stroke Blood is found in brain tissue in 10% of stroke patients and the recurrence rate ranges from 5 to 30%, while SAH features 6%, with a 4% risk of rebleeding within the first 24 hours and 1% per day thereafter for the first 2 weeks after hemorrhage.151,152 According to its etiology, hemorrhagic stroke is divided into primary or secondary, while clinically it is classified as described in Table 33.3. A non-contrast CT scan is required for hemorrhagic stroke diagnosis. The term primary hematoma must be restricted to unknown etiology (Table 33.14). The most common cause of hemorrhage in basal ganglia is the degeneration and rupture of small penetrating arteries
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Table 33.12 Management of the most common medical complications of stroke Complication
Prophylaxis
Aspiration Hypoventilation Pneumonia Oximetry monitoring Myocardial ischemia Cardiac arrhythmias Pulmonary embolism
Kinesiotherapy
Deep vein thrombosis
Urinary infections Decubitus ulcers Contractures Stiff joints Malnutrition Infection Gastropathy
Continuous cardiac monitoring Intermittent pneumatic compression of the leg Elastic stockings Low-dose heparin (5000 IU twice daily) or low molecular weight heparin subcutaneously Urinalysis monitoring Early mobility Evaluation of swallowing to guide nutrition Aggressive fever control Gastric protection
(a)
following chronic insult due to hypertension. Lobar hematoma in frontal and parietal areas in the elderly is often due to amyloid angiopathy.153 The clinical presentation reflects both the general effects of increased ICP and the neurological deficits that result from the specific location of the hemorrhage. Hypertensive hematomas are preferentially located in basal ganglia, mesencephalon, and cerebellum. Acute hematoma in the putamen often presents with atypical aphasia (L), foreign accent syndrome, articulation difficulty (L), dysphonia,
Table 33.13 Management of the most common neurological complications of stroke (a) Intracranial pressure monitoring techniques Intraventricular catheter Epidural monitor Parenchymal optic fibre Subarachnoid bolts (b) Pharmacological treatment Raising bed 30 º Blood pressure control Osmotherapy Coma induced by barbiturates Hypocapnia Hypothermia (c) Surgical treatment Ventriculostomy Temporal lobectomy Hemicraniectomy Craniotomy Decompressive craniectomy
(b) Figure 33.19 Ischemic stroke 12 hours after onset (NIHSS score 15 p.): (a) computed tomographic scan on admission indicating decompressive surgery; (b) severe edema at control after left craniectomy (NIHSS score 25 p.). The patient died a few days later.
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ISCHEMIC STROKE
Clinical classification (Table 33.3) Review CT scan (Table 33.8) Laboratory test (Table 33.6)
Onset time
< 6 hours
> 6 hours
Thrombolysis
Anticoagulation Antiaggregation Neuroprotection Ancrod
< 3 hours i.v. (Table 33.7) i.v. and i.a. IA (Tables 33.9 and 33.10) Mechanical
> 3 hours i.v. + i.a. i.a. (Tables 33.9 and 33.10) Mechanical
Post-thrombolysis management (Table 33.11)
Any time endovascular
Management of complications Medical (Table 33.12) Neurological (Table 33.13)
Figure 33.20 Algorithm for the management or patients with ischemic stroke. CT: computed tomography; i.v.: intravenous; i.a.: intraarterial.
Table 33.14
Frequent causes of hemorrhagic stroke
Lipocollagenosis (hypertension) Arteriovenous malformations Cavernous angioma Durai fistula Aneurysms Neoplasias Infarction Coagulopathy Amyloid angiopathy Cerebral venous thrombosis
depression, contralateral hemineglect (R) and hemiparesis. In thalamus hematoma, there is inattention, dementia, contralateral neglect, and disturbances in the sleep-wake cycle, as well as behavioral, emotional, memory and language symptoms. Hemisensory, hemiparesis and abnormal oculomotor movements occur when blood spreads to nearby structures. Pons hematoma features acute tetraplegia and pinpoint pupils, personality changes, dysarthria, mutism, behavioral, and emotional symptoms; and hematoma in the cerebellum features vertigo, nausea, and gait and equilibrium disorders. All such manifestations start with headache and are closely related to decreasing awareness.
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(b)
(b)
c
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Figure 33.21 (a) Digital subtraction angiography with small saccular aneurysm, poorly visible in a two-dimensional study; (b) three-dimensional images disclose anatomical details for a more accurate therapeutic strategy.
(a)
(b)
(c)
Figure 33.22 Patient with subarachnoid hemorrhage due to a ruptured aneurysm, Fisher III. At 7 days of evolution. she presented with symptomatic vasospasm refractory to medical and endovascular treatment: (a) digital subtraction angiography, anteroposterior view: severe multifocal proximal and distal vasospasm; (b) control computed tomographic scan with bihemispheric infarcts.
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Table 33.15
Management of hematoma
Brain hematoma NlHSS < 07/42, stable with volume < 10 cm3 NIHSS > 07/42, progressive with volume > 10 cm3 Cerebellar hematoma Volume > 3 cm 3
Medical treatment Surgery
Surgery
NIHSS: National Institutes of Health Stroke Scale.
Treatment for cerebral hematoma remains controversial (Table 33.15). It may require surgery according to its volume, as well as to its interrelated localization and etiology.154 Volume depends on variables such as vascular diameter, rupture size, vessel reactivity, arterial pressure, clotting status and adjacent tissue resistance.155 The management of intracerebral hemorrhage involves two main issues: the treatment of increased ICP and the choice between medical and surgical therapy.154 The greater the volume of secondary edema, the poorer the functional outcome in patients with hyperacute supratentorial intracranial hemorrhage.156 Aggressive treatment of hypertension is useful for both primary and secondary hematoma. However, corticosteroids fail to alter the neurological outcome significantly. In patients with impaired awareness, intracranial monitoring may provide valuable information.154 The classification of cerebral vascular malformation provides useful data to determine the risk of each malformation and enables decision making about the appropriate therapy.157 Intraventricular hemorrhage remains associated with high mortality; therapy with external drainage fails to modify outcome, although recently intraventricular urokinase has been reported to improve this condition.158,159 Suboccipital craniectomy with hematoma evacuation is recommended for cerebellar hemorrhage larger than 3 cm. Surgery fails to improve the outcome in cases of comatose status, brainstem dysfunction, and signs of herniation, while in the basal ganglia the benefit has not been conclusive.158 Only in lobar hematoma does surgery lower mortality compared with medical treatment.153 A rim of ischemic penumbra around the hematoma explains the reversal of neurological defects.154,160 On occasion, neurosurgeons have used a hyperbaric chamber in patients with hemorrhagic stroke; if the acute defect improves with a hyperbaric chamber session, the hematoma is then evacuated, taking the surrounding ischemic penumbra as the target.161 Independent predictors of mortality in acute cases include hematoma volume with a GCS score > 8 points (Table 33.16), systolic blood pressure > 200 mmHg and pineal displacement > 3 mm. Prophylaxis measures include bed rest, pain and agitation control, and stool softener. Seizure prophylaxis is not used as it is controversial.154 Recent advances in catheter, guidewire, coil, and stent technology have enabled more selective intervention. Following diagnosis of a ruptured cerebral aneurysm, immediate treatment is to secure the aneurysm by an
(a)
(b)
(c) Figure 33.23 Localization of cerebral infarcts secondary to vasospasm due to subarachnoid hemorrhage: (a) tandem in deep watershed area; and (b) focal cortical area; and (c) multifocal corticai and focal superficial watershed area.
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Spontaneous To verbal stimulus: speech To pain No response
endovascular route, to reduce the risk of rebleeding. Hemorrhagic stroke due to a ruptured aneurysm is infrequent. The relative and absolute risk reductions in dependency or death after allocation to an endovascular versus a neurosurgical treatment are 22.6 and 6.9%, respectively. In the International Subarachnoid Aneurysm Trial (ISAT) study,162 the risk of rebleeding from the ruptured aneurysm after 1 year was 2 per 1276 and 0 per 1081 patient-years for endovascular versus neurosurgery, respectively.
Table 33.17 hemorrhage
281
Fisher grading scale for subarachnoid
Grade
CT scan: blood
1 2 3 4
None Diffuse subarachnoid Clot > 1 mm thick Intraparenchymal or intraventricular clot
Cerebral vasospasm is a pathological luminal narrowing of the arteries that occurs in 60% of patients after SAH, which disturbs cerebral autoregulation, ischemia due to such narrowing leads to a clinical syndrome developing in 25% of SAH patients. This group performs continuous velocity monitoring after SAH, once a day during the first 5 days and more frequently during the period of vasospasm. Control frequency is related to the Fisher Grading Scale (Table 33.17), a CT scan classification for non-traumatic SAH. The higher the score, the greater the likelihood of symptomatic vasospasm. An alternative grading system for SAH is the Hunt and Hess scale (Table 33.18). The treatment of cerebral vasospasm following hemorrhage by standard medical therapy is unsuccessful.163 Angioplasty with balloons of proximal cerebral vessel shows improvement in neurological status, although it is not advised with evidence of infarcts > 12 hours since onset. In small vessels beyond the circle of Willis, vasospasm may be reversed with calcium blockers or nitroglycerine. Nimodipine by
(a)
(b) Figure 33.24 Hemorrhagic stroke: (a) computed tomographic scan and magnetic resonance image (MRI) showing bilateral thalamic hemorrhage and thrombosis of the internal cerebrai vein; (b) Neurological defects disappeared entirely without treatment, with persistence of venous occlusion on control MRI.
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HEMORRHAGIC STROKE
Repeat clinical classification (Table 33.3) Review laboratory test (Table 33.6) Hemorrhagic cause (Table 33.8)
Reverse antiocagulants Reverse bleeding disorders Treatment of hypertension
Management of brain hematoma
Management of SAH
Assess GCS (Table 33.16) Repeat NIHSS Review CT scans Consult neurosurgery
Assess FGS (Table 33.17) HHS (Table 33.18) Repeat NIHSS score Monitoring vasospasm with TCD
Treatment
Vasospasm
Surgical (Table 33.11)
Medical (Tables 33.12 and 33.13)
Asymptomatic Calcium channel Antagonists
Symptomatic CT scan DSA
Proximal
Distal
Angioplasty (1) Mechanical (2) Pharmacological:
High blood pressure Triple H NeuroFlo* HBO*
Nimodipine Papaverine Nitroglycerine* Acetylchorine* (3) 1 and 2 (4) NeuroFlo
Rehabilitation
Figure 33.25 Algorithm for the management of patients with hernorrhagic stroke. SAH: subarachnoid hemorrhage; GCS: Glasgow Coma Scale; NIHSS: National Institutes of Health Stroke Scale; CT: computed tomography; HHS: Hunt and Hess Scale; TCD: transcranial Doppler; DSA: digital subtraction angiography; HBO: hyperbaric oxygen; *compassionate use or protocol under investigation.
the oral route has proven effective to prevent vasospasm, but subsequent arterial hypotension limits its use.164 Some patients with symptomatic vasospasm improve their neurological defect by increasing mean arterial pressure (MAP). The increased level to which they respond is highly individual; below this level they worsen, proving MAP sensitive. Since inotropic drugs that frequently cause serious adverse effects are required to increase MAP this therapeutic procedure is restricted,154 particularly in the elderly and patients
with heart disease, abdominal aorta aneurysm, renal failure, and chronic cerebrovascular disease. Triple H treatment, hypertension with hypervolemia and hemodilution, carries the same problem.152,163,165 Some patients present vasospasm refractory to all treatment, with a malignant behaviour similar to malignant infarct due to MCA occlusion. Hemorrhagic stroke in the spinal cord is uncommon. It arises from vascular malformations (fistulae, AVMs and cavernomas), and congenital or acquired clotting defects.1
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The stroke unit Table 33.18 Hunt and Hess scale of subarachnoid hemorrhage (SAH): medical classification of nontraumatic SAH Grade
Description
1 2
Asymptomatic, mild headache, slight neck rigidity Moderate to severe headache, neck rigidity, no neurological deficit other than cranial nerve palsy Drowsiness or confusion, mild focal neurological deficit Stupor, moderate to severe hemiparesis Coma, decerebrate posturing
3 4 5
Add one grade for severe systemic disease or marked vasospasm at angiography
Its treatment is anecdotal and controversial. When the spinal cord is compressed by the hematoma, methylprednisolone 1 g/day is administered and decompressive surgery considered. Hemorrhagic stroke in cerebral venous thrombosis occurs in less than half of the cases. The main arms of treatment are symptomatic, antithrombotic, and etiological. A welldocumented case has been reported in which improvement occurred after the initiation of heparin administration, recommended when patients deteriorate despite symptomatic treatment.166 Initial anticoagulant treatment is with heparin given by either continuous intravenous infusion or subcutaneous injections. Caution is required in patients with homozygous protein C and S deficiencies because of the risk of hemorrhagic skin necrosis induced by oral anticoagulants if not fully anticoagulated with heparin before starting with oral drugs.167 Intravascular thrombolytic treatment is a useful alternative in worsening cases; however, clinical effectiveness needs to be confirmed.168 it is essential to treat the underlying cause as it influences the immediate outcome and long-term prognosis.166
Discharged patients After 7 days of evolution, the patient may be considered to be in the subacute period, when research, recurrence prevention and therapy exceed the scope of this chapter.169 Nevertheless, patients who require endovascular therapeutic procedures beyond the acute period are attended in the stroke unit, Following acute care, patients are discharged either home or to the neurorehabilitation ward, since early hospital discharge and home-based rehabilitation have proven to be a less costly alternative to conventional care for patients with stroke. The role of rehabilitation service in the stroke unit is to promote recovery from depression, immobility, skin injury, urinary and fecal incontinence, aphasia, focal weakness, and emotional and behavioural disorders. Early initiation improves functional outcome.145,170–172 Out of the 75% of patients who survive their stroke, 15–30% are placed in a nursing home, 5–20% are admitted to rehabilitation units and 35–60% are discharged home.173,174
283
Table 33.19 Glasgow Outcome score: assessment of outcome after severe brain damage Grade
Description
5
Good recovery: resumption of normal life despite minor deficits Moderate disability (disabled out independent): can travel by public transport; can work in sheltered setting Severe disability (conscious but disabled): dependent for daily support Persistent vegetative state: unresponsive and speechless, after 2–3 weeks may open eyes and have sleep/wake cycles Death
4 3 2 1
Before discharge, functional independence measurements are used to assess a patient with appropriate scales such as the Folstein Mini Mental State.175 Glasgow outcome score (Table 33.19) and modified Rankin scale (Table 33.20). The next step in the stroke unit project is to determine the long-term outcome for acute stroke patients in terms of their self-sufficiency level.176,177 In summary, acute therapy for stroke is entirely feasible, particularly in the context of rapidly progressing advances. Medicine based on evidence is a sound assistance orientation resting on probabilities rather than on certainties, as shown by the necessary number of patients to be treated to achieve results. There are useful treatments for pathologies whose relative rarity prevents appropriate studies being undertaken. For several decades, atheromatous cervical stenosis has been successfully operated on and cerebral aneurysms treated by the endovascular route. However, both treatments are no longer regarded as controversial, following the NASCET and ISAT studies. Paradoxically enough, in medical practice the conclusions of such studies are duly respected but the selection criteria leading to those results are often neglected. The dilemma of how and when to treat a patient with stroke is hardly solved by means of an algorithm; the therapeutic decision should be grounded on experience, evidence, anecdotes, actual possibilities, and above all, the evaluation of each particular case. The well-known aphorism is still valid: there are no illnesses but only people who are ill. Table 33.20
Modified Rankin scale
Grade
Description
0 1
No symptoms at all No significant disability despite symptoms, able to carry out all usual duties and activities Slight disability, unable to carry out all previous activities, but able to look after own affairs without assistance Moderate disability, requiring some help, but able to walk without assistance Moderately severe disability unable to walk without assistance, and unable to attend to own bodily needs without assistance Severe disability bedridden, incontinent, and requiring constant nursing care and attention
2 3 4 5
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Nussbaum ES, Heros R, Solien E et al. Intra-aortic ballon counterpulsation augments cerebral blood flow in a canine model of subarachnoid hemorrhage-induced cerebral vasospasm. Neurosurgery 1995; 34: 879–86 Wang J, Lynette L, Lim Y et al. Influence of admission body temperature on stroke mortality. Stroke 2000; 31: 404–9 Kraff R Frietsch T, Lenz C et al. Mild and moderate hypothermia do not impair the coupling between local cerebral blood flow and metabolism in rats. Stroke 2000; 31: 1393–401 Maekawa T, Tateishi A, Sadamitsu D et al. Clinical application of mild hypothermia in neurological disorders. Minerva Anesthesiol 1994; 64: 537–40 Georgiadis D, Schwarz S, Kollmar R et al. Endovascular cooling for moderate hypothermia in patients with acute stroke: first results of a novel approach. Stroke 2001; 32: 2550–3 Schwab S. Georgiadis D, Berrouschot J et al. Feasibility and safety on moderate hypothermia after massive hemispheric infarction. Stroke 2001; 32: 2033–5 Langhorne P, Stott DJ, Robertson L et al. Medical complications after stroke. A multicenter study. Stroke 2000; 31: 1223–9 Chan BP AIbers GW. Acute ischemic stroke. Curr Treat Options Neurol 1999; 1:83–95 Hill MD, Hachinski V. Stroke treatment: time is brain. Lancet 1998; 352(Suppl III): 10–14 Doerfler A, Schwab S, Hoffmann TT et al. Combination of decompressive craniectomy and mild hypothermia ameliorates infarction volume after permanent focal ischemia in rats. Stroke 2001; 32:2675–81 Georgiadis D, Schwarz S, Aschoff A, Schwab S. Hemicraniectomy and moderate hypothermia in patients with severe ischemic stroke. Stroke 2002; 33: 1584–8 Engelhorn T, von Kummer R, Reth W et al. What is effective in malignant middle cerebral artery infarction: reperfusion, craniectomy, or both? Stroke 2002; 33: 617–22 Neau JR, Ingrand P, Couderq C et al. Recurrent intracerebral hemorrhage. Neurology 1997; 49: 106–13 Flemming KD, Brown RD, Wiebers DO. Subarachnoid hemorrhage. Curr Treat Options Neurol 1999; 1: 98–112 Massaro AR, Sacco RL, Mohr JP et al. Clinical discriminator of lobar and deep hemorrhages: the stroke data bank. Neurology 1991; 41: 1881–5 Seestedt RC, Frankel MR. Intracerebral hemorrhage. Curr Treat Options Neurol 1999; 1: 128–37 Kazui S, Minematsu K, Yamamoto H et al. Predisposing factors to enlargement of spontaneous intracerebral hematoma. Stroke 1997; 28: 2370–5 Gebel JM, Jauch EC, Brott TG et al. Relative edema volume is a predictor of outcome in patients with hyperacute spontaneous intracerebral hemorrhage. Stroke 2002; 33: 2636–41 Morgenstern LB, Frankowski RF Shedden P et al. Surgical treatment for intracerebral hemorrhage (STICH): a single-center, randomized clinical trial. Neurology 1998; 51: 1359–63 Liliang PC, Liang CL, Lu CH et al. Hypertensive caudate hemorrhage prognostic predictor, outcome, and role of external ventricular drainage. Stroke 2001; 32: 1195–200 Naff NJ, Carhuapoma JR, Williams MA et al. Treatment of intraventricular hemorrhage with urokinase. Effects on 30-day survival. Stroke 2000; 31: 841–7 Castillo I, Davalos, Alvares-Sabin J et al. Molecular signatures of brain injury after intracerebral hemorrhage. Neurology 2002; 58: 624–9 Kanno T, Nonomura K. Hyperbaric oxygen therapy to determine the surgical indication of moderate hypertensive intracerebral hemorrage. Minim Invasive Neurosurg 1996; 39: 56–9 International Subarachnoid Aneurysm Trial Collaborative Group. International Subarachnoid Aneurysm Trial of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomized trial. lancet 2002; 360: 1267–74 Molyneux AI, Kerr RS. The future management of subarachnoid haemorrhage. J Neuroradiol 2002; 29: 74–5 Ahmed N, Nasman P, Wahlgren NG et al. Effect of intravenous nimodipine on blood pressure and outcome after acute stroke. Stroke 2000; 31: 1250–5 Thomas JE, McGinnis G. Safety of intraventricular sodium nitroprusside and thiosulfate for the treatment of cerebral vasospasm in the intensive care unit setting. Stroke 2002; 33: 486–92 Bousser MG, Russel RR. In: Cerebral Venous Thrombosis Treatment. WB Saunders, Philadelphia, PA, 1997; 142–57 Samama M, Horellou MH, Soria J et al. Successful progressive anticoagulation in a severe protein C deficiency and previous skin necrosis at the initiation of oral anticoagulant treatment. Thromb Haemost 1984; 51: 132–3
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169. 170. 171. 172.
Wasay M, Bakshi R, Kojan S et al. Nonrandomized comparison of local urokinase thrombolysis versus systemic heparin anticoagulation for superior sagittal sinus thrombosis. Stroke 2001; 32: 2310–17 Holloway RG, Benesch C, Rusch SR. Stroke prevention. Narrowing the evidence-practice gap. Neurology 2000; 54: 1899–906 Anderson C, Mhurchu CN, Rubenach S et al. Home or hospital rehabilitation? Results of a randomized controlled trial. Stroke 2000; 31: 1032–7 Strand T, Asplund K, Eriksson S et al. A non intensive stroke unit reduces functional disability and the need for long-term hospitalization. Stroke 1985;16: 29–34 Beech R, Rudd AG, Tilling K, Wolfe CDA. Economic consequences of early inpatient discharge to community-based rehabilitation
173. 174. 175. 176. 177.
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for stroke in an inner-London teaching hospital. Stroke 1999; 30: 729–35 Garraway M. Stroke rehabilitation units: concepts, evaluation and unresolved issues. Stroke 1985; 16: 178–81 Ryglewicz D, Hier DB, Weissbein T et al. Factors predicting 30-day mortality in the Warsaw Stroke Registry, Cerebrovasc Dis 1995; 5: 72–7 Folstein M, Folstein S, McHugh PR. Mini-Mental State: a practical method for grading the cognitive state of patients for clinician. J Psychiatr Res 1975; 12: 189–98 Langhoeme R Duncan P. Does the organization of postacute stroke care really matter? Stroke 2001; 32: 268–72 Wardlaw JM, del Zoppo G, Yamaguchi T. Thrombolysis for acute ischemic stroke, ACP J Club 2002; 136: 50
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Interventional treatment of acute ischemic stroke: past, present, and future CS Eddleman, ZA Hage, DL Surdell, EI Levy, RM Samuelson, YA Mikhaeil, and BR Bendok
Introduction and rationale Acute ischemic stroke (AIS) continues to be a major cause of morbidity and mortality worldwide. In North America, it is estimated that 700,000 new ischemic strokes occur annually with a healthcare cost burden of over $50 billion. While mortality from AIS in North America exceeds 150,000 deaths per year, over 4 million AIS survivors currently live with some form of disability from a prior stroke.1–6 While conventional medical therapy of AIS has gained moderate ground in outcome improvement, there continues to be high morbidity and mortality. Based on the experience in the cardiac literature with coronary ischemia, the use of thrombolytics has become an integral modality of therapy in the management of AIS. Various thrombolytics have been used in stroke trials and include streptokinase, urokinase, recombinant tissue plasminogen activator (rtPA), recombinant pro-urokinase (r-proUK), retavase, and reteplase. At this point, the only intravenous (IV) trial to date that has been shown to benefit acute stroke patients has been the National Institute of Neurological Disorders and Stroke (NINDS) trial, which resulted in the 1996 FDA approval of IV use of tissue plasminogen activator (tPA) within 3 hours of stroke onset. Compared to placebo patients, those patients given IV tPA were 30% more likely to have minimal neurological symptoms or no disability at 90 days.7–10 However, the symptomatic intracerebral hemorrhage (ICH) rate 24–36 hours after tPA administration was higher, with a 6.4% incidence versus 0.6% of the patients in the placebo group. Despite these promising results, it is still currently estimated that less than 3–5% of all patients who present with AIS receive this drug for therapy.1–6 This is thought to be due to the lack of education of the public and perhaps medical personnel regarding stroke symptoms, lack of promptness of evaluation in emergency departments, and lack of appropriate training and awareness of those personnel who evaluate and eventually treat AIS patients.11 Despite the improvement AIS patients potentially gain with IV thrombolysis, patients suffering large vessel occlusions have a lower rate of recanalization and subsequent worse outcomes. Del Zoppo et al. found that recanalization rates significantly decreased the larger the diameter of the 288
occluded vessel (Table 34.1).12 Furthermore, in a stroke subtype analysis of AIS patients in the NINDS trial, poorer outcomes were reported in relation to larger vessel occlusions.7 In fact, good outcomes defined as a National Institutes of Health stroke scale (NIHSS) score of ≤ 1 at 90 days occurred in 47% of small vessel occlusions, 33% of large vessel occlusions, and in 29% of cardioembolic strokes.7 This is thought to be mainly due to the large clot burden in larger proximal vessels as well as the resultant ineffective recanalization of IV thrombolysis. Re-establishing large cerebral vessel flow would be expected to reduce morbidity and mortality in large vessel occlusions if completed before irreversible ischemic damage occurs. In addition, many of these patients with large vessel occlusions are ineligible for IV thrombolytic therapy due to their presentation after the 3-hour time window has expired. Therefore, an alternative therapeutic choice in the treatment of AIS was desired, namely the local administration of thrombolytics utilizing endovascular techniques. Several factors made intra-arterial (IA) administration of thrombolytics an attractive option, including the extended time window within which patients could be treated, the direct infusion of thrombolytics within the thrombus, and the decreased systemic concentrations of thrombolytics leading to a decreased risk of systemic hemorrhagic complications and possibly increased efficacy rates of recanalization. Furthermore, advancements in endovascular technology have provided novel alternatives, in particular mechanical thrombolysis, in addition to local pharmacologic thrombolysis that physically affect thrombi, either by removal or maceration, thereby leading to vessel recanalization. Intra-arterial thrombolysis provides several theoretical advantages over IV thrombolysis, including the ability to deliver higher concentrations of thrombolytics locally to the thrombus while reducing the systemic concentrations, thus potentially avoiding the complications associated with IV administration, the need for exact anatomical knowledge of the surrounding vasculature and patterns of circulation as well as precise timing of recanalization, and some degree of mechanical disruption of the thrombus.3,6,13,14 However, IA thrombolytic administration also has some theoretical disadvantages. These include the requirement of specialized centers necessary for such therapy; procedural costs; complications of
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Interventional treatment of acute ischemic stroke: past, present, and future Table 34.1 Overall recanalization rates in ICA vs. MCA occlusions reported by del Zoppo et al. the difference in recanalization rates according to occlusion site is significant Overall recanalization ICA MCA stem Distal MCA
8% 26.1% 38.1%
angiographic procedures requiring manipulation of endovascular catheters, which could lead to increased hemorrhage risk and vessel injury; and the delay of thrombolysis in order to perform the diagnostic angiogram.15–17 Intra-arterial mechanical thrombolysis has as its main advantage the potential to obviate the need for pharmacologic thrombolytics, thereby avoiding the possible side-effects of those agents. However, mechanical devices have the clear potential disadvantage of being physically injurious to vessels with either deployment or manipulation within the vessel.18 Regardless of intra-arterial modality, the approach to thrombolysis in AIS patients has taken a step forward. Currently, many interventional alternatives exist to treat AIS. As endovascular intervention for stroke becomes available at increasingly more hospitals and academic centers, the treatment of the growing number of patients who suffer AIS with these interventional therapies will be increasingly feasible. In this chapter, we will review the multiple modalities of interventional stroke therapy available today as well as therapeutic developments on the horizon.
Literature review Initial evaluation and grading of AIS The diagnosis of AIS first has to be determined, often using multiple techniques, before any interventional therapy for stroke is considered. Computed tomography (CT) scans are often the initial step in evaluating AIS patients and are Table 34.2
available at most hospital and academic centers. Initial CT scans evaluating ischemic regions were initially not shown to correlate with stroke outcome studies regardless of therapy.19–25 However, using a more detailed analysis of initial CT scans, for example the Alberta Stroke Program early CT score (ASPECTS), initial CT scans have been shown to be valuable when determining which patients will benefit from interventional therapy and likely result in improved neurological outcomes.19,22 Additionally, diffusion–perfusion mismatch imaging techniques, namely MR perfusion or CT perfusion, which can demonstrate potentially salvageable penumbra, have also been shown to be helpful in predicting which patients will benefit from interventional therapy.23,24,26 Demonstration of ischemic and non-infarcted areas of brain serves as an indication that successful recanalization may benefit the patient, thereby improving neurological outcome.1,23,25,26 Once it has been determined that the patient has suffered an AIS event, has presented within the 6-hour treatment window, and may, in fact, benefit from interventional therapy, the patient is taken to the angiographic suite for a cerebral angiogram. Cerebral angiograms are usually performed via a transfemoral approach using standard diagnostic angiographic catheters to determine important characteristics about the acutely occluded arterial segment, including specific location, length of occluded segment, and degree of distal flow occlusion. Interventional grading of AIS currently lacks a standard convention regarding the critical endpoint of cerebral revascularization after IA thrombolysis has been undertaken. The terms “recanalization” and “reperfusion” are frequently used interchangeably despite defining two distinct clinical situations. Recanalization is defined as the state of the primary arterial occlusive lesion (AOL) after treatment. Reperfusion is defined as blood flow distal to the occlusive lesion. Several scales have been created in an attempt to allow for standard reporting of AIS; however, their use is often not consistent with the reported clinical endpoints described.27,28 The thrombolysis in myocardial infarction (TIMI) score was created, modified, and adopted from the cardiac literature and describes angiographic contrast passage or lack thereof across or through the occlusive lesion (Table 34.2).29 The thrombolysis in brain
Thrombolysis in myocardial infarction (TIMI) classification scales, original and modified
Grade
Original TIMI
Modified TIMI
0
No perfusion or flow beyond the point of occlusion. Penetration without perfusion: contrast passes beyond occlusion site but fails to opacify the entire coronary bed distally. Partial perfusion: contrast passes distal to the occlusion site and opacifies the coronary bed. However, the rate of entry of contrast into the vessel distal to the occlusion site or its rate of clearance from the distal bed (or both) is perceptibly slower than other well perfused areas. Complete perfusion: Flow into and clearance from the distal coronary bed is equal to other well-perfused areas.
No perfusion of flow beyond the point of occlusion.
1 2
3
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Penetration with minimal perfusion: contrast passes beyond occlusion site but fails to opacify the entire coronary bed distally. Partial perfusion: contrast passes distal to the occlusion site and opacifies the coronary bed. However, the rate of entry of contrast into the vessel distal to the occlusion site or its rate of clearance from the distal bed (or both) is perceptibly slower than other well perfused areas. Complete perfusion: Flow into and clearance from the distal coronary bed is equal to other well-perfused areas.
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ischemia (TIBI) scale was subsequently created using transcranial Doppler (TCD) measures to describe similar parameters in cerebral vessels (Table 34.3).30 Given the difficulty of obtaining TCD measurements during cerebral angiography, the thrombolysis in cerebral infarction (TICI) scale was created using angiographic measures of flow through the occlusion site (Table 34.4).28 Finally, the original TIMI scale was modified by Qureshi and colleagues to more appropriately describe recanalization states using an angiographic scale (Table 34.5).31 All of the above scales refer primarily to reperfusion measures but have been used to describe recanalization. A recent scoring system, the arterial occlusive lesion (AOL) recanalization score, was created to focus primarily on recanalization (Table 34.6).28 It remains to be seen what clinical effect the use of different descriptions of recanalization or reperfusion will have on trial or study outcomes. However, what is clear is that interventional treatment of AIS is beneficial for patients who present within 6 hours of symptom onset.7–10 Many trials and clinical studies have been undertaken to demonstrate the effectiveness of IA thrombolysis for AIS in terms of TIMI, TIBI, and AOL scores as well as well-established outcome scores, for example modified Rankin score, NIHSS, and Barthel Index. In the following sections, we will describe the literature with regard to the various treatment strategies and outcomes of interventional therapy of AIS.
Intra-arterial pharmacologic thrombolysis The English language stroke literature has seen a multitude of reports utilizing IA administration of thrombolytics for large vessel recanalization after AIS.3,6,13 For those patients who present within 6 hours of AIS symptom onset and are taken to the angiographic suite, the thrombosed segment is localized and the occlusion grade is determined. Subsequently, an endovascular catheter is placed proximal to and directly within the thrombus (Figure 34.1). Intra-arterial pharmacologic thrombolysis usually involves direct administration of thrombolytics proximal to, within, and beyond the thrombus. Adjunctive administration of low-dose IV heparin may potentiate the action of some thrombolytics (we prefer to keep the ACT no higher than 200). Thrombolytics are often infused directly into the thrombus for 30–120 minutes. To assess the degree of recanalization, periodic angiograms are performed,
Table 34.3
although the number of contrast injections is minimized due to the possible correlation to increased hemorrhage rates.6,32 Cessation of IA thrombolytic therapy occurs when systemic concentrations of thrombolytic are reached (usually not exceeding 20 mg of IA tPA), significant recanalization occurs, or no clear benefit of continued IA therapy is determined (Figure 34.2). Initial trials of IA thrombolytic administration in cases of AIS were positive, although the small population of patients investigated precluded definite therapeutic guidelines with regard to safety and efficacy.15,17,20,25,33–38 Early trials of patients with AIS treated within 6 hours of onset utilized urokinase and tPA in doses of up to 2 million U or 80 mg, respectively, with complete thrombolysis in 39% and partial thrombolysis in 36%. Posterior circulation occlusion was sometimes treated within 12 hours of onset. Symptomatic ICH occurred in approximately 4% of patients.13 These encouraging results prompted two randomized, double-blinded, prospective, multi-center trials in which the safety, recanalization frequency, and clinical efficacy of direct IA infusion of r-proUK versus placebo (prolyse in acute cerebral thromboembolism, PROACT I) with or without heparin (PROACT II) in symptomatic proximally occluded MCA segments were studied. The PROACT I study was performed from 1994 to 1995 and involved a total of 105 eligible patients out of 1314 who were screened.39 Clinical inclusion criteria required patients to have had an AIS consistent with an MCA territory occlusion within 6 hours of symptomatic onset, age 18–85 years, and a NIHSS score of ≥ 4 except for isolated aphasia or isolated hemianopsia. Clinical exclusion criteria included stroke within 6 weeks, minor stroke symptoms, seizures at stroke onset, subarachnoid hemorrhage, intracranial hemorrhage or tumor, uncontrolled hypertension, septic emboli from endocarditis or other etiology, surgery or trauma within 30 days, head trauma within 90 days, active or recent hemorrhage within 14 days, hematologic dyscrasia, international normalized ratio (INR) > 1.5, and a NIHSS > 30. Radiographic exclusion criteria involved the presence of ICH, significant mass effect with midline shift, and evidence of intracranial tumor. Once a patient was determined to have passed clinical and radiographic inclusion, a cerebral angiogram was performed. Angiographic inclusion criteria were TIMI grade 0 or 1 of either the M1 or M2 segment of the MCA. Clinical outcome was based on the NIHSS, modified Rankin score (mRS), and
Thrombolysis in brain ischemia classification using transcranial Doppler assessment
Grade
Description
Grade 0 Grade 1
Absent flow: Lack of regular pulsatile flow signals despite varying background noise Minimal flow: Systolic spikes of variable velocity and duration Absent diastolic flow Blunted flow: Flattened systolic flow acceleration of variable duration Positive end diastolic velocity and pulsatility index < 1.2 Dampened flow: Normal systolic flow acceleration Positive end diastolic velocity Decreased mean flow velocity (MFV) by > 30% Stenotic flow: MFV > 80 cm/s AND velocity difference > 30% compared to controls OR MFV < 80 cm/s but a difference of MFV > 30% from controls AND signs of turbulence Normal flow: Similar waveforms compared to controls < 30% mean velocity difference compared to controls
Grade 2 Grade 3 Grade 4 Grade 5
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Thrombolysis in cerebral ischemia (TICI) classification scale
Grade
Description
0 1
No perfusion of flow beyond the point of occlusion Penetration with minimal perfusion: contrast passes beyond occlusion site but fails to opacify the entire cerebral bed distally Partial perfusion: contrast passes distal to the occlusion site and opacifies the cerebral bed. However, the rate of entry of contrast into the vessel distal to the occlusion site or its rate of clearance from the distal bed (or both) is perceptibly slower than other well perfused areas Only partial filling (less than two-thirds) of the entire vascular territory is visualized Complete filling of all of the expected vascular territory is visualized, but the filling is slower than normal Complete perfusion: Flow into and clearance from the distal cerebral bed is equal to other well-perfused areas
2 2a 2b 3
Table 34.5
Arterial occlusion and recanalization grading scheme proposed by Qureshi et al.
Grade
Description
0 1 2 3 3A 3B 4 4A 4B 5
No occlusion MCA occlusion (M3 segment) ACA occlusion (A2 or distal segments) 1 BA/VA branch occlusion MCA occlusion (M2 segment) ACA occlusion (A1 or A2 segments) ≥ 2 BA/VA branch occlusions MCA occlusion (M1 segment) Lenticulostriate arteries spared and/or leptomeningeal collaterals visualized No sparing of lenticulostriate arteries nor leptomeningeal collaterals visualized ICA occlusion (collaterals present) BA occlusion (partial filling direct or via collaterals) Collaterals fill MCA Anterograde filling Collaterals fill ACA Retrograde filling ICA occlusion (no collaterals) BA occlusion (complete)
Table 34.6
Arterial occlusive lesion (AOL) recanalization score definition
Score
Description
0 1 2 3
No recanalization of the primary occlusive lesion Incomplete or partial recanalization of the primary occlusive lesion with no distal flow Incomplete or partial recanalization of the primary occlusive lesion with any distal flow Complete recanalization of the primary occlusion with any distal flow
(a)
291
(b)
(c)
Figure 34.1 80-year-old gentleman who presented to the emergency department within 6 hours of symptom onset, which consisted of left-sided weakness: (a) right internal carotid injection (anterolateral projection) showing an acute occlusion in the proximal portion of M1 (arrow); (b) unsubtracted digital image of same plane as A showing end of catheter at the proximal portion of thrombus (asterisks); and (c) unsubtracted digital angiogram image of B with injection of the right internal carotid artery, demonstrating the relationship of the catheter tip and the site of acute occlusion.
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(a)
(b)
(c)
(d)
Figure 34.2 18-year-old male who presented to the emergency department within 6 hours of symptom onset with left-sided weakness: (a, b) Digital subtraction angiogram (right internal carotid injection: A, anteroposterior plane; B, lateral plane) demonstrating acute occlusion of the proximal M1 segment; (c, d) digital subtraction angiogram (right internal carotid injection: A, anteroposterior plane; B, lateral plane) demonstrating recanalization of right M1 segment after IA thrombolysis for 65 minutes.
the Barthel index at 7, 30, and 90 days after treatment. All patients were given IV heparin for 4 hours after angiographic verification of occlusion. Of the 105 AIS patients who satisfied clinical and radiographic criteria, 40 had complete occlusions of the main MCA, M1, or M2 segments and completed treatment and follow-up, of which 26 patients received 6 mg of IA r-proUK therapy. Of the latter patients, 15 (57.7%) had partial or complete recanalization as compared to only 2 of 14 patients given placebo (14.3%) (p = 0.0085). Five patients (19.2%) given IA r-proUK had complete recanalization as compared to none from the placebo group. Hemorrhagic complications within 24 hours occurred in 42.3% of the r-proUK group and 7.1% in the placebo group, of which only 15.4 and 7.1% were symptomatic, respectively. The first 16 patients were initially given a high-dose heparin therapy, which was subsequently
changed to a low-dose heparin regimen due to frequency of acute ICH. Outcome analyses demonstrated a 10–12% absolute increase in good neurological outcome in the r-proUK group compared with the placebo group at 90 days after IA therapy. The PROACT II study involved 54 North American and Canadian centers where 12,323 patients with AIS were screened, 474 underwent angiography, and ultimately 180 patients were subsequently randomized into a group ratio of 2:1 to receive 9 mg of IA r-proUK and low-dose heparin (similar to PROACT I), or low-dose heparin alone in the control group. Inclusion and exclusion criteria were similar to PROACT I, with the addition of the European Cooperative Acute Stroke Study (ECASS) CT exclusion criteria, which involved hypoattenuation or sulcal effacement in more than one-third of the MCA territory.40
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Interventional treatment of acute ischemic stroke: past, present, and future Of the 180 patients with AIS who presented within 6 hours of onset and were randomized, 121 received r-proUK and 59 were only given low-dose heparin. Diagnostic angiography was performed 120 minutes after infusion, and CT scans were obtained at baseline, 24 hours, and 7–10 days after therapy. Clinical outcome was assessed using mRS, NIHSS, and Barthel index at 7–10 days, 30 days, and 90 days. The recanalization rate of the r-proUK group was 66 and 18% for the control group (p < 0.001), with complete recanalization in 19 vs. 2%, respectively (p < 0.003). Increasing the dosage of r-proUK from 6 to 9 mg improved recanalization by 26% but also increased the symptomatic ICH rate by 4%. The incidence of ICH at 10 days was 68% in the r-proUK group and 57% in the control group, which was not significantly different. Good clinical outcomes (mRS £ 2) at 90 days were seen in 40% of the r-proUK group and 25% of the control group (p = 0.43), which represented an absolute benefit of 15% and a relative benefit of 58%. Several post-hoc analyses were subsequently conducted and provided further evidence for the efficacy of IA thrombolytic therapy. The dynamic physiological response to IA and IV thrombolytic recanalization has been studied using diffusion–perfusion imaging, which demonstrated that early recanalization after ischemic onset can salvage not only areas of oligemia experiencing minimal or no cellular bioenergetic compromise (diffusion–perfusion mismatch), but also parts of the region of early neuronal tissue injury itself (diffusion abnormality).23,24 Further analysis of the PROACT II data demonstrated that the treatment effect of IA thrombolysis is consistent over the range of baseline risk levels. However, treatment effect has been shown to be larger for women than men, due to the nullification of reported worse outcomes for untreated women compared to men.41 Despite these promising results of IA administration of r-proUK in AIS patients, r-proUK has not been approved for use in the US. Several single center experiences have been published regarding the effects of IA thrombolytics outside the realm of clinical trials. Reteplase, a recombinant plasminogen activator derived from rtPA, which has been shown to be safe and effective to recanalize coronary arteries in acute myocardial infarction, has been examined as an alternative to urokinase. Qureshi et al. reported in a small study that IA reteplase resulted in partial or complete recanalization rates of 65% but had a symptomatic ICH rate of 5% when IA reteplase was either used alone or in combination with an IV-administered glycoprotein IIb/IIIa inhibitor (abciximab) and/or mechanical clot disruption.42 However, when low-dose reteplase and mechanical clot disruption have been used in combination, a high rate of recanalization (84%) with no symptomatic ICH resulted, suggesting that a lower-dose thrombolytic strategy may result in lower rates of complications while maintaining acceptable rates of recanalization.43 In a comparison study between IA reteplase and urokinase, Sugg et al. examined, in a retrospective study, 55 patients (33 patients received IA reteplase compared to 22 patients receiving IA urokinase) who presented with AIS and who had not received any other IV thrombolytic therapy. The inclusion criteria were presentation > 3 hours from symptomatic onset, minimal ischemic changes on initial CT scan (< 1/3 of the MCA territory), disabling neurological deficit (NIHSS ≥ 6 or complete aphasia), evidence on TCD of large vessel arterial occlusion or stenosis, and no
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evidence of intracranial hemorrhage on initial CT scan. In addition, patients included in the analysis did not receive IV tPA, had TICI < 1 of the BA, ICA, or MCA by cerebral angiography, and received either urokinase or reteplase. Intra-arterial thrombolytics were administered until either recanalization was obtained or maximum dose limits were achieved (6U reteplase or 2,000,000 U urokinase). Recanalization rates of reteplase-treated patients were 82% as compared to 64% of the IA urokinase-treated (p = 0.13).44 Symptomatic ICH rates were 12% for reteplase patients and 4.5% with urokinase patients (p = 0.5). Although the statistical power of this study was limited, the trend demonstrated that both recanalization and symptomatic ICH rates were higher for the patients treated with reteplase. However, recanalization, outcome, mortality, and ICH rates were not statistically significant between the two IA therapies.44
Combinational IV–IA thrombolysis Intra-arterial thrombolysis has been shown to improve patient outcomes with lower complication rates; however, the initiation of IA therapy is not immediate. It is known that the duration of impaired cerebral perfusion is associated with the degree of infarction and the time from the impaired perfusion onset to treatment initiation is an important outcome predictor in thrombolysis. With IA thrombolysis, there exists a significant delay between the time of diagnosis and actual treatment, during which the mobilization of personnel and equipment for IA thrombolysis can require greater than 60 minutes before initiation of IA treatment can commence. In contrast, IV thrombolysis has the advantage of more rapid administration after the decision has been made to treat a patient with AIS. In an attempt to utilize the advantages of both modes of thrombolytic administration, the combination of the two therapies has been investigated. The first phase 1 trial to examine the combination of IV and IA thrombolysis was the Emergency Management of Stroke (EMS) Bridging Trial, where 35 patients who presented within 3 hours of stroke onset were randomized into groups receiving either 0.6 mg/kg IV tPA or placebo followed by cerebral angiography and IA thrombolysis with an additional 20 mg tPA if the vessel remained occluded.45 Of the 35 patients, one patient did not undergo angiography due to access problems. Of 34 patients who underwent angiography, 22 had a residual thrombus identified. Arterial reperfusion, described using TIMI grades, was more frequent in patients who received IV and IA thrombolytics than in patients who received IA tPA alone (54% vs. 10%, respectively). The frequency of symptomatic hemorrhagic complications in the combination group was 11.8%, similar to that observed with IA tPA alone.45 However, there was no significant difference in the primary clinical outcome as measured by improvement of NIHSS, GOS, mRS, or Barthel index. Therefore, the authors concluded that improvement in reperfusion, as demonstrated by the increased reperfusion scores in the combined therapy group, did not translate into an improved clinical outcome as compared to IA tPA alone. The authors also further discussed several limitations and confounding factors with this study, which included the small number of patients involved, an excess of adverse events unrelated to treatment, and an imbalance of randomization resulting in a
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disproportionately large number of patients with severe deficits being assigned to the combined therapy group. Despite these limitations, the study did conclude that combinational therapy was safe and did not result in additional adverse complications despite using both IV and IA thrombolysis.45 In another combinational trial funded by the National Institutes of Neurologic Diseases and Stroke (NINDS), the Interventional Management of Stroke (IMS I), which began in 2001, examined through 17 centers the feasibility and safety of a combined IV and IA approach to recanalization using rtPA in 80 subjects with AIS with a baseline NIHSS ≥ 10 who were treated within 3 hours of symptom onset.46 The complete recanalization rate (TIMI 3 flow) for the 62 patients who received a combination of IA rtPA (0.6 mg/kg) and IV rtPA (0.6 mg/kg) was 11% (7/62); the rate of partial or complete recanalization (TIMI 2 or 3 flow) was 56% (35/62), after 2 hours of infusion at the most. Thirty-four percent of the patients achieving TIMI 2 or 3 flow had a favorable outcome (mRS of 0–1 at 3 months) as compared to 12% of those only achieving TIMI 0 or 1 flow (p = 0.013). Forty-three percent (7/16) of patients who were administered IA rtPA within 3 hours of symptom onset had a mRS of 0–1 at 90 days as compared to 13% (3/24) of subjects who were given IA rtPA within 3–4 hours and 27% (6/22) of those who received IA rtPA after 4 hours. The 3-month mortality in IMS I was numerically lower but not statistically different than the mortality of placebo and rtPA-treated patients in the NINDS rtPA trial. The rate of symptomatic ICH was higher than the placebo group of the NINDS trial (6.3 vs. 1%) but not statistically different than the IV rtPA-treated patients (6.3 vs. 6.6%). However, the rate of asymptomatic ICH was significantly higher in the IMS I trial than the IV rtPA NINDS trial (43 vs. 6%).27,46 Similar to standalone IA thrombolytic therapy, combinational IV–IA thrombolytic therapy of AIS has been examined outside of clinical trials in several published case series.32,47–52 Keris et al. reported on 45 patients with acute onset of hemispheric stroke who were randomized to receive combined IV and IA thrombolysis or IV heparin alone. Good clinical outcomes (mRS 0–3) were seen at 1 month in 67% (8/12) of patients who underwent combined IV and IA thrombolysis and 21% (7/33) in the control group and in 83% and 33% of patients, respectively, at 12 months. Intracranial hemorrhage occurred in 17% of patients treated with combined IV and IA thrombolysis and 6% of patients in the control group. Mortality at 30 days was 17% in the combined treatment group as compared to 48% in the control group.49 Flaherty et al. reported on combined IV–IA thrombolysis in 44 patients in which 59% (26/44) achieved TIMI 2–3 after combinational therapy. In patients 80 years of age or less treated with an IV–IA approach, 54% (20/37) achieved a mRS score of 0 to 2 at the 90-day outcome analysis. In this same group, mortality was 16% and symptomatic ICH was 8%.47 While combinational therapy has been shown to result in favorable outcomes when compared to IA thrombolysis alone, further clinical studies are necessary to establish treatment guidelines and patient selection.
Intra-arterial mechanical thrombolysis Promising results for improved neurological outcome for recanalization and reperfusion of AIS patients have been
demonstrated with both IV and IA thrombolytic as well as combinational therapy. However, many patients are still ineligible for thrombolytic therapy, have large vessel occlusions that are unaffected by thrombolytic therapy, or present to the hospital in an untimely fashion. As a result, alternative endovascular therapies have been developed, in particular mechanical devices designed to potentially obviate the need for thrombolytics by mechanically either dissolving the offending clot or removing it from the occluded vessel. Mechanical thrombolytic devices can dissolve, macerate, or remove clot in a manner of minutes, whereas pharmacologic thrombolysis can take as long as 2 hours to dissolve a thrombus.18 This accelerated time to recanalization has encouraged the use of long treatment windows in trials of AIS treatments. In addition, IA-delivered devices theoretically result in lower rates of intracranial hemorrhage compared to pharmacological thrombolysis.18,53 Several thrombolytic devices have entered clinical trials or studies using various thrombolytic mechanisms, including suction-creating saline jets, laser energy, ultrasound, and corkscrew or snare removal systems. In this section, we will review the thrombolytic devices and known clinical data. The AngioJet system (Possis Medical, Minneapolis, MN) uses saline jets that are directed back into the catheter to create a low-pressure zone around the catheter tip, inducing suction that pulls the clot into the exhaust lumen and removes it from the vessel. Between April 2000 and July 2003, 22 patients were enrolled in the Thrombectomy in Middle Cerebral Artery Embolism (TIME) trial, which resulted in several vessel perforations, leading to termination of the trial.54,55 The Latis laser device (Latis Inc., Coon Rapids, MN) was designed to utilize laser energy to ablate thrombi in arteries 2–5 mm in diameter. Enrolment in a safety and efficacy trial was terminated due to the numerous delivery problems of the system.54,55 The first mechanical thrombolytic device for which safety and feasibility results were reported in AIS patients was the Endovascular Photo Acoustic Recanalization (EPAR) laser system (Endovasix Inc., Belmont, CA). The low energy laser power source was delivered by means of fiber optics at the catheter tip where absorption of laser light by darkly pigmented materials in the clot resulted in the conversion of photo energy to acoustic energy, eventually emulsifying the thrombus inside the catheter tip. Berlis et al. reported on 34 patients whose inclusion criteria included a minimum NIHSS score of 4, stroke onset of £ 6 hours in the anterior circulation and £ 24 hours in the posterior circulation, and occlusion of the ICA, MCA, PCA, basilar, or vertebral arteries with a minimum diameter of 2 mm and TIMI 0 to 1 flow, where the recanalization rate was 41.1% (14/34). However, only 18 patients received complete EPAR treatment with 11 (61.1%) resulting in complete vessel recanalization; 6 of the 18 patients received IA rtPA during EPAR treatment. Symptomatic ICH within 24 hours of treatment occurred in two (5.9%) patients, one of whom had received adjuvant IA rtPA. Thirty days after treatment, 22.2% (4/18) of the patients who received complete treatment recovered to mRS score 0 to 2.56 Mortality was 38.2%, and NIHSS improved by 50% or greater in 22.2% of treatment-complete patients. The EPAR device was deemed safe and technically feasible without significant complications during therapy and provided the necessary
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Interventional treatment of acute ischemic stroke: past, present, and future data to enroll patients in an important phase II study; however, the loss of funding terminated further clinical testing. The combination of IA thrombolytic therapy with a mechanical device was further developed into the Ultrasound Thrombolytic Infusion Catheter (EKOS Corporation, Bothell, WA), which combined the use of an ultrasound transducer in conjunction with infusion of pharmacological thrombolytic therapy through the same microcatheter, which theoretically increases the permeability of the thrombus, resulting in not only a pressure gradient to move thrombolytics into the clot but also to provide increased effectiveness of the thrombolytic. Mahon et al. reported on the use of the EKOS MicroLys US infusion catheter device in a safety and feasibility trial that resulted in no adverse events due to technical deployment of the device.57 Ten patients with anterior-circulation occlusions who presented within 6 hours of symptom onset and four patients with posterior-circulation occlusions who presented within 24 hours of symptom onset were treated. The median initial NIHSS score was 19.5. Eight patients (57%) attained TIMI flow of 2 to 3 within 1 hour of treatment, which included an initial 2 mg bolus of IA tPA at the site of the clot followed by a continuous infusion of IA tPA 0.3 mg/min to a maximum of 20 mg with simultaneous ultrasound transmission for as long as 60 minutes. Symptomatic ICH occurred in 14%, mortality rate was 36%, and 90-day outcome with mRS £ 2 was 43% as compared to 10%, 25%, and 40%, respectively, in the PROACT II study. Although the numbers in this study were small and unable to demonstrate statistical significance, the results were encouraging. As a result, the EKOS MicroLys US infusion catheter device has been incorporated in the IMS II trial, which has recently been completed, and results are waiting to be published. The device has also been included in the current IMS-III trial, which is a phase III, randomized, multicenter, open-label clinical trial that will examine whether a combined IV and IA approach to recanalization is superior to standard IV thrombolytic therapy when initiated within 3 hours of AIS symptom onset. The only FDA-approved mechanical device for IA thrombolysis is the MERCI (Mechanical Embolus Removal in Cerebral Ischemia) retrieval system (Concentric Medical Inc., Mountain View, CA), which consists of a flexible tapered nitinol wire with five helical loops that are embedded into the thrombus followed by gentle retraction of the clot into the microcatheter (Figure 34.3). A distal protection balloon is inflated before clot retrieval occurs. The Part I Safety and Efficacy Clinical Trial consisted of 28 patients treated within 8 hours of symptomatic AIS onset. Successful recanalization (TIMI 2 or 3) occurred in 12 patients (43%) with the device alone and in 18 (64%) with additional IA tPA administration. No symptomatic ICH occurred in this trial.58 In the Part II MERCI trial, consisting of 25 participating hospitals, 141 patients were treated with a mean NIHSS of 20.1 and a mean time of symptomatic onset of 4.3 hours.59 Revascularization was achieved in 48% (68/141) of patients, and device-related clinically significant complications occurred in 7.1% (10/141) of patients (Figure 34.4). Symptomatic ICH occurred in 7.8% (11/141) of patients; however, major adverse events (death, MI or new stroke at 30 days) occurred in 30% of patients with successful recanalization and in 49% of patients with unsuccessful recanalization. The 90-day outcome (mRS) was 0–2 in 46% of patients who were successfully recanalized as compared to 10% of those who were not recanalized.59
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Figure 34.3 Diagram showing the stages of clot extraction using the MERCI retriever. The thrombus is first approached by the catheter followed by carefully passing the guidewire beyond the thrombus. Some versions of the MERCI retriever have distal protection balloons to catch any emboli. The conical spring is slowly advanced beyond the thrombus. Once fully expanded, the retriever is slowly retracted to engulf the thrombus. Once the thrombus is trapped with the retriever, it is withdrawn into the catheter and removed from the vasculature.
Since the MERCI trial had reported efficacy of the MERCI retriever in patients ineligible for IV rtPA, patients who were eligible for IV rtPA therapy but failed to recanalize after IV thrombolytic therapy were thought to potentially benefit from mechanical thrombectomy in addition to IV thrombolysis. As a result, the Multi MERCI trial was undertaken to examine the combination of IV, IA thrombolysis with and without the use of the MERCI retriever.60 In Multi MERCI, 111 patients with a mean NIHSS of 19 who presented within 8 hours of symptomatic AIS were treated with the device. Intravenous rtPA was administered in 27% (30/111) of patients, all of whom failed to recanalize. Additional IA rtPA was administered in 43% (13/30) of patients who received IV rtPA. Successful recanalization with the retriever alone was achieved in 54% (60/111) of treatable vessels and in 69% (77/111) after all adjunctive therapies, for example IA rtPA or mechanical. Symptomatic ICH occurred in 9% (10/111) with clinically significant procedural complications occurring in 4.5% (5/111) of patients.60 The Multi MERCI study demonstrated that combining IV rtPA with endovascular thrombectomy did not substantially increase the risk of hemorrhage or serious adverse events. The NINDS has currently funded a randomized trial of the MERCI retriever compared with medical therapy as long as 8 hours after AIS symptom onset, called Magnetic Resonance and Recanalization of Stroke Clots Using Embolectomy (MR RESCUE), which will stratify the effects
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Figure 34.4 31-year-old male who presented to the emergency department within 5 hours of symptom onset: (a) digital subtraction angiogram (right vertebral artery injection, anteroposterior view) demonstrating acute right proximal PCA occlusion; (b) fluoroscopic view of MERCI retriever in the right PCA; and (c) digital subtraction angiogram (right vertebral artery injection, anteroposterior view) demonstrating restored flow in the right PCA segment.
of therapy by the presence of a penumbra on MRI at randomization and is the first study to address the comparison of clinical outcomes and financial impact of these devices with medical therapies.
Future directions in intra-arterial thrombolysis The treatment of AIS with IA thrombolysis by pharmacological, mechanical, or combinational means has shown great promise for a serious healthcare burden. Unfortunately, many people who suffer from AIS still either do not qualify or arrive at centers that do not offer such advanced treatment for stroke. As further clinical trials progress and education is enhanced, the availability of such technology to treat AIS will certainly become more widespread. At the same time, future developments aimed at either improving current methods or the development of more advanced techniques will certainly flourish. Future developments in IA thrombolysis generally fall into two categories: improving the pharmacological agents used in IA thrombolysis and the development of newer and more effective mechanical means of thrombolysis. Recombinant tissue plasminogen activator remains the only FDA-approved thrombolytic accepted for intra-arterial thrombolysis. Combinational IA therapy has been shown to be as effective and safe as IA rtPA alone. The combination of IA thrombolytics and IV therapy using newer agents, such as glycoprotein IIb/IIIa inhibitors, which inhibit platelet aggregation and mechanical thrombolysis, is showing promise. In a study by Lee at al., 16 patients were given IA urokinase alone and 10 patients were given IV abciximab, a monoclonal antibody to glycoprotein IIb/IIIa receptors, in combination with IA urokinase.61 Nine of ten patients (90%) in the combined urokinase and abciximab group demonstrated arterial recanalization compared with 44% (7/16) given IA urokinase alone. There was no significant difference in the incidence of symptomatic ICH between the two groups. In a study by Mangiafico et al., 21 patients were treated with IV tirofiban, another glycoprotein IIb/IIIa receptor inhibitor, and heparin followed by IA urokinase coupled with mechanical thrombolysis. Complete recanalization was noted in 74% (14/19), and the 90-day functional outcome was favorable
(62% had mRS 0–2).62 These studies and many like them demonstrate that the combination of different agents beyond thrombolytics will likely be developed and will enhance the recanalization rates as well as outcomes of AIS treatment with IA thrombolytics. Mechanical thrombolysis will continue to evolve as more devices are either improved or developed. The MERCI retriever continues to be the only mechanical thrombolysis device approved by the FDA, yet it too has evolved, which has lead to improved results. In the Multi MERCI Trial, the older devices (X5/X6) showed lower rates of recanalization when compared with the newer generation (L5) of MERCI devices.60 Other devices, such as intracranial stents, are beginning to show promise in the treatment of AIS recanalization, especially in light of the potential complications with IA thrombolysis such as IPH, inability to dissolve platelet-rich clots, and the often lengthy times required for recanalization.63 Furthermore, intracranial stents can be used when other efforts at pharmacological or mechanical thrombolysis have failed (Figure 34.5). In a retrospective analysis of 19 AIS patients (median NIHSS score of 16) whose occluded vessels were resistant to standard thrombolytic techniques, Levy et al. demonstrated that intracranial stent placement across the occluded arterial segment resulted in 79% of patients achieving TICI flow of 2 to 3. Patients in this study who achieved TICI grade 2 or 3 flow were significantly more likely to have a favorable discharge outcome.64 The continued maturation of intracranial stents and improvement in navigation within the torturous intracranial vasculature will certainly lead to further studies and possibly improved results when treating AIS with stent-assisted recanalization. Probably the most important future development in the IA thrombolytic treatment of AIS is the continued improvement of imaging modalities to aid in patient selection. Innumerable reports that have demonstrated the promising results of IA thrombolysis continue to describe a subpopulation of patients who do not do well regardless of the modality of AIS therapy. Patient selection has become the single most important predictor of success with IA thrombolysis. Imaging technology as well as imaging analysis continues to evolve to aid the stroke physician in selecting the appropriate patients who will most likely benefit from AIS treatment. Computed tomography remains the most used imaging modality in acute stroke and
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Figure 34.5 27-year-old female who presented to the emergency department within 4 hours after acute onset of left-upper extremity weakness and slurred speech: (a) digital subtracted angiogram (right common carotid injection, anteroposterior view) demonstrating a proximal M1 occlusion (arrow); (b) digital subtracted angiogram (right common carotid injection, enlarged anteroposterior view) demonstrating the radio-opaque markers (arrows) on either end of the intracranial stent. There is TIMI 2 recanalization with good flow distal to the stent. Lateral view (not shown) identified diminished flow in angular artery distribution.
is available in most hospitals. Dynamic contrast-enhanced CT (CT perfusion) has recently been shown to be sensitive and specific when identifying patients who possess salvageable brain tissue and thus could potentially benefit from IA thrombolysis. The further implication of this study is that the arbitrary time window of 3 and 6 hours that is commonly used for stroke therapy may be eliminated, and the amount of salvageable brain tissue determined from dynamic imaging may dictate whether a patient can benefit from stroke therapy regardless of the time from symptom onset.
Conclusion Although IA thrombolysis, both pharmacological and mechanical, has been shown to be beneficial in the treatment
of AIS, the recognition and timely initiation of therapy for AIS patients remains the most crucial aspect of therapy. Continued education of the public as well as other physician services that evaluate these patients will likely offer the most pronounced benefit to AIS patients, especially in light of the extraordinarily small numbers of AIS patients treated today. Continued refinement of current techniques as well as the development of newer pharmacological agents and devices will likely greatly enhance the treatment of AIS patients using IA thrombolysis.
Acknowledgments The authors thank Mr. Paul H. Dressel for preparation of the illustrations and Mrs. Jessica Kazmier for her editorial assistance.
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Interventional treatment of acute ischemic stroke: past, present, and future 55. Lutsep HL. Mechanical thrombolysis in acute stroke. eMedicine November, 2006 56. Berlis A, Lutsep H, Barnwell S, Norbash A, Wechsler L, Jungreis CA, et al. Mechanical thrombolysis in acute ischemic stroke with endovascular photoacoustic recanalization. Stroke. 2004;35(5): 1112–6 57. Mahon BR, Nesbit GM, Barnwell SL, Clark W, Marotta TR, Weill A, et al. North American clinical experience with the EKOS MicroLysUS infusion catheter for the treatment of embolic stroke. AJNR Am J Neuroradiol. 2003;24(3):534–8 58. Gobin YP, Starkman S, Duckwiler GR, Grobelny T, Kidwell CS, Jahan R, et al. MERCI 1: a phase 1 study of Mechanical Embolus Removal in Cerebral Ischemia. Stroke. 2004;35(12): 2848–54 59. Smith WS, Sung G, Starkman S, Saver JL, Kidwell CS, Gobin YP, et al. Safety and efficacy of mechanical embolectomy in acute ischemic stroke: results of the MERCI trial. Stroke. 2005;36(7): 1432–8
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60. Smith WS. Safety of mechanical thrombectomy and intravenous tissue plasminogen activator in acute ischemic stroke. Results of the multi Mechanical Embolus Removal in Cerebral Ischemia (MERCI) trial, part I. AJNR Am J Neuroradiol. 2006;27(6):1177–82 61. Lee DH, Jo KD, Kim HG, Choi SJ, Jung SM, Ryu DS, et al. Local intraarterial urokinase thrombolysis of acute ischemic stroke with or without intravenous abciximab: a pilot study. J Vasc Interv Radiol. 2002;13(8):769–74 62. Mangiafico S, Cellerini M, Nencini P, Gensini G, Inzitari D. Intravenous glycoprotein IIb/IIIa inhibitor (tirofiban) followed by intra-arterial urokinase and mechanical thrombolysis in stroke. AJNR Am J Neuroradiol. 2005;26(10):2595–601 63. Sauvageau E, Levy EI. Self-expanding stent-assisted middle cerebral artery recanalization: technical note. Neuroradiology. 2006;48(6): 405–8 64. Levy EI, Ecker RD, Horowitz MB, Gupta R, Hanel RA, Sauvageau E, et al. Stent-assisted intracranial recanalization for acute stroke: early results. Neurosurgery. 2006;58(3):458–63; discussion –63
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Carotid angioplasty and stenting under protection: techniques, indications, results, and limitations M Henry, A Polydorou, I Henry, Ad Polydorou, and M Hugel
Introduction Stroke represents the third leading cause of death in the US and the most common and disabling neurological disorder in the elderly population. Occlusive disease of the extracranial circulation is responsible for about 30% of cases. Medical therapy (e.g. antiplatelets and lipid-lowering agents) have a continuing role in reducing cardiovascular risk, but randomized controlled trials1−6 have shown that carotid endarterectomy (CEA) is superior to medical therapy alone and have demonstrated the efficiency of CEA in reducing the risk of stroke and death in symptomatic and asymptomatic patients. After the North American Symptomatic Carotid Endarterectomy Trial (NASCET) published in 1991,1 CEA was considered to be the gold-standard treatment for symptomatic carotid stenosis. After the Asymptomatic Carotid Atherosclerosis Study (ACAS) and the Asymptomatic Carotid Surgery Trial (ACST), surgery was also considered better than medical therapy for some subgroups of asymptomatic carotid stenosis.4−5 However this operation is not without drawbacks and always at risk in high- or low-risk patients. The stroke and death rate at 30 days in these trials ranged from 5.8 to 7.5% in the symptomatic patients and from 2.3 to 4.3% in the asymptomatic patients. However, the benefits of the procedure are critically dependent on the rate of peri-operative complications.5−7 In higher risk patients, particularly those with severe coronary artery disease, perioperative morbidity and mortality has been reported in up to 18% of patients.7−17 Rothwell et al.8 reported an overall mortality of 1.62% and a risk of stroke and/or death of 5.64% with CEA. The risk was higher in studies in which patients were assessed by a neurologist after surgery (7.7%) and lower in studies without neurological assessment (2.3%). In a series of 3061 procedures, Ouriel et al.18 described a stroke, myocardial infarction, and death rate of 7.4% in high-risk patients and 2.9% in low-risk patients. Carotid angioplasty and stenting (CAS) has been proposed as an alternative to surgery and the popularity of CAS has steadily risen partly due to the perceived benefits of the less invasive nature of the procedure, less procedural discomfort, and faster convalescence when compared to CEA. In the past few years, endoluminal devices used in CAS have been referred to to improve treatment success and reduce 300
procedural complications. Several studies suggest that CAS, even without cerebral protection, can be performed with an acceptable peri-operative stroke/death rate of 2.9−8.2%.19−29 Two randomized studies comparing carotid angioplasty and CEA30−31 showed comparable results. Restenosis is fortunately rare after CAS, between 3 and 5%, and the long-term results are encouraging.22−28 So CAS may be a substitute for surgery and may be proposed to the majority of patients suffering from a carotid stenosis, in particular high-risk patients. However, embolic stroke, even with a meticulous technique and experienced operators, represents the major drawback of the procedure. The majority of neurological complications are due to intracerebral embolism of plaque fragments or thrombus during different procedural steps. Embolic particles can be created at any time and dislodged from every plaque during CAS despite advanced techniques. Medication, improvements in technique, and careful selection of patients and lesions may reduce the embolic risks, but the stent alone cannot provide sufficient protection. Cerebral protection techniques that retain particles and debris generated during the procedure can reduce the frequency of neurological complications. Vitek32 and Theron33 were leaders in the concept of cerebral protection in the 1980s. From their studies, three types of cerebral protection devices were developed to reduce the incidence of embolic events and several recent studies demonstrated a reduction in neurological complications during CAS. The routine use of cerebral protection can achieve similar or even better results compared to the best surgical series and particularly in high-surgical-risk lesions, so the indications of this percutaneous technique could be extended, especially for lesions with high embolic risks.34−75 New techniques and new protection devices should also, as we will discuss, enlarge the indications of CAS to low-risk patients. However all protection devices are not equivalent and cannot prevent all neurological complications. If transcranial Doppler sonography (TCD) has shown a reduction in embolic load with some protection devices,38,76,77 Vos78 has recently reported that CAS yields more microemboli in patients treated with filters than in unprotected procedures. Furthermore, silent brain infarcts are often detected on DW-MRI performed after CAS and more frequently than after CEA.79−80 Nevertheless, there is now a consensus among specialists to perform all CAS under protection. This technique
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Carotid angioplasty and stenting under protection: techniques, indications, results, and limitations is now the standard of care40 and the routine use of cerebral protection seems beneficial.44−45 CAS should be the first treatment to be proposed to a patient presenting with a carotid stenosis in the near future, but in contrast to many endovascular peripheral arterial interventions, CAS represents a more challenging procedure requiring complex catheter-based skills and an extensive learning curve what explains the poor results of CAS in some published studies,81−85 particularly in the EVA 3S study,86 where the interventionists were unexperienced, as we will discuss later.
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Current indications and contraindications for CAS Preprocedure assessment They are based on a rigorous selection of the patients and the lesions. Before a CAS, several examinations are indispensable. Whatever the circumstances of discovery of a carotid stenosis, whether the patient is symptomatic or asymptomatic, it is always important to perform a complete examination before the angioplasty procedure. This examination will influence the technique of the angioplasty to be chosen, and should include the following: ●
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A careful clinical examination is necessary, not only of the neurological system, but also of the cardiovascular system. Cardiac diseases, coronary diseases, and more particularly peripheral vascular diseases are often associated with carotid disease and may contraindicate the procedure or prevent certain access sites from being used. Multivascular patients are being diagnosed more and more and it is essential to define what the first lesion to be treated should be. A hematological and chemistry examination should be undertaken. Coagulation and renal function should be checked. Gruberg et al.87 recently reported, in a series of 253 procedures, that patients with even mild chronical renal insufficiency (CRI) demonstrated an overwhelmingly
(a) Figure 35.1
(b) Different aortic arch types, level 1−3.
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high rate of neurological complications. Patients with severe CRI are at higher risk for major neurological complications. Hepatic examination. Neurological examination, and consultation by a neurologist who will be able to follow the patient post-procedure, with a clinical examination using neurological scales: the N-scale, the Rankin tests, or the NIH score scale. A carotid echo Doppler examination and transcranial Doppler examination so as to quantify the stenosis and to assess its morphological characteristics, looking for potential associated lesions of supra-aortic vessels. The characterization of plaque echodensity according to Nicolaides’ criteria is very useful to define high-risk lesions.47−49 Echolucent plaques carry a higher risk than hyperechogenic plaques and could lead to different techniques. Ultrasound examination of other arterial locations in case of suspicion of disease based on prior physical examination. This may lead to complementary angiographic examination. CT scan/MRI are also mandatory before any CAS. Silent infarcts can be detected in asymptomatic patients. Complete angiographic examination of the aortic arch and of all supra-aortic vessels with intracranial arterial imaging. Three types of aortic arch are described (Figure 35.1). With type A, it is easy to catheterize the common carotid artery but with types B and C, the access could be difficult and necessitate specific diagnostic catheters or guiding catheters. The angiographies will also show the degree of tortuosities of the different arteries, which could lead to some contraindications for CAS in case of very tortuous arteries. It is also indispensable to have a good imaging of the carotid bifurcation and of the carotid stenosis to define the technique (protection device, stent, etc.).
All these examinations help the interventionist to select both patients and the best technique, as well as to define high-risk patients.
(c)
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Indications
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Selection criteria for carotid revascularization indications Conventional indications are based on the results of several randomized controlled trials which demonstrated the efficacy of CEA and its superiority compared to the best medical treatment. The same selection criteria can be used for CEA and CAS. They are usually based on degree of stenosis, neurological symptomatology, age, and gender. Emerging parameters appear to be important to discuss and to use if we want to improve the indications and identify the patients who could benefit from carotid revascularization. One of the most important problem is that of asymptomatic patients. We have to keep in mind that 700,000 new strokes occur every year in the US. Five to twelve percent of them result from angiographically demonstrated carotid stenoses. But out of these atheroembolic strokes, 75−80% occur without a warning stroke or a TIA. It is therefore of critical importance to better target carotid revascularization therapies in asymptomatic patients to those who have a high risk of future stroke. We also have to discuss specific selection criteria depending on some anatomical situations which could be a contraindication for CAS, and on associated co-morbidities with the problem of high-surgical-risk patients who seem better treated with CAS. Conventional indications Symptomatic trials. Three studies were the cornerstone for developing international guidelines: the North American Symptomatic Carotid Endarterectomy Trial (NASCET), the European Carotid Surgery Trial (ECST) and the Veterans Affairs study (VA). They evaluated the respective role of CEA and the best medical therapy in recently symptomatic patients with ipsilateral carotid diseases.1−3 The databases of these trials were combined in the Carotid Endarterectomy Trialists Collaboration (CETC) and should now be considered the true gold standard.88−90 From these studies we can conclude that carotid stenoses > 50% gained no benefit from CEA. However CEA did confer moderately significant benefit in patients with 50−99% stenoses (70−99% ECST). The maximum benefit was observed in patients with 70−99% stenoses (85−99% ECST) provided there was no evidence of near occlusion/string sign. Indications for symptomatic patients were recently well summarized by Naylor.91 CEA can be proposed in patients with a symptomatic stenosis > 50%. However, not all symptomatic patients with a stenosis > 50% gain equivalent benefit. The following subgroups gained less benefit: ● ●
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patients aged < 65 years with 50−69% stenoses; females with 50−69% stenoses in whom > 2 weeks has elapsed since the last event; females with 70−99% stenoses in whom > 4 weeks has elapsed since the last event.
CEA conferred highly significant benefit in the following subgroups: ● ●
male; contralateral occlusion;
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aged > 75 years; hemispheric symptoms; recent symptoms; incremental stenosis but not near occlusion; plaque irregularity; tandem disease; no intracranial collateral recirculation.
Asymptomatic trials. Five randomized trials (MACE, CASANOVA, VA, ACAS, and AC5T) compared immediate CEA (plus best medical therapy) against deferred CEA (plus best medical therapy).4−6,92,93 The most important of these (regarding their overall impact on developing guidelines in asymptomatic patients were ACAS and AC5T). From these trials, we can conclude that in patients with a 60−99% asymptomatic stenosis, the 5-year risk of stroke is about 12%, which can be reduced to about 6% provided CEA is performed with a < 3% risk. From ACAS trial some concerns were pointed out.94−97 ●
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There was no evidence that CEA significantly reduced disabling or fatal stroke. Men benefited considerably from surgery, but women derived no benefit at all. There might be harm conferred by prophylactic CEA in the presence of contralateral occlusion.
However the publication of the AC5T trial in 2004 appeared to provide definitive answers to many of the concerns raised by ACAS5 and this trial concluded that immediate CEA significantly reduced the risk of fatal or disabling strokes by 50%, males and females appeared to gain significant benefit from prophylactic CEA, and immediate CEA only benefited asymptomatic patients if aged under 75 years. Naylor91 recently summarized the implications for practice. ●
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Males with 60−99% asymptomatic stenoses (who are otherwise fit and aged under 75) gain significant benefit from prophylactic CEA. Females with 60−99% stenoses (who are otherwise fit) gain significantly less benefit from CEA than males. Emerging evidence suggest that the threshold for recommending intervention may have to be reduced to perhaps < 70 years to optimize the rate risk/benefit. If the operative risk exceeds 4%, all long-term benefit from CEA cease. This includes patients considered as being high-risk patients for CEA.
As pointed out by Naylor,91 none of these randomized studies has defined any clinical or imaging features that identify a cohort of asymptomatic patients or plaques as being “higher risk” for strokes than others. This concept is of course totally different to being “higher risk” for CEA. Emerging parameters Several reports47−49,98−100 pointed out that the degree of a carotid stenosis and the presence or absence of neurological symptoms are not reliable selection criteria for conventional or endoluminal repair of carotid stenoses in the prevention of brain ischemia and do not sufficiently and accurately identify the real risk presented by the patient.101 Other parameters
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Carotid angioplasty and stenting under protection: techniques, indications, results, and limitations should be used to define the best indications, particularly in asymptomatic patients, as recently pointed out.101,102 Echographic plaque characteristics. Echography, assessed according to the Grey−Wealey−Geroulakos classification,103,104 can reliably register areas with a lot of echoes (hyperchoic or echogenic) and areas with few echoes (hypoechoic or echolucent). It was well demonstrated in an ex vivo model that echolucent plaques are at higher risk of embolization during CAS.105 Through the advent of high-resolution B mode scanners, it is now possible to achieve a more reliable analysis of echogenicity and to distinguish between echogenic and echolucent carotid lesions. Furthermore, as reported by Biasi,101 the improvement in ultrasonography allowed several authors to demonstrate in more than 8000 patients that carotid plaque echolucency is an important factor in determining future neurological events.106−110 Further improvement in a carotid echographic evaluation has been achieved through the introduction of a computer-assisted objective grading of the echogenicity of carotid plaques, namely the grayscale median (GSM).47,48,111,112 GSM is a measure of the overall plaque echogenicity which is a quantitative index of the echoes registered from the plaque. Low-GSM plaques generated a higher number of embolic particles following CAS35 and there is a direct correlation between the number of particles generated during CAS and the incidence of new clinical and subclinical lesions on DW-MRI imaging and the risk of stroke during CAS.113,114 According to Biasi et al.47,48 the plaque echogenicity measured by the GSM can be a useful indicator of embolic potential in the carotid arteries and a better selection of CAS candidates may be performed with this echographic assessment. In the ICAROS study, Biasi et al.49 demonstrated that patients with a GSM = 25 (echolucent plaques) had a higher risk of stroke during CAS than patients with a GSM > 25 (echogenic plaques) (7.5 vs. 1.5%). Twenty-five appeared as the best cut-off value to predict brain embolism risk. In this study, GSM and degree of stenosis appeared as significant independent predictors of stroke. Following these important reported data, we consider that a good echographic evaluation of the carotid stenosis with GSM study is mandatory before the CAS procedure to identify patients at a higher risk of stroke, particularly during the procedure. These new parameters allow us to decide the best therapeutic options and should lead to modifications of the technique, and in particular to choosing the best protection device. As mentioned by Biasi et al.101 those findings bring to the conclusion that these two parameters − degree of stenosis and presence/absence of neurological symptoms − are obsolete and no longer adequate for correctly indicating any carotid procedure. Characterization of the plaque by echography appears indispensable, especially in asymptomatic patients when it has to be decided who could benefit from the treatment. In addition, echolucent carotid plaques with low GSM values have: ● ● ●
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a higher risk of future coronary events;115 a higher risk of restenosis development;116 a higher incidence of brain ischemic lesions detected on DW-MRI;80,81,117 more rapid plaque progression.118
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Echodoppler evaluation is also interesting to appreciate the evolution of a stenosis. A rapid progression could lead to revascularization, particularly in asymptomatic patients. Transcranial Doppler monitoring (TCD). Spencer et al.119 studied 319 asymptomatic carotid stenoses with TCD embolus detection for up to 1 hour on two occasions a week apart. Patients were followed for 2 years. Ten percent of patients had microemboli at baseline. Patients with microemboli were more likely to have a stroke during the first year of follow-up (15.6 vs. 1%) and could benefit from CEA or CAS. Patients without microemboli could not benefit from CAS or CEA unless it can be done with a risk < 1%. So this technique may allow identification of a particular high-risk group of patients with carotid stenosis, particularly in asymptomatic patients who benefit from carotid revascularization. Silent brain infarcts. Silent MRI infarcts are an independent risk factor for future stroke120 and at 3-year follow-up a discrete subcritical or critical infarction confers an unfavorable prognosis in patients with a carotid stenosis who are either symptomatic or asymptomatic.121 So the detection of silent brain infarcts on DW-MRI or CT scan could reinforce the indications of CAS or CEA especially in asymptomatic patients. Cerebrovascular reserve. Silvestrini et al.122 studied 94 patients with asymptomatic carotid artery stenosis and measured their cerebrovascular reactivity in response to CO2. Patients with impaired cerebrovascular reserve compared to those with normal reserve have a significantly higher incidence of ipsilateral ischemic events (14 vs. 4%). This technique may also be of great interest to identify patients who may benefit from carotid revascularization. Specific selection criteria Vessel anatomy: lesion selection Some anatomical situations may lead to difficulties in safely performing CAS due to access problems, increasing risk of the procedure. CEA could be better in some cases such as complex bifurcation disease with long, multifocal lesions, very angulated ICA, extensive aortic or brachiocephalic trunk plaque, severe tortuosities, severe calcifications of the aortic arch vessel, severe ulcerations, or heavy circumferential calcifications of the carotid bifurcation. A good knowledge of the vessel anatomy is indispensable to decide the appropriate approach way and the best techniques to use. We must know the exact anatomy of the aortic arch, of the carotid bifurcation, and of the distal part of the ICA. Distal loop, bends, and kinks may be a contraindication to some protection devices. If a clot is suspected, CAS is contraindicated if the interventionalist cannot use a reversal flow system as protection device. However indications for CAS depend on the experience of the interventionalist. Bovine arch severe tortuosities can be approached by experienced interventionists, but not by beginners. On the other hand, CAS is justified in patients ●
with surgically difficult or inaccessible lesions 䊊 bifurcation C3C2 䊊 proximal CCA 䊊 distal ICA 䊊 tandem stenoses
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with hostile neck 䊊 restenosis after CEA 䊊 radiotherapy 䊊 radical neck dissection 䊊 inflammatory or tumorous disease of the neck 䊊 contralateral pareses of recurrent nerve where the rate of cranial nerve injuries following surgery is higher in this subset of patients with high risk of cerebral ischemia during carotid clamping: occlusion of the contralateral ICA and abnormalities of the circle of Willis.
Medical co-morbidities: “high-risk patients” There is no definition of high-risk patient. But patients with exclusion criteria of NASCET for symptomatic and of ACST for asymptomatic can be considered “high risk.” The Food and Drug Administration (FDA) agreed that the definition of high-risk patient includes patients with: ●
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congestive heart failure (class III/IV) and/or known severe left ventricular dysfunction (LVEF > 30%); open heart or vascular surgery needed within 6 weeks; recent myocardial infarction (> 24 hours and < 4 weeks); cardiac valvular or rhythm abnormality likely to cause embolic cerebrovascular symptoms; unstable angina with EKG changes; multivessel coronary artery disease; severe pulmonary disease; contralateral carotid occlusion or severe contralateral carotid stenosis; renal insufficiency (creatinine > 2.5 mg/dl); uncontrolled hypertension or diabetes; age greater than 79 years; contralateral laryngeal nerve palsy, radiation therapy to the neck, restenosis, high cervical ICA lesions or CCA lesions below the clavicle, severe tandem lesions, cervical spine immobility, intracranial hypoperfusion, or tracheostomy; recent TIA.
CAS should treat all high-risk patients for surgery. The complications rate of the procedure is demonstrated by recent studies60−69 to be lower than that of surgery. FDA approved in September 2004 CAS for high-risk patients with a symptomatic stenosis ≥ 50% or an asymptomatic stenosis ≥ 80%. The indications for asymptomatic patients and low-surgicalrisk patients are more controversial. However, all the large published series28,70,74 showed results that are at least similar to surgical results and several studies have shown that we can treat high- and low-risk patients with the same security.72,74 Some patients should be considered as contraindicated for a revascularization procedure: ● ●
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patients with cerebral atrophy or multiple cerebral infarcts; patients with dementia, intracranial aneurysm, or hemorrhage; patients with crescendo TIA or stroke in evolution.
In these cases, it is better to wait for at least 3 weeks. Patients with a total occlusion of the ICA are classically considered as a contraindication for any revascularization procedure but some
interventionists try to reopen the artery in some specific cases, after precise evaluation of the brain circulation and perfusion.
Advice to beginners Carotid angioplasty is more widely utilized and several specialties are involved in this field: vascular surgeons, radiologists, cardiologists, neurosurgeons, and neuroradiologists, sometimes with different approaches. Whatever the specialty, a good knowledge of different techniques is indispensable before beginning CAS: ●
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the traditional approach to diagnostic angiography of supra-aortic vessels and a good knowledge of supra-aortic and intracerebral vessel anatomy; large experience in angioplasty and stenting either in the coronary or peripheral field; experience with different approach ways.
The training requirements are significantly different in CAS. For diagnostic angiography, we use low-profile preshaped catheters. For carotid angioplasty we need larger and stiffer catheters, large access conduits, and the safe placement of this large access conduit is essential for the successful completion of the stenting procedures to avoid ischemic neurological events. Multiple catheters and guidewire exchanges in the aorta or in the common carotid artery are needed, so the risk of scraping the arch vessels potentially exists, with the risk of brain embolism. Several important points must be emphasized. New techniques New techniques are developed to facilitate carotid access site, angioplasty, and stenting. New stents mounted on monorail system can be implanted through 6-French to 8-French systems, depending on the diameter of the stent. Predilatation of the lesion or dilatation of the stent can be performed with monorail balloons like for a coronary angioplasty. We advise beginners to use preferably monorail systems than over-thewire devices. This technique appears to be faster and safer. The team A team comprising a vascular surgeon, radiologist, cardiologist, anesthesiologist, neuroradiologist, and nurses, is important when performing CAS. To perform a CAS, a team of two interventionists (at least one well-trained), an anesthesiologist, and one well-trained nurse is recommended to give the best chance to the patient. At least one interventionist must know how to manage a neurological complication using fibrinolytic drugs, GP IIb IIIa inhibitors, and interventional intracranial procedures. Protection devices The risk of brain embolism during CAS remains the main concern of the procedure because cerebral embolism occurs in all procedures. So protection devices seem to be indispensable to perform CAS as recommended by the majority of interventionists. We advise beginners not to perform CAS without
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Carotid angioplasty and stenting under protection: techniques, indications, results, and limitations a protection device, either a protection balloon or a filter. CAS without protection seems, at the present time, unethical outside randomized controlled studies.
To perform CAS with the maximum of safety and efficacy, we would like to summarize several tenets an interventionist should know and have, as also pointed out by Myla.51 ●
The learning curve Begin CAS with low-risk patients; that is, those with: ● ● ● ● ● ● ● ● ●
easy access to carotid artery (type A or B aortic arch); focal stenosis of the internal carotid artery; concentric lesions; non-calcified lesions; contralateral carotid artery with no significant stenosis; good collateral circulation; carotid arteries without tortuosities, kinks, etc.; good landing zone to place the distal protection device; duplex scan with plaque characterization showing a lowrisk lesion according to Nicolaides’ criteria.47−49
The learning curve plays an important role and to be entitled to participate in trials, physicians must accumulate certain experience in CAS before becoming eligible as physician investigators. A minimum number of CAS procedures should be required, particularly with protection devices, because each additional step in an existing procedure assesses the possibility of an additional risk to the procedure. Several authors have pointed out the role of this learning curve.
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Ahmadi et al. in his series of 320 CAS reported a 30-day complications rate of 15% for the first 80 procedures and only 5% for the others. Lin P et al.123 evaluated the effect of the learning curve of CAS with neuroprotection over a 32-month period. They divided their patients in five groups: group 1 − cases no. 1−50; group 2 − cases no. 51−100; group 3 − cases no. 101−150; group 4 − cases no. 151−200; group 5 − cases no. 201−246. The complication rates were 8, 8, 2, 2, and 2%, respectively. In one of the early clinical trials comparing CAS and CEA, Allerts et al.81,82 randomized 219 patients. The 30-day stroke and death rate was 12.1% for CAS and 4.5% for CEA. This study was stopped prematurely due to the high complication rate for CAS but it was found that a majority of CAS-related complications was clustered around physician investigators with little or no previous CAS experience. Naylor et al.85 conducted a similar study which was also stopped prematurely for the same reasons. Numerous other clinical reports have highlighted the importance of the operator’s experience as a crucial factor in the clinical success of the carotid stenting procedure.20,26,55,124 Wholey et al.55 reported a particularly interesting review of the Global Carotid Artery Stent Registry including 12,254 CAS procedures performed in 53 institutions. It was noted that institutions that had performed fewer than 50 distally protected CAS procedures had a 4.04% combined stroke and death rate. In contrast, institutions with high CAS experiences, especially those with more than 500 cases of experience, reported a stroke and death rate of 1.56%. With all these reported data, we can consider that to be confident with CAS, experience of at least 50 procedures performed with a well-trained interventionist is required.
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Good knowledge of the lesion and of the patient. Good analysis of the angiography of the patient to evaluate the aortic arch level with respect to its curvature and the origin of great vessels to predict difficulties and choose appropriate technique as mentioned. With type A aortic arch, access to the carotid artery is generally easy. With type B it is more difficult and with type C (angulated take-off of the vessels) it could be very difficult. A bovine arch could lead to severe difficulties. Have an ability to identify and be aware of the “hostile” aortic arch. Good knowledge of the supra-aortic and intracerebral vessel anatomy and their anomalies. Apply antiplatelet therapy with aspirine/clopidogrel or ticlopidine. Adequate knowledge of equipment. Different types of catheter, guide catheters, sheaths, guidewires, angioplasty balloons, and stents must be available in the catheterization lab as well as equipment for intracerebral interventional procedure. Pay careful attention to equipment handling in the great vessels, and use the least possible amount of equipment manipulation. Use a minimum number of catheter exchanges. Each catheter and guidewire manipulation can lead to aortic plaque detachment, brain embolism, and neurological complications. Use a minimum amount of contrast and a minimum number of injections. Pay attention to frequent or continuous catheter flushing. Carry out anticoagulation with heparin (with efficient ACT which should be between 250 and 300 seconds). Bilavirudin may be used in place of heparin. Continuous neurological assessment of the patient during the procedure to detect rapidly any neurological complication. Continuous monitoring of blood pressure and heart rate. Appropriate drugs must be available in the cathaterization lab to correct any severe acute or chronic modifications. Be able to manage a neurological complication.
CAS under protection: techniques and how to prevent cerebral embolism CAS is at higher risk of cerebral embolism than CEA, as well demonstrated by Jordan et al.125 who reported an average of 74 emboli per stenosis after CAS and only 8.8 emboli per stenosis after CEA. Embolic particles can occur at any time during a CAS as well shown by Al-Mubarak et al.38 who studied the frequency of Doppler microembolic signals (MES) during CAS. Three critical phases with increased MES were identified: stent deployment, predilatation and post-dilatation. So it is important to protect the brain from embolism during CAS. Cerebral protection devices are mandatory for all CAS procedures but
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we also have to consider medication and the procedure itself with its technical problems. Medication The benefit of antiplatelet drugs was demonstrated for patients undergoing a carotid angioplasty procedure. Patients are placed on antiplatelet therapy with aspirin (100−300 mg/day) and ticlopidine (500 mg/day) or clopidogrel (75 mg/day) at least 3−4 days before the procedure. During the procedure, they are given a 5000−10,000 unit bolus of IV heparin, to have an ACT > 250. One mg of atropine (if no contraindication to this drug) is given to reduce the risk of bradycardia due to the compression of the carotid glomus during the balloon inflation and implantation of a temporary pacemaker is indicated only in case of severe conduction disorders or contraindication to atropine. Fibrinolytic drugs and glycoprotein IIb/IIIa inhibitors may be used in certain cases with particularly thrombogenic lesions; however, cerebral protection devices limit their use and we do not recommend systematically using IIb IIIa inhibitors in CAS because of the risk of brain hemorrhage. Bilavirudin has recently been recommended and used in place of heparin during CAS. The angioplasty is performed under local anesthesia, and mild conscious sedation. The anesthesiologist constantly monitors the patient’s heart rate, arterial pressure, and the level of consciousness. The neurological status is also checked frequently during the procedure, particularly after the critical steps for brain embolism (balloon inflation and stent dilatation). We use a simple method, which is to ask the patient to squeeze a musical toy with the hand opposite the involved artery. Transcranial Doppler may be performed during the procedure to detect brain embolism. Once the procedure is over, the patients are given aspirin (100 mg/day) indefinitely, and ticlopidine (500 mg/day) or clopidogrel (75 mg/day) for only one month. The procedure: access sites and basic technique The first step of the procedure is to place a guiding catheter or a long sheath into the common carotid artery. The technique is well known and has been largely described. We insist on the necessity to choose carefully the diagnosis catheter, guiding catheter, and guidewires, which will depend on the anatomy of the aortic arch, the carotid, and the take-off of the great vessel. Excessive catheter manipulations into the aortic arch should be avoided because of the risk of detaching atheromatous plaque, which could embolize to the brain. The aortic arch has its own set of embolic potential. In case of difficulty it is better to stop than to have a neurological complication. It is important to cross the lesion as atraumatically as possible with low-profile protection devices or steerable coronary guidewires, and low-profile coronary-type small balloons for predilatation. The diameter of the balloon should never be greater than that of the carotid artery. It is of the utmost importance not to overdilate the artery, as this is a factor of dissection and secondary thrombosis. Low-profile stents limit the risk of brain embolization. The blood pressure and heart rate must be monitored to avoid neurological events. The femoral access is the most commonly used access. We recommend it as first choice, since it may be used in the majority
of cases and with all protection devices. However, it may be contraindicated or may not be used due to severe aortoiliac lesions or occlusions that may not be crossed, or that may lead to high embolism risk, or due to very tortuous arteries or a hostile aortic arch, thus rendering the advancement of the catheter more difficult or dangerous. If this is the case, other access sites may be used: brachial or radial access, or direct carotid artery puncture. These approach ways should be known by any interventionist who wishes to perform this kind of angioplasty. The femoral access site (Figure 35.2) The different steps of this technique are as follows. Puncture of the femoral artery at the groin and placement of a 5- or 6French introducer is then followed by selective catheterization of the right or left CCA. Several 5-French catheters may be used (Figure 35.3): ● ● ● ● ● ● ●
Sidewinder or Simmons (Cordis, Roden, the Netherlands) Headhinter (Terumo, Tokyo, Japan) Hinck (Cook, Bloomington, IN) Right coronary Judkins catheter (JR4) Multipurpose catheter Benson (AngioDynamics, Glens Falls, NY) Vitek catheter (Cook Inc., Bloomington, IN)
They are mounted on 0.035-inch steerable guidewire, or on an angled 0.035-inch hydrophilic guidewire. The choice of the catheter depends on the anatomy of the aortic arch. With type A, a right Judkins or multipurpose catheter may be used. For type B or C, other catheters are better, particularly the Vitek or Simmons catheter. Once the catheter is introduced in the CCA, the guidewire is withdrawn, and hand injection of contrast medium is performed, thus enabling the precise location of the internal and external carotid artery. The road-mapping will also prove to be helpful for the following steps. The guidewire is reintroduced into the catheter and carefully placed distally in the external carotid artery, enabling introduction of the 5-French catheter into the external carotid artery. The steerable 0.035-inch or hydrophilic guidewire is exchanged for a long, rigid Amplatz 0.035-inch guidewire (Boston Scientific). The guidewire placed far in the external carotid artery provides good support. The 5-French catheter is withdrawn. Eight-French or nine-French guiding catheters (Cordis, Boston Scientific) or 6-French to 8-French long sheaths (Cook, Arrow International, Reading, PA) are advanced over the Amplatz guidewire. Once the sheath is changed at the groin, the 5- or 6-French sheath being replaced by another 8-French or 9-French sheath, when using a guiding catheter. The rigidity of the Amplatz usually allows easy passage of the guiding catheter or of the long sheath into the CCA. In case of difficulty, and more particularly in the presence of tortuous arteries, a coaxial technique (Figures 35.4) may prove to be useful: a long 5-French catheter (120 cm long) like the Vitek catheter is introduced into the guiding catheter or into the long sheath and both catheters are advanced over the Amplatz guidewire. This facilitates the progression of the guiding catheters or long sheaths as well as the crossing of curved segments. The 5-French catheter or long sheath is then
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Amplatz wire Glidewire
Diagnostic catheter placed at the ostium of CCA Stiff angled 0.035 glidewire advanced into ECA
Diagnostic catheter is withdrawn Amplatz wire remains into ECA.
(a)
Diagnostic catheter
.
(d)
Diagnostic catheter
Glidewire
Diagnostic catheter advanced into ECA over Glidewire
(b)
Diagnostic catheter
7-8-f guide catheter or 6-f guide sheath advanced over the Amplatz wire Amplatz wire is withdrawn
(e)
Guide catheter / guide sheath
Amplatz wire
Glidewire exchanged for 0.035 stiff Amplatz wire
Amplatz wire is withdrawn
(c)
Diagnostic catheter
(f)
Guide catheter / guide sheath
Figure 35.2 Carotid artery stenting (CAS), technique 1: (a) Diagnostic catheter placed at the ostium of CCA. Stiff-angled 0.035 Glidewire advanced into ECA; (b) diagnostic catheter advanced into ECA over Glidewire; (c) Glidewire exchanged for 0.035 stiff Amplatz wire; (d) diagnostic catheter is withdrawn and Amplatz wire remains in ECA; (e) 7−8-French guide catheter or 6-French guide sheath advanced over the Amplatz wire; and (f) Amplatz wire is then withdrawn.
removed, and the guiding catheter or the long sheath remains in place. We prefer guiding catheters, particularly the new Boston catheters with a soft, flexible atraumatic tip. We have a better torque control, which allows orientation of this guide catheter towards ICA, which is better in tortuous anatomy. New “Shuttle” guiding sheaths (Cook Inc., Bloomington, IN) with different shapes (JB1, JB2, Vitek, Simmons 2, M1) are now available and can facilitate the CCA catheterization. The tip of the guiding catheter or of the sheath is placed 1 or 2 cm below the carotid bifurcation. Once the Amplatz guidewire is withdrawn, digital subtraction angiography is performed, including multiple oblique angles. Thus we are able to obtain precise information including: ●
●
● ●
degree of the stenosis estimated using quantitative angiography techniques (the NASCET criteria are usually followed; length of the stenosis, and its extent through the carotid bifurcation, as well as downstream; its morphological characteristics: ulceration, calcifications; presence or absence of intracranial lesions.
This careful examination is necessary to determine the method of angioplasty to be performed and to assist in the choice of predilatation and dilatation balloons, as well as the type of stent. Direct internal carotid artery puncture (Figure 35.5) This technique is rarely used and only in case of failure of the other access ways. It is performed with the usual puncture needle, using arterial pulses, ultrasound localization (by duplex scan or with a “Smart Needle,” or after placement of a 4-French or 5-French catheter in the ascending thoracic aorta, with hand injection of contrast medium allowing precise localization of the CCA, the puncture being performed using “road-mapping.” A single wall puncture should be done in order to avoid any subsequent hematomas afterwards. Once the needle is in the arterial lumen, a short 0.035-inch guidewire is advanced into the internal carotid artery and a short 6- or 7-French introducer, 5.5 cm long, is placed. The procedure will continue as previously described for the femoral access. This technique may be used in upward direction to treat an internal carotid artery stenosis or in downward direction
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JUDKINS CATHETER 90° 120° HEADHUNTER H1
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(b)
(c)
(d)
(e) JB1 (f) JB2 (g) JB3
(e)
(f)
(g)
(h) MANI-VITEK (I) MANI-VITEK (J) HEADHUNTER H3
(h)
(i)
(j)
SIMMONS SIDEWINDER
(k)
(l)
(m)
Figure 35.3 CAS: technical aspects and choice of catheters: (a) Judkins catheter; (b) 90º; (c) 120º; (d) Headhunter H1; (e) JB1; (f) JB2; (g) JB3 (h) Mani-Vitek (i) Mani-Vitek; (j) Headhunter H3; and (k−m) Simmons Sidewinder.
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Amplatz wire Glidewire Diagnostic catheter Diagnostic catheter Guide catheter / guide sheath
Guide catheter / guide sheath
(a)
(e) Amplatz wire Diagnostic catheter
Diagnostic catheter Guide catheter / guide sheath
(b)
Guide catheter / guide sheath
(f)
Glidewire
Diagnostic catheter Guide catheter / guide sheath
Guide catheter / guide sheath
(c)
(g)
Glidewire
Diagnostic catheter Guide catheter / guide sheath
(d) Figure 35.4 CAS, technique 2: (a) Diagnostic catheter inside guide catheter or guide sheath over a stiff 0.035 angled Glidewire; (b) diagnostic catheter placed at the ostium of CCA; (c) Glidewire advanced into ECA; (d) diagnostic catheter advanced into ECA over Glidewire, which is then withdrawn; (e) Glidewire exchanged for 0.035 stiff Amplatz wire; (f) guide catheter or guide sheath advanced over diagnostic catheter and Amplatz wire (very good support); (g) Amplatz wire and diagnostic catheter are withdrawn.
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6-F Introducer Direct carotid artery poncture
Figure 35.5
CAS technique, direct puncture of CCA.
to treat a common carotid artery stenosis. It should be reserved for very rare situations, as the risk of hematoma is high. Brachial access (Figure 35.6) We recommend the use of the right brachial access for the catheterization of the left common carotid artery, and the left brachial access for the catheterization of the right common carotid artery. Three steps should be focused on:
Several types of catheter similar to those used in the femoral approach may be used and advanced over a steerable guidewire or a 0.035-inch hydrophilic guidewire. The 5-French catheter is placed into the external carotid artery using the same techniques as described for the femoral approach. Similarly, the guidewire is removed and replaced with an Amplatz 0.035inch stiff guidewire. A 6- or 7-French Cook sheath or Arrow Flex introducer and sheath is then progressively advanced over the guidewire. These sheaths are braided and do not kink in arterial curves which subsequently allows for easier passage of balloons and stents. The distal tip of the sheath is positioned 1−2 cm below the carotid bifurcation, as is the guiding catheter when using the femoral approach. The long introducer catheter is removed from the sheath, and the procedure then continues as previously described for the femoral approach. Radial access As described for coronary procedure, this access can be used for carotid angioplasty with the same techniques as for brachial access.
Cerebral protection: Different types of embolic protection devices Several techniques are proposed: ●
●
● ●
percutaneous puncture of the brachial artery in the elbow’s bend; placement of a 5-F catheter; selective catheterization of the CCA.
Catheter 7-F/8-F
(a) Figure 35.6
● ●
distal occlusion (derived from Theron’s technique, the first to prove the efficacy of brain protection during CAS);22,23,25,33,35,36,41,42,126−133 filters;45,46,53,55−58 flow reversal systems.37,75,76
Catheter 7F/8F
(b)
CAS technique, brachial approach: (a) left brachial access site; (b) right brachial access site.
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(a)
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(b)
(c) Figure 35.7
Distal protection devices.
Distal occlusion The different devices The concept is based on blockage of distal blood flow by placement of a sealing balloon downstream from the lesion of interest and inflated at low pressure. This redirects blood flow towards the ECA and results in a stagnant column of blood during intervention. The brain is protected from any embolic migration during the occlusion and the potential embolic debris trapped within it can be removed before releasing downstream occlusion. This debris generated by the dilatation and stent placement is then eliminated using aspiration or cleaning depending on the device used. Three devices employ this approach. The Percusurge Guardwire (Medtronic Inc., Santa Rosa, CA) (Figure 35.7a) This has been widely used.25,34,35,38,42 The Percusurge Guardwire system is constructed as a 0.014-inch hollow nitinol (nickel−titanium alloy) wire with a shapeable floppy distal tip (190 or 300 cm). Proximal to the floppy tip is a compliant elastomeric polyurethane occlusion balloon with a maximal crossing profile of 0.036 inches when deflated. Once the stenotic lesion is crossed with the Guardwire, the occlusion balloon is inflated to a variable size, ranging from 3 to 6 mm in diameter, using the handheld Microseal Adaptor and EZ Flator. The handheld system is then removed from the proximal end of the wire while the occlusion balloon remains inflated. This coaxial exchange set-up allows for over-the-wire (OTW) delivery of angioplasty balloons and stent systems.
Any embolic particles released during this portion of the procedure remain in the stagnant pool of blood below the occlusion balloon in the distal ICA. This column of blood is aspirated through the large-bore lumen of the Export catheter connected to a vacuum syringe. Two or three aspirations can be done through the stent and below the balloon to eliminate the maximum of debris. At the conclusion of the procedure, the occlusion balloon is deflated with the handheld device. Total occlusion times typically range from 5 to 15 minutes. The Tri Active FX (Kensey Nash, Exton, PA) (Figure 35.7b) This device has the ability to block, flush, and aspirate the debris generated during CAS. It consists of a 0.14-inch hypotube upon which an inflatable balloon (3−5 mm) is attached. This hypotube, like the PercuSurge Guardwire, serves as the interventional guidewire over which balloon and stents can be placed. The current version of the Triactive FX system uses a rapid CO2 exchange system, allowing for quick inflations and deflations. This allows for rapid re-establishment of antegrade flow. After the procedure is completed, the stagnant column of blood is removed using a distal saline infusion catheter (Flushcath) and active extraction. This active flush system allows for more aggressive particle removal from the walls of the vessel, stent struts, and area surrounding the distal balloon before the downstream vasculature is exposed to restoration of flow. Recently, Franke133 reported a prospective, non-randomized multicenter pilot study. Fifty patients were included with a procedural
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success of 94% and 2% of neurological complications at hospital discharge (one minor stroke). The Guard Dog (Possis Medical Inc., Minneapolis, MN) (Figure 35.7c) This was recently approved for work in the periphery and consists of a 0.035-inch guidewire that incorporates a 3−6 mm, CO2-filled compliant balloon at the tips. The balloon requires 0.7 atmospheres of pressure to be inflated and is used to seal off the distal vasculature. Removal of debris can then be performed using another device (AngioJet, Possis Medical Inc.) as desired. The Twin-One (Minvasys, Gennevilliers 92230 France) (Figure 35.8) This new system was recently proposed by Theron and is an evolution of his cerebral protection concept described many years ago.126−129 For this author, as well as for Castriota et al.,134 the only moment of real risk of embolic complication is the time of post-dilatation of the stent when the plaque is broken. So the goal of this new protection device is to focus the problem on the carotid bifurcation and to concentrate, from the beginning to the end of the procedure, all manipulations on a very limited anatomical space (Figure 35.8a). The various phases of the technique are as follows.
●
After having positioned the guiding catheter in the common carotid artery, the stenosis is passed with a 0.14-inch wire (Figure 35.8b). When a predilatation is necessary, it is performed with a 2-mm balloon without cerebral protection (Figure 35.8c). The stenosis is passed with the stent without cerebral protection. The stent is auto-expandable and its length is of 4 cm or more. It can be rapid-exchange or over-the-wire. Its diameter is 7−9 mm according to the artery. It is a delicate moment and the manipulations must be extremely soft (Figure 35.8d). The stent is deployed without cerebral protection. It is positioned covering the origin of the external carotid (Figure 35.8e).
●
●
●
●
●
(a)
(b)
(h)
Figure 35.8
Twin One.
(c)
(i)
●
●
●
●
●
●
●
The guiding catheter is introduced in the stent (Figure 35.8f). The delivery system of the stent and the wire are withdrawn (Figure 35.8g). The protection system is introduced (TwinOne) in the stent. It is a device combining a catheter loaded with an occlusion balloon with a rapid-exchange angioplasty catheter. Introduced as one tool, it is possible − after peeling away the sheath − to move each catheter separately to ensure best positioning of each item. There is no wire and the progression is particularly fast and simple when continuous frame stents are used. For the open-cell stents, a torquer facilitates the progression of the balloon. The system is positioned at the distal extremity of the stent (Figure 35.8h). The occlusion balloon is inflated in the stent and the angioplasty balloon is positioned at the narrowing of the stent (Figure 35.8i). An angiographic series is performed. Contrast should be gently injected to avoid forcing the contrast around the occlusive balloon and give a false impression of incomplete occlusion. The contrast must remain at the origin of the internal carotid if the closure is efficient (Figure 35.8j). Post-stenting dilatation is achieved. The angioplasty balloon is pulled back and withdrawn from the femoral or radial introducer. The guiding catheter is repositioned, when necessary on the site of the angioplasty and blood (one or two 20-cm3 syringes) is aspirated quickly through the guiding catheter (Figure 35.8l). A flush is not performed. The occlusion balloon is deflated and retrieved. The mean occlusion time is less than 5 minutes in most cases and may reach just 3 minutes with some experience. The guiding catheter is positioned, again in the common carotid artery, and control angiographic series are performed (Figure 35.8m).
(d)
(j)
(e)
(k)
(f)
(l)
(g)
(m)
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Carotid angioplasty and stenting under protection: techniques, indications, results, and limitations A first series of 45 CAS performed with this technique has been reported without complications and without any cerebral intolerance. This system can be used via a femoral or radial approach. Advantages of distal occlusion ● These devices have a very low crossing profile (< 3-French), high flexibility, good steerability and radio-opacity. ● They behave similarly to the steerable coronary guidewires, allowing the lesion to be crossed easily and decreasing technical failures. ● Technical failures are very rare (1−2%) and may be due to the impossibility of crossing a very tight stenosis (a predilatation is required) or the impossibility of placing the balloon above the lesion in case of important tortuosities. ● Protection balloons are rapidly inflated or deflated. They do not require a very large landing zone (9−10 mm) so there does not need to be much clearance distal to the lesion in order for the device to be placed properly. ● With these devices, we can aspirate particles of all sizes, and they are not limited in the amount of debris collected because there is no basket to fill up or become clogged. ● These devices give adequate support as the inflated balloon facilitates stent implantation and balloon dilatation.
● ●
●
Disadvantages of distal occlusion During CAS under protection with occlusion balloon, the flow is totally interrupted and oriented towards the ECA. Particles are blocked in the ICA. Nevertheless, some problems remain and embolic events may occur at all steps of the procedure (Figure 35.9). ●
●
The balloon protection device offers protection against embolism only after the lesion has been crossed by the wire. Some embolisms may occur during lesion crossing. The occlusion balloon may deflate or may be non-occlusive during the procedure, sometimes only during systole or
(a)
(b)
●
313
after dilatation of the stenosis (the increased flow may result in dramatic enlargement of the artery). So, some particles can migrate to the brain. It is very important to verify by contrast injection that the blood flow is totally blocked. In case the flow is not interrupted, it is better to place the balloon high in the ICA at the base of the skull. Some particles could be too large for suction (very rare). Below the inflated balloon there is a shadow zone where some particles may remain blocked and are difficult or impossible to aspirate with the aspiration catheter. These particles may migrate to the brain when the balloon is deflated. This area may be cleaned up by flushing with the aspiration catheter or with the Flushcath. But flushing vigorously at high pressure during the cleaning procedures may lead to reflux to the origin of the CCA (more critical on the right side since the length of the CCA is usually shorter) and/or to the right vertebral artery, with the risk of neurological deficit in this territory. The shadow zone may need to be flushed carefully in some circumstances, particularly in patients with a high risk of neurological complications. During ICA balloon occlusion, blood flow is redirected to the ECA with the potential for cerebral and retinal embolization through large collaterals (to the mid-cerebral artery and vertebral artery). Collateral circulation exists between the ECA and ICA through the ophthalmic artery, ascending pharyngeal artery and internal maxillary artery, and between the ECA and vertebral artery through the occipital and ascending pharyngeal arteries. The risk of brain embolism due to this collateral circulation must be recognized. It is important to obtain a good cerebral angiogram before the procedure to identify this collateral circulation, so that a different protection strategy can be envisaged (e.g. filters or flow reversal). Al-Mubarak et al.38 have described this complication well. Even after meticulous aspiration some debris may remain in the treated area, which may be cleaned up by flushing. However, this technique may lead to ischemic complications in cases of collateral circulation, as previously described. In our
(c)
(d)
Figure 35.9 Risks of embolization with protection balloon: (a) occlusive GW balloon during systole/diastole; (b) ineffective protection during systole/diastole, non-occlusive GW balloon; (c) ineffective protection during systole; and (d) ineffective aspiration, shadow zone.
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series, one neurological complication (amaurosis) appeared after flushing, after which flushing was discontinued. Intolerance to balloon occlusion could sometimes appear quickly after the beginning of the procedure with convulsions, syncope, and neurological deficit. Deflation of the balloon (after quick aspiration) to restore the flow could be necessary and after an adequate recovery time, reblockage of the ICA is often possible and the procedure is completed under protection. In our series, we always observed a complete neurological recovery after balloon deflation in a few minutes. These intolerances are seen in 4−8% of the cases (12/267 in our series), and particularly in patients with extensive intracranial disease or absence of adequate collateral flow from other vascular beds. These patients must be detected before choosing the protection device with a good four-vessel angiogram and imaging of the intracranial circulation. Some complications have to be mentioned: 䊊 Spasms could appear at the site of the balloon, easily treated with antispasmodic drug (3.8% in our series). 䊊 Dissection of the ICA has been rarely reported. We have to mention that angiographic assessment of the lesion is not possible during balloon inflation.
Filters Characteristics of a filter135 Filters offer the opportunity to trap the larger embolic debris while potentially maintaining perfusion of the ICA during angioplasty and stenting procedure. The majority of the distal filters incorporate very similar designs with minor modifications. These devices are essentially small basket filters mounted on 0.014-inch guidewire with a floppy, shapeable distal tip that can be easily torqued and passed across the stenosis. They offer the advantage of continued visualization by contrast injection during stent placement as well as the obvious perfusion advantage. The frame of the filter basket is typically constructed of expandable nitinol covered with a porous polyurethane membrane. The pores in the membrane are laser cut and range from 70 to 140 µm. Although the crossing profiles are variable, the designs are such that the filter is collapsed within a delivery sheath, which is retracted and discarded once the filter is in position beyond the stenotic arterial segment in the distal ICA. Two primary configurations of the delivery systems exist: over-the-wire (OTW) and monorail. Once the delivery sheath is retracted, the filter device “springs” open. The guidewire is then used for subsequent balloon angioplasty and stent placement. Ideally, the filter is designed to conform to the vessel lumen upon deployment and capture emboli released during angioplasty and stent placement. At the end of the procedure, a separate recovery or retrieval catheter is passed over the wire and used to envelop or capture the filter system (including trapped debris). The entire device is then removed. Different filters (Figure 35.10) Several filters are proposed, some are available on the market and FDA approved, while others are still being tested. The AccuNet system (Guidant, Indianapolis, IN) This filter was the first to gain FDA approval based on the results of the ARCHER trial.65 It comprises a 0.014-inch guidewire with a 3.5-cm-long shapeable floppy tip. Integrated on the guidewire
is the deployable filtration element comprising a four-wire nitinol basket. A thin porous polyurethane membrane with 120 µm pore size is fixed to the basket to capture emboli. The crossing profile ranges from 3.5 to 3.7 French. The size of the basket ranges from 4.5 to 7.5 mm in diameter (adapting to vessel lumen of 3.5−7.0 mm). The retrieval catheter (5.5 French) has a shapeable end, allowing the operator to deflect the tip away from stent struts during the recapturing step (working length 141 cm). This device is 6-French compatible. The Angioguard XP (Cordis, Warren NJ) This filter is currently available in an OTW and monorail configuration. It was used for the SAPPHIRE trial.36,37 The deployable filtration element is made out of an eight-wire nitinol basket attached to a 0.014-inch guidewire with a 3.5-cm-long shapeable platinum coil floppy tip. The basket has six radio-opaque markers for better visualization, one distal and one proximal to the basket for checking its position and four markers on the struts for checking whether the basket is open or closed. The filter membrane has a pore size of 100 µm. The crossing profile ranges from 3.2 to 3.9 French depending on the filter sizes. The filter diameter ranges from 4 to 8 mm. The crossing profile of the retrieval catheter is 5.1 French. This device is 7-French guide compatible with a landing zone of 18 mm. It is important to stress that the filter cannot be completely withdrawn into the pod. The Filter Wire EZ (Boston Scientific, Natik, MA) This has FDA approval for coronary angioplasty. A unique feature of this filter is the suspended loop filter (“fish mouth”) frame. The nitinol ring supports the polyurethane membrane “butterfly net,” which theoretically provides for complete circumferential contact with the arterial wall. The ring expands to accommodate a vessel diameter range of 3.5−5.5 mm. To improve the alignment with the vessel wall, the wire is kept in the center of the filter by a horizontal strut. A spinner tube underlying filter assembly allows the wire to rotate independently from the delivery sheath to enhance the system’s steerability. The pore size of the membrane is 110 µm, and the 150-cm delivery catheter has a crossing profile of 3.2 French. This device is 6-French guide compatible with a landing zone of 18 mm. The retrieval catheter has a crossing profile of 4.3 French. This filter wire has been validated in the Beach study.38 The Emboshield (Abbott) This is a device featuring a bare wire configuration. It allows crossing of the lesion with an independent filter delivery wire (0.014-inch) available in two lengths (190 cm and 315 cm). The filter is then separately delivered and deployed on the wire. This design allows the filter element to “float” freely on the wire below a distal stop. Guidewire movement is possible while the filter is in place. The crossing profile ranges from 3.7 to 3.9 French. The pore size of the membrane is 140 µm. This device is 6-French compatible. The filter diameter ranges from 3 to 6 mm and the retrieval catheter has a 6-French crossing profile. A new device was recently proposed, the Emboshield Pro with a crossing profile ranging from 2.8 to 3.2 French, 19 mm and 22.5 mm landing zone (for 2.5−4.8 mm and 4−7 mm sizes, respectively). The pore size is 120 µm. The effectiveness of the Emboshield filter has been validated in the Security study.66 The Spider RX (EV3, Plymouth, MN) This filter permits the use of a guidewire of choice for crossing the target lesion.
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(b)
(c)
(d)
(e)
(f)
(g) Figure 35.10
Examples of filters.
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Figure 35.11
Tight left ICA stenosis treated with EPI filter.
In a second step, the delivery catheter with a crossing profile of 2.9 or 3.2 French is introduced over the wire and placed distal to the lesion in the ICA. A stylet is used to create a transition from the delivery catheter to the primary guidewire. After removal of the central guidewire, the filter, which is mounted on a 0.014-inch guidewire (175 or 320 cm) is advanced through the delivery catheter and is strictly maintained in the same landing position distal to the lesion. After placement of the filter, the delivery catheter is withdrawn. In contrast to the systems previously mentioned, the basket of this device consists of a nitinol wire braid filter with “pores” ranging from 167 to 209 µm. The diameter of the basket ranges from 3 to 7 mm. This device is 6-French compatible and the filter heparin coated. A clasp at the entrance of the frame may ensure a better vessel wall apposition of the fish-mouth opening filter with a
Figure 35.12
CAS with EPI filter: predilatation.
radio-opaque gold ring. The retrieval catheter has a diameter of 4.2 French for filters of 3, 4, and 5 mm, and 4.9 French for the 6- and 7-mm filters. If necessary, the snap wire feature permits conversion of the 320 cm long wire to a 175-cm rapid-exchange length. This device has been validated in the Protect trial.136 The Interceptor Plus (Medtronic Inc., Santa Rosa, CA) This filter consists of a braided nitinol basket attached to a 0.014-inch steerable guidewire. Four pores are located at the entrance of the basket. Minimal pore size is 100 µm. The filter features a simplified, intuitive delivery system that does not require the use of a sheath for deployment. The filter system is offered in sizes to fit vessel diameters from 4.25 to 6.25 mm with a lesion crossing profile of only 0.036 inches. This filter features excellent conformity to vessel walls. It is 6-French guide compatible.
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Figure 35.13
CAS with EPI filter: implantation of a Wallstent and dilatation of the stent.
The Rubicon Filter (Rubicon, Salt Lake City, UT) This device has a unique design and is the only filter without a dedicated delivery catheter. It has a very low profile of 2.4 to 2.7 French. It is mounted on a 0.014-inch guidewire and deployed via a coaxial actuating wire at the proximal end of the guidewire. The pores have a size of 100 µm. The filter basket is supported by floating nitinol struts for optimal apposition. It is 6-French guide compatible. The Rubicon filter is available in sizes from 4 to 6 mm. The long toper design of the filter increases the volume to capture debris. The large-bore catheter retrieval system actuator (6 French) shows the exact status of the filter as it is being captured for removal, minimizing the risk of debris loss. To reduce snagging of the stent, it has a dilator-style inner
Figure 35.14
317
CAS with EPI filter: filter retrieval and final results.
sheath; telescopes over the filter basket minimize movement of the filter during its retrieval. Advantages of the filters (Figure 35.11-35.14) The major advantage is the preservation of the flow, allowing their use in patients with poor collateral circulation, total contralateral ICA occlusion, severe contralateral ICA stenosis, intracranial stenosis, or a poor circle of Willis. The ability to perform angiography during the procedure allows accurate placement of the stent. The new generation of filters has a very low profile that allows crossing the majority of the lesions without predilatation. Two filters, Emboshield and Spider, have an independent guidewire allowing crossing the lesion with the guidewire at
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(a)
(b)
(c)
(d)
Figure 35.15 Risks of embolization with filters: (a) microemboli; (b) ineffective protection during systole/diastole; (c) ineffective protection during systole (d) filter withdrawal.
first, which is an advantage with tight lesions and tortuous vessels. Disadvantages and limitations of filters (Figure 35.15) ● Some filters have a large crossing-profile, leading to difficulties in crossing tight, tortuous lesions. Some published series reported that it was impossible to cross the lesion with the filters in 2−12% of cases.137,138 Predilatation of the lesion with a coronary balloon can facilitate the placement of the filter but with a risk of brain embolism. A “buddy wire” can straighten the artery and facilitate the crossing of the lesion in tortuous arteries. With the new generation of filters, failure to cross the lesion is rare, and in our experience, less than 1% of the cases (one failure in 318 procedures). ● A filter should be placed via straight part of the vessel to have a good wall apposition. A minimum landing zone is required. ● A filter engulfment with consequent distal slow flow may occur. A filter may also plug up with a static column of
(a)
(b)
●
●
●
●
(c)
blood with suspended particles that will embolize if we retrieve the filter. In these cases before retrieving the filter we have to aspirate very carefully the blood below the filter and to clean the dilated area with either an aspiration catheter or the guiding catheter we advance inside the stent. The filter may thrombose: effective anticoagulation with activated coagulation time (ACT) > 250−300 seconds is recommended. The filter may cause spasm or dissection of the distal ICA, which could possibly lead to restenosis (Figure 35.16). Closure and retrieval of filters can dislodge their content collected during the procedure. Some difficulties in retrieving the filters have been reported, for example in 8.4% of cases.138 We may have difficulties to get the retrieval catheter in and the filter could get caught on the struts of the stents during retrieval. These problems occur more frequently with
(d)
Figure 35.16 (a) Right ICA stenosis treated under protection (EPI filter) and with Wallstent; (b, c) spasm after filter deployment and Wallstent implantation; and (d) final result after filter retrieval and anti-spasmodic drug injection.
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●
●
●
●
open-cell stent design. Some tips and tricks have to be well known to solve the problems (rotation of the head, pressure on the carotid bifurcation, introduction of the guiding catheter inside the stent lumen, etc.) As with occlusion balloons, filters cannot prevent all neurological embolic events. The filter can protect the brain only after the filter has crossed the lesion and has been deployed. This maneuver and the initial positioning of the guide catheter in the CCA can release embolic material. Some emboli may occur during the procedure if the filter is not well deployed or if the diameter of the filter is not sufficient during systole and diastole, and after predilatation of the lesion, which could increase the flow and the diameter of the artery. It is important to deploy the filter in a straight part of the vessel to have a good wall apposition of the filter to avoid embolism. Inadequate filter vessel apposition is not always angiographically detectable and complete protection from embolization may not be possible in oval or eccentric vessels. A filter can generally retrieve debris > 100 µm, most of the devices have a pore size of 100 µm or larger, which can allow smaller particles to go to the brain with the possibility of microinfarcts. Only a small number of particles are removed139 and macroscopically visible particles are retrieved in only 35.0−83.7% of the filters.138,140 Filters reduce the risk of brain embolism as demonstrated by TCD or diffusion-weighted magnetic resonance imaging (DW-MRI) but do not prevent all emboli from reaching the cerebral circulation. Asymptomatic or “silent” ischemic lesions detected with DW-MRI have been reported more frequently after CAS than after endarterectomy.141−143 Recently, Flach et al.79 published a 9% frequency of new hyperintense lesions in surgically treated patients and a 43% frequency in the CAS group. Although the clinical importance of silent lesions is yet unclear, Vermeer et al. recently found that silent brain infarcts are associated with cognitive dysfunction in the general population. An increased frequency of dementia, and neuropsychomatic changes could also be a consequence of these lesions.144−147 With all protection devices and all stents we may observe peri-procedural or delayed embolic events. Most of the
Figure 35.17
FiberNet filter.
●
319
time, these complications are due to plaque protrusion through the stent struts and embolization of plaque material. To avoid these problems, we can aspirate this debris inside the stent and below the filter with an aspiration catheter or the guiding catheter. It is better to aspirate and clean the dilated area for at least all symptomatic lesions and all echolucent plaques. Other issues have been demonstrated with current EPD. Recently, Vos et al.78 published interesting data showing that the role of some filters is unclear and associated with potential problems. By means of TCD, they detected a higher number of microemboli during filter-protected CAS but the number of particulate macroemboli was higher in the unprotected group. Distal thrombus formation occurred only in patients with filter protection. MacDonald et al.148 published similar data with the EmboShield filter.
New generation of filters To overcome some problems encountered with current filters, a new filter was recently proposed and is under experiment. This filter, the FiberNet (Figure 35.17), (Lumen Biomedical Inc., Plymouth, MN) consists primarily of polyester fibers located coaxially around the distal tip of a guidewire assembly. This filter is soft, conformable, and when activated expands radially to fill the vessel, providing excellent apposition to the vessel wall. Contained and captured emboli are recovered/removed both by aspiration through the retrieval catheter and also by retention within the filter fibers when the filter is closed and retracted into the retrieval catheter. Aspiration is achieved through the retrieval catheter using vacuum syringes to provide suction. This filter enables capture of emboli as small as 40 µm without compromising the flow through the filter, and can be delivered as a standard coronary guidewire. The possibility of suction through the retrieval catheter during device removal is probably one of the major improvements with this device, allowing cleaning of the dilated area and of the inner part of the stent. This technique allows aspiration of the debris, which can protrude through the struts of the stent after stent placement and dilatation and which could be one of the causes of the delayed embolic events. We performed the first human study in carotid and renal arteries with this new protection device. Sixty-two lesions
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AV shunt
Filter
Figure 35.18
A schematic sequence of Parodi’s anti-embolization catheter (PAEC).
(58 carotid and 4 renal) were treated in 61 patients. Visible debris comprising atheroma was detected in each case. It is important to state that nearly 30% of the debris was aspirated from inside the stent, which could potentially reduce delayed embolic events. We compared this device with other filters. With the FiberNet, we removed five times more debris. Thirty-four patients underwent CT or MRI before and at 30-day post-procedure. No changes were noted in the follow-up tests when compared to the baseline.149 Flow reversal technique Parodi anti-embolization catheter (Gore and Associates Inc., Flagstaff, AZ) (Figure 35.18) Description of the device.37,76 The Parodi anti-embolization catheter (PAEC) is a guiding sheath with an occlusion balloon attached at the distal end of the catheter. The main lumen has an inner diameter of 7.3 French that allows the passage of balloons and stents. Once the PAEC has been inserted in the CCA, a Parodi external balloon (PEB) is inserted and inflated in the ECA. Then, the occlusion balloon attached on the outer surface of the PAEC is then connected to a sheath that is percutaneously inserted into the femoral vein to create a temporary arteriovenous shunt. This shunt, along with the PEB, creates reversal of flow in the ICA. The deployment of the PEB is required to prevent retrograde flow from the ECA, which may cause prograde flow in the ICA. Particles of all sizes flow through the PAEC and are captured by a filter placed at the arteriovenous connection. The new device is 9-French sheath compatible. The working length of the Gore balloon sheath (0.035-inch guidewire compatible) is 91 cm. Advantages ● Complete protection can be achieved before manipulating the lesion. The risk of complications is reduced by never crossing the lesion unprotected. ● The lesion can be crossed with any guidewire of our choice under protection, avoiding brain embolism during this step.
●
● ●
● ●
●
Embolization to the brain is not possible during reversed flow. Particles of all sizes can be captured. Tight, tortuous lesions and stenosis with limited landing zone can be treated with any wires. The PAEC provides a treatment option for patients whose anatomy is unsuitable for the use of a distal filter. No damage is caused to the fragile intima of the distal ICA. The technique avoids flushing through the ECA with the risk of brain embolization in the case of collateral circulation between the ECA and ICA or vertebral artery. Complications associated with filter retrieval and filter related vasospasm in the ICA are eliminated.
Disadvantages and limitations ● The interruption of flow during protection may not be tolerated in some patients (5%), as with the distal occlusion balloon. ● The new generation of PAEC need a 9-French introducer. With the previous device a larger puncture side-hole was needed (11 French). ● The technique has the potential to cause spasm or dissection in the ECA or CCA. ● As with other protection devices, a brain embolism may occur during placement of the catheter in the CCA. This step cannot be protected. Seatbelt and airbag technique This technique was described by Parodi et al.150 in two patients. They used a flow-reversal system (Parodi anti-embolism system), which was first placed with a 260 cm exchange wire in the CCA 3 cm below the carotid bifurcation. Flow reversal was achieved by inflating the balloon in the ECA and CCA. Via an external connector a guidewire and an E Trap Filter (MSD, Pittsburgh, PA) were delivered to the distal ICA with active suction from a syringe on the PAES catheter. Once the filter was above the stenosis, the flow reversal was discontinued and the procedure proceeded under cerebral protection with the filter.
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Filters Occlusion Flow reversal
321
Advantages and disadvantages of different protection devices
Embolization during guidewire / catheter lesion Flow crossing decrease
ICA protection from emboli
Ability to perform angiography during protection
Embolization through ECA
Potential spasm /damage to ICA Tolerance
Easy to use
+++ ++ —
+ ++ +++
+++ — +++
— +++ —
+++ +++ —
+++ ++ +
+ ++ +++
+++ + +
ECA: external carotid artery – ICA: internal carotid artery
The combination of these existing cerebral protection devices could, at least in theory, achieve what neither of them could independently. Moreover, it may be feasible to avoid some drawbacks of the various systems. Because distal protection devices must cross the lesion, which may account for about 12% of all emboli generated during a procedure,12 Parodi et al. sought to provide protection during this step by initiating flow reversal through the ICA to prevent distal embolization. No cerebral embolization has been demonstrated on TCD monitoring during these procedures. This technique could be indicated for carotid stenoses that demonstrate a high potential for embolization, or in patients with an aberrant or a non-functioning circle of Willis or contralateral ICA occlusion, which may be intolerant to balloon occlusion. MOMA device The MOMA device is a “proximal flow blockage” cerebral protection device. Cerebral protection occurs by interruption of antegrade blood flow from the common carotid artery and retrograde blood flow through the ipsilateral ECA. This is achieved by a low-pressure balloon occlusion of the two vessels by means of a single device integrating the two occlusive balloons and a working channel for the delivery of interventional devices to the target lesion. One balloon occludes the ECA and the second balloon the CCA, so that passing the target lesion with the embolic protection system before starting the procedure is avoided. Debris are thus stopped at the carotid bifurcation and prevented from dislodging to the brain. Removal of debris is performed by spot (active) syringe aspiration which can be performed any time during the intervention through the working channel of the device.
Choice of protection device Table 35.1 summarizes advantages and disadvantages of the different protection devices. We know that all CAS should be performed under cerebral protection. The choice of the protection device depends on the interventionist, the lesion, the anatomy of the different vessels (aortic arch, carotid arteries, etc.), the intracranial circulation, and the collateral circulation.
Before deciding which protection device to use it is indispensable to assess carefully the anatomy at intracerebral level, the access site, and the lesion itself. Intracerebral circulation To decide on which protection device to use, a good angiography of the intracranial circulation is mandatory with four-vessel angiography and good assessment of the collateral circulation. Without sufficient collateralization, only distal filters can be used. Distal and proximal occlusions systems should not be used because cerebral perfusion will be inadequate during the procedure and intolerance episodes could happen. This could be the case in patients with severe contralateral carotid stenosis or occlusion. Distal occlusion is also contraindicated in patients with an anastomosis between the ICA, ECA, and vertebral territories. With sufficient collateralization distal occlusion can be used. Access site assessment Patients presenting with tortuous vessels or type III aortic arch require low-profile, flexible protection systems as it is difficult to reach the lesion site. Carefully selected low-profile, steerable, flexible devices should be used, like the distal occlusion system and some filters. Proximal occlusion systems seem inadequate due to their larger profile. Lesion site assessment ● Severe stenoses and irregular lesions can be treated under any kind of protection but very low-profile, steerable devices need to be selected. ● With very tortuous ICA, severely angulated ICA, or when there is little space between the lesion site and the cerebrum with lake of landing zone for the device, it is better to use proximal occlusion devices. ● If thrombotic lesion or thrombi are suspected, proximal occlusion devices offer a unique possibility of avoiding brain embolism. ● Some authors advise proximal occlusion systems to treat plaques with very high risk of brain embolism (soft, dyshomogenous plaques, plaques with a GSM of less than 25). However, very-low-profile, flexible, soft-tipped
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Figure 35.19
Crushing of a Palmaz stent and redilatation.
Figure 35.20
Ostial CCA stenosis: angioplasty and stenting with a Genesis stent.
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Periodic peak–peak flex connectors e.g.optimed Sinus 5f Periodic peak–peak non-flex connectors e.g. Cordis - Precise
Periodic peak-valley non-flex connectors e.g. Cook - Zilver
Rings connected by “bridges” Figure 35.21
Open-cell stents.
filters or distal occlusion systems can be used and the generation of protection devices such as FiberNet also seems very promising for these lesions with a greater tendency to embolize. Stent selection Different types of stents Two main types of stent are available: balloon-expandable and self-expandable stents. ● Balloon expandable stents like the Palmaz stent and coronary stents. Palmaz stents were used early on in our experience, but have now been abandoned at carotid bifurcation because of the risk of compression and crushing (Figure 35.19). These stents are only implanted at the ostium of the common carotid artery. Their precise placement and good radial force facilitates a good positioning (Figure 35.20). Coronary stents are used for distal intracranial lesions of the ICA to treat tandem lesions. ● Self expandable stents: two types are available: 䊊 A cobalt chromium alloy stent: Wallstent (Boston Scientific, Natik, MA), which is braided, has a closed-cell
Laser cut
Closed-cell pattern one-to-one cell relation e.g Abbott-XACT Boston-nexstent
Figure 35.22
Closed-cell stents.
䊊
design, is straight, and available in different lengths (20−40 mm) and diameters (6−10 mm). Nitinol stents with two designs: open-cell and closed-cell design. Examples of open-cell design stents include: Precise RX (Cordis, Warren, NJ), Acculink (Guidant, Indianapolis, IN), Zilver (Cook, Bloomington, IN), Protégé (EV3, Plymouth, MN), Conformex (Bard, Tempe, AZ), Exponent (Medtronic, Santa-Rosa, CA), and Sinus (Optimed, Ettingen, Germany).
Figure 35.21 shows how rings are connected by bridges for different open-cell stents. Figure 35.22 shows two types of closed-cell stents. The nitinol stents are available straight or tapered in different lengths and diameters (Table 35.2). Choice of stent All stents are not equivalent. They have specific characteristics depending on the design. It is therefore important to choose carefully the stent depending on the vessel anatomy, the lesion, and the plaque characteristics.
Braided
Woven tube one-to-one cell relation e.g Wallstent
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Table 35.2
Straight and tapered stents Tapered stents
Company
Stent
ø mm
Boston Boston
Wallstent Nexstent
Abbott Bard Cordis EV3 Guidant Medtronic Optimed Cook
XACT Conformex Precise Protege Acculink Exponent Sinus Zilver
Straight stents
L mm
4–9 Self tapering 10/8, 9/7, 8/6 12/8, 10/7, 8/6 10/7, 9/7, 8,6 10/7, 8/6 10/7, 8/6
30 30–40 30–40 30 30–40 30–40
10/7, 9/6
40
Table 35.3 summarizes the different characteristics of carotid Wallstent and nitinol stents. One of the most important is the foreshortening: nitinol stents allow precise placement, which is impossible with a Wallstent. Table 35.4 summarizes the geometric effects of the different stents. ●
●
●
●
A nitinol stent is more flexible than a Wallstent. Open-cell stents are more suitable for tortuous arteries. With more rigid stents such as a Wallstent, we straighten the carotid bifurcation and reduce the ICA tortuosity angle and offset, leading to longitudinal extension and upward displacement of the distal ICA with the possibility of kinking above the stent termination (Figure 35.23 and 35.24). The radial force may be a little better with nitinol stents. With open-cell nitinol stents, we have separation and protrusion of stent segments. The inner stent surface is not as smooth as that of other stents, and we can see protrusion of plaques or thrombus into the lumen reducing the surface sealing barrier to debris embolization and increasing the risk of brain embolization, particularly in the case of soft inhomogeneous plaques. For these lesions, it is better to choose a closed-cell stent, and it is important to post-dilate the stent to push up plaque material into the intimal layer and smooth the stented surface (longer inflations). Meticulous cleaning of the dilated area is indispensable (with an aspiration catheter or guiding catheter) to avoid procedural and delayed neurological events.
●
●
●
Braided Laser cut Foreshortening Accurate placement Repositionable Rapid exchange Radio-opacity Crossability
Carotid Wallstent
Nitinol stents
+ − +++ − + + +++ +++
+ + — +++ +/− +/− ++ ++
L mm
6–10 4–9
20,30,40 30
7–10 5–12 5–10 6–10 5–10 6–10 5–9 6–10
20,30 20,30,40 20,30,40 20,30,40,60 20,30,40 20,30,40 20,30,40 10–80
Open cell
Closed cell + +
+ + + + + + +
+
Nitinol tapered stents have a better adaptation to different vessel diameters and a better wall apposition. They should be used in cases of large difference between the ICA and CCA diameters. With open nitinol stents, we can encounter some difficulties introducing or retrieving the different protection devices. In tortuous vessels in particular, filter or protection balloon can get stuck or caught on the stent. Some tips and tricks have to be known to solve these problems (rotation of the head, pressure on the carotid bifurcation, introduction of the guiding catheter inside the stent lumen, etc.). In terms of neurological complications, regarding the restenosis rate there is no difference between the different stents.
Open-cell and closed-cell stents present some important differences. A closed-cell stent has some disadvantages such as ●
● ●
no stent struts protruding into the vessel lumen or into the vessel wall; less risk of balloon rupture; less risk of a problem related to retrieval of the stent delivery system or angioplasty balloon protection device.
With an open-cell stent, we also have some advantages: ● ● ●
Table 35.3 Different characteristics of carotid Wallstent and Nitinol stents
ø mm
better flexibility; better wall apposition; but risk of difficulty in retrieving or introducing devices.
A good choice of the stent is mandatory and it is important to have different types of stents in the catheterization laboratory to implant the stent better suited for the patients and the lesion. Table 35.5 summarizes the best indications for the different stents. Technique of stent implantation Angioplasty and stenting with predilatation A predilatation is recommended in cases of tight and calcified stenoses, to facilitate the passage of the stent through the lesion. Some interventionists also recommend predilatation with the Wallstent, due to its foreshortening during dilatation.
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325
The geometric effects of the different stents Nitinol stent Carotid Wallstent
Geometric effects Flexibility − adaptation to vessel tortuosities Straightening of the bifurcation Reduction ICA tortuosity angle and off set Longitudinal extension and upward displacement of the distal ICA Kinking above the distal stent termination Radial force Separation and protrusion of stent segments Smooth inner stent surface Protrusion of plaques or thrombosus into the lumen Surface sealing barrier to debris embolization Adaptation to different vessel diameters
+++ + +++ +++ +++ +++ ++ — +++ + ++ ++
Vessel wall apposition
+
Difficulties to retrieve devices from the ECA Difficulties to introduce or retrieve protection devices Neurological complications Restenosis rate
+ + + +
A coronary balloon of a size smaller than the diameter of the artery (2−4 mm) 2−4 cm long is advanced over the guidewire and short inflations (5−10 per second) are performed to predilate the lesion and allow the passage and placement of the stent. The deflation of the balloon must be done slowly to limit the risk of brain embolism. Once the predilatation balloon is withdrawn, a stent is implanted. Most of the time, we implant self-expandable stents, which can cover the carotid bifurcation without threatening the patency of the ECA. The length of the stent depends on the length of the lesion, but the diameter should be equal to the diameter of the upper part of the CCA. The dilatation of the stent is done with a balloon whose diameter is equal to that of the ICA. We recommend to never overdilate a stent to avoid dissection, which could compromise the patency of the ICA.
Open
+ ++ + + + + +++ — +++ + ++ + Tapered +++ ++ Tapered +++ + + + +
+ +++ + + + + +++ +++ + +++ + + Tapered ++ ++ Tapered +++ ++ ++ + +
Results: personal series From April 1995 to December 2006, 844 carotid angioplasties were performed in 786 patients, 187 without protection at the beginning of our experience, and 657 with protection in 614 patients (male: 461, female 153). The mean age was 70.9 ± 9.4 years (40−91). Forty-three bilateral angioplasties were performed. Symptomatic lesions were present in 64%. The etiology was as follows: atheromatous disease (n = 607), restenosis (n = 34), post-radiation (n = 11), inflammatory disease (n = 3), post-trauma aneurysm (n = 2). Three types of protection devices were used: ●
●
Angioplasty and primary stenting Implantation of a stent may be performed without predilatation with the assumption that it will reduce the risk of cerebral embolization. It may be performed in numerous cases, particularly with the new generation of low-profile self-expandable stents. In our experience, 90% of procedures can be done without predilatation of the lesion, and that is the technique we recommend. Once angioplasty and implantation of stent are performed, a control angiography is done using several angles in order to check the result of the procedure and potentially complete it if necessary. Extra inflations with a larger balloon or implantation of another stent may sometimes be necessary. Intracranial snapshots are also obtained to look for potential distal embolization, which may require complementary endoluminal interventions or administration of urokinase, rtPA, or Reopro.
Closed
●
Occlusion balloon: 334 䊊 Percusurge: 277 䊊 Theron’s technique: 47 䊊 Personal device: 10 Filters: 318 (two filters used in the same procedure) 䊊 EPI: 216 䊊 Angioguard: 28 䊊 Emboshield: 7 䊊 Accunet: 9 䊊 FiberNet: 58 Arteria: 6
Percusurge Guardwire technique Two hundred and seventy seven angioplasties were performed with this device in 251 patients. Technical success was 275/277. We had two failures due to very tight calcified stenoses in tortuous vessels. Twelve patients did not tolerate the occlusion of the ICA (4.4%). We should also mention that 64 patients presented with tight stenoses or occlusion of the contralateral ICA. We aspirated debris in all patients. The mean diameter was: 250 µm (56−2652); the mean number per procedure was 74 (7−145). Several types of particles were identified
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1
(a) Figure 35.23
(b)
Stents: geometric effects: (a) without stent; (b) nitinol stent; and (c) carotid Wallstent.
Filters Three hundred and eighteen angioplasties were performed under filter protection. We had only one failure to place the filter above the lesion due to very severe tortuosities of the ICA. In two cases, a predilatation of a very tight calcified 99% stenosis was needed before crossing it with the filter. In all other cases, filters were correctly placed without predilatation of the stenosis. Visible debris was retrieved in 70% of the filters. Three filters were totally blocked by debris. At 30 days, we observed 10 complications (3.1%):
by histological analysis: atheromatous plaques, cholesterol crystals, necrotic cores, macrophage foam cells, fibrin, platelets, thrombi. At 30 days, we observed 6 complications (2.2%): ● ● ●
●
3 TIA; 1 retinal embolism with amaurosis; 1 cerebral hemorrhage at day 3 in a patient treated with Reopro, leading to a major stroke; 1 death 3 weeks after the procedure due to a cardiac failure.
At 4 years follow-up 97% of the patients were free from any neurological symptom.
(a) Figure 35.24
(c)
● ●
2 TIA; 2 minor strokes;
(b)
Stents: geometric effects: (a) carotid stenosis; (b) rigid stent; (c) nitinol stent.
(c)
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Stent selection Nitinol open-cell
Nitinol closed-cell
Wallstent closed-cell
+++
+++
++
+
+++
+++
+ Tapered + + + +++
+ Tapered + + + +++
++ +++
+++
++
+
Hard / Calcified Radial force Soft / Dishomogenous Scaffolding Bifurcation Vessel wall adaptabllity Straight artery flexibility Tortuous artery flexibility
3 retinal embolisms (1 amaurosis fugax, 2 permanent amaurosis); 1 hyperperfusion syndrome with rapid recovery 4 hours after the procedure; 1 death at day 3 due to a hyperperfusion syndrome with cerebral hemorrhage in a patient under Reopro (the patient died after coronary angioplasty done for unstable angina); 1 myocardial infarction in a patient with unstable angina, treated before cardiac surgery.
●
●
●
●
Arteria system Our experience is limited with this device that we reserve to very specific indications. We used it in six cases with success and no complications. From our experience, we can point out some important points (Tables 35.6−35.10).
Table 35.6 protection
CAS: 30-day outcomes with and without
Without NP n = 187 TIA Minor stroke Major stroke Retinal embolus Hyperperfusion syndrome Death Fatal stroke Non-stroke death MI Death and stroke Embolic events
Death and stroke rate Symptomatic patients: Asymptomatic patients: Embolic complication rate Symptomatic patients: Asymptomatic patients:
p: > 0.05
327
●
●
●
●
●
If we compare carotid angioplasty with and without cerebral protection, the complication rate is significantly reduced. With protection, the 30-day death and stroke rate is 1%, the embolic complication rate 2%. Without protection, these rates are, respectively, 3.7% and 4.8% (p < 0.05). With cerebral protection, the 30-day death and stroke rate is 1.3% in symptomatic patients, 0.9% in asymptomatic patients, the cerebral embolic complications rate 2.5% in symptomatic patients, 1.8% in asymptomatic patients. These complication rates are inferior to the admitted rates by American Heart Association Guidelines, which advises a complications rate < 3% in asymptomatic patients and < 6% in symptomatic patients. We observed no statistical difference in the 30-day complications rate with the different protection devices. We did not observe any statistical difference when we treated high- and low-risk patients, whatever the protection device. As we have mentioned in the indications, we can now propose a carotid angioplasty to these two groups of patients with the same safety. With a good technique, a good choice of stent, there was no difference in terms of complication with the different types of stents. The embolic events, and death and
With NP n = 657
4 2% 3 1.6% 2 1% 0 0 2 1% 2 1% 0 7 3.7% 9 4.8%
6 3 1 4 3
0.9% 0.4% 0.2% 0.6% 0.5%
3 2 1 1 7 14
0.5% 0.3% 0.2% 0.2% 1% 2%
5 2
1.3% 0.9 %
10 4
2.5 % 1.8 %
Table 35.7 CAS: 30-day outcomes in symptomatic and asymptomatic patients Percusurge n = 277 TIA Minor stroke Major stroke Retinal embolus Hyperperfusion syndrome Death Fatal stroke Non-stroke death MI Death and stroke Embolic events p: N.S.
3 0 0 1 1 1 0 1 0 1 4
1% 0.3% 0.3% 0.3% 0.3% 0.3% 1.4%
Filters n = 318 2 2 0 3 2 1 1 0 1 2 6
0.6% 0.6% 0.9% 0.6% 0.3% 0.3% 0.3% 0.6% 1.9%
Arteria n=6 0 0 0 0 0 0 0 0 0 0 0
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Table 35.8 and stents
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Study
Cabernet69
Beach68
Maveric67
Archer 261,65
Security62,66
Capture162
Stent Protection devices Stroke/death/MI
Nexstent Boston Filterwire 3.8%
Wallstent Boston Filterwire 5.8%
Exponent Percusurge 5.2%
Acculink Accunet Filter 8.3%
X ACT Neuroshield 7.2%
Acculink Accunet 5.7%
stroke rates are similar with balloon expandable stents, self-expandable stents, Wallstents, or nitinol stents. With the new protection device we experimented in the first human study, we treated 57 patients (58 lesions) with a procedural success rate of 98% (57/58). In one patient, we were unable to cross one tight lesion with a severe angle just distal to the lesion. Four instances of TIMI 1 flow and 1 TIMI 0 flow were noticed. TIMI 3 flow was restored after aspiration and filter removal. In all cases visible debris were caught. The average area for FiberNet debris capture was 63.8 mm2 and the number of particles < 100 µm captured was 4976. We did the same study with other filters and with these the average area for debris captured was 12.2 mm2 and the number of particles > 100 µm captured was 2752. Visible debris was caught in only 43% of the cases. The FiberNet seems much more efficient in terms of debris captured. FiberNet captured five times more debris than other filters. Atheromatous material is found in both aspirate and filter samples. Thirty percent of the emboli are aspirated through the stent, which proves the importance of aspiration after placement of the stent and before filter removal to avoid peri-procedural and delayed embolic events. In this short series we had one minor stroke at the beginning of our experience and with the first generation of the device we had one amaurosis fugax, and two permanent amaurosis. One patient developed a post-procedure hemianopsia and one patient who had a partial hemianopsia before the procedure developed a full post-procedure hemianopsia due to either a hypotension episode or embolization. We have to point out that there were no changes in 30-day follow-up CT/MRI in 36 patients controlled.
Table 35.9 CAS: 30-day outcomes in high- and low-risk patients (657 procedures) High risk n = 417 TIA Minor stroke Major stroke Retinal embolus Hyperperfusion syndrome Death Fatal stroke Non-stroke death Death and stroke MI Embolic events
4 3 1 2 2
Low risk n = 240
p value
1% 0.7% 0.3% 0.5% 0.5%
2 0.9% 0 0 2 0.9% 1 0.4%
N.S. N.S. N.S. N.S. N.S.
2 0.5% 2 0.5%
1 0.4%
N.S. N.S. N.S. N.S. N.S. N.S.
6 1.4% 1 0.3% 10 2.4%
1 0.4% 1 0.4% 0 4 1.7%
Discussion Several randomized trials1−6,151,152 have proved the efficacy of surgical CEA for severe symptomatic and asymptomatic extracranial carotid artery stenosis and its superiority over medical treatment. However, the benefits of the procedure are critically dependent on the rate of peri-operative complications.8,9,153 The 30-day stroke and death rate in these trials ranged from 5.8 to 7.5% in the symptomatic patients and from 2.3 to 4.3% into the asymptomatic patients. CEA always carries a risk. In a series of 3061 procedures, Ouriel et al. described a stroke, myocardial infarction, and death rate of 7.4% in high-risk patients and 2.9% in low-risk patients.18 For CAS to be considered as an alternative to surgery, its complication rate should parallel that of CEA. Early clinical series of carotid stenting have led to the assumption that carotid stenting is a promising alternative to CEA due to a low morbidity and mortality rate. Since then only a few randomized studies comparing carotid stenting to CEA have been published. The CAVATAS trial30 was the first to give comparable results for angioplasty and CEA, despite only one-fifth of the patients receiving a stent. In 504 patients enrolled, the stroke rate at 30 days was 10% for angioplasty and 9.9% for CEA. CEA was associated with an 8.7% rate of cranial nerve palsy and 6.7% of hematomas. Brooks et al.31 published a small trial and also found comparable results for surgery and stenting. These two randomized studies were performed without protection devices. Considering these results, CAS could be proposed in an increasing number of patients with a carotid artery stenosis and several series have been published with an acceptable peri-operative stroke/death rate.19−26, 29, 38, 39, 154,155 In a series of 528 consecutive patients published by Roubin et al.,26 the major stroke rate was 1% and the minor stroke rate 4.8%. The overall 30-day stroke and death rate was 7.4%. However even for experienced interventionists, the risk of embolic stroke, a devastating complication, remains the main limitation of the procedure. The frequency of debris migration and distal embolism has been demonstrated by ex vivo human carotid stenting techniques45 and confirmed in clinical studies.8,26,38,39,74 The number of embolic particles generated by percutaneous techniques seems to be much higher than by endarterectomy.74,125,132 Although the clinical significance of such particles has not been documented74,156 their presence will not have any beneficial effect for the brain. Furthermore, the minimum particle size capable of producing ischemic events has not been determined. Various patients and plaque characteristics have been suggested as predictors of debris generation and embolic events49,133 to define high-risk groups for the CAS procedure. In our study, debris was extracted from all patients, even
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CAS: 30-day outcomes in high- and low-risk patients with percusurge and filters (594 arteries) Percusurge
Filters
High-risk n = 178
Low-risk n = 99
Total n = 277
High-risk n = 201
Low-risk. n = 117
Total n = 318
2 0 0 0 1 0 0 0 0 0 2
1 0 0 1 0 1 0 1 1 0 2
3 (1%) 0 0 1 (0.3%) 1 (0.3%) 1 (0.3%) 0 1 (0.3%) 1 (0.3%) 0 4 (1.4%)
1 2 0 2(1.1%) 1 1 1 0 3 1 5(2.5%)
1 0 0 1(1%) 1 0 0 0 0 0 2
2 (0.6%) 2 (0.6%) 0 3 (0.9%) 2 (0.6%) 1 (0.3%) 1 (0.3%) 0 3 (0.9%) 1 (0.3%) 7 ( 2.2%)
TIA Minor stroke Major stroke Retinal embolus Hyperperfusion syndrome Death Fatal stroke Non-fatal stroke Death and stroke MI Embolic events p = N.S. For high-risk /low-risk /all patients
in lesions theoretically at low-risk of cerebral embolism (restenosis, echogenic plaques, concentric lesions), suggesting that the risk of embolization is independent of the nature of the plaque.34,35 Stent deployment does not provide sufficient protection against the migration of embolic plaque debris. In all series of CAS, the embolic risk exists regardless of the implantation technique and the stent characteristics. Manninen et al.157 compared endovascular stent placement with PTA of carotid arteries in cadavers in situ and found no difference with respect to distal embolization. Protection devices are a unique way to protect the brain for embolization and several protection devices have been proposed for use during CAS. Therefore in almost all centers, embolic protection devices are applied routinely and CAS under protection is the standard of care. Unfortunately, there are no randomized trials comparing CAS with protection to CAS without protection. However, many series and registries revealed a benefit of protection devices, as we saw with our personal series. Kastrup et al.58 reviewed trials from 1990 to 2002 with a total of 2537 procedures without protection devices and 896 CAS procedures performed with an embolic protection device.
Table 35.11
The combined stroke and death rate at 30 days in patients treated with cerebral protection was 1.8% compared with 5.5% in patients treated without protection devices (p < 0.001). A world registry55 described a peri-operative stroke and death rate of 5.29% in the 6688 procedures performed without protection (minor stroke: 2.88%; major stroke 4.61%; death 0.82%) and 2.27% in the 4005 procedures performed with protection devices (minor stroke: 1.10%; major stroke: 0.72%; death: 0.45%). For symptomatic patients, the stroke/death rate is 6.07% without protection (n = 4223) and 2.82% with protection (n = 1949) and for asymptomatic patients 3.97% without protection (n = 2465), 1.75% with protection (n = 2056). Roubin et al.70 reported a series of 809 procedures performed without protection and 588 procedures with protection. The 30-day stroke/death rate was 6.2% without protection and 2.4% with protection (p < 0.05). The benefit is major for elderly patients older than 80 years (16.5 vs. 2.4%). Furthermore, there is no difference between the different protection devices (2.3% with balloon occlusion, 2.6% with filters).
CAS: 30-day outcomes with different types of Stents
SE Stent BM Stent n = 293 TIA Minor stroke Major stroke Retinal embolus Hyperperfution syndrome Death Fatal stroke Non-fatal stroke Embolic events MI Death and stroke *same patient
7 1 2 1 1 3 2 1 11
2.4% 0.3% 0.6% 0.3% 0.3% 1% 0.6% 0.3% 3.8% 0 6 2%
Wallstent n = 296 2 0.7% 2 0.7% 1 2* 1 1*
Nitinol n = 258 1 3 1 2
0.4% 1.2% 0.4% 0.8%
p value N.S. N.S. N.S. N.S N.S.
0.3% 0.7% 0.3% 0.3%
1 0.4% 1 0.4%
N.S.
5 1.7% 0 4 1.4%
7 2.7% 1 0.4% 4 1.5%
N.S. N.S. N.S.
Total n = 847 10 6 3 4 3 5 4 1 23 1 14
1.2% 0.7% 0.4% 0.5% 0.4% 0.6% 0.5% 0.1% 2.7% 0.1% 1.7%
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Mathias et al.71 also reported a large series of CAS (1621 patients/1799 procedures): 1222 were performed without protection with a 30-day stroke/death rate of 3.8%, and 577 with protection with a death/stroke rate 1.7%. Cremonesi et al.56 published a series of 442 consecutive patients treated with CAS under embolic protection. Only 1.1% of the patients experienced either a stroke or death within 30 days. Reimers et al.57 published in 2004 a multicenter study with 808 successful stent procedures in 753 patients. The rate of stroke and death within 30 days after the procedure was 3.8% for symptomatic lesions and 3.2% for asymptomatic lesions. Parodi et al.156 reported the first 100 patients treated with PAES with no embolic complications during the procedure. Post-operative TIA (1 month) occurred in four patients, and the mortality rate was 2% (one brain hemorrhage, one myocardial infarction). Sievert et al.158 published a multicenter study in which 302 carotid artery stenoses were treated with PAES with a technical success of 97.7%, a tolerance rate of 93.3%. The procedural cerebral complication rate was 0.99% (minor stroke) and the post-procedural complication rate 4.7% (TIA: 1.7%; minor stroke: 0.7%; hemorrhagic stroke: 0.7%; contralateral stroke: 0.3%; myocardial infarction: 0.1%; death: 1%). The MOMA Trial54 enrolled 157 patients. The procedure was technically and angiographically successful in all procedures. In 79.6% there was macroscopic evidence of debris after filtering the aspirated blood. The stroke/death rate at discharge was 2.55% and within 30 days 5.73%. Cremonesi et al. recently published a series of 78 patients with high-risk soft plaques (GSM < 25) treated with proximal protection devices (MOMA: 66; PAES: 12). Technical success was 100%. Debris was collected in 93.6% of the cases. During the procedure, two TIA were reported. Stroke/death rate at 30 days was 2.56% (1 death, 1 minor stroke). An interesting study was recently reported, the CARESS study.59 This trial is intended to represent the real world of carotid disease treatment, and is the only trial that will enroll low, medium, and high-risk patients. Two hundred and fifty four patients were treated with CEA, 143 with CAS under protection. Sixty-eight of the patients were asymptomatic. There was no significant difference in the 30-day combined all-cause mortality and stroke rate between CEA (2%) and CAS (2%). There was no significant difference in the secondary endpoint of combined 30-day all-cause mortality, stroke, and myocardial infarction between CEA (3%) and CAS (2%). Several randomized studies have recently been reported comparing CAS and CEA. The first study was the SAPPHIRE study60,63,64 comparing CEA with CAS with distal protection (Angioguard XP Emboli Protection Guidewire and Precise Nitinol Stent, Cordis) in high-surgical-risk patients. Three hundred and seven patients were treated: 156 by CAS, 151 by CEA. At 30-day follow-up, major adverse events (MAE) (death, stroke, myocardial infarction) were 5.8% for CAS and 12.6% for CEA. At 1-year follow-up MAE were 11.9% for CAS, 19.9% for CEA (p = 0.048) and at 2 years 20.1%, 26.7%, respectively. A subset analysis of diabetic patients found a 2.4% stroke incidence at 30 days versus 6.8% for the CEA arm. At 1 year MAE. were 4.8% for CAS, 25% for CEA. This SAPPHIRE study is in favor of CAS at least for high-surgicalrisk patients and particularly diabetic patients.
The EVA 3S study86 is a randomized non-inferiority trial to compare CAS with CEA in patients with a symptomatic carotid stenosis of at least 60%. This trial was first suspended in 2001 because of an excess stroke risk in CAS patients (15% overall, 26% following unprotected CAS and 10% after protected CAS). The trial was then restarted but all CAS procedures had to be performed with a protection device. This trial was stopped a second time prematurely after the inclusion of 527 patients for reasons of both safety and futility. The 30-day incidence of any stroke or death was 3.9% after CEA and 9.6% after CAS. The 30-day incidence of disabling stroke or death was 1.5% after CEA and 3.4% after CAS. At 6 months, the incidence of any stroke or death was 6.1% after CEA and 11.7% after CAS, but there were more systemic complications (mainly pulmonary) after CEA and more cranial nerve injuries. If this trial showed better results with CEA than with CAS, important criticisms must be pointed out: ●
●
The vascular surgeons had to have performed at least 25 CEA in the year before enrolment. It is mentioned by the authors that the 30-day incidence of stroke and death after CEA was lower in the EVA 3S trial than in previous trials of CEA in symptomatic patients. This lower risk is unlikely to be explained by the selection of the surgeons with a higher level of expertise. Unfortunately, it is not the same with interventionists who had to have performed at least 12 CAS or at least 35 stenting procedures in the supra-aortic vessels of which at least 5 were in the carotid artery. It is obvious that these interventionists were inexperienced, which could explain the high neurological complication rate in this study. As we have seen previously, the learning curve is important in CAS, and also exists for the use of any embolic protection device. It is surprising that in this EVA 3S study, two stenting procedures with any protection device before its use in the trial were considered as sufficient.
Another multicenter randomized trial, the SPACE trial159 (595 patients) with CAS (605 patients) was recently reported. The trial failed to prove the non-inferiority of CAS compared with CEA, expressed as the rate of ispilateral ischemic stroke or death within 30 days after treatment (6.8% with CAS, 6.34% with CEA). We have to point out that only 27% of the patients were treated with an embolic protection device and that the interventionists were not very well experienced, because they had to show proof of 25 successful consecutive PTA or stent procedures, which for a lot of interventionists does not seem sufficient. The peri-procedural risk in this trial was much the same in young patients (absolute risk difference: 0.02%) and in men (0.04%) but more different in older patients (3.5%) or women (1.7%). Similar findings with respect to age were reported in the lead in phase of the CREST trial.160 Of the 749 patients treated with CAS, those younger than 80 years had a 30-day stroke and death rate of 3% compared with 12% in patients older than 80 years. Opposite results were recently reported by Setacci et al.161 CAS procedures (1222) under cerebral protection were analyzed in two groups according to age: under 80 (n = 1078) and 80 and older (n = 144). The 30-day stroke and death rate was 2.12% in the older group and 1.11% in the younger
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Carotid angioplasty and stenting under protection: techniques, indications, results, and limitations group, so CAS with protection has proven to be safe and effective in elderly patients. The same conclusions were drawn by Roubin et al. 26 Several registries were recently reported concerning high-surgical-risk patients.68, 69,72−75 Table 35.8 summarizes the 30-day stroke/death/myocardial infarction rate obtained with different protection devices and stents. All these published series, as well as our personal data, show favorable results at least equal if not better than the results of historical surgical controls. These favorable results were recently confirmed by a meta-analysis done by Burton et al.,163 including 26 studies (2992 patients treated by CAS under protection). Within this patient group, the pooled peri-operative rate of any type of stroke was 2.4 ± 0.3%. The 30-day minor stroke rate was 1.1 ± 0.2%, the 30-day major stroke rate 0.6 ± 0.2%, and the 30-day mortality rate 0.9 ± 0.4%. These studies have provided considerable evidence that the use of an embolic protection device has dramatically lowered the incidence of cerebral embolic events during CAS in both symptomatic and asymptomatic patients and has become an integral part of CAS. Although the benefits of routine use of cerebral protection have not been confirmed by level 1 evidence, a consensus supports such use.164 However, cerebral protection cannot prevent all plaque debris migration and embolic events that may occur at all steps of the procedure. Mathias et al.39 studied 70 carotid angioplasties without protection and 102 carotid angioplasties with protection, by TCD monitoring during the procedure and MRI of the brain before and 24 hours after CAS. By TCD the number of high-intensity transient signals (HITS) for the patient was calculated during the different steps of carotid angioplasty. HITS were registered even with protection, but the number of HITS was much greater without protection, and the most critical steps for brain embolism are predilatation, stent placement, and in-stent dilatation. By MRI it was noted that new signalintense lesions were more frequent with unprotected angioplasties (28.5 vs. 8.2%). This study showed that cerebral protection reduced the rate of neurological complications during CAS by 60% (3.5 vs. 1.3%). No major strokes occurred after cerebral protection. Al-Mubarak et al. published similar results 38 with a greater number of emboli in the control groups of patients treated without protection. Schluter et al.165 studied 21 patients by DW-MRI before and within 24 hours after elective CAS. They found no sign of cerebral ischemia before the procedure, but new ischemic foci in five patients (23.8%) with no clinical signs. The etiology of this silent focal cerebral ischemia remains to be established and there seems to be no link with the type of protection system used. Recently, Flach et al.79 reported a prospective study using DW-MRI before and after carotid intervention. They found new hyperintense lesions in 43% of CAS cases, but only in 9% of CEA cases. The majority of the detected lesions did not cause neurological deficit. However we do not know exactly the clinical importance of these new DW-MRI lesions, if they could damage the brain or cause neuropsychological deterioration. These silent brain infarcts could be associated with cognitive dysfunction, increased frequency of dementia, or neuropsychomatic changes.144 Some other concerns should be pointed out with the current embolic protection devices. Vos78 recently published interesting data showing that the role of some filters is not clear and
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is associated with potential problems. Using TCD during 151 protected CAS with filters and 197 unprotected ones, he reported a higher number of microemboli during filterprotected CAS, but the number of particulate macroemboli was higher in the unprotected group. Distal thrombus formation occurred only in patients with filter protection. Another important problem is the delayed embolic events. Cerebral protection cannot prevent late embolic phenomena: 30% of TIAs occurred between 2 and 10 days after the procedure, while 30% of minor strokes occurred 4−10 days after stent placement.27 These late TIAs and minor strokes may have been related to dislodged plaque and/or thrombus from between the stent struts or adjacent to the stent. To avoid these delayed complications, we think that a meticulous cleaning of the dilated area and inside the stent must be done after stent implantation and dilatation. Aspiration of the debris remaining through the struts may be performed with an aspiration catheter or the guiding catheter or long sheath in all patients, or at least in all symptomatic patients or patients with high-embolic-risk plaque. The new embolic protection device FiberNet we have experimented on could overcome most of these problems, due to the possibility of capture debris of 30−40 µm, the possibility of suction delivered through the retrieval catheter allowing a meticulous cleaning of the dilated area and of the inner part of the stent. This technique explains the absence of modifications of CT/MRI at 30-day follow-up in our series and the absence of delayed neurological complications. Cerebral protection cannot prevent brain hemorrhage, which may occur after the procedure and is encountered in most of the published series. Most of the time, this is a catastrophic event with poor prognosis, which can appear despite blood pressure control and can be due to cerebral hyperperfusion following successful CAS. This syndrome is thought to be a failure of normal cerebral autoregulation of blood flow secondary to longstanding decrease perfusion pressure.163 Several factors may favor the hyperperfusion syndrome: severe ipsilateral stenosis ≥ 90%, impaired collateral blood flow secondary to advanced occlusive disease in other extracranial cerebral vessels or an incomplete circle of Willis, peri-operative hypertension, and the use of antiplatelet agents or other type of anticoagulation.27 Fibrinolytic agents may promote a brain hemorrhage. Despite their marginal success (in about 40% of the cases) they are the appropriate treatment in catastrophic events with angiographic evidence of occlusion,27 which are generally due to large, plaquelike emboli. These plaques are not effectively dissolved by thrombolytic agents, which reinforce the need for distal protection during carotid stenting. With the use of protection devices, the indications for glycoprotein IIb/IIIa inhibitors are very limited. The long-term results of CAS have to be discussed but do not depend on the use or not of cerebral protection device. The restenosis rate after CAS and after surgery seems comparable (3−6%). However only 3% of the restenoses require a second intervention. The CAVATAS trial compared the results of CEA to endovascular treatment after 3 years. The death or disabling stroke rate in any territory after 3 years is 14.3% in endovascular groups and 14.2% in the surgical groups. So angioplasty and CEA are comparable concerning long-term results. The SAPPHIRE study showed better results for CAS than for CEA at 2 years follow-up, especially in diabetic patients.63,64
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In the world registry,55 Wholey et al. reported a rate of neurological events including TIA, stroke, and neurologicalrelated death of 2.8% during the 6−12 months follow-up period, and 4.5% at 4-year follow-up. The neurological event rate was 1.36, 1.3, and 1.72% at 1, 2, and 3-year follow-up, respectively. In their report of 513 patients Wholey et al.166 described a 3-year freedom from all fatal and ipsilateral non fatal strokes excluding the 30-day peri-procedural period of 95% for balloon mounted stents and 95.2% for self-expendable stents during a mean follow-up of 20.6 months. Roubin et al.26 reported a 3-year freedom from all fatal and non fatal strokes of 88 ± 2% and taking into account only these patients who survived the 30-day peri-procedural period, a 3-year freedom of 95 ± 2%. During follow-up, 3.2% of the patients developed a stroke. Recent publications confirm that long-term results of CAS are competitive with surgery. Bergeron et al.167 reported a series of 193 patients (221 CAS) and found at 10 years a 96% rate for stroke freedom, a 98% rate for fatal stroke freedom, and a primary assisted patency rate of 95%. Sugita et al.168 reported the ELOCAS registry, in which 2172 patients were selected over four high-volume centers. The stroke/death rate was 4.1, 10.1, and 15.5% and the restenosis rate 1, 2, and 3.4% after 1, 3, and 5 years respectively. All these recent data showed that the long-term results of CAS are excellent and at least comparable to surgery.
Conclusion: indications for cerebral protection devices Although cerebral protection devices cannot prevent all neurological events, the majority of series published recently have shown a large reduction (at least 60%) in the neurological complication rate with these devices, with few or no major strokes in most of the studies. Embolization occurs during all procedures. Protection devices are indispensable in performing CAS and should be routinely used. CAS under protection seems to be the standard of care and is maybe becoming the gold standard treatment for a carotid stenosis, at least in some subgroups of patients. Indications for symptomatic and high-risk patients are well accepted. Indications for asymptomatic and low-risk patients are more discussed, but a lot of published data show comparable results if not better with angioplasty than with surgery in these patients. Some improvements have to be done. The best protection device and the best stent have yet to be determined. New protection devices currently in experiment seem promising. Randomized studies comparing all devices are needed to define the best system for the patient and/or the lesion. One remaining problem with these devices is their high cost. CAS is a safe procedure giving excellent short-term and long-term results comparable to surgery.
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Complications of internal carotid artery stenting and their management DL Surdell, ZA Hage, CS Eddleman, S Das, E Duckworth, MK Eskandari, IA Awad, HH Batjer, and BR Bendok
Introduction Stroke is the leading cause of disability in adults in the US and the third leading cause of death after cardiovascular disease and cancer.1 Atherosclerotic stenosis of the carotid artery near the bifurcation causes 20% of all ischemic strokes and transient ischemic attacks.2 Carotid endarterectomy (CEA) reduces stroke risk in select patients with both symptomatic and asymptomatic extracranial carotid artery stenosis.1 Four randomized trials: the North American Symptomatic Carotid Endarterectomy Trial (NASCET), the European Carotid Surgery Trial (ECST), the Asymptomatic Carotid Atherosclerosis Study (ACAS), and the European Asymptomatic Carotid Surgery Trial (ACST) have demonstrated the additional benefit of CEA over medical therapy for select patients.1 NASCET demonstrated that, among symptomatic patients with high-grade stenosis (70–99%), those who underwent carotid endarterectomy had an absolute reduction of 17% in ipsilateral stroke at two years.3 ACAS demonstrated a statistically significant difference in the estimated 5-year ipsilateral stroke rate of 5.1% for the surgical group versus 11.0% for the medical group.4 ACST showed that for patients up to 75 years of age with severe carotid stenosis, CEA halved their net 5-year risk of stroke.5 ECST showed a benefit to surgery for symptomatic carotid stenosis above 70–79%.6 However, many patients at considerable risk of stroke were excluded from receiving surgical therapy because of stringent eligibility requirements.1 Certain medical co-morbidities place these patients at higher risk and include: history of myocardial infarction within 20 days, unstable angina with EKG changes, angina with two-vessel coronary artery disease, NYHA class III–IV congestive heart failure, ejection fraction less than 30%, heart or vascular surgery required within 30 days, COPD with less than 30% predicted FEV in 1 second, and age greater than 75 years.1 Anatomic considerations placing patients at higher risk for surgical treatment include: high cervical or intrathoracic stenosis, prior ipsilateral CEA, history of radical neck dissection or irradiation, bilateral carotid stenosis, contralateral occlusion, contralateral cranial nerve palsy after CEA, cervical spine immobility, crescendo or recent TIA, tandem stenoses, intracranial hypo-perfusion, and tracheostomy.1 In these patients, the risk of surgery may outweigh the benefits of CEA (Table 36.1). 336
More recently, carotid artery angioplasty and stenting (CAS) has emerged as an alternate treatment for carotid occlusive disease. A randomized study of patients considered at high surgical risk showed it was not inferior to CEA.7 CAS is currently being evaluated for symptomatic patients with ≥ 50% stenosis or asymptomatic patients with ≥ 80% stenosis with risk factors placing them at high risk. The general indications for CAS are: ●
● ● ●
high-risk surgical candidates requiring carotid revascularization; symptomatic patients with ≥ 50% stenosis; asymptomatic patients with ≥ 80% stenosis; reference diameter of target vessel 4–5 to 9 mm, depending on the stent.
With continuing improvements in stent technology, pretreatment medication, and proper patient selection, CAS will likely be used increasingly in both primary and secondary treatment of carotid occlusive disease to prevent stroke. Due to the success of CEA for treating both symptomatic and asymptomatic carotid disease, care must be taken when utilizing new technology such as CAS. Ideally, patients should not be exposed to an intervention that has more risk than the natural history of the disease itself, or than alternate treatments such as medical or open surgical management. It is important for anyone performing CAS or caring for a patient who had CAS to know the possible complications of CAS and employ strategies to avoid complications, thereby minimizing patient risk and improving patient outcome.
Complications reported in registries and trials CAS has emerged as a viable treatment alternative for carotid stenosis in patients who are poor candidates for carotid endarterectomy.8 This has been demonstrated by trials such as ACCULINK for Revascularization of the Carotids in HighRisk Patients (ARCHER), Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE), Evaluation of the Medtronic AVE SelfExpandable Carotid Stent System with Distal Protection in the
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Complications of internal carotid artery stenting and their management Table 36.1
Factors generally considered high risk
Medical Myocardial infarction within 20 days Unstable angina with EKG changes Angina with two vessel coronary disease NYHA class III–IV CHF EF less than 30% Heart or vascular surgery required within 30 days COPD with less than 30% predicted FEV Anatomic High cervical or intrathoracic stenosis Previous ipsilateral CEA History of radical neck dissection or radiation Bilateral carotid stenosis Contralateral occlusion Contralateral CN palsy after previous CEA Cervical spine immobility Crescendo or recent TIA Tandem stenosis Intracranial hypoperfusion or tracheostomy
Treatment of Carotid Stenosis (MAVERIC), Carotid Artery Revascularization Using the Boston Scientific Filter Wire EX/EZ and the Endo Tex Nex Stent Trial (CABERNET), and the Registry Study to Evaluate the Neuroshield Bare Wire Cerebral Protection System and X-Act Stent in Patients at High Risk for Carotid Endarterectomy (SECURITY).8 The ARCHER trial studied the ACCULINK carotid stent and the ACCUNET embolic protection device. It involved a sequential series of three prospective, non-randomized, multi-center registries enrolling 581 patients from May 2000 to September 2003. The patients were pretreated with 325 mg aspirin twice a day and 75 mg clopidogrel or 250 mg ticlopidine twice a day for 48 hours before the procedure, or loaded with 650 mg aspirin and 450 m clopidogrel at least 4 hours before the stenting. The patients were required to take 325 mg aspirin daily for a year and either 75 mg clopidogrel daily or 250 mg ticlopidine daily for a minimum of 2 weeks. The primary endpoint was a composite of all deaths, strokes, and nonfatal myocardial infarctions within 30 days. In addition, the trial recorded ipsilateral strokes between 31 and 365 days. Only 24% of the trial population had symptomatic carotid disease. The trial found a 15/581 (2.6%) access site event rate (12 required blood transfusion and 4 required surgical repair).9 In addition, there were five device placement complications involving failure to retrieve the filter device. Three were retrieved via endovascular means, one was sandwiched against the original stent with a second stent, and one was retrieved surgically. There were no neurological sequelae from these events. Primary endpoint outcome was 9.6% compared to a historical control rate of 14.4% in high-risk surgical patients, leading to the establishment of non-inferiority between CAS using ACCULINK/ACCUNET and CEA. Further breakdown of the complications showed the 30-day combined safety endpoint of death, stroke, or myocardial infarction to be 8.3%; and the 30-day rates for symptomatic and asymptomatic patients were 13.1 and 6.8%, respectively. Minor stroke accounted for 23/32 neurologic events (4.0%), with myocardial infarction and death accounting for 2.4 and
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2.1%, respectively. At 30 days, the rate of major or fatal stroke was 1.5%.9 The rate of ipsilateral stroke between 31 and 365 days was 1.3%. In addition, 5% of patients at 12 months had significant restenosis (> 70%). Ninety-five percent of the patients who sustained a minor peri-procedural stroke did not have deficits at 1 year. They concluded that CAS in highsurgical-risk patients is safe and may be considered to be an effective alternative to CEA.9 The SAPPHIRE7 trial was a randomized trial directly comparing CAS with a distal protection device to CEA. Both the CAS and CEA groups were treated with 81–325 mg aspirin daily, starting at least 72 hours prior to the procedure, and during the procedure the patients were treated with heparin to achieve an ACT of 250–300 seconds. Patients undergoing stent placement were also treated with 75 mg clopidogrel daily, starting 24 hours before and continuing for 2–4 weeks after stenting. The primary endpoints of death, stroke, or myocardial infarction within 30 days of the procedure, or death or ipsilateral stroke between 31 and 365 days, were evaluated. The study enrolled patients between August 2000 and July 2002, and 334 patients underwent randomization. Of those assigned to the CEA group, 151/167 received the treatment, and of those assigned to the CAS group, 159/167 received the treatment. The primary endpoint occurred in 20 of the 167 patients randomly assigned to stenting (12.2%) and in 32 of the patients randomly assigned to surgery (20.1%). This trial showed that CAS was not inferior to CEA in high-risk surgical patients. The 30-day cumulative incidence of stroke, myocardial infarction, or death was 4.8% for those receiving CAS versus 9.8% for CEA. There were no cranial nerve palsies at 1 year in the CAS group, compared to 4.9% in the CEA group. The estimated rate of target-vessel revascularization was 0.6% for CAS versus 4.3% for CEA. The trial investigators further broke down the data for symptomatic carotid artery stenosis. The cumulative incidence of primary endpoint at 1 year was 16.8% for CAS versus 16.5% for CEA, with post-procedural period cumulative incidence of primary endpoint at 30 days among these patients of 2.1% for CAS and 9.3% for CEA. For patients with asymptomatic carotid artery stenosis, the cumulative incidence of primary endpoint at 1 year was 9.9% for CAS and 21.5% for CEA. The peri-procedural cumulative incidence of death, myocardial infarction, or stroke was 5.4% for CAS and 10.2% for CEA. The authors therefore concluded that CAS with a distal embolic protection device (Angioguard) was not inferior to CEA for high-risk surgical patients.7 The Carotid Artery Revascularization Using the Boston Scientific Filter Wire and the Endo Tex Nex Stent (CABERNET) trial looked at symptomatic patients with greater than or equal to 50% stenosis by ultrasound or angiogram and asymptomatic patients with stenosis of greater than or equal to 80% by ultrasound and 60% by angiogram. They found a 30-day composite major adverse event rate for CAS, defined as stroke, death, or myocardial infarction, of 3.8% (death 0.5%, stroke 3.4%, and myocardial infarction 0.2%).10 The Carotid Revascularization Using Endarterectomy or Stenting Systems (CaRESS) trial was a multicenter, prospective, non-randomized equivalence cohort study designed to assess the safety and effectiveness of CAS with embolic protection compared with CEA in a broad risk population with symptomatic and asymptomatic carotid stenosis.8 The primary endpoint of
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the phase I trial was mortality of any cause or stroke within 30 days and 1 year of the procedure. The secondary endpoints included a composite of 30-day all-cause mortality, stroke, or myocardial infarction and 1-year all-cause mortality or stroke, residual stenosis (more than 50% in the target lesion after the index study procedure), restenosis (75% narrowing documented by ultrasonography or symptomatic narrowing greater than 50% that required secondary treatment), repeat angiography and carotid revascularization at 30 days and 1 year, and quality of life changes at 1 year. Three hundred and ninety seven patients (254 CEA (33% symptomatic/87% high risk) and 143 CAS (31% symptomatic/84% high-risk) were enrolled. The primary endpoints of all-cause mortality or stroke at 1 year demonstrated no statistically significant differences between CEA and CAS, although CAS primary endpoints were consistently lower. The 30-day stroke rate was 3.6% for CEA and 2.1% for CAS, and the 1-year stroke rate was 9.8% for CEA and 5.5% for CAS. The death rate remained comparable at 30 days (0.4% for CEA and 0.0% for CAS) and 1 year (6.6% for CEA and 6.3% for CAS). None of the results were significant; however, seven cases of myocardial infarction were observed (five (2.4%) in the CEA group and two (1.7%) in the CAS group) with two of the five in the CEA group occurring within 30 days of the procedure. Secondary endpoint outcome showed that the CAS group had higher rates of residual stenosis (0.9% CAS vs. 0.0% CEA), restenosis (6.3% CAS vs. 3.6% CEA), repeat angiogram (3.6% CAS vs. 2.1% CEA), and carotid revascularization (1.8% CAS vs. 1.0% CEA), but none were statistically significant. The trial investigators concluded that this phase I study suggests that the risk of death or stroke 1 year after CAS using distal protection is equivalent to that of CEA in a broad population with carotid stenosis.8 For a summarized list of peri-procedural and post-procedural complications, please refer to Table 36.2.
Complication avoidance Preprocedural complication avoidance Patient selection for CAS versus CEA is the first step to provide patients with effective treatment to prevent stroke. Narnis and Illig reported that relative to CEA, the results of CAS seem favorable in patients with certain anatomic considerations that make surgery more difficult, such as restenosis after prior endarterectomy, prior radical neck surgery, or previous radiation therapy involving the neck.11 The results of stenting are
Table 36.2
CAS complications
Intraprocedural complications ●
●
● ●
Bleeding from access site (requiring blood transfusion or surgical repair) Device placement complications: failure to retrieve filter device Stroke Myocardial Infarction
Post-procedural complications ●
● ●
● ●
Myocardial Infarction Stroke Residual stenosis Restenosis Death
also favorable in patients with severe concomitant cardiac disease. As demonstrated by multiple clinical studies, CAS may be considered as a safe and effective mechanism for stroke prevention in patients who are considered to be poor candidates for CEA. Patients selected to undergo CAS need baseline EKG, Chem 7, PT, INR, PTT, and CBC. Another issue to be considered is the appropriate timing to perform CAS or CEA after a TIA or stroke has occurred. When considering timing of CEA after an ischemic event, this decision remains controversial as some authors recommend waiting at least 4 weeks, while others perform the procedure at an earlier time. Rockman et al. reported their experience on 1046 non-urgent CEA cases and found that those that were operated on earlier than 4 weeks after a TIA or stroke had a significantly higher rate of peri-operative stroke when compared to CEA performed after 4 weeks (5.1 vs. 1.6%, p = 0.004). The authors concluded that a 4-week waiting period is recommended for patients undergoing CEA for stroke management.12 On the other hand, in their thorough review of the literature, Baron et al. conclude that the current evidence supports the safety of using CEA earlier than 4–6 weeks in patients with mild to moderate ischemic deficits. This, however, remains a controversial area when tackling crescendo TIAs. The timing of CEA was also assessed for other types of stroke.13 In a different study, Kastrup et al. evaluated the risk factors for recurrent ischemia in patients waiting to have CAS for symptomatic carotid stenosis. The authors found that the risk of early recurrent ischemia was highest in patients who experienced motor symptoms and in those that had a contralateral carotid occlusion. The authors advocated the prompt use of CAS in these high-risk patients.14 While timing of CEA for management of stroke patients has been well studied, data regarding timing of CAS remains scarce, and further studies are surely warranted. At our center, we favor early intervention (within several days) when the presentation is a TIA or minor stroke. If there is a large stroke on the CT scan, particularly with mass effect, we prefer to wait several weeks. Hemorrhagic conversion of a stroke is also grounds for waiting. The distinction between “minor” and “major” stroke is not clearly defined in the literature in this context. “Clinical judgment” is needed in the absence of clearer guidelines. Stroke is one of the major complications of CAS. Steps to prevent this complication are taken long before the patient undergoes the procedure. The patient is started on a dual regimen of anti-platelet agents. Bhatt et al. found that dual antiplatelet therapy with clopidogrel plus aspirin in patients undergoing CAS is associated with a low rate of ischemic events, and that clopidogrel (Plavix) appears superior to ticlopidine.15 Five days prior to the procedure, the patient is started on 75 mg clopidogrel daily and 81 mg aspirin daily. During the procedure, the patient is heparinized to achieve an ACT of 250–350 seconds to prevent thrombus forming on the catheters or wires during the procedure. Alternatively, patients can be treated with 0.75 mg/kg IV bolus bivalirudin (Angiomax, The Medicines Company, Parsippany, NJ) followed by 2.5 mg/kg/hour IV infusion during the procedure in addition to the dual antiplatelet regimen.16 Nonetheless, the use of antiplatelet therapy is not without complications, and drawbacks include prolonged bleeding from hematoma formation at the access site, intracerebral hemorrhage, thrombocytopenia, and genitourinary and gastrointestinal complications.17,18
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Complications of internal carotid artery stenting and their management Intraprocedural complication avoidance Despite these prophylactic measures, stroke can still occur intraprocedurally, even with a distal protection device in place. Some authors recommend intraoperative monitoring using transcranial Doppler ultrasonography, which can detect microemboli.19 Others report using intravascular ultrasound in association with specialized virtual histology software to identify, preprocedurally, lesions at high risk for embolizations and also to detect emboli during the actual procedure.20 It is critical to management of distal emboli that the practitioner understands the anatomy of the particular vessel being treated and the territory of the brain at risk of stroke. This guides the management. In general, in patients with distal embolus with an obvious vessel occlusion, we consider the use of low-dose abciximab (1–5 mg IA) or low-dose tPA (5–10 mg IA) via a microcatheter as close to the lesion as can be safely achieved. For “large vessel” occlusion, another option is mechanical thrombolectomy with the MERCI (Concentric Medical Inc., Mountain View, CA). Recent results from the MERCI and Multi MERCI trials suggest that a high recanalization rate of the intracranial internal carotid artery (53% with MERCI alone and 63% with MERCI and adjunct endovascular treatment) led to improved post-stroke clinical outcome.21 These are off-label application uses of FDA-approved drugs and devices. Other maneuvers performed to open an occluded intracranial vessel include angioplasty and snare maneuvers.22,23 Stenting has also been used for refractory cases.24 Whether to intervene pharmacologically and/or interventionally in the setting of intraprocedural thromboembolism depends on a clear understanding and assessment of the clinical exam, the particular vessel which may be occluded, and the ability of the operator to handle intracranial thrombolysis. It is recommended that a neurointerventional specialist be involved for such management. In patients with intraprocedural stroke, a post-procedure CT of the head should be obtained to rule out hemorrhage. An MRI will assess the extent of stroke. We recommend that a vascular neurologist and/or neurosurgeon be consulted. The patient is monitored in the ICU and often treated with mild hypertension and slight hypervolemia to improve perfusion. It is our preference to perform CAS with the help of an anesthesiologist. The main role of anesthesia is to monitor and treat hemodynamic alterations. We have found this to be valuable in many regards. Patients feel more comfortable knowing a physician is closely monitoring them while the procedure is being performed. We place an arterial line prior to the procedure, and thus the anesthesiologist is able to closely monitor the patient’s hemodynamic status during CAS and treat appropriately, such as prompt initiation of pressors for hypotension or atropine for bradycardia. Prior to starting the procedure, we administer antibiotics, typically cefazolin (1 g IV) or clindamycin (900 mg IV) if penicillin-allergic. A standard time-out procedure is performed to discuss the procedure with those involved and answer any final questions. We localize the access site by placing a needle driver over the lower third of the femoral head and confirm it radiographically (Figure 36.1). We start with a 5-French 25-cm sheath; once the sheath is in place, the patient is heparinized to achieve an ACT of 300–350 seconds. All catheters are connected to heparinized saline flush (2000 units/1 liter bag)
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Figure 36.1 An instrument located over the lower third of the femoral head is used to localize an entry point below the inguinal ligament.
at the rate of one drip/second. We use a 5-French catheter and a 0.035-inch wire to image the common carotid artery and the bifurcation. We then measure the stenosis and the internal carotid artery beyond the stenosis (Figure 36.2). Here we take care not to bring the wire through the stenotic portion of the carotid artery. All devices to be utilized are prepared and organized in order of use so that the CAS is done in a careful and efficient manner. Using a road map, we navigate a diagnostic catheter to the external carotid, and an exchange length wire is placed through the catheter into the external carotid artery. We make sure the wire remains in a large branch of the external carotid on the road map to avoid perforation of the artery. We then remove the catheter and short access sheath and place a 6-French sheath, which is attached to heparin flush through a rotating hemostatic valve (RHV), into the common carotid artery below the stenosis. The introducer and wire are removed and allowed to back-bleed approximately 20 cm3. It is critical to avoid placing the sheath too close to the lesion. Simultaneous AP and lateral fluoroscopy can be very helpful in sheath placement. The first step in CAS is placement of the embolic protection device (EPD) (Figure 36.3). EPDs have proven to be valuable in protecting against procedure-related thromboembolic events.25 (Of note, only distal filters have a labeled use for CAS.) Careful technique is needed to avoid negating the benefits of distal protection. It is important to size the device carefully. Oversizing can result in dissections or vasospasm, and undersizing may decrease the efficiency of capturing the emboli and debris. It is important that the filter be below the base of the skull. We typically place the filter at the level of C1. It is also important to keep the filter beyond the lesion and the stent landing zone to avoid trapping the filter. Also, we make sure the EPD moves minimally during the procedure.
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Figure 36.2 Carotid artery angiogram and measurements for carotid artery stenosis.
Figure 36.3 Placement of EPD below the skull base above the lesion (arrow).
In their review of 2357 cases of CAS without EPD versus 896 cases of CAS with EPD, Kasturp et al. reported a 30-day cumulative death and stroke rate of 5.5 versus 1.8%.25 This appeared to be due to a decrease in minor and major stroke through the use of EPD.25 In their series of 442 patients treated with carotid angioplasty and/or stent with EPD, Cremonesi et al. found a protection device-related complication rate of 0.9%: one case of abrupt closure of the internal carotid artery because of dissection (0.2%), one case of a trapped guidewire (0.2%), and two cases of intimal dissection (0.5%).26 Transient loss of consciousness, tremors, and fasciculations were present in 6 of 40 patients (15%) where occlusive protection devices were used. Of note, the authors found macroscopic debris in the protection device in 69% of cases. None of the patients in the Cremonesi series had any long-term detrimental events from the EPD-related complications. The patient with the spiral dissection had an occluded carotid and good collateral flow, and tolerated the injury clinically. The patient with the trapped guidewire underwent surgery for removal of the device without incident. The patients with intimal dissections were treated with further stenting. This is necessary in patients with flow-limiting lesions. Cremonesi et al. also reported transient spasm in 7.9% of patients treated with an EPD, all managed with intra-arterial nitroglycerin with resolution in all cases.26 Another potential complication that has been reported is blood flow interruption due to occlusion of the filter pores by the embolic material.27 If there is difficulty removing the EPD through the stent at the end of the CAS procedure, the guide catheter or sheath can carefully be brought through the stent to in-sheath the distal protection device; the catheter and EPD are then removed as a unit. Two other methods of protection systems that can be used during CAS are distal occlusive balloons and proximal occlusive balloons.27 In the first method, a balloon is inflated distal to the carotid stenosis until blood flow is totally interrupted, and CAS is performed. Following the procedure, the column of blood in the occluded arterial segment is aspirated by a catheter, along with any floating debris, and the balloon is then deflated. The disadvantages are that 6–10% of patients do not tolerate the occlusion, and it is not possible to image the vessel with contrast injection during balloon inflation.27 The second method involves the inflation of a balloon in the internal carotid artery (ICA), proximal to the lesion. A second balloon is then inflated in the external carotid artery, thus allowing for back-pressure through the collateral flow of the circle of Willis and preventing antegrade flow in the ICA. Again, following CAS and before both balloons are deflated, the blood in the ICA with potential debris is aspirated. Nevertheless, this procedure is not always tolerated (Table 36.3).27 It is important to size the stents accurately. Oversizing could risk in-stent stenosis and vessel tear. Undersizing could risk stent migration. Each stent system has different “guidelines” for stent sizing, and the operator is encouraged to refer to the “information for use” document for specific guidelines. After the EPD is in place, pre-stent angioplasty is performed (Figure 36.5). To prevent complications of thromboembolism or post-in-stent restenosis, we prefer pre-stent angioplasty with a 3–4 × 30 mm balloon. A longer balloon is used to cover the entire length of the plaque, thereby pushing the plaque against the walls. We prefer a longer balloon to avoid the risk of forcing plaque to embolize forward, or
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Complications of internal carotid artery stenting and their management Table 36.3
CAS protection systems and some of their potential complications
Embolic protection device (filter) ● ● ● ●
Arterial dissection Trapped guidewire Vasospasm Flow interruption through the filter due to occlusion of pores by embolic material
Distal occlusive balloons ●
ICA occlusion not tolerated
●
●
Procedure not tolerated Vasospasm
Vasospasm
Immediate post-procedural complication avoidance We angiogram the head and neck post-procedure to rule out vasospasm, which we would consider treating with vasodilators; clot on stent, which we would consider treating with ReoPro (abciximab, Eli Lilly Cooperation); dissection, which we would consider treating with heparin and coumadin versus further stent and antiplatelet agents; and distal embolization, which we would consider treating with thrombolytics versus mechanical thrombectomy, as described previously (Figure 36.6). Angioplasty and placement of a carotid stent are associated with hemodynamic effects, including hypertension, hypotension, and bradycardia. Transient bradycardia and lowering of the systolic blood pressure were seen in one study in 5–10% of cases of CAS despite prophylaxis with atropine.28 In a series by Yadav, 71% of 107 patients were reported to have bradycardia,
Figure 36.4
Proximal occlusive balloons ●
“watermelon seeding.” Following CAS, we typically use a smaller 4–5 × 20 mm diameter balloon and choose a length that does not go beyond the length of the stent placed. This decreases the possibility of adjacent re-stenosis. The majority of stents are 30–40 mm in length and consequently routinely jail the ECA.
(a)
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with one requiring permanent pacemaker.29 Pappada et al. reported in their review of 51 cases that post-procedural hypertension occurred in 10% of cases.30 They report that hypotension and bradycardia occurred in 10% of cases and that transient peri-procedural bradycardia was seen in 19 cases or 37%, with only one patient having severe bradycardia without hypotension.30 For these reasons, we recommend aggressive correction of hemodynamic issues intraprocedurally. Having an A-line and adequate access makes this more readily feasible. We usually recommend 12–24 hours of ICU monitoring for these issues. It is important to adjust antihypertensive therapies post-procedurally since the angioplasty may alter the baroreceptors. We typically consult with the patient’s internist in this regard. Persistent hypotension may also be a sign of an access site complication (i.e. retroperitoneal hematoma). CAS is also associated with the risk of hyperperfusion syndrome, which was initially described following CEA. This clinical syndrome involves atypical migraines, transient focal seizure activity, and intracerebral hemorrhage.31 The risk of death seems especially high when associated with intracerebral hemorrhage. In their study regarding hyperperfusion syndrome, Coutts et al. reported on 129 consecutive CEA cases and 44 consecutive CAS cases. Hyperperfusion syndrome was
(b) EPD in place to prevent emboli during carotid artery stent placement: (a) AP view; and (b) lateral view.
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(a) Figure 36.5
(b) Pre-stent angioplasty (arrow) with EPD in place: (a) AP view; and (b) lateral view.
described in 3.1% of CEA cases and in 6.8% of CAS cases. They proposed a redefinition of this syndrome as a hemispheric neurologic deficit or seizure following revascularization, ipsilateral to the treated vessel, with no association to thromboembolism and no evidence of new infarction on MRI. Furthermore, perfusion MRI or CT scans should note the presence of hyperperfusion in the ipsilateral hemisphere.31 The pathophysiology behind this syndrome is still poorly understood. Nonetheless, it is thought that hyperperfusion syndrome is caused by abnormal autoregulation of cerebral blood flow following long-standing hypoperfusion through
Figure 36.6
Final lateral image post-stenting.
the diseased ICA. A reaction to this hypoperfusion is maximal dilation of the cerebral arterioles, which do not constrict adequately after normal perfusion is restored.17,31 A possible role for calcitonin gene-related peptide (CGRP), substance P, and neurokinin A as mediators of vasodilation has been proposed.17 Risk factors for hyperperfusion syndrome include severe carotid stenosis, bilateral stenosis, previous stroke, peri-procedural hypertension, and poor collateral blood supply.31 The treatment is usually empirical and often includes aggressive blood pressure control.31 This is another reason for proactive monitoring and management of patient hemodynamics intraprocedurally and post-procedurally. Following the procedure, the patient is taken to the ICU and monitored closely. Each patient has a post-procedure EKG, cardiac enzymes, CBC, Chem 7, PT, PTT, and INR. Patients are treated for hypertension, if needed. The femoral artery access site is checked regularly as well as distal pulses. Delayed complication avoidance In-stent stenosis is one long-term complication of CAS.32 In-stent restenosis is defined as a greater or equal to 50% increase in narrowing of the lumen within the stent compared to the immediate post-treatment lumen diameter.32 The incidence of in-stent stenosis is considered to be 5%33 to 16%.34 Patients who are asymptomatic with ≥ 80% in-stent stenosis or those with symptoms and ≥ 50% stenosis are recommended for treatment.32 Currently, in-stent stenosis is treated with angioplasty.35 There have been publications supporting cutting balloon angioplasty for the treatment of restenosis after CAS,32 and it appears that the incisions made by the cutting balloon cause less trauma to the vessel wall during dilation and lessen elastic recoil that can be seen in lesions with fibrotic plaque.36 Zhou et al. reviewed 208 CAS procedures in patients with carotid stenosis ≥ 80%.34 Over a 17-month follow-up period, 33 (15.9%) in-stent restenosis
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Complications of internal carotid artery stenting and their management (ISR) of 60% or greater was found, by Doppler criteria. Among them, seven patients (3.4%) developed high-grade ISR (≥ 80%) and required further endovascular interventions. Six of the seven patients with high-grade restenosis were asymptomatic, whereas one patient presented with a transient ischemic attack. Five of seven cases of ISR occurred within 12 months of CAS, and two occurred at 18 months follow-up. Treatment indications for initial CAS in these seven patients included recurrent stenosis after CEA (n = 4), radiation-induced stenosis (n = 1), and high-cardiac-risk criteria (n = 2). Treatment modalities for ISR included balloon angioplasty alone (n = 1), cutting balloon angioplasty alone (n = 4), cutting balloon angioplasty with stent placement (n = 1), and balloon angioplasty with stent placement (n = 1). Technical success was achieved in all patients with no complications. Two patients with post-CEA restenosis developed restenosis after ISR interventions, both of whom were successfully treated with cutting balloon angioplasty at 6 and 8 months. The remaining five patients showed an absence of recurrent stenosis or symptoms during a mean follow-up of 12 months (range: 3–37 months).34 It is important that patients with COD have modifiable risk factors for atherosclerosis treated. These include tight control of hypertension and diabetes. Often these patients need to be on medication to manage cholesterol. Additionally, it is important to encourage patients to stop smoking. These patients need to be followed closely by their primary physicians to reduce the progression of their atherosclerotic disease. For a summary of complication avoidance, please refer to Table 36.4.
Table 36.4
Complication avoidance (our strategy)
Pre-op Internal medicine/cardiology evaluation Evaluate/treat modifiable risk factors for atherosclerosis Pre-medicate with 5 days of aspirin and clopidogrel Obtain baseline EKG, Chem 7, CBC, PT, PTT, INR Confirm devices available Pre-op antibiotics given Intra-op “Time-out” procedure Consider anesthesiology for close hemodynamic monitoring Check lines for bubbles Connect sheath and catheters to heparinized saline flush Localize femoral head Heparinize (ACT 250–350 seconds) once sheath placed Do not pass wires through stenosis until ready to place EPD Use EPD whenever possible Keep EPD below the skull base and immobile Sheath kept below stenosis, allowing room for stent Use 3–4-mm × 30-mm balloon for pre-stent angioplasty Stent: cover lesion (we routinely go into common) Use a 5–6mm × 20-mm diameter balloon for post-stent angioplasty Post-stent angioplasty balloon length less than the stent length Do not trap EPD Post-op Admit to ICU and control blood pressure Chem 7, CBC, PT, PTT, INR, EKG, cardiac enzymes Continue aspirin and plavix Evaluate for restenosis at 1-month, 6-months, and yearly Follow-up with PCP for medical TX of atherosclerosis risk factors
Conclusion CAS has emerged as a treatment option for stroke prevention for high-risk surgical candidates, and is being evaluated currently as a primary treatment for symptomatic and asymptomatic patients with COD. Complication avoidance is critical because patients need to be offered low-risk procedures that do not exceed the risk of medical management or open surgical therapy. Patient selection for CAS is the important first step. Preoperative treatment with dual antiplatelet agents has made CAS safer, as has the use of an EPD. Regardless, the primary complications of death, stroke, myocardial infarction, restenosis, and bradycardia are seen despite efforts to avoid their occurrence. It is therefore important to continue to recognize these and other complications, to work to avoid them, and to manage these complications as they occur to allow patients to have their best possible outcome. Patients with carotid occlusive disease must be evaluated for factors that place them at risk for the development of atherosclerosis, and these factors modified when possible. Finally, patients who have
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Imaging Measure thrombosis Get best views Biplane preferable but not absolutely necessary Minimize angiograms Document final result Image cranial circulation pre- and post-treatment
been treated with CAS need evaluation with carotid ultrasound on a regular basis. We monitor for restenosis at 1 month, 6 months, and yearly thereafter.
Acknowledgment The authors thank Mrs. Jessica Kazmier for her editorial assistance.
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Sunit Das RJP, Bernstein RA, Alberts MJ et al. Update on carotid artery stenting: Part I. contemporary neurosurgery. 2004; 26(12):1–4 Endovascular versus surgical treatment in patients with carotid stenosis in the Carotid and Vertebral Artery Transluminal Angioplasty
3.
Study (CAVATAS): a randomised trial. Lancet 2001; 357(9270): 1729–37 Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. North American Symptomatic Carotid Endarterectomy Trial Collaborators. N Engl J Med 1991; 325(7): 445–53
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6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17. 18.
19.
20.
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Textbook of peripheral vascular interventions Endarterectomy for asymptomatic carotid artery stenosis. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. JAMA 1995; 273(18): 1421–8 Halliday A, Mansfield A, Marro J et al. Prevention of disabling and fatal strokes by successful carotid endarterectomy in patients without recent neurological symptoms: randomised controlled trial. Lancet 2004; 363(9420): 1491–502 Randomised trial of endarterectomy for recently symptomatic carotid stenosis: final results of the MRC European Carotid Surgery Trial (ECST). Lancet. 1998 May 9; 351(9113): 1379–87 Yadav JS, Wholey MH, Kuntz RE et al. Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med 2004; 351(15): 1493–501 Carotid revascularization using endarterectomy or stenting systems (CaRESS) phase I clinical trial: 1-year results. J Vasc Surg 2005; 42(2): 213–9 Gray WA, Hopkins LN, Yadav S et al. Protected carotid stenting in high-surgical-risk patients: the ARCHeR results. J Vasc Surg 2006; 44(2): 258–68 Carotid Artery Revascularization Using the Boston Scientific FilterWire and EndoTex NexStent. 2006, available from: The Internet Stroke Center Narins CR, Illig KA. Patient selection for carotid stenting versus endarterectomy: a systematic review. J Vasc Surg 2006; 44(3): 661–72 Rockman CB, Maldonado TS, Jacobowitz GR et al. Early carotid endarterectomy in symptomatic patients is associated with poorer perioperative outcomes. J Vasc Surg 2006; 44(3): 480–7 Baron EM, Baty DE, Loftus CM. The timing of carotid endarterectomy post stroke. Neurol Clin 2006; 24(4): 669–80 Kastrup A, Ernemann U, Nagele T, Groschel K. Risk factors for early recurrent cerebral ischemia before treatment of symptomatic carotid stenosis. Stroke 2006; 37(12): 3032–4 Bhatt DL, Kapadia SR, Bajzer CT et al. Dual antiplatelet therapy with clopidogrel and aspirin after carotid artery stenting. J Invasive Cardiol 2001; 13(12): 767–71 Lin PH, Bush RL, Peden EK et al. Carotid artery stenting with neuroprotection: assessing the learning curve and treatment outcome. Am J Surg 2005; 190(6): 850–7 Arab D, Yahia AM, Qureshi AI. Use of intravenous abciximab as adjunctive therapy for carotid angioplasty and stent placement. Int J Cardiovasc Intervent 2003; 5(2): 61–6 Bendok BR, Padalino DJ, Levy EI et al. Intravenous abciximab for parent vessel thrombus during basilar apex aneurysm coil embolization: case report and literature review. Surg Neurol 2004; 62(4): 304–11 Rangi PS, Markus HS, Punter MN, Clifton A. The use of intraoperative monitoring and treatment of symptomatic microemboli in carotid artery stenting: case report and discussion. Neuroradiology 2006; 49(3): 265–9 Wehman JC, Holmes DR, Jr., Ecker RD et al. Intravascular ultrasound identification of intraluminal embolic plaque material
21. 22. 23.
24.
25. 26.
27. 28. 29. 30. 31. 32. 33. 34. 35. 36.
during carotid angioplasty with stenting. Catheter Cardiovasc Interv 2006; 68(6): 853–7 Flint AC, Duckwiler GR, Budzik RF, Liebeskind DS, Smith WS. Mechanical thrombectomy of intracranial internal carotid occlusion. Pooled results of the MERCI and Multi MERCI Part I trials. Stroke 2007; Gonzalez A, Mayol A, Martinez E, Gonzalez-Marcos JR, Gil-Peralta A. Mechanical thrombectomy with snare in patients with acute ischemic stroke. Neuroradiology 2007; 49(4): 365–72 Qureshi AI, Siddiqui AM, Suri MF et al. Aggressive mechanical clot disruption and low-dose intra-arterial third-generation thrombolytic agent for ischemic stroke: a prospective study. Neurosurgery 2002; 51(5): 1319–27; discussion 27–9 Levy EI, Horowitz MB, Koebbe CJ et al. Transluminal stent-assisted angiplasty of the intracranial vertebrobasilar system for medically refractory, posterior circulation ischemia: early results. Neurosurgery 2001; 48(6): 1215–21; discussion 21–3 Kastrup A, Groschel K, Krapf H et al. Early outcome of carotid angioplasty and stenting with and without cerebral protection devices: a systematic review of the literature. Stroke 2003; 34(3): 813–9 Cremonesi A, Manetti R, Setacci F, Setacci C, Castriota F. Protected carotid stenting: clinical advantages and complications of embolic protection devices in 442 consecutive patients. Stroke 2003; 34(8): 1936–41 Reimers B PP, Favero L, Pasquetto G, Cernetti C, Sacca S. Current techniques of carotid artery stenting. Endovasc Today 2004; 3(8): 42–52 Phatouros CC, Higashida RT, Malek AM et al. Carotid artery stent placement for atherosclerotic disease: rationale, technique, and current status. Radiology 2000; 217(1): 26–41 Yadav JS, Roubin GS, Iyer S et al. Elective stenting of the extracranial carotid arteries. Circulation 1997; 95(2): 376–81 Pappada G, Beghi E, Marina R et al. Hemodynamic instability after extracranial carotid stenting. Acta Neurochir (Wien) 2006; 148(6): 639–45 Coutts SB, Hill MD, Hu WY. Hyperperfusion syndrome: toward a stricter definition. Neurosurgery 2003; 53(5): 1053–58; discussion 8–60 Bendok BR, Roubin GS, Katzen BT et al. Cutting balloon to treat carotid in-stent stenosis: technical note. J Invasive Cardiol 2003; 15(4): 227–32 Wholey MH, Wholey M, Bergeron P et al. Current global status of carotid artery stent placement. Cathet Cardiovasc Diagn 1998; 44(1): 1–6 Zhou W, Lin PH, Bush RL et al. Management of in-stent restenosis after carotid artery stenting in high-risk patients. J Vasc Surg 2006; 43(2): 305–12 Chakhtoura EY, Hobson RW, 2nd, Goldstein J et al. In-stent restenosis after carotid angioplasty-stenting: incidence and management. J Vasc Surg 2001; 33(2): 220–5; discussion 5–6 Lary BG. Coronary artery incision and dilation. Arch Surg 1980; 115(12): 1478–80
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Which patients should be referred for surgical endarterectomy and not have carotid stenting FJ Criado and C Gallagher
Introduction
Current status of CAS
Carotid endarterectomy (CEA) is one of the most significant and arguably among the best vascular reconstructive operations in our specialty. It is also nothing short of an icon for evidencebased medicine. But it is not without challenge. An estimated 10–20% of CEA procedures are done on so-called “high-risk” (HR) patients – especially those with unfavorable vascular or neck anatomy. Medical co-morbidities (mainly cardiac and pulmonary) can also increase risk or even preclude performance of CEA, albeit infrequently. Another difficult question is whether community-based and low-volume operators can reproduce the surgical results achieved at centers of excellence. And last but not least, CEA – as good as it may be – is “another” standard open operation, and as such is viewed with suspicion and increasing disdain by those who glorify all things endovascular and less invasive. This was the backdrop against which carotid stenting (CAS) evolved over a 20-year period. But it was really during the past 6 to 8 years that CAS “came of age,” due in large part to the development of embolic protection technologies that have since become a critical component of every carotid stent procedure. Further improvements in techniques and equipment will undoubtedly occur, but they are likely to be evolutionary and not revolutionary. We can state with some confidence today that the degree of technical standardization and equipment refinement that have been achieved so far with CAS are quite impressive and (perhaps) near optimal. They provide a solid foundation for a discussion of the topic at hand. Those who are strong proponents of CAS do not hesitate to express the view that the procedure may be equivalent to CEA, offering patients a valuable and potentially better treatment alternative when high-risk factors (for CEA) exist. Furthermore, it is unmistakable that CAS champions (mostly those of a non-surgical background) wish to advance the concept that carotid stent intervention is a procedure that can replace CEA for the majority of patients. Unfortunately for them, it is hard to deny that CAS has been dealt a definite setback in the recent past as the cumulative impact of international randomized clinical trials is beginning to be felt. Many experts would agree today on the fact (and reality) that the pendulum has definitely swung back to CEA (Figure 37.1) – at least for now.
What we know today is as follows (summarized in Table 37.1). ●
●
●
●
●
●
CAS has been shown to be non-inferior to CEA in the treatment of HR patients. The non-inferiority concept is one that sounds obscure and somewhat foreign to most clinicians. However, it is a well-accepted term in clinical research and statistical circles. The underlying thought is that a non-surgical percutaneous procedure need not be superior to an open surgical operation to be accepted and embraced – but it does need to be reasonably comparable and generally safe. Most of us can agree on this. However, significant disagreement remains on the magnitude of the HR patient cohort, and on the fact that cardiac events (largely subclinical) have accounted for most of the difference in favor of CAS in such patient population. Distal-filter embolic protection seems effective in preventing CAS-related major ipsilateral stroke (< 2% incidence). On the downside, these filters do allow the passage of small particles. The clinical consequences of such microembolization to the brain are still unclear. Increasingly, however, well-respected experts are suspicious of its negative impact. This may be particularly significant in the elderly (> 80 years of age) who may have diminished brain reserve and a much lower threshold for complications in the face of ischemic injury. Symptomatic patients (with a history of recent TIA or stroke) undergoing CAS are at increased neurological risk when compared with those who are asymptomatic. This is likely related to both the nature of their stenosing carotid plaque and the status of the brain itself. “The jury is still out” on the issues of safety and appropriateness of CAS on elderly patients. Stroke and mortality rates would appear to be significantly higher for octogenarians, and we would not be surprised if general consensus is reached soon on advising against CAS for such patients – especially those with asymptomatic carotid stenosis. Incidence of peri-procedural MI events, mostly non-Q wave, is definitely lower after CAS than after CEA surgery, but the true clinical significance of such finding remains suspect. CAS avoids cranial nerve injury (CNI) altogether. Again, a finding of doubtful significance since contemporary 345
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Figure 37.1
Meta-analysis of completed randomized carotid trials.
results in centers of excellence reporting CEA-related CNI rates of well under 5%. Occurrence of post-CAS restenosis requiring reintervention appears to be infrequent, with an incidence that may be lower than that following CEA. However, very little if any meaningful data exist after 2 years. Long-term (> 5 years) stroke prevention after CAS remains largely unknown.
●
●
●
●
Where we are today: selecting patients who should be referred for CEA and not have CAS It would be hard to deny that CAS remains largely unproven in the treatment of the majority of patients in need of carotid revascularization. It is the senior author’s (FJC) firm view today that, outside the confines of well-controlled clinical trials, the following findings should dictate referral for surgical endarterectomy instead of carotid stenting. Good-risk patients without any significant medical or anatomic issues that would make CEA difficult or risky.
●
Table 37.1 Carotid angioplasty-stenting (CAS): what we know today (2007) ● ● ●
● ● ● ●
CAS is not inferior to CEA in treatment of HR patients Distal filters minimize occurrence of ipsilateral stroke Microembolization to the brain may well have consequences MI events are very infrequent Restenosis incidence is low Vascular anatomy is a major limitation Symptomatic and > 80 patients are at increased risk
● ●
In other words, low-risk candidates for CEA should have surgery! And this is especially so for symptomatic patients who have had a recent stroke or TIA. Patients with unfavorable anatomy for CAS as demonstrated by angiography: type B+ or C aortic arch, severely angulated common carotid artery, marked loops and/or angulations in the proximal or mid-ICA precluding safe filter deployment. Patients with unfavorable carotid lesions; that is those that are extremely tight (“string-sign”), heavily calcified, or very long or extensive. Patients over the age of 80. Patients with very difficult or impossible endovascular access for CAS because of aortoiliac arterial occlusion or multiple previous femoral operations and the like.
The future of carotid revascularization: What will the next 5 years bring? The carotid revascularization landscape will surely continue to change. CAS techniques and technologies are likely to evolve, perhaps dramatically, with the potential for overcoming some if not all of the issues that limit its applicability at the present time. Embolic protection and access techniques and devices rank very high in the shortlist of critical CAS components where further advances are necessary if carotid stenting is ever going to be fully competitive with surgical endarterectomy. Data from several important trials will emerge within the next 5 years and provide a more solid foundation for clinical decision-making. We do not see CEA going away, but its role is likely to change in the years to come as CAS becomes more competitive. For now though, CEA’s pre-eminence remains largely unchallenged.
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REFERENCES 1.
2.
3. 4.
5.
6. 7. 8.
North American Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade stenosis. N Engl J Med 1991; 325: 445–53 European Carotid Surgery Trialists’ Collaborative Group. MRC European Carotid Surgery Trial: interim results for symptomatic patients with severe (70–99%) or with mild (0–29%) carotid stenosis. Lancet 1991; 337: 1235–43 Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA 1995; 273: 1421–8 Wennberg DE, Lucas FL, Birkmeyer JD, Bredenberg CE, Fisher ES. Variation in carotid endarterectomy mortality in the Medicare population: trial hospitals, volume, and patient characteristics. JAMA 1998; 279: 1278–81 Biller J, Feinberg WM, Castaldo JE et al. Guidelines for carotid endarterectomy: a statement for healthcare professionals from a Special Writing Group of the Stroke Council, American Heart Association. Circulation 1998; 97: 501–9 Ouriel K, Hertzer NR, Beven EG et al. Preprocedural risk stratification: identifying an appropriate population for carotid stenting. J Vasc Surg 2001; 33: 728–32 Cebul RD, Snow RJ, Pine R, Hertzer NR, Norris DG. Indications, outcomes, and provider volumes for carotid endarterectomy. JAMA 1998; 279: 1282–7 Hannan EL, Popp AJ, Tranmer B et al. Relationship between provider volume and mortality for carotid endarterectomies in New York State. Stroke 1998; 29: 2292–7
9. 10. 11. 12. 13. 14.
15.
16.
Badner NH, Knill RL, Brown JE, Novick TV, Gelb AW. Myocardial infarction after noncardiac surgery. Anesthesiology 1998; 88: 572–8. [Erratum, Anesthesiology 1999; 90: 644.] Kim LJ, Martinez EA, Faraday N et al. Cardiac troponin I predicts short-term mortality in vascular surgery patients. Circulation 2002; 106: 2366–71 McFalls EO, Ward HB, Santilli S et al. The influence of perioperative myocardial infarction on long-term prognosis following elective vascular surgery. Chest 1998; 113: 681–6 Yadav JS, Wholey MH, Kuntz RE et al. Protected carotid-artery stenting versus endarterectomy in high-risk patients. N Engl J Med 2004; 351: 1493–501 Gray WA, Hopkins LN, Yadav S et al. Protected carotid stenting in high-surgical-risk patients: the ARCHeR results. J Vasc Surg 2006; 44: 258–68 White CJ, Iyer SS, Hopkins LN et al. BEACH Trial Investigators. Carotid stenting with distal protection in high surgical risk patients: the BEACH trial 30-day results. Catheter Cardiovasc Interv 2006; 67(4): 503–12 Mas JL, Chatellier G, Beyssen B et al. on behalf of the EVA-3S Investigators. Endarterectomy versus stenting in patients with symptomatic severe carotid stenosis. Engl J Med 2006; 355: 1660–71 SPACE collaborative group; Ringleb PA, Allenberg J, Bruckmann H et al. 30-day results of the SPACE trial of stent-protected angioplasty versus carotid endarterectomy in symptomatic patients. Lancet 2006; 368: 1239–47
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Common carotid artery: PTA stenting J Franke, G Robertson, and H Sievert
Introduction
Outcomes/complications
Eighty-five percent of all strokes are ischemic events. Thirty percent of ischemic strokes are from carotid thromboembolic events from atherosclerotic disease at the carotid bifurcation.1 Significant atherosclerotic disease is less commonly isolated to the common carotid artery. Although atherosclerosis is the predominant cause of this vascular disease, Takayasu arteritis, a subset of giant-cell arteritis, can also result in significant narrowings in young adults.2–4 Takayasu’s arteritis is a rare chronic inflammatory disease of unknown etiology involving the aorta and supra-aortic vessels. It occurs more often in females in the second decade of life. It presents with an acute symptomatic systemic phase from its inflammation. The chronic phase involves the formation of fibrosis in the intima, media, and adventitia often resulting in stenoses, occlusions, or aneurysms. This phase, when resulting in a significant stenosis and when inflammation ceases, can be treated surgically or with PTA/stenting. There are no data to guide us as to when to intervene in this subset of patients or that reveals superiority of a specific treatment modality. Surgery is technically difficult in this anatomical location whereas carotid stenting by experienced operators is usually more straightforward. It is probably reasonable to at least partially extrapolate the randomized controlled trial data from bifurcation carotid disease treatment to help answer when to treat. This would be to consider treatment for symptomatic 50% stenoses and possibly asymptomatic 70% stenoses.
There is a paucity of published work on endovascular treatment of the common carotid artery. Chio et al. reported on the treatment of 42 consecutive, proximal, and ostial common carotid lesions in 37 patients with stent implantation in 2003.5 Procedural success was high (95%, 40 of 42 vessels) and two patients suffered a minor stroke (4.7%). There were no peri-procedural major strokes. During a mean follow-up period of 24 months the following neurological events occurred: one transient ischemic attack, two contralateral minor strokes and one cerebral hemorrhage associated with long-term warfarin therapy occurred. The stroke/death rate during follow-up was 7.1%. The restenosis rate was 5.1%. The prospective registry performed by Sullivan et al. included 14 cases of left common carotid artery stenting.6 All stenoses were of atherosclerotic etiology. The mean patient age was 63 years. Ischemic strokes occurred in 2 of 14 common carotid interventions (14.3%), both of which were performed in conjunction with ipsilateral carotid bifurcation endarterectomy. Of the 11 patients available for follow-up examination, 10 remained stroke-free at a mean of 14.3 months. The authors concluded that endovascular repair of common carotid artery lesions can be performed with a high degree of technical success, but should be approached with caution when performed in conjunction with ipsilateral bifurcation endarterectomy. A total of nine common carotid stent implantations performed under cerebral protection were published by Peterson et al.7 Cerebral protection was achieved with
Table 38.1
Clinical series
Outcome of clinical series
Method of treatment
Sullivan et al. Stent (1998) implantation Chio et al. Stent (2003) implantation Peterson et al. Stent implantation (2006) under cerebral protection Archie (1999) Bypass surgery
348
Procedural PeriLesions Mean age success procedureal Follow-up (n) (years) (%) stroke (%) (months) 14
63
85.7
42
NN
95
9
68
100
29
68
96.6
14.3 4.7 0 3.4
Stroke in follow-up (%)
Restenosis (%)
Mean follow-up (months)
14.3
9
NN
14.3
24
7.1
5.1
24
1
0
0
1
12
0
7
12
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Figure 38.1 Ostial lesion of the right common carotid artery. The tip of the guiding catheter is kept very proximal, away from the diseased ostium of the right common carotid artery.
Figure 38.2 Ostial lesion of the left common carotid artery. The guide or sheath is kept in the aorta, away from diseased left common carotid artery ostium. Stabilizing 0.035-inch buddy wire is sometimes used.
either a distal embolic filter device or with open surgical occlusion of the distal common carotid artery. At 30-day follow-up, there were no deaths, myocardial infarctions, strokes, or restenoses.
The catheter is gently pulled back until it slips into the brachiocephalic trunk. However, when there is ostial disease the guiding catheter is maintained just outside the ostium, often requiring a stabilizing 0.035-inch supportive buddy wire maintained in the aortic arch. Thereafter, the stiff hydrophilic wire is advanced into the right common carotid artery. Keeping the wire in position, the catheter is advanced into the common carotid artery over the wire and positioned proximal to the disease. When the stenosis is in the distal CCA, the guiding catheter is then advanced only a short distance for maximal support. To enter the left common carotid artery the catheter is pulled back very slowly from the ostium of the brachiocephalic trunk. It should be turned 20∞ counter-clockwise to have the tip of the catheter pointing slightly anteriorly. As soon as the catheter enters the ostium of the common carotid artery it is turned clockwise 20∞. In elongated aortic arches, the origin of the left common carotid artery migrates posteriorly. In this case the catheter may have to be rotated posteriorly instead of anteriorly. Its final position depends on the anatomical location of the disease. When there is ostial disease the guiding catheter remains in the aortic arch. Due to elastic compressability of ostial lesions and the need for precise stent placement, balloon-expandable stents are recommended. When the ostium of the right CCA is the stenosis for treatment, we prefer not to stent across the subclavian ostium if possible. Peri-procedural distal embolization of debris and/or thrombus is a major potential limitation to CCA interventions.
Technique Identification of common carotid anatomy and significant disease occurs through standard MRA, CT angiography, or conventional angiography. Simple or complex catheter forms or sheaths are chosen according to operator preference for the individual anatomy. Eight-French guides are generally preferred due to maximally offered support. Patients should be pretreated with aspirin and clopidogrel and fully heparinized. Special care is taken to avoid engaging the diseased portion of the common carotid artery with the guide. When patients have already been shown to have an ostial brachiocephalic or CCA stenosis prior to catheterization laboratory arrival, the operator may prefer to begin with a guiding catheter to minimize catheter induced trauma. When placed in the lower aortic arch, the tip of one of the above-mentioned catheters (simple designs such as Bernstein, right Judkins, Vitek, and Headhunter, or complex designs like Sidewinder or Simmons) should point or be placed over a guidewire inferiorly. This prevents traumatizing the aortic arch intima and prevents the catheter from being trapped in vessel ostia. The catheter is then turned around 180∞, which places the tip in a vertical upright position (Figure 38.2).
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Balloon dilatation, stenting, and manipulation of the vessels through catheters and wires are likely to release debris that can cause severe damage through distal embolization. Although the data showing less embolization when EPD is used with carotid artery stenting is from bifurcation carotid disease, it is reasonable to speculate its protective advantage when used for all carotid interventions.
Surgical options Only a few reports on common carotid artery surgery exist. Archie reported axillary artery-based bypass grafting in 23 cases on symptomatic atherosclerotic common carotid artery occlusions and 6 cases of long ostial stenosis of > 90%. Saphenous vein grafts were used in 25 procedures, and synthetic grafts were used in 4. There were no peri-operative deaths; one stroke occurred (3.4%). The 1-year stenosis-free rate for 50% or greater stenosis was 93%, and the 5- and 10-year rates were 87%. No late ipsilateral strokes occurred.8
No randomized clinical trial has ever been performed to compare the outcome of common carotid surgery versus common carotid angioplasty/stenting.
Restenosis and its treatment Restenosis is a known limitation of coronary and peripheral interventions. However, the restenosis rate after internal carotid artery stenting is remarkably low. Various series found that the rate of restenosis ranges between 2.39 to 5%.10 This data is limited for isolated CCA anatomy. The authors have reported rates between 07 to 5.1%,5 whereas the 0% rate of restenosis was reported at 30-day follow-up and the 5.1% rate after a mean follow-up of 24 months. Stent compression has also been described during follow-up. Technically, repeat angioplasty for restenosis is safe and routine. In cases where the restenosis is located at the distal end of the stent a second stent may be necessary.
(a)
(b)
(c)
(d)
Figure 38.3 Procedural angiograms: (a) Ostial stenosis of the right common carotid artery; (b) positioning of the stent at the ostium; (c) balloon dilatation of the stent; and (d) result after stent implantation.
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(b)
(c)
(d)
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Figure 38.4 Procedural angiograms: (a) high-grade ostial proximal brachiocephalic stenosis; (b) predilatation with a 6-mm PTA balloon; (c) 8-mm balloon-expandable stent placement; and (d) minor residual stenosis.
Summary Significant narrowing can occur in the common carotid arteries from atherosclerosis in older patients or inflammatory arteritis – Takayasu’s – in younger patients. Although these diseases are of different etiology and affect patients in different age groups, both can be treated by the same endovascular method of angioplasty/stent implantation. This is a challenging anatomical area for traditional surgery.
Despite it requiring meticulous endovascular technique especially when involving the ostium of the supra-aortic vessels, experienced operators can achieve a high rate of success. There is a paucity of published work for this subset of patients and hence a void of outcome science to guide the practitioner. Additional data is needed to prove the safety and long-term effect of common carotid artery angioplasty/stent implantation.
REFERENCES 1. 2. 3.
American Heart Association. Heart Disease and Stroke Statistics— 2007 Update. Dallas: American Heart Association, 2007 Bali HK, Bhargava M Bhatta YK et al. Single stage bilateral common carotid artery stenting in a patient of Takayasu arteritis. Neurol India 2001; 49(1): 87–90 Murakami R, Korogi Y, Matsuno Y et al. Percutaneous transluminal angioplasty for carotid artery stenosis in Takayasu arteritis: persistent benefit over 10 years. Cardiovasc Intervent Radiol 1997; 20(3): 219–21
4. 5. 6.
Rath PC, Lakshmi G, Henry M. Percutaneous transluminal angioplasty using a cutting balloon for stenosis of the arch vessels in aortoarteritis. Indian Heart J 2004; 56(1): 54–7 Chio FL Jr, Liu MW, Khan MA et al. Effectiveness of elective stenting of common carotid artery lesions in preventing stroke. Am J Cardiol 2003; 92(9): 1135–7 Sullivan TM, Gray BH, Bacharach JM et al. Angioplasty and primary stenting of the subclavian, innominate, and common carotid arteries in 83 patients. J Vasc Surg 1998; 28(6): 1059–65
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Peterson BG, Resnick SA, Morasch MD et al. Aortic arch vessel stenting: a single-center experience using cerebral protection. Arch Surg 2006; 141(6): 560–3; discussion 563–4 Archie JP Jr. Axillary-to-carotid artery bypass grafting for symptomatic severe common carotid artery occlusive disease. J Vasc Surg 1999; 30(6): 1106–12
9. 10.
Willfort-Ehringer A, Ahmadi R et al. Single-center experience with carotid stent restenosis. J Endovasc Ther 2002; 9(3): 299–307 Chaktoura EY, Hobson RW, Goldstein J et al. Instent restenosis after carotid angioplasty-stenting: incidence and management. J Vasc Surg 2001; 33(2): 220–25
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Percutaneous transluminal angioplasty of the subclavian arteries M Henry, I Henry, A Polydorou, Ad Polydorou, and M Hugel
Introduction
General considerations
Clinically significant atherosclerotic occlusive diseases involving the supra-aortic vessels have been managed by surgical procedures (bypass, endarterectomy, arterial transposition, extra anatomical reconstruction) with an acceptable complication rate along with an excellent patency rate and long-term symptomatic relief. Despite these good results, over the last 15 years, percutaneous transluminal angioplasty (PTA) of the supra-aortic vessels, especially the subclavian and innominate arteries has progressed from an experimental procedure to an accepted means of treatment with an outcome equal or superior to surgery in selected groups of patients.1–4 Today, angioplasty is considered as the treatment of choice for the majority of the cases by most interventionists.3,5 Placement of endoprotheses broadens the indications towards total occlusions1 and improves the results.6 The first subclavian artery angioplasty was performed by Mathias et al.7 in 1980 and in the same year another case was reported by Bacham et al.8 Thereafter, many subsequent reports have confirmed its efficacy.1,9–23 With an experience of 237 consecutive patients who underwent PTA of subclavian or innominate arteries, we would like to discuss the technique, and the immediate and long-term results.
Clinical signs The lesions (stenosis or occlusion with, in most cases, subclavian steal syndrome) (Figure 39.1) may be asymptomatic or symptomatic, and it is essential to distinguish these two forms. This division is usually the deciding factor for selecting the appropriate treatment option. The subclavian and innominate arteries supply the brain as well as the arm with blood. Both vascular territories compete for the flow distribution in case of a proximal stenosis or occlusion (Figure 39.1). Therefore, the patient may suffer from symptoms of the arm or the brain24 and several clinical situations are encountered. The steal of blood from the vertebrobasilar circulation may be asymptomatic or symptomatic with symptoms of impaired perfusion of the posterior cerebral circulation (subclavian steal syndrome). Clinically manifest vertebrobasilar insufficiency is caused by a unilateral obstruction, when the dominant vertebral artery is supplied by a stenotic subclavian artery. A stroke as a consequence of a subclavian artery obstruction is an unusual event when the carotid arteries are patent. Patients with acute arterial insufficiency of the upper extremity present with the same signs as with acute arterial
(a) Figure 39.1
(b)
(c)
(a) Left subclavian artery stenosis; (b) and (c) left subclavian artery occlusion with subclavian steal syndrome.
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insufficiency of the lower extremities: pulselessness, pallor, paresthesia, pain, and paralysis. A subclavian artery stenosis can be at the origin of thromboembolism with acute ischemia of the upper extremity. Chronic arterial insufficiency of the upper extremity is diagnosed when the patients complain with disabling exertional arm discomfort. A coronary steal syndrome may have its origin in subclavian artery stenosis. Patients with mammary artery anastomosis will develop angina when the blood flow in the subclavian artery is impaired.25–33 Hemodialysis shunts, and extra anatomic axillofemoral bypass grafts are endangered by a proximal subclavian artery obstruction. Atherosclerotic disease is the most frequent etiology of subclavian and innominate obstructions and the predilection site is the proximal part of the artery. Atherosclerotic plaques may extend to the aortic arch or involve the origin of the vertebral artery. The stenosis may be short or tubular, long, concentric or eccentric, ulcerated, or calcified. The occlusion always extends from the aortic arch to the origin of the vertebral artery. The arm symptoms are more severe when the obstruction is located distally to the origin of the vertebral artery because of the poor collateral circulation.7 Besides atherosclerotic disease, subclavian artery obstruction may be caused by disease processes; for example, fibromuscular dysplasia, neurofibromatosis, arteritis (Takayasu’s disease), radiation, post-traumatic scarring, and compression syndromes.34–38 Diagnosis Clinically, with a blood pressure difference greater than 20 mmHg between the two arms we may suspect a subclavian artery obstruction. Duplex scanning of the supra-aortic vessels enables the diagnosis of subclavian artery obstruction and subclavian steal syndrome and allows the diagnosis of associated lesions of other arteries like carotid arteries. Ultrasound provides both anatomical and physiological information regarding a lesion and is the best initial test to establish the hemodynamic significance of a stenosis. In particular the direction of vertebral artery blood flow is easily determined and is a prerequisite for the diagnosis of subclavian steal. Transcranial Doppler may also be useful to provide information about how a lesion is affecting the cerebral circulation in symptomatic patients. The diagnostic imaging work-up of patients should include magnetic resonance imaging (MRI) with or without magnetic resonance angiography (MRA) or computed tomographic scan of the brain with close evaluation of the posterior fossa and brain stem. MRA could be useful as a screening test to evaluate stenoses of both intracranial and extracranial vessels. However, MRA commonly overestimates the degree of vessel stenosis, which limits the ability of MRA to function as the sole test prior to interventions. Spiral computed tomography (CT) is an additional method of evaluation and allows for three-dimensional reconstruction of the aorta and supra-aortic vessels. CT angiography (CTA) may be a good alternative to MRA but requires contrast injection. Angiography remains the gold standard for the diagnosis but is always associated with some degree of risk. A global arteriography and a selective arteriography of supra-aortic
vessels with multiple views allow us to assess the type, the morphology, and the extent of the lesion, its relationship to the other arteries, and the origin of the internal mammary artery. We prefer to use the femoral approach for angiographic diagnosis. The brachial approach using contralateral access may be used while the ipsilateral brachial approach is avoided for diagnosis purposes. Angiography is important not only for diagnosis of subclavian artery obstruction but also to diagnose associated lesions and particularly extracranial or intracranial carotid artery lesions. A neurological examination by an independent neurologist is indispensable before and after the procedure and during the follow-up.
Indications for interventions Indications for PTA are the same as for surgery. However because of its low risk, angioplasty is preferred. In symptomatic patients, indications seem to be licit in patients with the following. ●
●
●
●
●
Neurological signs, vertebrobasilar insufficiency (syncope, ataxia, blurred vision, dizziness, etc.) transient ischemic attacks, or stroke. The presence of a subclavian steal syndrome is a favorable indication since it prevents the risk of vertebral embolization. The subclavian steal is rarely bilateral (5% of the cases).39 Recurrent angina following coronary bypasses grafting with the internal mammary artery (coronary steal syndrome).6,30,32,33,40–46 The incidence of coronary steal syndrome has been reported to be 0.4%.46 Marques et al. reported this incidence to be 0.7%.30 Treatment of the lesion (nine in our series) usually improves the symptoms. Signs of ischemia of the upper limb (significant arm claudication, distal embolization). Lower-limb ischemia secondary to a stenosis above axillary femoral bypass.
In asymptomatic patients, the indications are more debated because of their favorable evolution47,48 and low risk of aggravation of the neurological or ischemic signs. In these patients, we recommend subclavian angioplasty in the following situations. ●
●
●
Angioplasty of subclavian stenoses before other cardiovascular interventions – coronary bypass, axillary femoral bypass, and preservation of the vasculature for other angioplasty procedures, more particularly coronary procedures. In all patients referred for coronary angiography, 3.5% demonstrate significant stenosis and of those referred for coronary bypass grafting, 5.3% demonstrate hemodynamically significant stenosis. Recently Wood et al. published two cases of subclavian angioplasty and stenting performed by transcranial approach, allowing successful coronary stenting as part of the procedure.49 Subclavian or innominate angioplasty prior to arteriovenous fistula creation or to maintain the function of an arteriovenous fistula (stenosis proximal to hemodialysis graft).
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SUBCLAVIAN ARTERY STENOSIS
FEMORAL APPROACH 8F GUIDING CATHETER OR 6F LONG SHEATH 0.035” STEERABLE OR HYDROPHILIC GUIDE WIRE 0.018” – 0.020” STEERABLE GUIDE WIRE
FAILURE
SUCCESS ISOLATED STENOSIS
ADJACENT TO VERTEBRAL ARTERY 2 STEERABLE GUIDE WIRES (vertebral 0.014”, subclavian 0.018”)
PREDILATATION
PRIMARY STENTING
GOOD RESULTS
KISSING BALLOON ANGIOPLASTY
INSUFFICIENT RESULTS
GOOD RESULTS
STENT
BALLOON ANGIOPLASTY ALONE
Figure 39.2
●
●
BRACHIAL APPROACH SURGERY
INSUFFICIENT RESULTS
STENT
BALLOON ANGIOPLASTY ALONE
Subclavian artery stenosis, femoral approach.
Severe innominate or subclavian artery stenosis > 80%, particularly in young patients in whom the coronary risk is high since the stenosis may render the bypass more difficult starting from the internal mammary artery. Preservation of the cerebral perfusion. The treatment of subclavian lesions was proposed when there existed other arterial lesions at the level of the supra-aortic vessels, especially the carotid vessels, so as to improve cerebral flow.14,15,18,50
Techniques of angioplasty (Figures 39.2–39.4) A femoral or a brachial approach may be used interchangeably in most of the cases for the treatment of subclavian or innominate artery obstructions.7,51 Sometimes it is helpful to use two arterial accesses simultaneously to approach the lesion from both sides. It depends on the type of lesion – stenosis or occlusion – and its location, as well as the patency of the iliac arteries.
SUBCLAVIAN ARTERY STENOSIS
FIRST INTENTION
BRACHIAL APPROACH OR RADIAL APPROACH
AFTER FAILURE OF FEMORAL APPROACH
6 OR 7 F LONG INTRODUCER OR GUIDING CATHETER 0.035" STEERABLE OR HYDROPHILIC GUIDE WIRE 0.018"– 0.020" STEERABLE GUIDE WIRE SUCCESS
PRIMARY STENTING
FAILURE PREDILATATION
FEMORAL APPROACH
SUCCESS GOOD RESULTS
BALLOON ANGIOPLASTY ALONE
Figure 39.3
FAILURE
INSUFFICIENT RESULTS
STENT
Subclavian artery stenosis, brachial or radial approach.
SURGERY
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PRESENCE OF A NIPPLE
ABSENCE OF A NIPPLE
FEMORAL APPROACH
BRACHIAL APPROACH
FEMORAL APPROACH
LONG SHEATH INTRODUCER OR 7 F GUIDING CATHETER
GUIDING CATHETER STEERABLE HYDROPHILIC GUIDE WIRE HYDROPHILIC CATHETER
0.014” or 0.035” STEERABLE HYDROPHILIC GUIDE WIRE CROSSED DILATATION + STENT
Figure 39.4
NOT CROSSED OR FALSE LUMEN
BRACHIAL APPROACH
UNCROSSABLE
DILATATION + STENT
SURGERY
Subclavian artery occlusion.
Recently the radial access has been proposed.33,49,52 In the majority of the cases subclavian artery angioplasty can be performed by the femoral route. Recanalization of an occluded subclavian or innominate artery normally requires a brachial or radial approach because the femoral route gives insufficient support to the catheter to penetrate the occluded artery segment.7,12,51–53 The brachial approach is also indicated in case of severe tortuosities of aorta, iliac, and subclavian artery or bilateral occlusion of the iliac arteries. When the subclavian artery is occluded, the puncture of the humeral or radial artery may be difficult. Sonographic or angiographic guidance may help the arterial puncture.
(a)
CROSSED
(b)
Femoral approach technique The femoral access may be used at first intention in the majority of the cases. Several techniques can be used to cross the lesion with a guidewire. Technique 1 (Figure 39.5) A 7- or 8-French guiding catheter (multipurpose type or a right coronary Judkins), is placed at the ostium of the subclavian artery. This guiding catheter allows injections of the contrast medium and localization of the stenosis which is crossed with a guidewire, either a 0.035-inch steerable or rarely a hydrophilic 0.0035-inch, a 0.020-inch, or a 0.018-inch for a very tight stenosis.
(c)
Figure 39.5 Subclavian artery angioplasty and stenting, technique 1: (a) 0.014–0.035 guidewire, 7/8-French guiding catheter; (b) balloon dilatation, 7/8-French guiding catheter; and (c) BE stent, SE stent 7/8-French guiding catheter.
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(b)
(d)
(e)
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(c)
Figure 39.6 Subclavian artery angioplasty and stenting, technique 2: (a) 0.014–0.035 guidwire, 5-French catheter; (b) 0.014–0.035 guidwire, 5-French catheter; (c) 0.035 Amplatz stiff wire, 5-French catheter withdrawn; (d) 6–8-French catheter, 6-French long sheath inserted; and (e) stent, 6–8-French guiding catheter, 6-French long sheath.
Technique 2 (Figure 39.6) If the subclavian artery cannot be catheterized with a guiding catheter, it may be catheterized with a selective catheter (Vitek, Sidewinder, or a multipurpose or vertebral catheter), generally 5 French, and the stenosis is crossed with a 0.035–inch, 0.020-inch, or 0.018-inch steerable guidewire (and rarely with a hydrophilic one in the presence of a very tight irregular anfractuous stenosis). The catheter is then advanced into the axillary artery and pressure gradients are assessed. The guidewire is replaced by a rigid 0.035-inch Amplatz-type guidewire. The 5-French catheter is withdrawn and a 7- or 8-French multipurpose-type guiding catheter, or a 6-F long-sheath advanced over the rigid guidewire up to the subclavian artery. As previously, selective injection of contrast medium enables us to locate the lesion.
After placing a long sheath or a guiding catheter and crossing the lesion with a guidewire, we have to choose the technique: ●
Balloon angioplasty alone. The diameter of the balloon is selected to be equal to that of the artery. Overdilation may cause dissection or rupture of the vessel. The stenosis is dilated, the balloon deflated and withdrawn, then a control angioplasty performed as well as an assessment of the pressure gradient. When possible, a balloon position over the origin of the vertebral artery should be avoided to prevent occlusion of the artery by shifted atherosclerotic material. The risk of permanent vertebral artery occlusion is increased in patients with ostial stenosis of the artery.
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If the result is unsatisfactory (residual pressure > 5 mmHg or residual stenosis > 20% on angiography), a stent is implanted. Stent implantation should be performed carefully and should avoid covering the vertebral artery or the internal mammary artery. Predilatation of the lesion with a smaller balloon (4.5 mm in diameter) in case of very tight or calcified stenosis, then stenting. Direct stenting, which reduces the risk of dissection and potentially the risk of embolization.
Technique 3 (Figure 39.7) A third technique is currently used for direct stenting in particular. It consists of the same technique as the one described above to catheterize the subclavian artery, but long 5-French catheters (120 mm) are placed in a guiding catheter, generally
(a)
(b)
(d)
(e)
7 or 8 French or in a 6-French sheath (coaxial technique). Once the guidewire has crossed the lesion, both the 5-French diagnostic catheter and the guiding catheter or the sheath are advanced and usually cross the stenosis easily. The 5-French catheter is then withdrawn and a stent is advanced over the guidewire, “protected” by the guiding catheter, which is then progressively withdrawn and placed above the lesion. The endoprosthesis may then be deployed. Hand injections of contrast medium are performed for an accurate positioning of the stent. This technique could be difficult and even dangerous (risk of embolization) in cases of a tight, calcified, ulcerated stenosis. Special attention should be paid to avoid excessive catheter manipulations in the aorta. The aortic arch has its own set of embolic potential. Special attention is also paid to lesion crossing so that the risk of dissection is minimized. Dissection in the supra-aortic region may not be well tolerated.
(c)
Figure 39.7 Subclavian artery angioplasty and stenting, technique 3 “coaxial technique”: (a) 0.018–0.035 guidewire, long 5-French catheter, 6–8-French guiding catheter, 6-French long sheath; (b) 0.018–0.035 guidewire, long 5-French catheter, 6–8-French guiding catheter, 6-French long sheath; (c) guidewire, guiding catheter and 6-French long sheath; (d) guidewire, stent inserted, guiding catheter and long 6-French sheath withdrawn; and (e) BE stent, SE stent, 7/8-French guiding catheter, long 6-French sheath.
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Brachial approach technique (Figure 39.8) By brachial approach we can place a long 6- or 7-F sheath close to the lesion, which allows injection of contrast medium to locate the lesion. The technique is the same as the femoral approach concerning crossing the lesion, balloon angioplasty, and stenting. Treatment of subclavian artery occlusion (Figure 39.9) When the occlusion does not begin at the ostium of the subclavian artery and when there is a nipple, recanalization may then be attempted using the femoral approach. In case of failure the brachial approach is used. When the occlusion begins at the ostium of the subclavian artery it is usually impossible to cross the occlusion using the femoral approach. The brachial approach is then used. A catheter placed in the ascending aorta allows injection of contrast medium and localization of the lesion. Hydrophilic guidewires (0.035-inch Terumo J wire) are then used to cross the lesion in combination with a multipurpose, curved diagnostic catheter. Controlled force is often necessary to cross the occluded artery segment especially in cases with calcified aortic arches.7,51–54 After successful passage of the obstruction the balloon is placed at the level of the occlusion and inflated. Stenting is performed after using this access. In some cases (very tight calcified lesions) the guidewire is in the good lumen but it is impossible to progress and cross the lesion with the dilatation balloon. The hydrophilic wire may be exchanged for a stiff Amplatz wire inside a glide 4- or 5-French Terumo catheter. This wire gives better support when crossing the lesion with the balloon. In case of failure, once the guidewire has crossed the lesion it may be advanced into the aorta and placed in a femoral artery. It may be caught back with a lasso through a femoral introducer and the procedure (angioplasty plus stenting) may be continued through either the femoral access or the brachial access. By pulling the guidewire at its two extremities, crossing the lesion with the balloon is facilitated. This “pull-through technique” provides dual access and may facilitate accurate stent placement in cases of extreme vessel tortuosity and severely calcified lesions. Associated vertebral artery stenosis (Figure 39.10) When the vertebral artery originates at the level of the stenosis it is important to protect it with a 0.014-inch or a 0.018-inch coronary-type guidewire during the angioplasty procedure. In the presence of an associated vertebral artery stenosis the angioplasty may be performed using the kissing technique. Two balloons are placed at the site of the vertebral artery and subclavian artery stenoses, and simultaneously inflated. Decision for stent placement is made by evaluation of the angioplasty results after deflation and withdrawal of the balloons. The complication rate from embolization of plaques material is low10,58–60 and could be lowered by improving technique57–61 but brain embolization is always a possible complication of these procedures. Analyzing the site of plaques and stenoses in vertebral and subclavian arteries, Staikov et al.62 described a special double balloon PTA technique, which may be helpful in high-risk situations when a
Figure 39.8 Subclavian artery angioplasty and stenting: rightsided transbrachial approach for innominate artery intervention.
vertebral artery stenosis is associated with a subclavian artery stenosis to avoid brain embolism. The double balloon technique for PTA of the subclavian and vertebral arteries has been employed previously.59 Two selective PTA catheters are used simultaneously, one by femoral approach and one by brachial artery approach. The brachial catheter is exchanged over a coronary wire for a balloon catheter and the balloon placed at the origin of the vertebral artery. The balloon in the vertebral artery is inflated to protect the vertebrobasilar territory from potential emboli when the subclavian artery stenosis is crossed by the guidewire and then by the dilatation balloon. The subclavian artery stenosis is dilated while the vertebral artery dilatation balloon is inflated. After dilatation of the subclavian stenosis the transfemoral balloon is deflated first and withdrawn to the origin of the subclavian artery. The restored blood flow therefore flushes potential debris into the brachial artery. The vertebral artery balloon is then deflated. The result of the PTA of the subclavian and vertebral arteries is evaluated by injection of contrast medium. If the result is not satisfactory, the procedure can be repeated or a stent can be placed by the transfemoral or transbrachial approach in the subclavian or the vertebral artery. When PTA has been successful, all catheters and guidewires are removed. Stenting Several types of stents may be implanted. For the prevertebral portion of the subclavian artery or the innominate artery a balloon-expandable stent like a Palmaz (P154, P204, P304) stent seems a good option because of its excellent radial
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(b)
(a) (d)
(c) (f)
VERTEBRAL ARTERY
(g) (e)
AFTER FIRST STENT (PALMAZ STENT) AFTER SECOND STENT (PALMAZ STENT)
Figure 39.9 Left subclavian artery occlusion and subclavian steal syndrome: (a) occlusion; (b) after recanalization; (c) after dilatation; (d) after first stent (Palmaz stent); (e) after second stent (Palmaz stent); (f) normal flow in the vertebral artery (g) Palmaz stents.
strength, radio-opacity, accurate positioning, and the possibility of flaring the proximal part, which originates from the aorta. The stent should be protruding into the lumen of the aorta by 1 or 2 mm to well cover the ostium and avoid restenosis. The more flexible Cordis Corinthian stent (Cordis, Warren, NJ), also seems to be a good indication, as well as the new Boston Express stent (Boston Scientific, Natik, MA). Other balloon-expandable stents may also be used. Self-expandable stents, like the Wallstent have also been implanted in this location, but with a lesion located at the offspring of the subclavian artery it is difficult to place the stent exactly without protrusion into the aortic arch or innominate artery.43 For this reason, nitinol self-expandable stents seem better. These nitinol stents may be placed at a precise location. Good results were also reported with the Strecker stent.64 For the post-vertebral location, we recommend self-expandable stents (to avoid compression of the stents), the Wallstent, and nitinol stents.
As previously mentioned, it is recommended not to cover the vertebral and mammary arteries. Cerebral protection Cerebral protection is routinely used for carotid stenting but not for subclavian artery angioplasty and stenting, because the risk of embolization is low. Cerebral protection is not necessary for the majority of procedures. Nevertheless, in some specific situations with high-risk patients for brain embolism, cerebral protection like occlusion balloon or filter could be used and placed in the vertebral artery to protect the brain. Medication Before the procedure, the patients received 100 mg of aspirin and 15,000 units of heparin per 24 hours. Five thousand units
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(b)
(d)
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(c)
Figure 39.10 (a) Vertebral and subclavian artery stenoses; (b) kissing balloon technique; (c) Palmaz stent in vertebral artery; (d) Palmaz stent in vertebral artery and Wallstent in subclavian artery; (e) final result and 1-year follow-up.
of heparin were also given as a bolus during the procedure and heparin perfusion was continued for 24 hours after the procedure. Aspirin at a dose of 100 mg/day was continued after that. In case of stent implantation, ticlopidine (250 mg/day) or clopidrogel (75 mg/day) was given for 1 month.
Results Patients From January 1988 to June 2006, 307 patients (males: 175; females: 132) underwent PTA of the subclavian or innominate arteries: 70 right subclavian arteries (23%), 15 innominate arteries (5%), and 222 left subclavian (72%). The mean age of patients was 65 ± 12 years (range: 25–87 years). The mean age of males was: 66.3 ± 12.5 years (range: 40–81 years) and of females was 62.6 ± 13.3 years (range: 25–87 years). In the majority of the cases (301 patients) the lesions were of atheromatous etiology. Dysplasia seemed to be the etiology in two patents, post-radiation in two patients and Takayasu’s disease in two cases. In one of the patients treated for dysplasia, angioplasty was performed for severe restenosis, which appeared 5 years after surgical endarterectomy. The main risk factors were: hypertension (58%), smoking (63%), dyslipidemia (41%), and diabetes (21%).
A multivascular arterial disease was found in numerous cases: coronary disease (64%), peripheral arterial disease (39%), carotid artery stenosis (18%), and renal artery stenosis (6%). In 232 cases, we found a tight stenosis (> 70%) and in 75 cases a total occlusion. The mean percentage of stenosis was: 82.6 ± 7.6% (range: 70–100); the mean lesion length was: 23.6 ± 8.8 mm (range: 10–50); and the mean arterial diameter was: 7.1 ± 0.7 mm (range: 5–9). One hundred and fifty-nine lesions were calcified, 162 were eccentric and 97 were ulcerated. Twenty-seven vertebral arteries were also stenosed on the side of the subclavian lesion, and 4 originated from the stenosed segment. Two hundred and fifty-five lesions were prevertebral lesions, 33 were post-vertebral, and 19 were both pre- and post-vertebral lesions. We found arterial blood pressure asymmetry in all patients on the diseased side. The difference for the systolic blood pressure was always greater than 20 mmHg, mean: 3.8 ± 18 mmHg. The indications for angioplasty were: superior-limb ischemia in 157 patients (subacute ischemia in 8 patients, chronic ischemia in 149 patients), and symptoms and signs of vertebrobasilar insufficiency in 160 patients. Vertebrobasilar insufficiency and superior-limb ischemia were associated in 83 patients. Fourteen patients who had undergone a bypass procedure presented with signs of angina due to coronary steal. Thirty-six asymptomatic patients were also treated
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because the lesion was very tight and because of the associated coronary arterial disease that may have required myocardial revascularization by internal mammary anastomosis. The preangioplasty examination consisted of: ● ●
●
duplex scan of all the supra-aortic vessels; global and selective angiography of the supra-aortic vessels; CT scan and neurological examination by an independent neurologist before the procedure.
The mean length of the stents was 27.3 mm ± 11.4, which indicated that the stents correctly covered the lesions. The mean diameter of the stents was 7.1 mm ± 0.8, which is equal to the diameter of the treated artery. After the procedure, the mean residual pressure gradient was of 3.4 ± 3 mmHg (Table 39.1). There was no longer any significant difference in the blood pressure between the two arms. All treated patients had symptomatic relief acutely. Complications
We diagnosed: ● ● ● ● ● ●
isolated stenoses: 174 subclavian steal syndrome: 119 coronary steal syndrome: 14 associated vertebral stenoses: 27 associated carotid stenoses: 61
●
Technique The femoral access was used alone in 221 patients with a 7- or 8-French guiding catheter according to the technique previously described. The brachial access was used alone in 61 patients using a 7-French introducer and allowing easy stent placement. A combined approach (brachial and femoral) was used in 25 cases in the presence of a total occlusion and in four cases the “pull-through technique” was used with success. It is worth noting that at the beginning of our experience we implanted stents (Palmaz P204 or P 304) in case of suboptimal results (residual pressure gradient > 5 mHg or residual stenosis > 20% on the angiography), but we now implant stents routinely, regardless of the result of angioplasty. Direct stenting may also be performed without predilatation as we did in 96 patients. Immediate technical results (Figures 39.13–39.15) Immediate technical success was obtained in 292 patients (95%). We were able to successfully treat stenosis of subclavian artery (232 patients) with 100% success. However, we were able to treat only 60 total occlusions out of the 75 (80%). Thus, total occlusion of the subclavian artery remained a difficult problem. An isolated balloon angioplasty was performed in 59 cases. We implanted 196 balloon-expandable stents (Palmaz stents: 89, first case in 1989; Corinthian: 58; Express: 49), 52 self-expandable stents: nitinol: 42; Wallstent: 10.
Table 39.1
Before PTA After PTA After PTA and stent
●
●
Local complications. We report three hematomas at the femoral puncture site without any significant consequences and one brachial thrombosis at the puncture site that required surgical treatment. Neurological complications: 2 (0.7%). We report one TIA with diplopia after treatment of a prevertebral lesion without subclavian steal syndrome and one major stroke with a hemiplegia occurring 2 hours after the procedure in a patient presenting with bilateral carotid lesions. This patient died 4 days after the procedure. One subclavian thrombosis occurred after 24 hours in a patient presenting with a dysplasic arterial lesion. The artery could not be recanalized. Since the patient refused surgery, he was treated medically. One subclavian thrombosis occurred at day 30 in a patient presenting with post-radiation stenosis, and was treated by a new PTA and stenting with success.
Follow-up All our patients were followed-up on duplex scan at 24 hours. At 6 months, a duplex scan and an angiography were routinely performed. Then a duplex scan was performed every 6 months, and an angiographic assessment was done only when restenosis was suspected. Our mean follow-up was 68.8 months ± 35.5; the maximum follow-up was of 14.8 years. We had 35 restenoses (12%), 13 occurred following angioplasty alone (18.8%), and 19 following angioplasty and stent implantation (8.4%) (p < 0.01). Stent implantation seems to lower the restenosis rate. Twenty-six restenoses occurred in prevertebral lesions, 4 in post-vertebral lesions, and 5 both in pre- and post-vertebral lesions. We treated these restenoses by another angioplasty (20 cases), angioplasty and stent placement (8 cases), surgery (carotidosubclavian bypass) (7 cases). In a post-vertebral tight
Results after PTA Stenting of Subclavian Arterial Diseases
Mean % stenosis
Mean arterial diameter (mm)
Mean lesion length (mm)
Mean peak systolic gradient (mmHg)
82.6 ± 7.6 11.6 ± 9.7 4.2 ± 3.6
7.1 ± 0.7 7 ± 2.7 7.1 ± 0.8
23.6 ± 8.8 – 27.3 ± 11.4
48 ± 33 5.1 ± 3.8 3.4 ± 3
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(c) Figure 39.11 (a) Right subclavian artery restenosis inside Palmaz stent/right ostial vertebral artery stenosis (b) vertebral artery angioplasty; and (c) result after angioplasty.
restenosis inside a Palmaz stent (implanted for restenosis after surgical endarterectomy), we implanted another self-expandable stent (Optimed, Medcare, Conflans Ste Honorine, France) with a very good result at 6 years (Figure 39.10 and 39.11). Primary (PI) and secondary (PII) patencies (Table 39.2) on an intention-to-treat basis at 10 years follow-up were 78.5 and 84.7%, respectively. In patients without initial stent placement, the rates were 67.5 and 75.5%, while in those with stents, the rates rose to 90.3 and 97.1% (p < 0.01). Primary patency rate for all recanalized lesions were 85.1, 79.1% without stent, 90.3% with stent (p < 0.04) and secondary patency 91.8, 88.5, 97.1% respectively (p < 0.02). Stents seem to improve long-term patency.
Table 39.2
Discussion Subclavian artery stenosis accounts for 2–17% of significant aortic arch artery stenoses although it is frequently associated with various symptoms.25,52 In most cases, the subclavian lesions are of atheromatous etiology and are frequently part of a multivascular arterial disease. Other etiologies may be found such as fibromuscular dysplasia, post-radiation, Takayasu’s disease,65 or other inflammatory arterial diseases. Until now, the surgical treatment was considered as the reference. It involved either an intra- or extrathoracic bypass procedure. Although it was highly effective when successful, transthoracic surgical approaches carry a reported complications rate that could be as high as 23–25%. They included carotid embolization, cerebral
Primary (PI) and secondary (PII) patency 10-year follow-up All lesions
Nb PI (%) PII (%)
Recanalized lesions
Global
Without stent
With stent
p
Global
Without stent
With stent
p
307 78.5 84.7
59 67.5 75.5
248 90.3 97.1
— p < 0.01 p < 0.01
292 85.1 91.8
59 79.1 88.5
233 90.3 97.1
— p < 0.04 p < 0.02
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(a)
(b)
(c) Figure 39.12 (a) Result after balloon angioplasty of right subclavian artery restenosis and vertebral artery angioplasty and stenting; (b) and (c) Optimed stent implantation inside the Palmaz stent.
ischemia, chylothorax, endarterectomy thrombosis, pneumothorax, pleural effusions, wound infection, neck lymph fistula, phrenic nerve palsy, and the most serious, Horner’s syndrome, with a mortality of up to 8%.66,67 The mortality of extra-anatomic bypass is lower, but a complication rate of 8–15% has been published.67–69 More recently, Abu Rahma et al. reported a 20-year series of PTFE carotid subclavian bypasses.70 The morbidity was 6% without stroke or death and the long-term patency excellent. Primary patency of 1, 3, 5, and
(a) Figure 39.13
10 years was 100, 98, 96, and 92% respectively, and the secondary patency 100, 98, 98 and 95%, respectively. For subclavian transpositions, Ballotta et al. demonstrated 2.5% mortality and 2.5% morbidity without stroke with 100% immediate relief of symptoms in 39 patients followed during a mean duration of 6.8 years.71 Endovascular treatment offers a promising alternative with low morbidity, shorter hospitalization, and a high rate of success. The initial technical success rate is of 97% in the series of
(b)
(a) Left subclavian artery stenosis; (b) result after angioplasty and stenting.
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(a) Figure 39.14
Figure 39.15 and stenting.
365
(b)
(a) Tight left subclavian artery stenosis with subclavian steal syndrome; (b) result after angioplasty and stenting.
(a)
(b)
(c)
(d)
(a) and (b) Left subclavian artery stenosis with subclavian and coronary steal syndromes; (c) and (d) after angioplasty
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Mathias,51 92% in the combined series of more than 400 cases reported by Becker et al.,72 94% for Bogey et al.73 and 94% in the data pooled from several studies.19 These results are comparable to the initial result of surgery.14 Recently, Nakamura et al. reported a technical success of 100% in a series of 215 patients.33 This technical success rate depends on the status of the lesion. In the presence of a subclavian stenosis, the success rate is nearly 100%.1,9,18,52,74 However, in the presence of an occlusion, the success rate is much lower in most of the series: 46% for Motarjeme et al.,1 56% for Hebrang et al.,11 55.6% for Prezwlocki et al.,52 69% in our series. However, Mathias et al.51 obtain a success rate of 83% in a series of 46 patients, and Kumar et al. 100%.23 More recently Mathias et al.63 in a series of 416 patients with SA stenosis and 68 with SA occlusion published a primary success rate of 98.8% in SA stenosis, 76.5% in SA occlusion. MacNamara et al.75 in a review of 25 publications of subclavian artery stenoses in the literature (968 patients, 992 lesions) found an initial success rate of 95% and in a review of six publications of subclavian artery occlusions (80 patients) found an initial success rate of 74%. Schillinger et al.76 in a series of 115 patients reported a PTA success in 85% of these patients. Complete occlusion of the vessel and long lesions (≥ 2 cm) correlated with a lower success rate. In the 27 completely occluded vessels, angioplasty via the brachial artery was more often successful than with the transfemoral percutaneous technique (10/14 vs. 3/13, p = 0.02). A fibrinolysis performed before the procedure does not improve the recanalization rate.1 Surgery is indicated in case of failure of recanalization of a subclavian occlusion. The results at the level of the innominate arteries seem similar to those obtained at the initial part of the subclavian arteries.1,23 The complications rate of these procedures remains low, particularly the embolic complications. Concern for the use of PTA in this disease has centered largely on the potential for the release of embolic debris during the procedure. However, significant embolic complications are relatively rare.77 In addition, Ringelstein and Zeumer78 have shown that it takes a significant period of time (20 seconds to 20 minutes or more) for flow in the vertebral artery to change from retrograde to antegrade after successful PTA and they have postulated that this serves as a protective mechanism against cerebellar embolization. Becker et al.72 reported only three neurological complications and four peripheral embolizations in their series of more than 400 procedures. It also appears that the neurological ischemic accidents are mostly transient.79,80 In a review of the literature with 1018 subclavian artery angioplasties, Kachel64 reported a complication rate of 2.8% and an incidence of stroke of 0.2%. Mathias et al.51 observed in 3 of 484 procedures (0.6%) a transient ischemic attack. All of them occurred in the carotid territory and were probably provoked by embolism from the aortic arch. MacNamara et al.75 reported a stroke rate of 0.4% and arm embolism in 0.3% with SA stenosis and an arm embolism rate of 2.5% with SA occlusion. More recently Nakamura et al.33 and Przewlocki et al.52 reported no peri-procedural major complications in their series of, respectively, 215 and 57 patients. A very rare complication was described by Pucillo et al.81: a cerebral hyperperfusion syndrome in the posterior cerebral
circulation after angioplasty and stenting of a totally occluded left subclavian artery. If peri-procedural complications are generally rare and usually minor when treating a stenosis, some life-threatening complications such as aortic arch dissection can occur during the recanalization of a subclavian occlusion. A meticulous technique is needed to treat these lesions. Mathias et al. described three false SA aneurysms treated surgically (0.6%).51 This complication could be now treated by placing prosthetic stent-grafts. Vitek et al. have addressed the question of potential occlusion of the vertebral artery while performing subclavian PTA.10 In their experience, there have been no vertebral artery complications as long as the vertebral artery originates from a non-stenotic segment of the subclavian artery, including both normal appearing segments and segments with post-stenotic dilatation. In the presence of an associated vertebral stenosis, it is better to perform a simultaneous angioplasty procedure using the “kissing” technique, or at least protect the artery with a guidewire kept in place in its lumen during the subclavian artery angioplasty procedure. The technique described by Staikov et al. may be useful in selected high-risk patients for embolism.62 The new techniques of brain protection could also be proposed for these patients. We recently treated a patient presenting with a very tight prevertebral stenosis and a visible thrombus under protection with an EPI filter (Boston Scientific) deployed in the vertebral artery. No neurological complications appeared (Figure 39.16). The restenosis rate after subclavian angioplasty averages 13% after a mean follow-up period of 30 months.22,72 Duber et al. reported restenoses higher after treatment of occlusions (50%),12 but Hebrang et al. reported results that were comparable to those achieved in PTA of stenoses.11 The combined series of Becker et al. suggest about a 19% recurrence rate.72 For MacNamara et al.,75 the restenosis rate is 5.7% at a mean follow-up of 54 months for subclavian artery stenosis and 12% for subclavian artery occlusion at a mean follow-up of 33 months. Nakamura et al. reported a 0.5% restenosis rate in 179 of 195 patients who underwent angiographic follow-up 6–12 months after the procedure.33 For Przewlocki et al. the restenosis rate was 9.4%.52 In our series the restenosis rate was 12%, but was 18.8% after angioplasty alone and only 8.4% after angioplasty and stenting with a mean follow-up of 65.8 months. If a restenosis occurs, a repeat balloon angioplasty can be performed sometimes with additional stent placement. A cutting-balloon angioplasty may also be done with the new large peripheral cutting balloons. The long-term results of this procedure are satisfactory and 1-year patency rates of greater than 85% are consistently reported in the literature.1,12,51,74,75,82–85 More importantly, long-term symptomatic relief is achieved in the majority of cases. Recently Bates et al. reported an overall patency rate of 96, 91, 86, 77, and 72% for years 1 through 5,85 and Wilms et al. reported an 86% clinical success rate at 25 months,13 while Hebrang et al. reported 80% success at 4 years.11 In Mathias’ series after 2-year follow-up a primary patency of 78.8% was found. The results for the subgroup varied considerably between 76 and 84% with the best outcome in the patients
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(a)
(b)
(c)
(d)
(e)
(f)
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Figure 39.16 (a) Left subclavian artery stenosis with thrombus above the stenosis; (b) and (c) EPI filter in the vertebral artery; (d) Palmaz stent implantation under protection; (e) stent dilatation (Palmaz stent); (f) final result.
with subclavian artery stenosis and angioplasty combined with stent placement. The same subgroup had also the best patency rate after 5 years with nearly 77%. The highest recurrence rate was observed in patients with SA occlusion treated only by angioplasty. Forty-six patients had a second angioplasty with stent placement in 41% of them. This secondary patency after 5 years was 76%. In general, long-term patency is better following the treatment of a stenosis than of an occlusion51,82–84 and better in men than in women.85 According to Mathias’s results and our results a prosthesis seems to improve the long-term patency rate and could be implanted after all subclavian artery
angioplasty procedures and at least after the revascularization of any occluded subclavian artery.1,51,82,84 Schillinger et al. recently reported different results.76 The 1-year patency after stenting was significantly better compared to PTA alone due to higher technical success (95 vs. 76%). However, long-term results in stented arteries were less favorable. The 4-year patency rates were 59% in arteries with stent and 68% in arteries without. Long lesions, residual stenosis after PTA, occlusions, and stent implantation were independent predictors for restenosis after successful intervention. In patients with stenosis distal to the vertebral artery, restenosis occurred more frequently compared to proximal lesions.
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Kumar et al.23 propose routine primary stenting because it achieves better results than balloon angioplasty, prevents intimal tear and abrupt vessel closures, theoretically could prevent debris embolization by trapping atherosclerotic material between the stent struts and the arterial wall, prevents possible particulate embolization into the vertebral artery, and possibly lowers the restenosis rate. As far as we are concerned, we currently tend to perform primary stenting in the presence of subclavian lesions and our results showed better long-term patency rates with stents than without stents. Several types of stents may be implanted. Balloon-expandable stents are superior to self-expanding stents for ostial and postvertebral subclavian artery lesions. The deployment of these stents is more precise and this is beneficial in ostial lesions in which a 1–2 mm of “overhang” of the stent in the aorta is desired. Balloon-expandable stents have a good radial force, which may be beneficial because ostial lesions are generally more calcified. Because of the risks of compression, self-expandable stents are better for post-vertebral lesions. If possible it is important to avoid covering the vertebral and mammary arteries. The angioplasty technique of the subclavian artery has several particularities. The approach way should be discussed. The femoral access site is usually used at first intention in the presence of a stenosis. If crossing of the lesion fails, or if the femoral approach cannot be used, brachial access is used, or possibly radial access. This access may also be used to decrease the risk of vertebral embolization during a right subclavian artery angioplasty. In the presence of an occlusion, the brachial or radial access is preferred to the femoral access, more particularly if the occlusion begins at the origin of the subclavian artery.
Combined accesses (femoral plus brachial or radial) are often mandatory.
Conclusion Angioplasty is currently the treatment of choice for lesions of the subclavian and innominate arteries. It should be proposed as the primary treatment because it is associated with low risks, a high initial success rate and good long-term results. The treatment of total occlusions of the subclavian arteries remains difficult and if crossing of the lesion fails, surgery should be opted for. The indications of this procedure are still debated, and yet the subclavian artery deserves to be preserved because it is an axis of cerebral perfusion, and an access site for other angioplasty procedures. In addition, the internal mammary artery, which is of the utmost importance as regards myocardial revascularization, originates from it. Stenting seems to improve the long-term results and we will possibly have to recommend it for all lesions. (We are waiting for controlled randomized studies.) However, at least subclavian artery occlusions should be treated with stents. Balloon-expandable stents with good radial force give an excellent result at the prevertebral level, and self-expandable stents are recommended at the post-vertebral level in order to avoid the possibility of post-vertebral compression. In the future, coated stents might limit the restenosis rate and the new large cutting balloon could avoid some stent implantations and help the treatment of calcified lesions and restenoses.
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Courtheoux P, Theron J, Maiza D et al. L’angioplastie endoluminale percutanée des sténoses athéromateuses des troncs supraaortiques proximaux. Tronc artériel brachiocéphalique, artères sous-clavières. J Mal Vasc 1986; 11: 113–9 Mathias KD, Luth I, Haarmann P. Percutaneous transluminal angioplasty of proximal subclavian artery occlusions. Cardiovasc Interv Radiol 1993; 16: 214–8 Przewlocki T, Dieniazek P, Kaslas-Ziembicka. Endovascular treatment of subclavian artery stenosis: technical efficacy and symptom protection. Am J Cardiol 2004. (Abstracts); 94: 127 E Dorros G, Bates MC, Palmer L et al. Primary stent deployment in occlusive subclavian artery disease. Cathet Cardiovasc Diagn 1995; 34: 281–5 Martinez R, Rodriguez-Lopez J, Torruella L et al. Stenting for occlusion of the subclavian arteries. Technical aspects and follow-up results. Tex Heart Inst J 1997; 24: 23–7 Motarjeme A, Keifer JW, Zuska AJ. Percutaneous transluminal angioplasty of the vertebral arteries. Radiology 1981; 139: 715–17 Théron J. Angioplasty of brachiochepalic vessels. In: Vinuela F, ed. Interventional Neuroradiology: Endovascular Therapy of the Central Nervous System. New York: Raven Press, 1992: 167–80 Kachel R, Endert G, Basche S et al. Percutaneous transluminal angioplasty (dilatation) of carotid, vertebral, and innominate artery stenosis. Cardiovasc Interv Radio 1987; 10: 142–6 Nasim A, Sayers RD, Bell PRF et al. Protection against vertebral artery embolisation during proximal subclavian artery angioplasty. Eur J Vasc Surg 1994; 8: 362–3 Schroth G, Do DD, Remonda L et al. Spiezielle Techniken der Angioplastie brachiocephaler Gefässe. Fortschr Röntgenstr 1997; 167: 165–73 Sharma S, Kaul U, Rajani M. Identifying high-risk patients for percutaneous transluminal angioplasty of subclavian and innominate arteries. Acta Radiol 1991; 32: 381–5 Higashida TR, Tsai FY, Halbach W et al. Transluminal angioplasty for atherosclerotic disease of the vertebral and basilar arteries. J Neurosurg 1993; 78: 192–8 Staikov IN, Daido D, Remonda I et al. The site of atheromatosis in the subclavian and vertebral arteries and its implication for angioplasty. Neuroradiology 1999; 41: 537–42 Mathias K, Jäger H. PTA Proximal subclavian artery obstruction. In: Henry M, Amor M, eds. 10th Internal Course Book of Peripheral Vascular Intervention. ETC Paris, 1999: 607–16 Kachel R. Subclavian arteries and veins. In: Sigwart U, Bertrand M, Serruys PW, eds. Handbook of Cardiovascular Interventions. New York: Churchill Livingstone, 1996: 855–69 Hodgins GW, Dutton JW. Transluminal dilatation for Takayasu’s arteries. Can J Surg 1984; 27: 355–7 Samoil D, Schwartz JL. Coronary subclavian steal syndrome. Am Heart J 1993; 126: 1463–6 Beebe HG, Stark R, Jonson ML et al. Choices of operation for subclavian–vertebral artery disease. Am J Surg 1980; 139: 516–23 Gerely RL, Andrus CH, May AG et al. Surgical treatment of occlusive subclavian artery disease. Circulation 1981; 64 (suppl 11): 228–30 Aburahma AF, Robinson PA, Khan MZ et al. Brachiocephalic revascularization: a comparison between carotid–subclavian artery bypass and axilloaxillary artery bypass. Surgery 1992; 112: 84–91 Aburahma AF, Robinson PA, Jennings TG et al. Carotid subclavian bypass grafting with PTPE grafts for symptomatic subclavian artery stenosis or occlusion: a 20 year experience. J Vasc Surg 2000; 32: 411–9 Ballotta E, Da Giav G, Abbruzzese E et al. Subclavian carotid transposition for symptomatic subclavian artery stenosis or occlusion. A comparison with the endovascular procedure Int. Angiol 2002; 21: 138–44 Becker GJ, Katzen BT, Dake MD. Noncoronary angioplasty. Radiology. 1989; 170: 921–40 Bogey WM, Demasi RJ, Tripp MD et al. Percutaneous transluminal angioplasty for subclavian artery stenosis. Am Surg 1994; 60: 103–6 Henry M, Amor M, Henry I et al. Endoluminal treatment of subclavian occlusive diseases. Percutaneous angioplasty and stenting (abstract). Circulation 1997; 96(8): 1–284 MacNamara TO, Greaser LE, Fisher JR et al. Initial and long term results of treatment of brachiocephalic arterial stenoses and occlusions with balloon angioplasty, thrombolysis, stents. J Invasive Cardiol 1997; 9: 372–83 Schillinger M, Haumer M, Schillinger S et al. Risk stratification for subclavian artery angioplasty: is there an increased rate of restenosis after stent implantation? J Endovasc Ther 2001; 8: 550–7
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Sullivan TM, Gray BH, Bacharach JM et al. Angioplasty and primary stenting of the subclavian, innominate and common carotid arteries in 83 patients. J Vasc Surg. 1998, 28: 1059–65 Reekers JA. Subclavian artery stenosis is best managed by PTA and stent. In: Greenhalgh RM, ed. The Evidence for Vascular and Endovascular Reconstruction. London: Saunders, 2002: 101–5 Sheiban I, Dharmadhikari A, Melissano G et al. Subclavian artery stenting: immediate and mid-term clinical following results. Int J Cardiovasc Intervent 2000; 3: 231–5 Bates MC, Broce M, Lavigne PS et al. Subclavian artery stenting: factors influencing long term outcome. Catheter Cardiovasc Interv 2004; 61: 5–11
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Percutaneous transluminal angioplasty and stenting of extracranial vertebral artery stenosis V Polydorou, I Henry, A Polydorou, M Henry, Ad Polydorou, J Stephanides, M Hugel, and S Anagnostopoulou
Introduction Sundt et al. reported the first successful treatment of a basilar artery stenosis by percutaneous transluminal angioplasty (PTA) in 1980.1 Since then a large number of centers have reported excellent clinical, angiographic, and hemodynamic improvement after treatment of extracranial and intracranial lesions2–15; and since the early 1990s, PTA has been more frequently used to treat stenoses of the vertebral artery. The risk of neurological complications remains high for intracranial lesions. The reason for this is that the intracranial vertebral and basilar arteries are difficult to access and PTA carries a high risk of damage of the perforating arteries that arise from this region.6 PTA for this territory is still uncommon16–18 and the outcome often not good.19 Patients in the chronic stage who showed no response to medical therapy should be considered for PTA.19 There are only a few reports concerning the application of this procedure to these territories during the acute stage.1,7,10,20,21 The treatment of extracranial vertebral artery lesions is easier and can be proposed. A variety of surgical procedures has been described over the years but they are technically demanding and have been associated with a high frequency of complications.13–15,20 However, PTA of these lesions and particularly ostial vertebral artery lesions can now be proposed with safety and efficacy for the treatment of vertebrobasilar ischemia or vertebrobasilar insufficiency (VBI). This is an underdiagnosed condition and the incidence of significant vertebral artery stenosis has been underappreciated.13 The complication rate from embolization of plaque material to the central nervous system can be lowered by improving techniques in microballoon catheter technology, high-resolution radiographic imaging, proper neurological monitoring, and patient selection.8,9,19,22–25 Balloon angioplasty alone has been limited by severe elastic recoil, poor improvement in the luminal area, high propensity for restenosis, and failure to achieve less than 50% stenosis of the final lumen diameter.2,13,19,22,26–29 The use of stents seems to improve immediate and long-term results. The vertebral artery is divided into four segments (Figure 40.1). The first segment V1 includes the origin of the vertebral artery (ostium or V0) up to the level of entry into the
foramen of the transverse process of the cervical vertebral body, usually C6. The second segment V2, or neck segment, courses up to the level of the foramen of the C2 transverse process. Distally to this level up to the atlanto-occipital membrane, where the vertebral artery enters into the subarachnoidal space, this is the V3 segment. The V4 segment is the intracranial portion of the vertebral artery. We will describe the endovascular treatment of the extracranial portion of the vertebral artery and the ostial segment in particular.
General considerations VBI denotes global ischemia of the territory supplied by the basilar artery due to inadequate blood flow. Atherosclerosis is the most common underlying problem in VBI. Other causes are rare: vertebral artery dissection, fibrous banding in the neck, extrinsic compression, vasculitis. Plaque formation results in stenosing lesions that may affect the vertebral artery at any level but are most common at its origin.30 Plaques in the
V.4 V.3
V.2
V.1
V.0 :OSTIUM
Figure 40.1
Vertebral artery stenosis location.
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vertebral artery show the same degenerative features as plaques that appear elsewhere, such as ulceration, intra-plaque hemorrhage, and surface thrombus. The growth of a plaque may ultimately result in thrombosis of the vertebral artery. The vertebral artery lesions may lead to insidious onset with potentially disabling or deadly consequences. The true incidence of this condition is unknown in the general population, but approximately 25–40% of patients with cerebrovascular disease are affected.31,32 One-quarter of all ischemic strokes occur in the territory of posterior circulation.33 Twenty percent of posterior circulation infarcts are thought to be cardioembolic in origin and a further 20% due to intra-arterial embolism, usually from the vertebral artery.34 Seventy percent of vertebral and basilar occlusion is related to tight arterial stenoses.35 In a series of 35 patients with occipital infarction, six had vertebral atheroma with presumed distal embolism.36 So there is evidence that posterior circulation atherosclerosis is implicated in ischemic events. In an angiographic study of 4748 patients with ischemic stroke, some degree of proximal extracranial vertebral artery stenoses was seen in 18% of cases on the right and 22.3% on the left.31
●
symptoms (over hours to days). Thrombotic lesions are often associated with a focal stenosis or an ulcerated plaque which predisposes to platelet aggregation and thrombus formation. Low-flow hemodynamic symptoms may result from critical stenosis or tandem stenoses leading to a reduction in distal perfusion pressure, but are also often positional, brief in duration, generally triggered by changes in the position of the patient’s body or neck, and can be relieved by lying down.
These transient episodes can be caused by etiologies such as isolated atherosclerosis or cervical spondylosis resulting in narrowing of the transverse foramina.30,48 If prolonged ischemia occurs, it can lead to infarction. VBI may also be caused by a subclavian steal syndrome resulting from a highgrade stenosis or an occlusion of the subclavian artery. Hemodynamic stroke is less commonly due to vertebral artery stenosis49 because both vertebral arteries feed into one basilar artery. Also, in contrast to the internal carotid artery, the vertebral artery gives off numerous branches in the neck, therefore facilitating a considerable collateral blood supply which often reconstitutes the distal artery after occlusion at the origin.49
Clinical findings Clinically patients may present with posterior fossa transient ischemic attacks (TIAs) or strokes and/or repetitive symptoms of VBI, including dizziness, diplopia, ataxia, nausea, vomiting, vascular headaches, bifacial numbness, cortical blindness, memory disturbance, nystagmus, and drop attacks. Other symptoms referable to posterior circulation ischemia include homonymous hemianopsia, poor hand–eye coordination, visual agnosia, vertical gaze nystagmus, alternating hemiparesis and hemianesthesia, cranial nerve dysfunction, lethargy, and altered mental status.36–39 Symptoms of VBI are often not well recognized by physicians potentially leading to delay in treatment and other mismanagement. A wide variety of symptoms are reported by the patients and these symptoms are often similar to those attributable to other body systems. A large number of patients with vertebral artery disease may remain asymptomatic but 50% present with a stroke alone and 26% present with TIA rapidly followed by stroke.40 Patients suffering from TIA have a 22–35% stroke risk over 5 years41–43 and the mortality associated with a stroke is 20–30% greater than for a carotid stroke.44–46 Vertebrobasilar ischemia can result from embolic, thrombotic, and low flow hemodynamic mechanisms. ●
●
Embolism (same as with internal carotid artery disease) is the most frequent cause for vertebrobasilar ischemia and is most frequently associated with a vertebral artery lesion.32,34 It manifests with sudden maximal onset of neurological symptoms. These symptoms can resolve quickly especially if rapid spontaneous lysis of the embolus occurs. Post-infarction intracerebral hemorrhage is more common with an embolic source than with thrombotic or low-flow hemodynamic source of stroke.47 Thrombotic cerebral ischemia has a slower, more fluctuating course prior to the development of maximal neurological
Diagnostic imaging work-up The diagnostic imaging work-up of patients suspected of VBI may begin with a duplex examination and should include magnetic resonance imaging (MRI) with or without magnetic resonance angiography (MRA) or computed tomographic scan of the brain with close evaluation of the posterior fossa and brainstem. For the prognosis it is important to determine whether the patient has suffered a stroke as opposed to an ischemic event, which can be reversible. It is also important to determine if the stroke is hemorrhagic or non-hemorrhagic. MRA could be useful as a screening test to evaluate stenoses of both intracranial and extracranial vessels.50–54 Angiography is essential with a complete four-vessel arteriogram as well as the intracranial portion of both the posterior and anterior circulation before deciding whether a patient is a suitable candidate for PTA. This is necessary to ascertain whether symptoms are secondary to ischemia from a hemodynamically critical stenosis or a thromboembolic stroke with occlusions of an intracranial vessel. Angiography is also necessary to determine the extent of the lesion and evaluate it for evidence of ulceration, degree of stenosis, and presence of fresh intraluminal thrombus. More than 90% of the vertebral artery pathology occurs at the origin of the vertebral artery and this anatomy is involved in approximately 40% of all patients with symptoms of VBI. Angiography is also essential to evaluate possible associated lesions in carotid and subclavian arteries. Imaging of the cervicocerebral arch is also essential when planning access for any neurointerventional procedure.
Indications for vertebral angioplasty Classically patients should be managed initially by conventional medical therapy. Only patients who fail to respond to
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Percutaneous transluminal angioplasty and stenting of extracranial vertebral artery stenosis this therapy should be considered for PTA.37,55–59 A complete neurological history and examination must be performed on all patients by an independent neurologist before and after the procedure and during the follow-up. The current indications for the correction of extracranial vertebral artery lesions require:13,60 ●
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●
●
●
symptomatic (transcient ischemic attack or non-disabling ischemic stroke in the vertebral artery system) significant bilateral vertebral artery stenoses causing > 60% diameter reduction; asymptomatic unilateral significant stenosis of a dominant vertebral artery; asymptomatic significant vertebral artery stenosis or tandem lesions with evidence of resting posterior fossa hypoperfusion or diminished cerebrovascular reserve may be considered for treatment due to high risk for infarction; significant stenoses in an asymptomatic patient who needs collateral support (for example concurrent carotid artery occlusion); asymptomatic patients with high grade (> 70% stenosis) lesions or progressive severity of the stenosis are associated with an increased risk for stroke and would benefit from treatment, especially those with disease of either the dominant vertebral artery or a singular vertebral artery.60
Angioplasty and stent placement The procedure is performed under local anesthesia and intravenous conscious sedation and analgesia. Continuous neurological monitoring throughout the procedure is performed to quickly recognize any neurological complication.
(a)
(b)
373
Access Percutaneous access through the femoral artery is used in the majority of cases.4,8,12,13 Brachial access is used in cases of severe lower extremity atherosclerosis, severe arterial tortuosities, unfavorable anatomy of the aortic arch with severe angulation of the vertebral artery origin, and when femoral access fails.13 The radial approach has recently been proposed.61 Techniques The techniques used in angioplasty and stent placement are illustrated in Figures 40.2–40.5. By the femoral approach, a 6-French to 8-French guide catheter or long introducer sheath (depending on the artery and the lesion) is inserted and a systemic anticoagulation is achieved by administrating intravenous heparin starting with 50–70 units/kg to attain an activated coagulation time > 250 seconds. An appropriately shaped guide catheter (multipurpose, VBA catheter, right Judkins) is positioned in the subclavian artery just proximal to the ostium of the vertebral artery to be treated. For better control and support and to prevent the guide catheter from losing its position, an 0.018-inch extrasupport buddy wire can be placed in the ipsilateral axillary artery.13 Quantitative angiography is performed to evaluate the lesion, the degree of the stenosis and measure the diameter of the vessel to size balloons and stents. The degree of the stenosis is calculated in relation to the adjacent distal normal vessel diameter (analogous to the North American Symptomatic Carotid Endarterectomy Trial method for grading carotid artery stenosis) and calibration of the measurement is performed using the contrast-filled guide catheter as the reference. The balloon diameter is determined by measuring the normal caliber of the vessel but below and above the site of the
(c)
(d)
Figure 40.2 Left V0 vertebral artery stenosis: (a) before angioplasty; (b) balloon angioplasty; (c) result after balloon angioplasty; and (d) final result after coronary stent implantation (NIR stent).
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(a)
(b)
(c)
(d)
Figure 40.3 Left V0 vertebral artery stenosis: (a) before angioplasty; (b) balloon angioplasty; (c) result after balloon angioplasty: residual stenosis; and (d) final result after stent implantation (Palmaz stent).
stenosis so that it approximates but does not exceed this measurement. The diameter of the vertebral artery varies from 3 to 6 mm. The stenosis is crossed with a 0.014-inch or 0.018-inch coronary wire. The wire should be positioned far enough distally so that it is stable. The tips of the wire should be
(a)
(b)
visualized during the entire procedure to reduce the risk of perforation. Two techniques may be performed: ●
●
predilatation of the stenosis followed by stent implantation; direct stenting.
(c)
Figure 40.4 Left V0 and V1 vertebral artery stenosis: (a) before angioplasty; (b) after angioplasty and stenting of V0 lesion (Corinthian stent); and (c) final result after balloon angioplasty of V1 lesion.
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Percutaneous transluminal angioplasty and stenting of extracranial vertebral artery stenosis
(a)
(b)
(d)
(e)
375
(c)
Figure. 40.5 Vertebral and subclavian artery stenosis: (a) before angioplasty; (b) kissing balloon techniques; (c) Palmaz stent implantation in vertebral artery; (d) final stent result after Palmaz stent implantation in vertebral artery and Wallstent in subclavian artery; and (e) 1 year follow-up: excellent patency of both arteries.
Predilatation is useful in cases with a very tight or calcified stenosis. Angioplasty is performed with a coronary balloon. The balloon should be inflated for no more than 10 seconds to avoid induction of further ischemia in an already compromised area. After angioplasty, an angiography control is done to evaluate its results and choose the stent. The choice of the stent is largely governed by the location of the lesion and its anatomy. Balloon-expandable stents may be used to treat vertebral artery stenoses. For large vessels (> 4 mm in diameter) peripheral stents such as the Palmaz stent, Palmaz Corinthian (Cordis, Warren, NJ), Boston Express (Boston Scientific, Natik, MA) Medtronic AVE (Medtronic, Santa Rosa, CA) or other stents can be implanted and mounted on Speedy balloon (Boston Scientific) or other low-profile balloon. For smaller vessel any coronary stent can be used. Stents are deployed at high pressure (10–18 atmospheres). Self-expanding stents are reserved for vertebral arteries with large diameters (> 5 mm). Stents with monorail design are preferable to
over-the-wire stents to simplify the technique. The stent diameter should be sized to the vertebral artery distal to the lesion. Overdilatation can cause dissection or increase the risk of embolization. The stent length should be sized to cover the entire lesion. Contrast media injection through the guide catheter facilitates the precise positioning of the stent. For ostial lesions the stent must be placed no more than 1 mm inside the lumen of the subclavian artery. Protrusion of the stent into the subclavian artery is necessary to treat plaque within the subclavian artery that is contributing to the vertebral artery ostial lesions. After placement of the balloon-mounted stent, the balloon can be partially withdrawn, then reinflated at higher pressure to flare the proximal part of the stent. By the brachial approach the same technique is used after insertion of a 6-French or 7-French sheath in the humeral artery. Whatever the technique, a post-procedure arteriogram is performed to evaluate the results of the procedure and the intracranial circulation for evidence of complication and
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distal embolization. Close neurological evaluation is performed during and immediately after the procedure and the day after. Patients are followed neurologically at 6 months post-procedure. Doppler ultrasound is performed before the procedure, at day 1 and 6 months later. Angiographic control is also performed at 6 months with CT scan evaluation. In case of association of vertebral artery stenosis and subclavian artery stenosis (Figure 40.5), a kissing-balloon technique can be performed by femoral approach. A coronary wire is placed into the vertebral artery and a coronary balloon advanced over this wire. Another guidewire is placed in the subclavian artery with a dilatation balloon over it. The two balloons are placed at the site of the vertebral artery and subclavian artery stenoses and simultaneously inflated. Decision for stent placement is made by evaluation of the angioplasty results after deflation and withdrawal of the balloons. With these techniques, the complication rate from embolization of plaque material is low22,27,29,62 and could be lowered by improving techniques18,22–25 but brain embolization is always a possible complication of these procedures. Analyzing the site of plaques and stenoses in vertebral artery and subclavian artery, Staikov described a special double-balloon PTA technique which may be helpful in high-risk situations and particularly when a vertebral artery stenosis is associated with a subclavian artery stenosis to avoid brain embolism.8 The double-balloon technique for PTA of the subclavian artery and vertebral artery has been employed previously.24 Two selective PTA catheters are used simultaneously, one by the femoral approach and one by the brachial artery approach. The brachial catheter is exchanged over a coronary wire for a balloon catheter and the balloon placed at the origin of the vertebral artery. The balloon in the vertebral artery is inflated to protect the vertebrobasilar territory from potential emboli when the subclavian artery stenosis is crossed by the guidewire and then by the dilatation balloon. The subclavian artery stenosis is dilated while the vertebral artery dilation balloon is inflated. After dilatation of the subclavian stenosis the transfemoral balloon is deflated first and withdrawn to the origin of the subclavian artery. The restored blood flow therefore flushes potential debris into the brachial artery. Then the vertebral artery balloon is deflated. The result of PTA of the subclavian artery and the vertebral artery is evaluated by injection of contrast medium. If the result is not satisfactory the procedure can be repeated or a stent can be placed by the transfemoral or transbrachial approach in the subclavian artery or the vertebral artery. When PTA has been successful, catheters and guidewires are removed. A cerebral protection device (protection balloon, filter) could be used to protect the brain in specific situations with patients at high risk for brain embolization. Nevertheless, some difficulties to recover the device could occur in unfavorable angulation of the vertebral artery origin after stent deployment. We recommend the use of distal protection devices in large vertebral arteries (diameter > 3.5 mm), favorable geometric orientation of the vertebral artery origin, highrisk ulcerated plaques in patients with documented embolism.
before the procedure and the same treatment is continued for 4 weeks. Thereafter only aspirin is given.
Results Patient characteristics Sixty vertebral artery angioplasties were attempted in 58 vessels in 55 patients. There were 40 males, 15 females, ranging in age from 22 to 82 years (mean age: 67.5 ± 6.8 years). One patient had 3 lesions in the same vertebral artery at V0, V1, and V2 segments. One patient had 2 lesions in V0 and V1 segments. Two patients had bilateral vertebral artery stenosis at V0 segment. In total, 55 lesions at V0 segment (ostium), 4 at V1 segment, and 1 at V2 segment were treated (left: 31, right, 29). Fifty-eight lesions were atheromatous, 2 due to inflammatory arteritis. All patients were symptomatic: dizziness (n = 55), bilateral weakness (n = 9), visual changes (n = 8) diplopia (n = 8), drop attacks (n =), TIA (n = 5), ataxia (n = 4), and dysarthria (n = 1). Eleven vertebral artery stenoses were associated with severe subclavian artery stenoses. Three lesions involved the origin of the vertebral artery; 8 were located at the ostium of the subclavian artery. These subclavian artery stenoses were responsible for arm claudication in 9 cases and recurrent angina pectoris in 2 patients presenting with left internal mammary artery bypasses. These vertebral artery stenoses were treated during the same procedure. Other associated diseases were present: 39 patients (71%) had carotid stenoses, 38 (69%) coronary diseases, 15 (27%) peripheral vascular diseases, and 10 renal stenoses, necessitating interventional procedures. Other co-morbidities included 31 patients (56%) with hypertension, 26 smokers (47%), 25 (45%) with elevated cholesterol (> 200 mg/dl), 13 (24%) with diabetes mellitus, and 8 (15%) with obesity. Four patients (7%) were in congestive heart failure, 3 (5%) had renal insufficiency, 3 (5%) pulmonary insufficiency. Technique Femoral access way was used in all cases. Failure to access the vertebral artery occurred in two cases (3.3%) owing to severe tortuosities of iliac arteries and supra-aortic vessels. In these cases catheterization of the vertebral artery was attempted by a humeral approach which also failed due to the same problem of vessel tortuosities. These high-risk patients were treated medically. Six lesions were treated by PTA alone: ● ● ● ●
Fifty-three lesions were treated with stents: ● ● ●
Medication Aspirin (160 mg/day) and either ticlopidine (250 to 500 mg/day) or clopidorel (75 mg/day) are given at least 3 days
3 V0 lesions (the first 3 patients) 2 V1 lesions 1 V2 lesion 1 V0 lesion in a patient presenting with inflammatory arteritis was treated with cutting balloon.
● ●
11 with Palmaz stent (Cordis, Warren, NJ) 4 with Medtronic AVE (Medtronic, Santa Rosa, CA) 1 with Corinthian (Cordis) 35 with coronary-type stents 2 (for V1 lesions) with Optimed self-expandable stent (Optimed, Germany).
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Percutaneous transluminal angioplasty and stenting of extracranial vertebral artery stenosis Thirty-five lesions were treated by direct stenting, 18 after balloon angioplasty. Eleven subclavian artery stenoses were treated during the same procedure. Eight lesions located at the ostium were treated with balloon expandable stents and three lesions involving the origin of the vertebral artery at first by kissing balloon technique by femoral approach, then stented. The vertebral artery lesions were treated with balloon selfexpandable stents (Wallstent, Boston Scientific). A protection device (EPI filter, Boston Scientific) was used in three cases in patients presenting with tight ulcerated ostial vertebral artery stenoses associated with diffuse lesions of the subclavian and vertebral artery. No difficulties were observed in placing and removing the filter. Visible debris was seen in two cases. Angiographic results The results are illustrated in Figures 40.4 and 40.5. The vertebral artery reference size was 4.6 ± 0.6 mm (range: 4–6). The mean percentage stenosis before the procedure was 82.6 ± 7.9% (range: 70–98), the mean lesion length 9.4 ± 2.5 mm (range: 5–14) and the minimum lumen diameter (MLD) 1.12 ± 0.49 mm. Procedural success, defined as < 20% diameter stenosis without any major neurological event, emergency surgery, or death after angioplasty and stent placement, was achieved in 58/60 cases. The post-stent MLD was 4.55 ± 0.8 mm, the mean residual stenosis 2.2 ± 3.5%, and the acute gain 3.43 ± 0.7 mm (Table 40.1). Procedure: related results and complications There were no direct procedure-related myocardial infarctions, strokes, or deaths during the 30 days following the procedure. None of the patients experienced cranial nerve palsies, wound infection, bleeding requiring transfusion, significant brachycardia, hypotension, or loss of consciousness after treatment with balloon inflations. In all patients we observed a significant clinical improvement with complete resolution of the clinical symptoms. Follow-up Patients had a careful follow-up after the procedure. Vertebral duplex sonography, neurological examination were performed the day after the angioplasty, at 1 month, 6 months, 1 year and each year thereafter. A control angiography was also programmed at 6 months. The results of clinical follow-up are available for 50 patients at a mean of 27.3 ± 26.1 months (three patients died, two were lost at follow-up). During this time, four patients (8%) have had neurological symptoms due to a restenosis as confirmed by duplex scan and angiography. These restenoses included one total occlusion of the vertebral
Table 40.1
Immediate Results
MLD (mm) % diameter Acute gain (mm)
Baseline
Post-stenting p value
1.12 ± 0.49 82.6 ± 7.9
4.55 ± 0.8 2.2 ± 3.5 3.43 ± 0.7
< 0.001 < 0.001
377
artery treated medically, and three tight restenoses (stenosis > 70%), which were treated successfully by new angioplasty. The clinical symptoms resolved after the procedure. Three restenoses appeared in our first three patients treated by PTA alone, one restenosis after PTA and stent.
Discussion Vertebrobasilar insufficiency is probably an underdiagnosed clinical condition13 because patients often have non-specific symptoms. The new non-invasive techniques (duplex scan, MRI, CT scan) facilitate the diagnosis and a stenosis of the vertebral artery is increasingly suspected, leading to angiography which remains the main technique to confirm the presence of a lesion in the vertebral artery territory. Medical treatment alone has been the standard treatment for patients suffering from VBI, including antiplatelet therapies or anticoagulation with warfarin or a combination of these two treatments.63–65 Only in the most severe cases after failure of medical treatment have surgical options been considered, because of the potential complications and complexity of the procedure. A variety of surgical techniques have been developed for the treatment of the stenosis in the proximal vertebral artery, including endarterectomy, vertebral reimplantation into the common carotid artery or the subclavian arteries,66,67 and bypass from the carotid or subclavian arteries using prosthetic grafts or autologous veins. In general, a supraclavicular approach is used, although occasionally, a transthoracic approach is necessary. In a series of 165 vertebral artery operations, published by the Joint Study of Extracranial Arterial Occlusion,67 the mortality rate was 4.2%, the incidence of peri-operative vertebral artery occlusion 6%. In another series,66 109 vertebral artery operations were performed with a 3% mortality rate and 2% of immediate thrombosis. Results of 369 extracranial vertebral artery reconstructions69 (252 proximal, 117 distal) found a combined stroke-and-death rate for proximal reconstruction of less than 2% and cumulative patency rates of 92% at 10 years followup. In addition, the complications of surgery were considerable, with an incidence of Horner’s syndrome of 10% and a similar frequency of lymphoceles. Other series have described vocal cord paralysis, phrenic nerve injuries, and potential pulmonary complications from the thoracotomy.66,67 Given the difficulties in operating on the vertebral artery, a percutaneous endovascular approach, angioplasty, has been proposed to treat a vertebral artery stenosis. The initial radiological and clinical results were uniformly reported beneficial to the patients.2,3,26–29,70,71 However in most of the cases the stenosis was not fully dilated to the normal diameter of the vertebral artery.29 If one carefully reviews previous reports on vertebral ostial angioplasties, most illustrations carry residual stenosis after the procedure. It has been well recognized that certain lesions, particularly those located at the ostia of coronary and renal arteries, have severe elastic recoil that limits the success of PTA.13,72–74 At ostial vertebral artery level, this may be due in part to adjacent subclavian plaque encroaching on the orifice of the vertebral artery The stenosis at the ostium of a relatively small artery which originates from a significantly larger artery has a natural tendency for elastic recoil. This is exacerbated by the fact that the atherosclerotic plaques usually
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overlap the origin of the vessel and are extended into the wall of the larger artery, thus impeding the mechanism of PTA, such as sharing the intima and media and cracking the atherosclerotic plaque. The use of larger balloons to gain greater luminal area has been proposed but often results in severe dissections that cause end-organ damage. Hence there is the need for an endovascular scaffold or stent to hold back the elastic recoil and prevent restenosis. Vertebral artery balloon angioplasty alone has been reported safely and is widely reported to help symptomatic patients.2,3,13,27,71 The largest reported series is from Higashida.71 Thirty-four vertebral angioplasties were performed with an 8.8% incidence of transient neurological complications and no permanent neurological complications. Follow-up angiography revealed restenosis in 9% of patients within 2–5 months of angioplasty, with an undisclosed angiography follow-up rate. Nevertheless, some other reports where PTA alone was performed for vertebral artery origin stenosis were associated with a marked incidence of restenosis comparable to that seen in PTA of ostial renal artery stenosis.15–75 Storey et al. reported that all three patients who underwent vertebral angioplasty alone developed systematic restenoses within 3 months.15 Stenting was subsequently undertaken in two patients with excellent results and no restenosis at 1-year follow-up. Cloud et al. reported also that a restenosis after balloon angioplasty had occurred in all four patients treated without stenting by one year.74 In contrast, only 1 of 11 arteries in which a stent was deployed showed restenosis over an average of 20 months of follow-up. In our series, our first three patients treated without stenting also developed a restenosis. To overcome the problem of elastic recoil and atherosclerotic plaque overlap into the subclavian artery and to improve the long-term results, stenting was proposed for the treatment of vertebral artery stenoses. From the coronary literature, there are some suggestions of improved rates of patency and restenoses in stented vessels and also diminished rates of thromboembolism when stents are used. This reduction in thrombus formation and thromboembolism occurrence is thought to be due to a protective
Table 40.2
layer of fibrous and neointimal tissues growing over the stent mesh and covering the atherogenic tissues of the vessel wall. Another advantage of primary stenting is a reduced rate of internal dissection.49 The ideal stent for any segment of the vertebral artery has to be discussed. For ostial lesions, balloon-expandable stents seem to be a good option, either peripheral or coronary stents, depending on the diameter of the artery. These stents have a good radial force, short length, good radio-opacity, and allow a precise positioning. When the proximal V1 segment is very tortuous or kinked, flexible stents may be used, especially coronary stents. A stiffer stent may possibly cause kinking of the artery after stenting. Appropriate placement of the stent in the ostium of the vertebral artery may need multiple angiographic projections to delineate the true ostium, since the artery comes off posteriorly and superiorly from the subclavian artery. For lesions in the V2 segment, with bone surrounding the vessel, selfexpandable stents like the Wallstent are better to avoid compression by the bone during the neck movements. For ostial lesions the most important technical detail of this technique is proper, precise stent placement. The stent is intentionally placed minimally projecting into the subclavian artery. Meticulous attention to the precise relationship of the proximal edge of the stent to the subclavian artery is essential before deployment. To date, the series with primary stenting of vertebral artery stenoses have shown high levels of technical success: 97–100% in most of the published series; and high levels of clinical success: the percentage of asymptomatic patients remained high during the follow-up period (Table 40.2), more than 90% in most of the series. The complication rate and the death-stroke event rate occurring during the inhospital stay was low (Table 40.2). Some TIA were reported.71,84,87 Stroke and death were rarely reported.12,76,79,81,87 The essential issues involved in the long-term follow-up of patients who undergo vertebral artery angioplasty and stenting are the frequency of in-stent recurrent stenoses and the presence or absence of symptoms of VBI. The rate of restenoses varies from one series to another (3–43%) and may be related to patient selection and of the duration of the
Vertebral Angioplasty and Stenting
Authors
Year
NBR Lesions
Tech. Suc.%
Mean F.U. Months
Restenosis %
Higashida Malek Chastain Jain Mukherjee Jenkins Chiras Cloud Albuquerque Mathias Lutsep Ko Janssens Kizilbilic Hauth
1993 1999 1999 2000 2001 2001 2002 2003 2003 2003 2003 2004 2004 2004 2004
34 13 55 73 12 38 13 10 33 278 14 25 16 14 16
100 100 98 97 100 100 100 100 97 97 94 100 100 100 87
N.A. 20.7 25 12 6.4 10.6 12 19.7 16.2 N.A. 6 25 30 N.A. N.A.
9 25 10 5.6 8.3 3 7.7 10 43.3 20-30 43 16 25 0 N.A.
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Percutaneous transluminal angioplasty and stenting of extracranial vertebral artery stenosis follow-up. But vertebral artery recurrent lesions are largely asymptomatic. The most important and recent published series are reported in Table 40.2. Chastain treated 55 vessels in 50 patients with a technical success of 98% and no direct procedure related myocardial infarction, stroke or death.13 A clinical follow-up review performed at a mean of 25 ± 10 months revealed two patients with recurrence of VBI symptoms. Six-month angiographic follow-up was completed in 90% of eligible patients with a 10% incidence of restenosis. Piotin treated seven patients with immediate resolution or improvements of symptoms in all patients.11 Malek performed 13 vertebral artery angioplasties and stent placement with improvements in symptoms in all patients except one who developed a stroke after the procedure due to a thrombotic occlusion of an untreated cavernous carotid artery stenosis.12 One patient had a transient ischemic attack (TIA). None had minor stroke. At long-term follow-up of the 13 patients (mean 20.7 ± 3.6 months) 11 (84.6%) remained symptom-free and two (15.4%) had persistent symptoms. There were no clinically evident infarcts during the follow-up period. Mukherjee et al. performed vertebral artery stenting in 12 patients with vertebrobasilar TIAs.83 All lesions were successfully stented, with no significant residual stenosis. Clinical follow-up showed resolution or improvement of symptoms in all patients. At follow-up (mean 6.4 months) all patients were alive and asymptomatic. One patient had symptomatic restenosis at 7 months and required repeat angioplasty. Jenkins et al. treated 38 vertebral artery stenoses in 32 patients.84 Success was achieved in all patients. One patient experienced a TIA 1 hour after the procedure. At follow-up (mean 10.6 months) all patients were alive and 31 (97%) asymptomatic. One patient had in-stent restenosis at 3.5 months and underwent successful balloon angioplasty. Zhang treated 16 patients with an angiographic success of 100% and one post-procedure TIA.85 The restenosis rate was 6.2% at 6-month angiographic follow-up. Maini et al. treated successfully 14 vertebral artery in 13 patients with coronary stents.87 One patient had an asymptomatic subarachnoid hemorrhage which resolved before discharge. At 20-month follow-up 66% (n = 6) of patients were totally asymptomatic, 22% (n = 2) had markedly decreased symptoms and 11% (n = 1) had persistent symptoms. In a multicenter registry,83 73 patients were enrolled, with a procedural success of 97%, and 3 in-hospital complications: 1 TIA, 1 stroke and 1 death. Sixty-six patients remain asymptomatic during a mean follow-up of 12 months (94.4%), 4 patients (5.6%) developed restenosis with recurrent symptoms. The series of Albuquerque involved angiographic follow-up in 30 of the 33 patients at a mean follow-up period of 16.2 months.88 Restenosis occurred in 43% of the patients. Among 21 patients with TIAs, 6 had complete resolution, 12 noted fewer events and 3 had no change in symptoms. There was no correlation with restenosis and recurrence of symptoms. In the SSYLVIA trial, 43% of the patients showed evidence of restenoses, half of which had complete occlusion of the vessel.76 All these series showed that the peri-procedural complication rate is low, but potential complications include emboli
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originating from atheromatous plaques like at the carotid bifurcation location. When emboli are washed into the vertebrobasilar system, stroke may result. Most workers believe that the risk of embolization is low22,27 but some feel that the risk is substantial and that PTA technique could be improved to lower the risk22–25,71 especially with plaques in the subclavian artery, close to the origin of the vertebral artery. The doubleballoon technique as described previously with the two approach ways seem useful (coronary devices), and the possibility of direct stenting should minimize the risk of complications. Brain protection devices could also be used in this field as for carotid angioplasty (protection balloons, filters), at least for high-risk patients. Microembolization is a very important concern in endovascular intervention of any arterial system supplying the brain, and emboli protection devices are likely to play an important role in vertebral artery stenting in the future.89 Antiplatelet and antithrombotic therapy before and during the procedure, and after the stenting is very important to prevent thrombus formation and distal embolization. It is the rational to premedicate the patients for 2–3 days with aspirin and ticlopidine or clopidogrel before the intervention and keep them on this medication for 1 month after the procedure. Abciximab was recently proposed for high-risk patients to reduce the risk of ischemic and embolic events.90 All these series also showed a significant variability of restenosis risk and the next stage of advancement in vertebral artery stenting could be the use of drug-eluting stents. These stents reduce dramatically the incidence of restenosis in coronary artery lesions especially in diabetic patients, but the results in peripheral arteries (SIROCCO study) were less promising. We have to wait for randomized studies in the vertebral artery territory. Biodegradable stents could also be useful in the future. Three controversial issues remain, well described by Chastain:13 ●
●
●
The need for intervention in asymptomatic patients found incidentally to have a stenotic vertebral artery lesion. These patients are treated because of the perceived need for the VB system to provide hemodynamic or collateral support. It is also necessary to consider that, although they are believed to be asymptomatic, many of these patients may have non-specific symptoms such as dizziness91,92 that may be alleviated by restoring adequate perfusion pressure to the VB system. The need for intervention in case of a stenotic vertebral artery with a normal contralateral vertebral artery. Although the hemodynamic effect of the stenosis on brainstem perfusion can be easily compensated for by the normal contralateral vessel, the risk of in situ thrombus formation and distal embolization is not eliminated. This pathogenic mechanism is reported to be a factor in approximately 25% of patients with VBI more frequently in these with unilateral lesions.40 Whether the intervention should be reserved for patients in whom medical therapy has failed. We have no prospective randomized data. The treatment with both antiplatelet and anticoagulating drugs is at low risk but does not treat the distal hemodynamic compromise caused by stenotic vertebral artery lesions. This is significant enough to have been reported to cause VBI in 16% of the patients with this diagnosis.40
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Conclusion Percutaneous angioplasty and stent placement seem a useful technique for the treatment of VBI and the first treatment to be proposed. This technique appears safe and effective for alleviating symptoms and improving blood flow to the cerebral circulation, with a low complication rate and good long-term results. However, this procedure needs experienced interventionists to choose the stent and have appropriate placement of
the stent in the ostium of the vertebral artery. The tortuosity of the vertebral artery may be technically challenging. The new coronary stents seem to be well suited to treat atherosclerotic lesions of the origin and of the proximal vertebral artery. A large variability of restenosis risk has been reported. Drugeluting stents may be the solution. Further prospective randomized studies are needed to demonstrate its clinical effectiveness in stroke prevention, its durability, and to define more clearly its indications.
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Sundt TM, Smith HC, Campbell JK et al. Transluminal angioplasty for basilar artery stenosis. Mayo Clinic Proc 1980; 55: 673–80 Courtheoux P, Tournade A, Theron J et al. Transcutaneous angioplasty of vertebral artery atheromatous ostial stricture. Neuroradiology 1985; 27: 259–64 Theron J, Courtheoux P, Henriet JP et al. Angioplasty of supraaortic arteries. J Neuroradiol 1984; 11: 187–200 Higashida RT, Hieshima GB, Tsai FY et al. Transluminal angioplasty of the vertebral and basilar artery. AJNR 1987; 8: 745–9 Schutz H, Yeung HP, TerBrugge K, et al. Dilatation of vertebral artery stenosis. N Engl J Med 1981; 304: 732 Nomoura M., Hashimoto N., Nishi S. et al. Percutaneous transluminal angioplasty for intracranial vertebral and/or basilar artery stenosis. Clin Radiol 1999; 54: 521–7 Lanzino G, Fessler R, Miletich R. et al. Angioplasty and stenting of basilar artery stenosis: technical case report. Neurosurgery 1999; 45: 404–8 Staikov IN, Dai Do D, Remonda L. et al. The site of atheromatosis in the subclavian and vertebral arteries and its implication for angioplasty. Neuroradiology 1999; 41: 537–42 Crawley F, Clifton A, Brown M M. Treatable lesions demonstrated on vertebral angiography for posterior circulation ischemic events. Br J Radiol 1998; 71: 1266–70 Kubis N, Houdart E, Merland J-J et al. Angioplastie des sténoses athéromateuses hémodynamiques des artères vertébrales intracrâniennes. Rev Neurol 1997; 153: 6–7, 386–92 Piotin M, Spelle L, Martin JB, et al. Percutaneous transluminal angioplasty and stenting of the proximal vertebral artery for symptomatic stenosis. AJNR 2000; 4: 727–31 Malek AM, Higashida RT, Phatouros CC et al. Treatment of posterior circulation ischemia with extracranial percutaneous balloon angioplasty and stent placement. Stroke 1999; 30: 2073–85 Chastain II H, Campbell M, Iyer S. et al. Extracranial vertebral artery stent placement: in-hospital and follow-up results. J Neurosurg 1999; 91: 547–52 Touho H, Karasawa J. Hemodynamic evaluation of the effect of percutaneous transluminal angioplasty for atherosclerotic disease of the vertebrobasilar arterial system. Neurol Med Chir 1998; 38: 548–55 Storey GS, Marks MP, Dake M et al. Vertebral artery stenting following percutaneous transluminal angioplasty. Technical note. J Neurosurg 1996; 84: 883–7 Honda S, Mori T, Fukuoka M et al. Successful percutaneous transluminal angioplasty of the intracranial vertebral artery 1 month after total occlusion – case report. Neurol Med Chir 1994; 34: 551–4 Nakano S, Yokogami K, Yamada R et al. Acute thrombolytic therapy and subsequent angioplasty for atherosclerotic stenosis of basilar artery – case report. Neurol Med Chir 1995; 35: 674–7 Nakatsuka H, Ueda T, Ohta S et al. Successful percutaneous transluminal angioplasty for basilar artery stenosis: technical case report. Neurosurgery 1996; 39: 161–4 Terada T, Yokote H, Tsuura M et al. Tissue plasminogen activator thrombolysis and transluminal angioplasty in the treatment of basilar artery thrombosis: Case report. Surg Neurol 1994; 41: 358–61 Touho H, Ohnishi H, Karasawa J et al. Percutaneous transluminal angioplasty for acute stroke due to stenosis of major cerebral vessels: Report of two cases. Surg Neurol 1994; 41: 362–7 Mori T, Kazitak, Mori K. Cerebral angioplasty and stenting for intracranial vertebral atherosclerotic stenosis. AJNR 1999; 20: 787–9
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Jones HR, Millikan CH, Sandok BA. Temporal profile (clinical course) of acute vertebrobasilar system cerebral infarction. Stroke 1980; 11: 173–7 McDowell FH, Potes J, Grosch S. The natural history of internal carotid and vertebral-basilar artery occlusion. Neurology 1961; 11 (4, pt 2): 153–7 Patrick BK, Ramirez-Lassepas M, Synder BD. Temporal profile of vertebrobasilar territory infraction. Prognostic implications. Stroke 1980; 11: 643–8 Fisher CM, Adams RD. Observations on brain embolism with special reference to hemorrhagic infraction. In: Furlan AJ, ed. The Heart and Stroke: Exploring Mutual Cerebrovascular and Cardiovascular Issues. Berlin: Springer-Verlag, 1987: 17–36 Hardin CA. Vertebral artery insufficiency produced by cervical ostheoarthritic spurs. Arch Surg 1965; 90: 629–33 Cloud GC, Markus HS. Diagnosis and management of vertebral artery stenosis. J Med 2003; 96: 27–34 Laub GA, Kaiser WA. MR angiography with gradient motion refocusing. J Comput Assist Tomogr 1988; 122: 377 Ruggieri PM, Laub GA, Masaryk TJ et al. Intracranial circulation: pulse sequence considerations in three-dimensional (volume) MR angiography. Radiology 1989; 171: 785 Hale JD, Valk PE, Watts JC et al. MR imaging of blood vessels using three-dimensional reconstruction: methodology. Radiology 1985; 157: 727 Masaryk TJ, Ross JS, Modic MT et al. Carotid bifurcations: MR imaging. Radiology 1988; 166: 461 Edelman RR, Mattle HP, Kleefield J et al. Quantification of blood flow with dynamic MR imaging and presaturation bolus tracking. Radiology 1989; 171: 551 Kistler JP, Roppor AH, Heros RC. Therapy of ischemic cerebral vascular disease due to atherothrombosis. N Engl J Med 1984; 311: 100 Weksler BB, Lewin ML. Anticoagulation in cerebral ischemia. Stroke 1983; 14: 658 Garde A, Samuelson K, Fahlgren H et al. Treatment after transient ischemic attacks: a comparison between anticoagulant drug and inhibition of platelet aggregation. Stroke 1983; 14: 677 Millikan CH. Treatment of occlusive cerebrovascular disease. In: Siekert RG, ed. Cerebrovascular Survey Report for Joint Council Subcommittee on Cerebrovascular Disease. Whiting Press: Rochester, 1976 Sandok BA, Furtan AJ, Whisnant JP, Sundt TM. Guidelines for the management of transient ischemic attacks. Mayo Clin Proc 1978; 53: 665 Wehman JC, Hanel RA, Gudot CA. Atheroslcerotic occlusive extracranial vertebral artery disease: indications for intervention, endovascular techniques. short term and long term results. J Interven Cardiol 2004; 17: 219–32 Fessler RD, Wakhloo AK, Lanzino G et al. Transradial approach for vertebral artery stenting: technical case report. Neurosurgery 2000; 46(6): 1524–7; discussion 1527–8 Théron J. Angioplasty of brachiocephalic vessels. In: Vinuela F, ed. Interventional Neuroradiology: Endovascular Therapy of the Central Nervous System. Raven Press, New York, 1992: 167–80 Caplan LR. Vertebrobasilar disease: should we continue the double standard of managing patients with brain ischemia? Heart Dis Stroke 1993; 2: 377–83 Caplan LR. Vertebrobasilar embolism. Clin Exp Neurol 1991; 28: 1–22 Caplan LR, Amarenco P, Rosengart A et al. Embolism from vertebral artery origin occlusive disease. Neurology 1992; 42: 1502–12 Imparato AM: Vertebral arterial reconstruction: a nineteen-year experience. J Vasc Surg 1985; 2: 626–34 Spetzler RF, Hadley MN, Martin NA et al. Vertebrobasilar insufficiency. Part 1: Microsurgical treatment of extracranial vertebrobasilar disease. J Neurosurg 1987; 66: 648–61
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Hass WK, Fields WS, North RR et al. Joint study of extracranial arterial occlusion. JAMA 1968; 203: 961–8 Berguer R. Vertebrobasilar ischemia: indications, techniques and results of surgical repair. In: Vascular Surgery, 5th edition. Philadelphia: WB Saunders, 2000: 1823–37 Schutz H, Yeung HP, Chiu MC et al. Dilatation of vertebral artery stenosis. N Engl J Med 1981; 304: 732 Higashida RT, Tsai FY, Halbach VV et al. Transluminal angioplasty for atherosclerotic disease of the vertebral and basilar arteries. J Neurosurg 1993; 78: 192–8 Zampieri P, Colombo A, Almagor Y et al. Resultss of coronary stenting of ostial lesions. Am J Cardiol 1994; 73: 901–3 Rees CR, Palmaz JC, Becker GI et al. Palmaz stent in atherosclerotic stenoses involving the ostia of the renal arteries: preliminary report of a multicenter study. Radiology 1691; 181: 507–14 Dorros G, Prince C, Mathiak L: Stenting of a renal artery stenosis achieves better relief of the obstructive lesion than balloon angioplasty. Cathet Cardiovasc Diagn 1993; 29: 191–8 Cloud GC, Crawley F, Clifton A et al. Vertebral artery origin angioplasty and primary stenting: safety and restenosis rates in a prospective series. J Neurol Neurosurg Psychiatry 2003; 74:586–90 Mathias K. Evaluation and Treatment of Chronic Vetebrobasilar Ischemia. Presented at the TCT Meeting, Washington, 2003 Lutsep HL, Barnwell SL, Maward M et al. Stenting of symptomatic atherosclerotic lesions in the vertebral or intracranial arteries (S SYLVIA): Study results (Abstract P83A). Stroke 2003; 34: 253 Ko YG, Park S, Kim JY et al. Percutaneous interventional treatment of extracranial vertebral artery stenosis with coronary stents. Yonsei Med J 2004; 45: 629–34 Hauth EA, Gissler HM, Drescherr et al. Angioplasty or stenting of extra and intracranial vertebral artery stenosis. Cardiovasc Intervent Radiol. 2004; 27: 51–7 Janssens E, Leclerc X, Gautier C et al. Percutaneous transluminal angioplasty of proximal vertebral artery stenosis: long term clinical follow-ups of 16 consecutive patients. Neuroradiology 2004; 46: 81–4 Kizlbilic CO, Oguzkurt L, Yildirim T et al. Endovascular treatment of vertebral artery origin stenosis in high risk patients. Tani Girisim Radyol 2004; 10: 252–8 Chiras J, Vallee JN, Spelle L et al. Endoluminal dilatations and stenosis of symptomatic vertebral arteritis. Rev Neurol 2002; 158: 51–7 Mukherjee D, Jadav JS. Endovascular therapy for symptomatic vertebral artery stenosis. Carotid Intervention 2002; 3: 66–9 Jenkins JS, White CJ, Ramee SR et al. Vertebral artery stenting. Catheter Cardiovasc Interv 2001; 54: 1–5 Zhang S, Jain S, Jenkins J et al. Aorta and long term results of vertebral artery stenting circulation 1999; 100 (suppl. 1): 1–674 Maini B, Villacorta R, Thomas C et al. Percutaneous coronary stent in the treatment of vertebral artery stenosis. Am Journal Cardiol 2001; 88 (suppl SA): 9G Jain S, Ramee S, White C et al. Treatment of atherosclerotic vertebral artery disease by endoluminal stenting: results from a US multicenter study. JACC 200: 84A Albuberque FC, Fioradella D, Hanp et al. A reappraisal of angioplasty and stenting for the treatment of vertebral origin stenosis. Neurosurgery 2003; 53: 607–16 Rocha-Singh K. Vertebral artery stenting: ready for prime time? Catheter Cardiovasc Interv 2001; 54: 6–7 Qureshi AI, Suri MF, Khan J et al. Abciximab as an adjunct to high risk carotid or vertebrobasilar angioplasty: preliminary experience. Neurosurgery 2000; 46(6): 1316–24 Baloh RW. Vertebrobasilar insufficiency and stroke. Otolaryngol Head Neck Surg 1995; 112: 114–7 Gomez CR, Cruz-Flores S, Malkoff MD et al. Isolated vertigo as a manifestation of vertebrobasilar ischemia. Neurology 1996; 47: 94–7
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Epidemiology of intracranial atherosclerosis Intracranial atherosclerosis is responsible for approximately 8–9% of ischemic strokes in population-based1 and hospitalbased studies.2–4 People of Asian (Japanese, Chinese, Korean),5–7 African2 and Hispanic1 descent seem to be at higher risk for intracranial atherosclerosis than those of European descent. Medical and behavioral risk factors associated with intracranial atherosclerosis include insulin-dependent diabetes mellitus, hypercholesterolemia, hypertension and cigarette smoking.8 Intracranial atherosclerosis generally occurs in the setting of widespread atherosclerosis.1,9,10
Dynamics of intracranial arterial stenoses Intracranial stenoses are typically discovered during the workup for an acute ischemic event. Data on the natural history of intracranial stenoses suggest that these are dynamic lesions that may progress, regress, or remain stable. Akins et al., using serial angiography, followed 21 patients with a total of 45 intracranial stenoses for an average of 26.7 months.11 They found that 40% of the stenoses remained stable, 40% progressed and 20% regressed. In that study, carotid siphon stenoses tended to remain stable over time, while lesions of the middle cerebral artery (MCA), anterior cerebral artery (ACA), or posterior cerebral artery (PCA), tended to progress. Data for vertebrobasilar stenoses were inconclusive owing to the low numbers in that series. The natural history of intracranial stenosis has also been examined using transcranial Doppler sonography (TCD). Schwarze et al. conducted a retrospective study of TCDs in 22 patients with a total of 29 stenoses diagnosed by angiography.12 At follow-up, 35% of the stenoses had progressed, while 7% showed evidence of regression. However, a limitation of that study is that the stenoses were diagnosed by angiography and the follow-up assessment was by TCD. Wong et al. used TCD to examine 17 patients with intracranial stenosis within 48 hours after stroke onset; 14 had MCA stenosis and three intracranial internal carotid artery (ICA) stenosis.7 Within 3 months of the stroke, 18% of stenoses had resolved, as shown by either 382
magnetic resonance angiography (MRA) or TCD. Again, the follow-up used different techniques and the results may therefore be flawed. Studies using TCD have also been performed looking specifically at MCA stenosis. Wong et al. followed 107 patients with MCA stenosis from a cohort of patients with acute ischemic stroke.13 MCA stenosis was defined as mild (systolic peak velocity 140–209 cm/second), moderate (systolic peak velocity 210–280 cm/second) or severe (systolic peak velocity > 280 cm/second). Owing to a lack of published validated data, the stenosis grade in other intracranial vessels was not assessed. Follow-up at 6 months using TCD demonstrated complete resolution of the MCA stenosis in 25% of patients, continued stenosis in 70% and progression to occlusion in 5%, The results by Wong et al. may not be representative for all stroke patients with intracranial atherosclerosis for some methodological reasons. Because of the need to examine patients at the neurosonology laboratory, Wong et al. excluded patients who required constant bedside monitoring, those who were confused or unable to comply physically with an examination, and those who were moribund. This introduces a selection bias, which may affect the overall results of the study. A study by Segura et al. examined 24 patients with a total of 28 MCA stenoses diagnosed by TCD in the setting of an acute ischemic stroke.3 An MCA was diagnosed as stenotic when the mean flow velocity reached 90 cm/second in patients younger than 70 years, or 75 cm/second in patients who were 70 years or older. The selected limits represent the 98th percentile of the control group in that particular Doppler sonography laboratory. Using these criteria, TCD at 6 months after the stroke showed that 25% of the MCA stenoses had completely regressed. The studies cited above demonstrate that intracranial stenoses are dynamic lesions. Clinicians can expect that a substantial percentage of intracranial stenoses diagnosed in the setting of acute ischemic events will resolve with medical treatment only. Unfortunately, it is not possible, using current imaging techniques, to establish the future course of a given lesion, nor is it possible to distinguish easily between local thrombosis and stenotic atherosclerosis. Lesion site may be an important determinant of stability, with ICA stenoses less likely to progress than other intracranial sites, but more data are needed to clarify this. Overall, the factors associated with progression, stabilization or regression have yet to be established.
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Morphology and features of atherosclerotic plaques As angioscopy and intravascular ultrasound of the intracranial vasculature are not possible, the in vivo disease process of intracranial luminal narrowing cannot be directly observed. However, autopsy studies demonstrate that in most cases narrowing is due to atherosclerotic plaque and that plaque morphology is similar to other vascular territories.14 Thus, in vivo observations of atherosclerotic plaque morphology in coronary and extracranial carotid arteries are likely to be applicable to the disease process in cerebral vessels. Angioscopy of coronary and carotid arteries reveals two types of plaque: white (stable) and yellow (unstable) plaques. Yellow plaques have thin fibrous caps with a lipid-rich core and low collagen content. They show a high degree of distensibility with compensatory enlargement.15.16 In contrast, white plaques have thick fibrous caps or are completely fibrous, and show minimal distensibility with paradoxical shrinkage.15 With time, yellow plaques change into white plaques, a process thought to represent healing.16,17 Yellow plaques, more than white ones, are associated with acute coronary syndromes.15.18.19 In one prospective study, there was a higher incidence of acute coronary syndromes during the follow-up period in patients with yellow plaques than in patients with white plaques.20 A probable explanation for these findings is that yellow plaques have a higher mechanical vulnerability than white plaques. Using intravascular ultrasound, Tanaka et al. demonstrated a higher occlusion rate of coronary arteries within minutes after successful coronary angioplasty in symptomatic echolucent plaques, which are thought to correspond to yellow plaques.21
Stroke in intracranial atherosclerosis Three mechanisms of ischemic stroke in the setting of intracranial atherosclerosis have been described: perfusion failure, local thrombosis at the site of the stenosis with or without subsequent arterioarterial thromboembolism, and occlusion at the origin of small penetrating arteries. In the following text each of these mechanisms will be discussed, and their relevance to angioplasty considered. Perfusion failure High-grade stenosis with inadequate collateral circulation may lead to a reduction in blood flow distal to the stenotic segment of a cerebral artery. This hemodynamic effect can be demonstrated, using cerebral angiography, by delayed flow or borderzone shift. An example of a patient with intracranial stenosis and perfusion failure is shown in Figure 41.1. The hemodynamic effects of cerebrovascular stenoses have been categorized into three stages (see Derdeyn et al. for review).22 ●
Stage 0, normal cerebral hemodynamics: owing to good collateral circulation, the occlusive lesion has no effect on the distal circulation.
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Stage 1 of hemodynamic compromise: collateral circulation is inadequate, and the perfusion pressure begins to fall. Reflex vasodilatation results, and with this an increase in cerebral blood volume (CBV) and a prolonging of mean transit time (MTT) occur. Cerebral blood flow (CBF) is maintained. Stage 2 of hemodynamic compromise, misery perfusion: vasodilatation is not adequate to maintain normal CBF. The brain increases the amount of extracted oxygen from the blood to maintain normal oxygen metabolism. A further decrease in perfusion pressure below that at which maximal oxygen extraction occurs, resulting in brain infarction.
However, a recent study by Derdeyn et al. demonstrated that the processes described above as stage 1 and stage 2 of hemodynamic compromise are actually effective at the time.23 Several studies have examined cerebral hemodynamics in the setting of intracranial arterial stenosis. In one of the earliest such studies, Naritomi et al. examined 36 patients with MCA stenosis by cerebral angiography and measurements of regional cerebral blood flow (rCBF) using xenon-133 (133Xe) inhalation.24 Patients with < 50% MCA stenosis showed normal cerebral hemodynamics and rCBF. In the patients with 50–74% MCA stenosis, angiography often revealed delayed filling of MCA branches, but with no significant reduction in rCBF. However, patients with 75–99% stenosis showed significant flow depression by both angiography and rCBF measurement. Three of the 11 patients with 75–99% stenosis had a large cerebral infarction in either the watershed zone or the cerebral cortex.24 This study demonstrates that altered cerebral hemodynamics tends to occur when MCA stenosis is > 50%, and that the degree of perfusion deficit is related to stenosis grade. In another study, Derdeyn et al. used positron emission tomography (PET) to examine five patients with MCA occlusion and five patients with MCA-M1 stenosis (50–83%). Their results indicated that MCA occlusion is associated with misery perfusion (stage 2), while MCA-M1 stenosis is not.25 In the group with MCA occlusion, three out of five patients had autoregulatory vasodilatation and four out of five patients had increased oxygen extraction fraction (OEF) distal to the lesion. In contrast, in patients with MCA-M1 stenosis, four out of five patients had normal hemodynamics, with one patient experiencing stage 1 of hemodynamic compromise. Based on these findings, Derdeyn et al. argued that stroke in MCA stenosis is more likely to be due to thromboembolism than to perfusion failure.25 Yet this study had limitations, which suggest that this conclusion may be premature. PET and angiography were not always performed on the same day (range 1–91 days), which is problematic given the highly dynamic nature of these lesions. Further, in a subsequent paper, Derdeyn et al. presented a patient with symptomatic 80% MCA-M1 stenosis who, when examined by PET immediately before angiography, had misery perfusion in the territory of the stenotic MCA.26 At 36 hours after a successful angioplasty (which resulted in a 40% residual MCA stenosis), normal hemodynamics were observed in this patient using PET. While large-scale studies that directly examine the association between perfusion failure due to intracranial atherosclerosis and subsequent increased stroke risk have yet to be published, there is substantial evidence to suggest that such an
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(a)
(e)
(b)
(f)
(c)
(g)
(d)
(h)
Figure 41.1 A 68-year-old woman with progressive vertebrobasilar insufficiency despite maximal medical therapy (aspirin, clopidogrel, warfarin, and i.v. heparin) developed postural syncopes. She was unable to rise from a horizontal position without fainting, (a) non-enhanced CT brain scan; (b) diffusion-weighted MRI demonstrating acute infarction in the right middle cerebellar peduncle (arrows); (c, d) complete cerebral arteriography including right vertebral arteriography in frontal and lateral projections demonstrating complete occlusion of the vertebral arteries (thin arrow) and reconstitution of the proximal basilar artery (thick arrow) via retrograde filling of the anterior spinal artery (arrowheads). The occlusion remained unchanged despite attempted thrombolysis using a total of 15 mg intraarterial recombinant tissue plasminogen activator; (e) Under general anesthesia, a microcatheter and 0.014-inch microguidewire were used to traverse gently the occluded segment. Arteriography through the microcatheter confirmed the patency of the basilar artery beyond the occlusion and intraluminal position of the microcatheter; (f) following angioplasty using a 3.0 mm balloon, the vertebral artery was patent but markedly irregular; and (g, h) a 3.5 × 15 mm stent was used to improve luminal diameter and maintain vessel patency. Stent placement was complicated by dislodgement of organized thrombus or plaque that initially occluded the basilar artery terminus. The embolus could not be retrieved with the retrieval devices available at the time. The embolus was forced distally into the right posterior cerebral artery beyond important thalamic and brainstem perforators. The patient suffered a small periventricular infarct in the right occipital lobe but did not lose vision.
association exists. Derdeyn et al. also examined a cohort of 117 prospectively studied patients with carotid occlusion and found that 38% had increased OEF distal to the occluded carotid.27 In a prospective, blinded, longitudinal cohort study by the same group, increased OEF was shown to be an independent risk factor for ipsilateral stroke.28 These studies suggest that hemodynamic compromise due to intracranial stenosis is a risk factor for ipsilateral stroke. While the presence of a high-grade stenosis or even occlusion does not always lead to perfusion failure, for the subgroup of patients who experience hemodynamic compromise, angioplasty may prove to be an effective treatment.
six different mechanisms for cerebral artery thrombosis associated with intracranial atherosclerosis: ● ●
●
●
●
●
Local thrombosis at the site of stenosis Numerous autopsy studies show that thrombosis related to intracranial atherosclerosis can complicate pre-existing stenosis.29 Evidence from angiographic,30,31 TCD,3,32 and autopsy33,34 studies demonstrates that local thrombus formation can result in distal arterioarterial embolism.33,35–37 Taken together, data from these two sets of studies suggest
plaque rupture followed by occlusive thrombus formation plaque rupture followed by occlusive thrombus formation, with subsequent distal embolization of thrombus and/or atheromatous plaque material intimal fibrosis causing stenosis, followed by lamellar thrombus formation and ultimate thrombotic occlusion intimal fibrosis causing stenosis, followed by lamellar thrombus formation and embolization of non-occlusive thrombus intimal fibrosis causing stenosis, followed by primary occlusive thrombus formation intimal fibrosis with intraplaque hemorrhage resulting in acute stenosis and vessel thrombosis.
These mechanisms parallel those observed in coronary and extracranial carotid artery atherosclerotic disease, and suggest plaque instability. Lammie et al. recently published an autopsy series that calls into question this association between unstable plaque and
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Elective endovascular revascularization of the intracranial cerebral arteries intracranial ICA thrombosis. On examining 14 cases of intracranial ICA thrombosis, they found no direct evidence for plaque instability.38 In these occlusions, there was either no atheroma or a mildly stenotic, stable, fibrous plaque. However, this study is limited by the fact that the autopsied subjects were mainly Caucasians, in whom the prevalence of intracranial atherosclerosis is lower than in non-Caucasians. Overall, it is reasonable to believe that, in the absence of perfusion failure, patients with stenotic intracranial atherosclerosis may obtain primary benefit from antithrombotic treatment and the application of statins and angiotensinconverting enzyme (ACE) inhibitors to prevent local thrombus formation and stabilize the plaque. Occlusion of small penetrating arteries at the site of stenosis Focal atherosclerosis of large intracranial arteries can lead to stenosis or occlusion of the small arteries found in the proximal and distal MCA (lenticulostriate arteries), the PCA (thalamogeniculate branches) and the basilar artery (median perforating and short or long circumferential arteries), This can result in infarctions in the deep structures of the cerebral hemispheres or brainstem.39, 40 Fisher published examinations of three autopsied patients with infarctions of the pons. In each case, the infarction was due to the occlusion of small arteries of the basilar artery, and this occlusion, in turn, was caused by the presence of atheromatous plaque at the small artery’s origin.41,42 An autopsy series of 11 patients with thrombotic MCA occlusion showed a similar occurrence, with one patient having an occlusion at the mouth of a basal perforating branch of the MCA caused by atherosclerotic stenosis.35 Evidence from clinical studies suggests that perforating arteries arising from a stenotic basilar artery frequently occlude. Bougousslavsky et al. demonstrated that 15 out of 23 patients (65%) with basilar artery stenosis by MRA had paramedian infarcts of the brainstem.43 Similarly, clinical studies have demonstrated the association of deep MCA infarctions with stenosis of the M1 and M2 segments. In the Extracranial/Intracranial (EC/IC) Bypass study, of the 166 patients who had infarctions in the MCA territory by CT scan, 39% with MCA stenosis and 25% with MCA occlusion had infarctions confined to deep structures (lenticulocapsular, corona radiata).14 Lyrer et al., in a retrospective series of 22 patients with ultrasonographic or angiographic evidence of isolated MCA stenosis, showed that 46% had deep infarcts in the basal ganglia and 27% had striatocapsular infarctions.45 Recently, a retrospective study of 102 consecutive Korean patients with small striatocapsular infarctions, published by Bang et al.,46 showed a high prevalence of MCA stenosis in these patients. Care must therefore be taken before proceeding with angioplasty to ensure, by imaging and clinical correlation, that the stenosis is not located at the origin of the penetrating arteries. However, this may not be possible, as very small penetrating arteries are invisible on standard angiography. Angioplasty of a stenotic plaque at the origin of the small arteries could result in complete obstruction and subsequent ischemic stroke in the territory of the penetrating arteries, resulting in an adverse outcome.
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Prognosis Patients with intracranial atherosclerosis The location and extent of intracranial atherosclerosis appear to be critical prognostic factors after stroke associated with intracranial stenoses. Most of what is known about prognosis in intracranial atherosclerosis is based on retrospective series, reviewed in the next section. Chimowitz et al. published a retrospective, multicenter study of symptomatic patients with angiographically proven intracranial stenosis of at least 50%.47 Patients in this study were treated with either warfarin (n = 88) or aspirin (n = 63). At the end of follow-up, 40 patients had reached an endpoint: 9% of patients had a stroke in the territory of the stenotic artery, 5% had a stroke in a site distant from the stenotic artery, and 13% either had a myocardial infarction or sudden death. The rate of major vascular events was 181 per 100 patientyears of follow-up in the aspirin group (stroke rate 10.4 per 100 patient-years, myocardial infarction or sudden death rate 7.7 per 100 patient-years), which was statistically higher than 8.4 per 100 patient-years of follow-up in the warfarin group (stroke rate 3.6 per 100 patient-years, myocardial infarction or sudden death rate 4.8 per 100 patient-years). Recurrent stroke rates seemed to correlate with the grade of stenosis; 6% of patients with 50–79% stenosis had a recurrent stroke in the territory of the stenotic artery, compared with 13% of patients with 80–99% stenosis. In another retrospective study of 52 patients with symptomatic intracranial atherosclerosis, 56% of whom failed antithrombotic therapy (either antiplatelet agents, warfarin or heparin), the median time to recurrent transient ischemic attack (TIA), stroke or death was only 36 days (95% confidence interval 13–59).48 Among the subgroup that failed antithrombotic therapy, the subsequent rate of stroke or death was extremely high, 45% per year. Older age seemed to predict antithrombotic therapy failure, while warfarin resulted in a decrease in stroke risk.48 It appears, therefore, that patients with symptomatic intracranial atherosclerosis are at a high risk for recurrent stroke or death. However, the early and high rates of medical failure suggested by this study contradict the results of older studies, reviewed below. Patients with intracranial carotid siphon stenosis The first detailed retrospective series of patients with angiographically proven ICA stenosis (≥ 50%) was published by Marzewksi et al.49 In this study, 70% of the 66 patient cohort presented with ischemic symptoms: 41% presented initially with ischemic events ipsilateral to the ICA stenosis, 24% had a tandem ICA stenosis and 16.7% had an intracranial ICA stenosis as the only apparent cause for their ischemic symptoms. The follow-up period averaged 3.9 years, during which 12.1% of the patients suffered an isolated TIA in the ICA territory and 15% suffered a stroke. The death rate was 12.8% per year and the ipsilateral stroke rate 3.1% per year.49 A retrospective series of 58 patients with angiographically proven intracranial ICA stenosis (≥ 30%) was published by Craig et al.4 In this series, 81% of the patients were initially symptomatic. During a mean follow-up period of 30 months, the ipsilateral stroke rate was 7.6% per year and the mortality rate 17.2% per year. A TIA or stroke occurred in 43% of
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patients during follow-up. Among those, 29% patients suffered an ischemic stroke, with 19% of patients experiencing stroke distal to the ICA stenosis. The rate of cerebrovascular events was 45% among symptomatic patients and 36% among asymptomatic patients. Forty-three percent of patients died during follow-up: 44% of deaths were due to cardiac disease and 36% to stroke. Death rates of symptomatic and asymptomatic patients were comparable. At the end of follow-up, only 33% of patients were alive or free from subsequent cerebrovascular events.4 Wechsler et al. published a retrospective series of 15 patients with angiographically proven carotid siphon stenosis (≥ 50%), 80% of whom were symptomatic.50 During an average of 51 months of follow-up, the mortality rate was 4.7% per year and the ipsilateral stroke rate 3.1% per year. Twenty-five percent of symptomatic patients suffered a stroke (three of the four strokes were ipsilateral to the stenosis), while none of the asymptomatic patients did. Twenty percent of the patients died during follow-up (two due to presumed myocardial infarction, one due to stroke). A main study finding was that ischemic symptoms at the initial clinical presentation correlated with the presence of hemodynamically significant stenosis. Five of the seven patients with TIAs at presentation had evidence of impaired flow on angiography, while only one of the five patients with stroke at presentation had evidence of impaired flow. Wechsler et al. argued that strokes were due to embolism distal to the stenosis, while TIAs were due to hemodynamic compromise. Bogousslavsky et al. published a series of 22 patients with siphon stenosis (≥ 30%).51 The follow-up averaged 40.4 months. The annual death rate was 9.5% (the cause of death was cardiac in six patients and stroke in one patient) and the annual ipsilateral stroke rate was 8.1%. Borozan et al. identified 93 patients with isolated carotid siphon stenosis (71 with unilateral and 22 with bilateral disease) among 885 consecutive patients with cerebral angiograms, and followed these patients for a mean duration of 22.5 months.52 The annual ipsilateral stroke rate was 5.1% and although the authors do not report the annual death rate, it can be extrapolated from their results to be 10.3%. During the follow-up period 22.5% of asymptomatic patients died (three due to myocardial infarction, three due to stroke, three due to carcinoma, and 44 due to unknown causes) and 23% of symptomatic patients died (known causes of death were myocardial infarction in three patients, stroke in one patient and carcinoma in one patient. The EC/IC Bypass study provides the only prospective study of patients with carotid siphon stenosis.53 Patients with stenosis of the ICA at or above the C2 vertebral body comprised one study subgroup, and it is probable that the majority of patients in the subgroup had a carotid siphon stenosis. Of the 72 medically treated patients with ICA stenosis (> 70%) at or distal to C2, 36% experienced a non-fatal or fatal stroke. It was not reported what percentage of these strokes was ipsilateral. Mean follow-up for the subgroup was not reported, but the average follow-up period for all patients in the study was 55.8 months. It is difficult, based on the available literature, to draw definitive conclusions regarding the short- and long-term prognoses of patients with carotid siphon stenosis. Available studies are limited for several reasons: (1) the cohorts were
highly selected because cerebral angiography was a main entry criterion into the studies;4,49–52 most stroke patients are not evaluated with cerebral angiography; (2) the degree of carotid stenoses required for inclusion varied, being as low as ≥ 20%;4,49–52 (3) the patient populations varied with respect to the proportions of unilateral versus bilateral intracranial carotid stenosis, and proportion of patients with intracranial and extracranial ICA tandem stenosis;49 (4) the severity of ipsilateral strokes due to carotid siphon stenosis was not clearly described in all cases;4,49 and (5) hemodynamic parameters, such as delayed flow distal to the stenosis, shift of the borderzone region or collateral flow, were often not presented.4,49 Patients with stenosis of the middle cerebral artery Unfortunately, there are limited data on the natural history of MCA stenosis. The data that exist come from small, retrospective studies. These studies suggest that the long-term risk of stroke or death is low in patients with MCA stenosis.30, 31, 54 Hinton et al. conducted a retrospective study of 16 patients with MCA stenosis (≥ 45%) diagnosed by angiography. At initial presentation 94% of these patients had TIAs and 69% had a minor stroke. Hemodynamic effects, evidenced by borderzone shift or delayed flow, were evident in all but two patients, During follow-up (range 1–72 months), only two patients experienced a severe stroke, and in both cases stroke occurred soon after diagnosis and before the start of treatment.30 Feldmeyer et al. published a retrospective series of 13 patients with angiographically proven MCA stenosis (≥ 34).54 In two of these patients MCA stenosis was not due to intracranial atherosclerosis (in one patient the cause was fibromuscular dysplasia, and in the other, radiation angiopathy). There was evidence of hemodynamic compromise in 77% of patients, and in 31% there was a probable mural thrombus. In 70% of patients there were additional stenoses in the proximal or distal ICA. During the average follow-up period of 63.6 months, the annual death rate for this cohort was 4.3% and the stroke rate was 1.5%. Three of the 13 patients died during study time-frame, with the causes of death reported as one basilar thrombosis, one carcinoma and one unknown. One patient had a fatal basilar stroke and a second patient suffered an MCA infarct (the side of the stroke, relative to the stenosis, was not reported). Corston et al. published a series of 21 patients with MCA stenosis as demonstrated by angiography (19 in the M1 segment and two in more distal branches).31 At initial presentation 67% had a stroke and 33% were experiencing TIAs alone. Eight out of the 14 patients with stroke at presentation had prior TIAs. Hemodynamic compromise was observed in 29% of patients, as demonstrated by borderzone shift or delayed flow, The mean follow-up period was 6.5 years (range 4 months–25 years), during which 29% of patients suffered a stroke (no information is given about the location of the strokes relative to the site of stenosis). During follow-up, ten patients died: four from recurrent stroke (in three of whom stroke was ipsilateral to the stenosis), two from myocardial infarction, three from cancer and one from unknown causes. The EC/IC Bypass study provides the only prospectively obtained data on the long-term outcome of patients with angiographically proven atherosclerotic MCA.44,53 In this
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Elective endovascular revascularization of the intracranial cerebral arteries study, 85 patients with MCA stenosis (who were treated medically with aspirin or warfarin, with management of risk factors), were followed for a mean of 43.3 months. All patients had a TIA or non-disabling stroke in the territory of the stenotic MCA within 3 months of study entry and none had a cardiac source of embolus or severe extracranial carotid stenosis. During the study follow-up, 21% of the patients had a stroke and 12% died (cause of death was stroke in three patients, coronary artery disease in two and other causes in five), The mortality rate was 3.3% per year, while the mean annual stroke rate was 5,9% for all vascular territories and 4.6% for ipsilateral stroke. As some patients experienced multiple strokes, the rate of stroke was 9.5% per patient-year for all vascular territories and 7.8% per patient-year for ipsilateral stroke. Of the patients who had a stroke, 71% with moderate MCA stenosis experienced warning TIAs, compared with 18% with severe MCA stenosis, The rates of stroke and death in patients with < 70% stenosis were comparable to those in patients with > 70% stenosis.44 In conclusion, although data on the prognosis of patients with MCA stenosis are limited, reported annual death rates (3.3–7.7%) and annual stroke rates (2.8–9.5%) are lower than observed in intracranial ICA stenosis. Patients with intracranial stenosis of the vertebrobasilar territory Data on the long-term prognosis of patients with intracranial posterior circulation atherosclerosis are also very limited, as most published studies are retrospective or use non-invasive techniques for the diagnosis of posterior circulation occlusive disease. Moufarrij et al. published a retrospective series of 44 patients with stenosis in the distal vertebral or basilar arteries (≥ 50%), as proven by angiography.55 The average follow-up period was 6.1 years, during which five patients had a non-fatal stroke (three in the vertebrobasilar territory) and eight patients died. The causes of death were stroke in the brainstem in two patients, stroke in another vascular territory in one patient, cardiac in two patients and other causes in three. Pessin et al. conducted a retrospective study of nine patients with stenosis of the mid-distal basilar artery (≥ 40%) shown by angiography (one patient had a tandem stenosis).56 All patients showed anterograde flow, with one patient demonstrating a slow filling through a 90% stenosis. During an average follow-up of 21 months, three patients died, two from a basilar artery stroke and one from alcohol abuse. The same group also published a retrospective series of six patients with PCA stenosis (50–80%).57 No hemodynamic abnormalities were noted in any of the patients during angiographic study. The mean follow-up period was 84 months, during which three patients died, one due to a large MCA infarction, one due to traumatic brain hemorrhage and one due to unknown causes. No patient developed an infarction in the ipsilateral territory of the PCA. The Warfarin–Aspirin Symptomatic Intracranial Disease (WASID) study provides a large retrospective series of 68 patients with vertebral or basilar artery stenosis (≥ 50%) demonstrated by angiography.58 Twenty percent of these patients had more than one stenotic lesion in the vertebrobasilar territory. The follow-up period averaged 13.8 months, during which 22% of patients had an ischemic stroke; in 15% of patients the
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stroke was in the territory supplied by the stenotic vessel. Of the seven patients who died, four had a fatal stroke and three had a fatal myocardial infarction or sudden death; the death rate was 6,1% per 100 person-years. An important finding of this study was the variation in stroke rates in the different stenotic arteries. The stroke rate in the territory of the stenotic artery (per 100 person-years) was 7.8 for vertebral artery stenosis, 10.7 for basilar artery stenosis and 6.0 for PCA/PICA (posterior inferior cerebellar artery) stenosis. The limited data on the natural history of intracranial vertebrobasilar artery stenosis suggest a mean death rate of 6.1–9.7 per 100 person-years, a mean stroke rate in any territory of 2.4–13.1 per 100 person-years, and a mean stroke rate in the territory of the stenotic artery of 0–8.7 per 100 person-years. Symptomatic patients with intracranial atherosclerotic stenosis At present, angioplasty and stenting is usually performed for patients with symptomatic intracranial stenoses. A detailed description of the different stroke syndromes is beyond the scope of this chapter and the interested reader can refer to standard textbooks on stroke and stroke syndromes.59,60 However, there are some general recommendations. An experienced stroke neurologist should evaluate all patients before any angioplasty to correlate each patient’s symptoms and clinical findings with the presumed symptomatic vessel and to exclude other potential diagnoses with alternative treatment options, e.g. cerebral vasculitis. Part of this evaluation should include the type and duration of medical therapy and adjustment of medical treatment as necessary. As outlined above, the clinical symptoms of intracranial stenosis may be due to perfusion failure or arterioarterial embolism. Perfusion failure manifests clinically by the presence of neurological symptoms attributable to the stenotic vessel when the patient changes body position, like an orthostatic reaction (Figure 41.1). A classical presentation of perfusion failure is orthostatic limb shaking from hypoperfusion in the carotid territory.61–63 Symptomatology in arterioarterial embolism distal to a stenosis depends on the vascular territory involved. The presence of ischemic lesions in the borderzone territories of major cerebral arteries suggests perfusion failure, In hemispheric disease due to MCA stenosis this may be visible as either non-confluent or confluent lesions in the ipsilateral supraventricular or paraventricular white matter.64 Careful analysis of the clinical syndrome and the results of neuroimaging should be performed to identify patients with perfusion failure due to proximal stenosis and to differentiate them from symptomatic penetrating artery disease at the site of the stenosis as the cause of ischemia, because patients with the latter condition may not benefit from angioplasty and stenting. In addition, an angiographically visible intracranial stenosis may not be hemodynamically significant and in these cases angioplasty may be of no value. The usual vascular work-up of stroke patients includes TCD or duplex sonography CT angiography, or MRI with MRA. Intracranial stenoses in the arteries accessible to angioplasty and stenting can be easily identified with any of these studies. In individual cases, verification of the findings of the non-invasive studies with conventional cerebral angiography may be necessary, Impaired cerebrovascular reserve as an indicator for perfusion
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Medical treatment of intracranial atherosclerosis (a)
(b)
Medical therapy for intracranial atherosclerosis is essentially the same as that used for atherosclerosis in other vascular territories. It includes the control of vascular risk factors (hypercholesterolemia, hypertension, diabetes, etc.) and the prescription of antithrombotics (platelet-active drugs or warfarin), statins and ACE inhibitors.
Symptomatic intracranial stenosis: surgical options (c)
(d)
Figure 41.2 A 51-year-old woman with hypertension and diabetes mellitus suffering a cerebral infarct with left hemiparesis. (a) diffusion-weighted imaging demonstrating abnormal signal in the posterior limb of the right internal capsule and lentiform nucleus. MRA examination (not shown) indicated stenosis of the right internal carotid within the skull base; (b) right common carotid arteriography in oblique lateral projection demonstrating a moderate, focal stenosis within the cavernous sinus segment (arrow); and (c, d) a microcatheter used to measure arterial pressures proximal and distal to the stenosis demonstrated no gradient: 79 mmHg distally (c) and 78 mmHg proximally (d). Although the histology of the stenosis remains uncertain, no intervention was indicated. Cerebral infarction was probably due to lenticulostriate (perforator) ischemia. The patient made a complete recovery without a revascularization procedure.
failure distal to the stenosis is diagnosed by several methods, each with its advantages and disadvantages (see Derdeyn et al. for a review).22 CBF can be evaluated at baseline and after a cerebral vasodilatory stimulus, such as hypercapnia, or acetacolamide. In the normal situation each of those stimuli results in an increase in CBF If the CBF response is muted or absent, pre-existing cerebral vasodilatation due to reduced cerebral perfusion pressure is assumed, CBF can be measured by several methods, including 133Xe by inhalation or intravenous injection, single-photon emission computed tomography (SPECT), stable xenon computed tomography (Xe-CT), PET, and CT and MRI perfusion studies after the injection of an adequate contrast medium.22,65–69 The changes in flow velocity as determined by TCD and carbon dioxide inhalation compared with baseline also serve to estimate reduced poststenotic vasoreactivity.70–72 However, for technical reasons all of these techniques allow only the diagnosis of stage 1 of hemodynamic compromise (see section on “Perfusion failure”). The diagnosis of stage 2 of hemodynamic compromise (increased oxygen extraction fraction) is currently only possible with PET using
Conventional surgical revascularization with craniotomy At present, extracranial-intracranial bypass surgery is not commonly used to treat intracranial stenosis or occlusion.53. 74 The EC/IC Bypass Study Group performed a randomized, controlled trial evaluating the efficacy of surgical revascularization for a variety of indications. The technique failed to demonstrate benefit for those enrolled in the trial. Particularly in the subgroup with MCA stenosis, surgical bypass from the superficial temporal artery to the distal MCA branches (M2–M4) met with the most disastrous results. M1–MCA stenoses treated with extracranial–intracranial bypass had the least favorable results, including basal ganglia and internal capsule infarction, due to thrombosis of the lenticulostriate arteries in proximity to the stenosis.75.76 The mechanism of infarction is loss of the hemodynamic pressure gradient across the stenosis following distal bypass surgery. Without the pressure gradient responsible for continued anterograde blood flow across the stenosis, loss of blood flow quickly leads to thrombosis of the MCA from the stenotic segment to the site of the surgical anastomosis. Perforating end-arteries including the lateral lenticulostriate branches occlude without likelihood for adequate collateral blood flow. Similarly, surgical series reporting bypass procedures for symptomatic vertebrobasilar stenosis have met with limited success.77 Nevertheless, there is renewed interest in the surgical treatment of patients with cerebral hypoperfusion demonstrated by blood-flow reactivity studies. Endovascular revascularization Remarkable developments in endovascular systems capable of treating coronary artery disease have recently been adapted to cerebral microcatheter technology. Miniaturized and more flexible systems now permit innovative endovascular neurovascular procedures and popularization of existing technology. The successful use of balloon angioplasty for the treatment of intracranial atherosclerosis has been demonstrated by physicians at many medical centres, predominantly academic centres and high-volume medical centres with significant
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Elective endovascular revascularization of the intracranial cerebral arteries neurovascular expertise. The technical results of endovascular revascularization therapy are encouraging. Nevertheless, the clinical management of patients with cerebral ischemia due to intracranial stenosis remains technically demanding at many levels, and treatment still carries a substantial risk. In general, most practitioners still reserve endovascular revascularization for patients who are refractory to maximal medical therapy. Not all patients with cerebrovascular stenoses are equivalent: careful neurological and imaging assessments are mandatory in planning a successful individualized treatment strategy. Moreover, treatment requires a multidisciplinary approach as weakness in any link of the chain can have devastating consequences, An important theme of this chapter is the customized approach needed to address each patient, No single operator works in a vacuum. Technically successful revascularization of cerebrovascular stenosis is only one step towards the achievement of acceptable treatment outcomes. Mori et al.78. 79 developed an arteriographic classification system to predict the outcome of cerebral revascularization with primary angioplasty alone. Although adapted to cerebrovascular disease, the categories are based on experience from the treatment of coronary artery disease. Lesions were categorized by high-resolution digital subtraction arteriography (DSA) according to length and geometry: ●
●
●
type A: short (≤ 5 mm in length); concentric or moderately eccentric; non-occlusive type B: tubular (5–10 mm in length); extremely eccentric; moderately angulated (curved) type C: diffuse (> 10 mm in length); extremely angulated (> 90 º); very tortuous proximal segment.
The endovascular treatment success rate is 92% in type A, 86% in type B and 33% in type C.78 The 1-year critical restenosis is 0% in type A, 33% in type B and 100% in type C. Overall, the more complex the target lesion, the less satisfactory the immediate and long-term outcomes using the currently available devices. The use of current stent technology resolves certain limitations inherent to angioplasty alone. Nahser et al.80 reported resolution of symptoms in 100% of patients treated with balloon angioplasty for posterior circulation stenoses. Improvements in luminal diameter (< 50% residual stenosis) and flow depicted on angiography following angioplasty have also been documented.81 In the second largest series on intracranial angioplasty to date, Mori et al.78 treated 42 patients with symptomatic intracranial stenoses of > 70% or occlusion failing maximal medical therapy, with a 76% technical success rate and 5% major complications (two cases). Specific risks of balloon angioplasty include thromboembolism, vascular dissection with acute or delayed occlusion, pseudoaneurysm formation, vessel rupture and occlusion of small perforators.82 The rate of procedure-related stroke varies from 8 to 50%.83–85 Vascular dissection has been observed in up to 38% of angioplasty cases performed for subarachnoid hemorrhage-induced vasospasm.86 In a series of 23 patients undergoing intracranial angioplasty,87 the annual rate for strokes in the territory of angioplasty was reduced to 3.2% during the mean follow-up period of 35.4 months. Eckard et al. reported a series of eight patients treated with angioplasty for intracranial carotid artery stenosis.81 Whereas all patients had been symptomatic before treatment,
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none experienced neurological symptoms in the distribution of the treated artery during follow-up, which ranged from 30 to 64 months. Connors and Wojak reported a series of 70 patients treated over 9 years and divided into three groups based on differences in technique used to perform angioplasty for intracranial stenosis.88 They experienced one procedural death due to vessel perforation, two cerebral hemorrhages, and seven vessel dissections in the most recent and largest grouping of 50 patients. Stent-assisted angioplasty Immediate complications of balloon angioplasty include plaque/vessel recoil, vessel dissection, acute closure, perforation and rupture. Stent-assisted angioplasty in the peripheral, extracranial cerebral and coronary circulation has been shown to have a superior safety profile and efficacy compared with balloon angioplasty alone, 89,90–93 Stents limit vessel wall recoil and the extent of iatrogenic dissection by compressing the intimal flap.94 The feasibility of stent-assisted angioplasty of the intracranial circulation was until recently limited by the inability of available stents to negotiate the tortuosity of intracranial vessels. Newer coronary stents are lighter and more flexible than their predecessors, providing the required performance for intracranial navigation. Moreover, thin struts that are widely spaced may have a theoretical advantage in preserving side-branches such as perforating arteries. The successful use of coronary stents, including the GRII (Cook, Bloomington, IN) 95,96 Multilink Duet (Guidant, Santa Clara, CA),94,97–99 and GFX I and II (Medtronic-AVE, Santa Rosa, CA),94,98–101 for the treatment of intracranial stenoses has been reported. Most applications have related to the vertebrobasilar system,94,95,98,99 with limited reports of their use in the MCA99 and intracranial ICA,96,98 Investigations using the INX stent (Medtronic-AVE), the first stent designed primarily for neurovascular use, were postponed. Guidant Corporation has conducted a successful clinical study of its own neurovascular stent, the results of which are forthcoming. Boston Scientific/Target has focused initially on the application of neurovascular stents for stent-supported coil embolization for wide-necked aneurysms, but plans to develop a device for the treatment of intracranial stenosis. Mori et al.98 primarily using the GFX stent (Medtronic-AVE) in 10 patients with 12 intracranial stenoses, reported a technical success rate of 83%. None of the procedures was complicated, and the restenosis rate at 3 months for type B and type C lesions was 0%. In a series of 12 patients who underwent stentassisted angioplasty for symptomatic basilar artery stenoses, 10 patients (83%) were asymptomatic after a mean follow-up period of 5.5 months.97 Rasmussen et al. reported eight patients treated with stent angioplasty for vertebrobasilar stenosis.92 Gomez et al. reported 12 patients treated for symptomatic basilar artery stenosis.99 Complications ranged from 12% to 25% over the short to intermediate term, No long-term follow-up information was given.
Technical considerations Patient selection Informed consent must be obtained in compliance with institutional policy and applicable law. The technical risk of vessel
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occlusion is in the range of 10% for anterior circulation lesions and up to 20% for the posterior circulation.101 Patient selection is a major factor in determining patient outcome. As the anatomical configuration of the lesion can affect technical outcome, the patient’s neurological and hemodynamic status certainly affects functional outcome. While patients failing maxima! medical therapy with anticoagulant and antiaggregate therapy comprise the treatment group for this procedure, patients with acute stroke and cerebral perfusion failure are at extremely high risk for per-operative complication, possibly approaching 50%. In this high-risk group, satisfactory functional outcomes can only be achieved with intensive medical management to complement the revascularization procedure. Patient preparation Cerebral arteriography remains the primary diagnostic modality required to evaluate cerebrovascular anatomy before endovascular revascularization, The spatial resolution cannot be reliably matched by other modalities. Most patients will also undergo non-invasive imaging, such as CT angiography, MRA and TCD ultrasound, inert xenon CT, nuclear medicine SPECT, or PET scanning, Although these non-invasive imaging modalities cannot reliably or accurately detect the presence or severity of intracranial vascular stenosis, only the non-invasive modalities can quantitatively assess the cerebral microvasculature. MRI with diffusion-weighted imaging is currently the optimal pretreatment imaging study to evaluate for acute cerebral infarction. Historically, the non-enhanced CT brain scan has been the screening tool used in major stroke therapy trials and is the most well-validated test to predict the risk of treatment in the presence of a recent cerebral infarction. Because fibrinolytic therapy may be required to treat the intraprocedural complications of cerebral revascularization, recent infarction remains a relative contraindication to angioplasty. Before the use of small-diameter stents (2.5–4 mm), antiaggregate therapy with strong antiplatelet medications could exacerbate the effects of intraoperative anticoagulation. For all the reasons described, a 6-week waiting period following cerebral infarction before proceeding with angioplasty has been suggested.102 This must be weighed against the risk of recurrent or progressive infarction if early revascularization is not achieved. Premedication Because the target population for endovascular revascularization therapy has failed maximal medical therapy, most patients are already on an antiplatelet regimen of aspirin and clopidogrel, dipyridamole, ticlopidine, or other combination therapy. Aspirin is a weak antiplatelet, but the benefits of its administration have been demonstrated.103 Aspirin therapy should be initiated at least 3 days before the procedure and continued indefinitely. Antiplatelet agents, typically clopidogrel or ticlopidine in addition to aspirin, are routinely administered 1-3 days before the procedure. Some operators also administer abciximab as a 0.25 mg/kg i.v. bolus before stent deployment, which is continued at a rate of 10 µg/minute for 12 hours. Others prefer to use Dextran 40 (10% w/v low molecular weight Dextran),98,101 Intra-arterial injection of isosorbide dinitrate via the guide
catheter may help to limit vasospasm. Preoperative administration of 10 mg i.v. dexamethasone and antibiotics has also been proposed.100 Heparin is given to achieve an activated clotting time (ACT) of 250–300 seconds throughout the procedure. An appropriate guide catheter is placed into the cervical ICA or vertebral artery via a standard transfemoral approach. Biplane digital roadmaps are obtained and the lesion is traversed with a floppy-tipped guidewire. A microcatheter is then advanced across the lesion and a small volume of contrast injected to confirm an intraluminal position. An exchange-length, floppy-tipped, hydrophilic guidewire is positioned with its tip sufficiently distal to the lesion to provide sufficient support for the stent. This usually requires the tip to be in the insular (M2) branches of the MCA for MCA stenoses97 P2 segments of the PCA for basilar artery stenoses99 or M1 segment of the MCA for distal ICA stenoses.96 Combination therapy with other anti-aggregate therapy has been demonstrated in the coronary and neurological literature to help to prevent early restenosis;104–106 its use has been extrapolated to the revascularization of neurovascular disease. Some operators administer low molecular weight Dextran 40 as an intravenous infusion (20–40 ml/hour) on the day before treatment, and continued this until the day after treatment.82,101 A neuroprotective effect may be provided by oral nimodipine, a calcium channel blocker (60 mg every 4 hours), beginning 12 hours before the procedure and continuing for 24 hours after the procedure.81 The benefits of nimodipine were previously demonstrated in the treatment of hemorrhagic stroke.107 Intraprocedural use of heparin, given as an intravenous bolus, is common in neurovascular procedures, although there is little consensus on the loading dose or rate of infusion. This group prefers a loading dose given as a bolus as 70 U/kg followed by an infusion of 1000 U/hour to achieve an ACT of 2.5–3.0 times baseline. Some operators routinely administer abciximab (ReoPro; Eli Lilly, Indianapolis, IN) as a 0.25 mg/kg i.v. bolus immediately before angioplasty and continue an infusion of 10 µg/minute for 12 hours. In general, strong intravenous antiaggregating agents are not well of characterized in the neurovascular literature. ReoPro is the only agent for which any substantial neurovascular experience has been obtained. Nevertheless, anecdotal complication rates in neurovascular revascularization applications have far exceeded those reported in the coronary literature, likely because of differences in the perfusion status of the brain between the two applications. If the use of ReoPro is warranted, most operators will opt for less anticoagulant effect with an ACT 2.0–2.5 times baseline value. A slow infusion of isosorbide dinitrate through the guide catheter82 or the application of 2 inches of nitroglycerine paste102 can be used to minimize iatrogenic vasospasm. The direct vasodilatory108 and cerebral protection effects109 of intra-arterial verapamil are under investigation. Anesthesia A complete discussion of the anesthetic considerations in the treatment of the neurologically symptomatic patient is beyond the scope of this text. For a more complete discussion, the reader may refer to one of many authorities on this subject.110
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Elective endovascular revascularization of the intracranial cerebral arteries In general, the anesthesiologist should be consulted in advance of the procedure and be aware of the goals of the procedure. The neurologically impaired patient will not tolerate periods of relative hypotension such as those that frequently occur after induction. The anesthesiologist should have a full complement of equipment during the procedure, not the subset that is often provided for cases off-site or outside the conventional operating room. These procedures have been performed successfully under general anesthesia94,100 or local anesthesia.97–99,101 Basilar artery lesions should be treated under general anesthesia as occlusion of the artery during balloon inflation can result in loss of consciousness and apnoea. In a series of 12 patients stented under local anesthesia, three (25%) complained of severe headache at the time of stent deployment, which subsided rapidly following balloon deflation.97 Most operators prefer to perform the procedure with the patient under general anesthesia to maximize safety and reduce procedure time.78.82,84 Four-vessel cerebral angiography is mandatory to determine the optimal working projection, assess collateral blood supply to the territory at risk, identify tandem lesions, characterize the length and geometry of the stenotic area, and guide further therapy if the revascularization procedure were to fail. Accurate and precise measurement of the stenosis, its length and normal vessel calibre adjacent to the stenosis are used to select the appropriate select balloon length and diameter. Patient motion artefacts limit the resolution, may lead to a need for repeat angiographic sequences, and increase contrast load. The injured brain can be intolerant of smaller doses of iodinated contrast than the uninjured brain. Non-ionic, iso-osmolar contrast dosage should be limited as much as possible, despite good renal function with a maximum total dose of 6 mg/kg. Guide catheter Adequate support for the microcatheter–guidewire assembly and the ability to inject contrast injection around the balloon catheter to evaluate the results of angioplasty and for digital roadmapping are essential. Small-bore (5–6 Fr) guide catheters may appear favorable relative to the size of the cervical vessels, especially the vertebral artery. Larger catheters (7–8 Fr), when safely placed directly or using an exchange technique with a 300 cm, 0.035–0.038-inch guidewire, can provide a more stable platform if necessary. The rapid-delivery, or monorail, systems now popular in cardiology catheterization laboratories, owing to their ease of use by a single operator, are distinctly suboptimal for intracranial navigation and revascularization procedures for three important reasons. First, the greater tortuosity of intracranial vessels and the longer distance from the orifice of the guide catheter to the target lesion compared with coronary procedures lead to a bowstring effect as additional forward pressure is required to advance the microcatheter device over the guidewire. Secondly, balloon dilatation catheters and balloon-mounted stents developed for coronary application remain excessively rigid for cerebral application. Tremendous research efforts are underway to design more malleable devices for intracranial navigation. Significant forward pressure is often needed to advance the available devices.
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Thirdly, softer guidewires are required for intracranial than for coronary application. The cerebral vessels are comparatively stationary and suspended in cerebrospinal fluid. Innumerable small perforating vessels (many < 250 µm in diameter and invisible even on high-resolution DSA equipment) arise from the larger cerebral arteries. Using even soft microcatheters and guidewires designed for cerebral applications, deformation of cerebral branches can easily avulse these small branches. Concurrent with the administration of strong anticoagulant and antiaggregate drugs, perforator branch injury can lead to catastrophic intracranial hemorrhage. By analogy, intracranial navigation for treatment of arteriovenous malformations is complicated by perforator branch injury and hemorrhage in up to 5% of procedures owing to the use of over-the-wire catheters. Consequently, many interventional neuroradiologists prefer the use of soft, flow-directed catheters for distal catheterization of tortuous vessels to these lesions. Unfortunately, the flow-directed systems used to treat high-flow vascular malformations are not applicable to the treatment of cerebrovascular stenosis. More flexible delivery systems may, in the future, make monorail systems as useful in the brain as they are in the heart. The microcatheter–guidewire assembly is passed through a rotating hemostatic valve into the guide catheter, Anterograde flow must be preserved in the cervical artery in which the guide catheter lies, Continuous forward flushing of the guide catheter with heparinized saline (3 U heparin/m1 normal saline at 1–2 ml/second) must be maintained. Digital roadmap images should be obtained in two projections determined by previously acquired arteriographic sequences to advance the microcatheter assembly to the skull base. Excessive trauma to the endothelium of the cervical vessels may lead to excessive platelet activation and suboptimal technical results. Lesion navigation and angioplasty Once the microcatheter assembly has been passed in proximity to the intracranial vessels, a second set of high-resolution, high-magnification (4.5–5 cm field of view) roadmap images is obtained in two planes by injection through the guide catheter. Coordination with the attending neuroanesthesiologist is imperative to maintain cerebral perfusion before revascularization and to provide additional cerebral protection, if appropriate. Burst-suppression doses of etomidate (0.3–0.6 mg/kg) may help to protect the brain from further ischemia during the brief time that the treatment device traverses the stenosis. For high-grade or tortuous stenosis, flow-arrest is not uncommon. Prior preparation and rapid execution of the treatment plan are necessary to ensure satisfactory outcomes. Although it is often tempting to use the treatment device (balloon catheter or balloon-mounted stent) and microguidewire to cross primarily and revascularize the stenosis, use of a microcatheter and soft microguidewire to cross the stenosis initially is technically superior. It is relatively rare that soft, steady forward pressure on currently available low-profile balloons and stent catheters will not cross an intracranial stenosis using an over-the-wire technique. Predilatation with a small, non-compliant balloon (1.5–2.0 mm) is seldom necessary, However, the risk of dissection and subintimal passage of the
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microguidewire in the cerebral circulation is significant. Little effort is required to dissect the delicate cerebral vessels. Operator error leading to subintimal dilatation or stent deployment in the cerebral circulation is generally unsalvageable. Typically, a low-profile, semicompliant balloon such as the Valor (Cordis, Miami Lakes, FL) is used with the Transend EX or Platinum Tip (BSC/SciMed, Maplegrove, MN) guidewire. Additional guidewire and balloon-catheter systems are being introduced on a regular basis, each with its own set of advantages and deficiencies. If superimposed thrombus is thought to be contributing to the degree of stenosis and recent infarction has been excluded, superselective infusion of 1–5 mg recombinant tissue plasminogen activator or 125,000 1U urokinase may reveal the true extent of the underlying lesion.102 However, this practice is highly controversial as the available thrombolytic agents have procoagulant properties mediated through the release of clot-bound thrombin and/or platelet activation.100 In addition, acute cerebral ischemia leads to poorly characterized vascular permeability owing to increased production of metalloprotetnases111–113 and endothelial injury,113 predisposing to catastrophic hemorrhage following the administration of thrombolytic agents. For the same reasons that administration of thrombolytic agents outside the treatment window for acute cerebral stroke leads to excessive risk of cerebral hemorrhage.115–118 administration of thrombolytic agents during cerebral revascularization in the symptomatic patient must be approached with extreme trepidation. Using a microcatheter designed for neurological applications, the lesion is carefully traversed under high-resolution roadmapping. To cross the lesion initially, a gentle curve on a soft-tipped microguidewire is preferable, allows greatest directional control and may be least likely to dislodge plaque or thrombus. Once across, the guidewire is gently removed. Under a blank roadmap image, a small amount of contrast (0.1–0.2 ml) is injected to confirm the intraluminal position of the microcatheter. An arteriographic sequence is useful to document the appropriate position of the microcatheter across the stenosis, within the true lumen of the target vessel distal to the stenosis, and to assess for flow arrest. An exchange-length, soft-type microwire is prepared with the J-curve on the distal tip of the guidewire. Under high-resolution road-mapping, the exchange-length microwire is passed into the vessel distal to the stenosis. The wire tip must be kept within the field of view throughout the procedure. Failure to maintain visualization of the wire tip is poor technique and may predispose to vessel perforation during the exchange process. Distal placement of the wire allows greater distribution of radial forces during passage of the treatment device and places a more structurally rigid segment of the wire across the site of stenosis. These factors must be balanced against the risk of vessel distortion, perforator avulsion and wall penetration. Careful assessment is made regarding the ease of wire advancement and the preferred path of the guidewire in relation to the roadmap and other radiographic landmarks to ensure an intraluminal position. An example of a catastrophic vessel rupture is shown in Figure 41.3. Primary stenting without predilatation may be feasible depending on lesion severity and morphology. Undersizing of the stent and angioplasty balloon if the lesion requires
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Figure 41.3 Catastrophic vessel rupture during stent-supported angioplasty for high-grade basilar artery stenosis and superimposed basilar artery thrombosis: (a–c) Arteriography following deployment of a 3.0 × 12 mm stent in the distal basilar artery demonstrating massive contrast extravasation in the basilar cisterns surrounding the angioplasty balloon. Despite reversal of heparin anticoagulation with protamine sulfate and intermittent reinflation of the balloon at the site of perforation, such lesions are generally irrecoverable and fatal; (d) CT brain scan without administration of additional contrast demonstrating extensive subarachnoid hemorrhage and severe hydrocephalus. The patient was clinically brain-dead and died hours later.
predilatation is recommended to minimize intimal trauma, Intimal damage is related to immediate occlusion and delayed restenosis, as previously discussed, This has particular implications in the current setting, as reangioplasty of a stented lesion may be difficult, if not impossible. The stent length should be selected to allow 2 mm of stent to protrude beyond each end of the stenosis. The stent is then positioned across the lesion and deployed using an insufflation device. After the balloon has been carefully withdrawn from the stent, post-procedural angiography is performed to define any residual stenosis and exclude branch occlusions. A screw-type inflation device is used to distend the balloon slowly and accurately over several minutes. Manual inflation using a 1 ml syringe alone is used with compliant balloons for treatment of vasospasm associated with hemorrhagic stroke. This technique is discouraged when using less compliant balloons for treatment of intracranial atherosclerosis, where fine pressure and temporal control are necessary. Gradually incremented inflations are continued in 0.5 atmosphere steps with a pause between each stage until a maximum pressure of 6–7 atmosphere is reached. Connors et al. reported immediate technical improvement and reduced short- and mid-term restenosis when slow inflation of the device was performed.101 Again, flow arrest is present throughout device inflation,
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Elective endovascular revascularization of the intracranial cerebral arteries The duration for which flow arrest will be tolerated by the involved vascular distribution varies on an individual basis according to cerebral metabolic status, presence of prior parenchymal injury and the degree of collateral CBF. In many cases, tolerance of prolonged flow arrest is not well characterized before the treatment procedure. Angiography is obtained with the deflated balloon in position across the site of stenosis by injection of contrast through the guide catheter. If required, the balloon can be withdrawn from the angioplasty site leaving the wire in place to reveal the true angiographic result. With primary angioplasty, modest restoration of luminal diameter is acceptable and to be expected given deliberate undersizing of the balloon. Increasing luminal diameter has an exponential effect (proportional to the fourth power of the radius) on flow rate, which is likely to be adequate even with modest improvement in the angiographic appearance. Primary placement of an appropriately sized stent device will immediately result in normal, or near normal, vessel calibre (Figure 41.4), Undersizing, the deliberate selection of a balloon at least 0.5 mm smaller in diameter than the normal vessel surrounding the stenosis, is recommended44,83 owing to the fragility of intracranial vessels that possess a thin muscularis and adventitia. Although this does not restore the lumen to its native diameter, the risk of vessel dissection and rupture, which is greater with eccentric lesions, is reduced to an acceptable level. Furthermore, restenosis is believed to be proportional to the degree of intimal damage produced119 and the rate at which dilatation is performed.102 At least 2 mm of the stent must extend beyond the proximal and distal margins of the stenosis for stable positioning to limit the risk of dissection. In either case, the microguidewire must be left in position across the stenosis until it is determined that hyperacute or acute vessel thrombosis will not occur. For this reason and any rescue procedure that may be required, an exchange-length microguidewire is a technical necessity. Once the guidewire has been removed, attempts at recrossing the recent angioplasty site with a guidewire should be resisted as selection of a false lumen may occur, Similarly, the smallest of stent devices may be displaced. Further dilatation, if required, may be performed at the 3-month follow-up, by which time the vessel will have healed. Reactive vasospasm at the angioplasty site can be treated aggressively with papaverine (3 mg/ml, maximum dose 150 mg per major vascular territory), nitroglycerine (10–25 µg /ml, maximum dose unknown) or verapamil (1 mg /ml, maximum dose unknown, but likely to be 8 mg per major vessel distribution). If refractory to medical therapy, a compliant balloon catheter designed for dilatation of cerebral vasospasm (Sentry, BSCI/Target Therapeutics, Fremont, CA; Commodore, Cordis Neurovascular, Miami Lakes, FL) may be used. It is important to observe the angioplasty site by performing intermittent angiography for 1 hour after the procedure, unless contraindicated. Exposure of subendothelial layers can stimulate malignant activation of the coagulation cascade, with platelet adhesion and activation of complement and the intrinsic clotting cascade. If thrombus is detected, an infusion of fibrinolytics typically clears the fresh red thrombus easily. Similarly, glycoprotein llb/llla inhibitors will also rapidly clear acute white thrombus formation, Either agent may be used for
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Figure 41.4 A 35-year-old man with focal right middle cerebral artery stenosis and episodic left arm weakness despite maximal medical therapy with aspirin, clopidogrel, and i.v heparin. He had been treated with cranial radiation therapy for craniopharyngioma 19 years previously. (a. c. d) Right internal carotid arteriography demonstrating severe narrowing of the proximal right middle cerebral artery; (b) left internal carotid arteriography demonstrating arterial supply to the right anterior cerebral artery distribution (arrowheads) via circle of Willis collaterals, but poor pial collaterals to the distal right middle cerebral artery distribution (short black arrows); (e, f) a 2.5 × 8 mm metallic stent was used to revascularize the right middle cerebral artery distribution.
emergency salvage in the presence of impending or acute occlusion, despite the certain risk of cerebral hemorrhage.
Post-procedural management It is often advantageous to extubate the patient in the neuroangiography suite and perform clinical assessment before transfer to the neurological intensive care unit. In certain situations, it may be advantageous to arouse the patient from general anesthesia in the intensive care unit if blood pressure instability mitigates towards continuous physiological monitoring. The patient transport process often exposes weaknesses in the ability to perform intensive pressure
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(a)
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Figure 41.5 A 54-year-old woman with severe expressive aphasia and right hemiparesis failing maximal medical therapy (aspirin, i.v. heparin). (a) T2-weighted and (b) diffusion-weighted MRI demonstrating deep white matter (watershed) and cortical ischemia (small arrows); (c, d) left internal carotid arteriography demonstrating tandem stenosis of the clinoid–supraclinoid (short arrows) and posterior cavernous (arrowhead) segments; (e, f) left internal carotid arteriography following stent-supported angioplasty of the cavernous stenosis using a 2.5 × 9 mm metallic stent (arrowhead) and primary angioplasty of the clinoid–supraclinoid stenosis (short arrow) using a 1.5 mm balloon under general anesthesia resulted in markedly improved cerebral perfusion. Note improved visualization of the left anterior cerebral artery distribution (open arrows). The patient recovered speech and use of the right leg, but the right arm remained weak. Three months later, the patient developed recurrent expressive aphasia; (g, h) left carotid arteriography demonstrating restenosis of both lesions (short arrows and arrowheads) requiring retreatment. The rate of cerebrovascular restenosis remains unknown. Early data suggest that the rate of restenosis is similar to the rate of coronary artery restenosis following treatment.
modulation often seen in the patient population requiring these procedures. After revascularization and catheter removal, blood pressure must be reduced by 25–30% in an effort to prevent hyperperfusion hemorrhage which may complicate up to 5% of technically successful procedures.120 Post-treatment perfusion studies such as TCD with evaluation of the pulsatility index,121,122 xenon CT123 or other perfusion studies, such as SPECT and MRI,124,125 may help to guide bloodpressure modulation in an effort to prevent the sequela of hyperperfusion.120 Unless contraindicated for cardiopulmonary reasons, antihypertensive agents such as metoprolol are optimal owing to α- and β-receptor blockage with a reduction in pressure and pulsatility. Heparin is continued for 24–48 hours to maintain a partial thromboplastin time of 60–80 seconds. Some operators add ticlopidine or clopidogrel to the antiplatelet regimen for 2–4 weeks.80,102 This group prefers administration of enteric-coated aspirin and clopidogrel for 6 weeks from the date of the procedure if not otherwise contraindicated, with aspirin administered indefinitely thereafter. Acute and subacute stent thrombosis may result from platelet aggregation on stent struts and damaged intima. Continuation of an antiplatelet regimen consisting of aspirin and clopidogrel or ticlopidine with or without abciximab minimizes the incidence of this complication.94 Some authors state that heparin can be discontinued
as persistent anticoagulation is unnecessary owing to the mechanism of early stent occlusion and superior restoration of luminal diameter compared with angioplasty alone,99,100 Unless an intravenous glycoprotein llb/llla inhibitor has been given, the present authors prefer to administer heparin for 1–3 days.
Follow-up Subacute-to-late restenosis is related to intimal hyperplasia (cellular proliferation) and vascular remodelling. MRI with MRA is useful for non-invasive surveillance80,81 but not all stenoses are detected with these modalities and measurements of stenosis severity can be inaccurate. The role of CT angiography in accurately depicting restenosis is uncertain but likely to be limited by beam-hardening artefacts. Some authors advocate rigorous angiographic follow-up beginning at 3 months,82,102,126 given the 33 and 100% incidence of restenosis for type B and type C lesions, respectively, at 1 year.126 It is recommended that conventional angiographic follow-up be obtained initially at 3 months, at which stage additional endovascular treatment can be undertaken if required.102 Depending on the patient’s age, medical condition and other angiographic risk factors, the value of aggressive arteriographic surveillance must be weighed against the potential complications.127
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Figure 41.6 Transcranial Doppler (TCD) findings in the same patient as in Figure 41.5. TCD findings are shown before (a–c) and after (e, f) the first angioplasty. (a) Blunted flow in the left middle cerebral artery measured at a depth of 50 mm with a mean flow velocity of 47 cm/second and a reduced pulsatility index of 0.54; (b) retrograde and accelerated flow in the left anterior cerebral artery measured at a depth of 66 mm (mean flow velocity 85 cm/second, pulsatility index 0.88) indicating compensatory collateral blood flow to the left middle cerebral artery; (c) anterograde and accelerated flow in the right anterior cerebral artery measured at a depth of 66 mm (mean flow velocity 103 cm/second. pulsatility index 0.60) indicating compensatory cross-filling to the left anterior and middle cerebral arteries; (d–f) TCD findings 5 days after the successful first angioplasty; (d) normalization of the flow velocity profile in the left middle cerebral artery measured at a depth of 50 cm (mean flow velocity 97 cm/second, pulsatility index 0.75); (e) orthograde but still accelerated flow in the left anterior cerebral artery measured at a depth of 66 mm (mean flow velocity 120 cm/second, pulsatility index 0.53) indicating restoration of blood flow in the left middle cerebral artery; (f) orthograde and normalized flow velocity in the right anterior cerebral artery (mean flow velocity 83 cm/second, pulsatility index 0.62). (See Color plates.)
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Barnett HJM, Mohr JP, Stein BM, Yatsu FM, eds. Stroke. Pathophysiology, Diagnosis, and Management, 3rd edn. (New York, Churchill Livingstone: 1998). Bogousslavsky J, Caplan L, eds. Stroke Syndromes, 2nd edn. New York Cambridge University Press: 2001). Yanagihara T, Piepgras DG, Klass DW. Repetitive involuntary movement associated with episodic cerebral ischemia. Ann Neurol 1985;18: 244–50 Tatemichi TK, Young WL, Prohovnik l et al. Perfusion insufficiency in limb-shaking transient ischemic attacks. Stroke 1990; 21: 341–7 Zaidat OO, Werz MA, Landis DM, Selman W. Orthostatic limb shaking from carotid hypoperfusion. Neurology 1999; 53: 650–1 Mull M, Schwarz M, Thron A. Cerebral hemispheric low-Flow infarcts in arterial occlusive disease. Lesion patterns and angiomorphological conditions. Stroke 1997; 28: 118–23 Lythgoe DJ, Ostergaard L, William SC et al. Quantitative perfusion imaging in carotid artery stenosis using dynamic susceptibility contrast-enhanced magnetic resonance imaging. Magn Reson Imaging 2000; 18: 1–11 Kim JH, Lee SJ, Shin T et al. Correlative assessment of hemodynamic parameters obtained with T2*- weighted perfusion MR imaging and SPECT in symptomatic carotid artery occlusion. AJNR Am J Neuroradiol 2000; 21: 1450–6 Kikuchi K, Murase K, Miki H et al. Measurement of cerebral hemodynamics with perfusion-weighted MR imaging: comparison with pre- and post-acetazolamide 133Xe-SPECT in occlusive carotid disease. AJNR Am J Neuroradiol 2001; 22: 248–54 Ozgur HT, Kent WT, Masaryk A et al. Correlation of cerebrovascular reserve as measured by acetazolamide-challenged SPECT with angiographic flow patterns and intra- or extra-cranial arterial stenosis. AJNR Am J Neuroradiol 2001; 22: 928–36 Furukawa M, Kashiwagi S, Matsunaga N et al. Evaluation of cerebral perfusion parameters measured by perfusion CT in chronic cerebral ischemia: comparison with xenon CT. J Comput Assist Tomogr 2002; 26: 272–8 Kleiser B, Widder B. Course of carotid artery occlusions with impaired cerebrovascular reactivity. Stroke 1992; 23: 171–4 Silvestrini M, Vernieri F, Pasqualetti P et al. Impaired cerebral vasoreactivity and risk of stroke in patients with asymptomatic carotid artery stenosis. JAMA 2000; 283: 2122–7 Cigada M, Marzorati S, Tredici S, lapichino G. Cerebral CO2 vasoreactivity evaluation by transcranial Doppler ultrasound technique: a standardized methodology. Intensive Care Med 2000; 26: 729–32 Mintun MA, Raichle ME, Martin WR, Herscovitch P. Brain oxygen utilization measured with O-15 radiotracers and positron emission tomography. J Nucl Med 1984; 25: 177–87 EC/IC Bypass Study Group: The International Cooperative Study of Extracranial/Intracranial Arterial Anastomosis (EC/IC Bypass Study): methodology and entry characteristics. Stroke 1985; 16: 397–406 Gumerlock MK, Ono H, Neuwelt EA. Can a patent extracranial– intracranial bypass provoke the conversion of an intracranial arterial stenosis to a symptomatic occlusion? Neurosurgery 1983; 12: 391–400 Gumerlock MK, Coull BM, Howieson J et al. Late stenosis of a superficial temporal–middle cerebral artery bypass: angiographic and histological findings. Neurosurgery 1985; 16: 650–7 Hopkins LN, Budny JL, Castellani D. Extracranial–intracranial arterial bypass and basilar artery ligation in the treatment of giant basilar artery aneurysms. Neurosurgery 1983; 13: 189–94 Mori T, Fukuoka M, Kazita K, Mori K. Follow-up study after intracranial percutaneous transluminal cerebral balloon angioplasty. AJNR Am J Neuroradiol 1998; 19: 1525–33 Mori T, Mori K, Fukuoka M et al. Percutaneous transluminal cerebral angioplasty: serial angiographic follow-up after successful dilatation. Neuroradiology 1997; 39: 111–16 Nahser HC, Henkes H, Weber W et al. Intracranial vertebrobasilar stenosis: angioplasty and follow-up. AJNR Am J Neuroradiol 2000; 21: 1293–301 Eckard DA, Zarnow DM, McPherson CM et al. Intracranial internal carotid artery angioplasty: technique with clinical and radiographic results and follow-up. AJR Am J Roentgenol 1999; 172: 703–7 Song JK, Eskridge JM. Intracranial angioplasty and thrombolysis. Neurosurg Clin North Am 2000; 11: 49–65, viii Alazzaz A, Thornton J, Aletich VA et al. Intracranial percutaneous transluminal angioplasty for arteriosclerotic stenosis. Arch Neurol 2000; 57: 1625–30 McKenzie JD, Wallace RC, Dean BL et al. Preliminary results of intracranial angioplasty for vascular stenosis caused by atherosclerosis and vasculitis. AJNR Am J Neuroradiol 1996; 17: 263–8
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Takis C, Kwan ES, Pessin MS et al. Intracranial angioplasty: experience and complications. AJNR Am J Neuroradiol 1997; 18: 1661–8 Eskridge JM, Newell DW, Winn HR. Endovascular treatment of vasospasm. Neurosurg Clin North Am 1994; 5: 437–47 Marks MR Marcellus M, Norbash AM et al. Outcome of angioplasty for atherosclerotic intracranial stenosis. Stroke 1999; 30: 1065–9 Connors JJ3, Wojak JC. Percutaneous transluminal angioplasty for intracranial atherosclerotic lesions: evolution of technique and short-term results. J Neurosurg 1999; 91: 415–23 Roubin GS, Yadav S, Iyer SS, Vitek J. Carotid stent-supported angioplasty: a neurovascular intervention to prevent stroke. Am J Cardiol 1996; 78(3A): 8–12 Theron J. [Protected carotid angioplasty and carotid stents]. J Mai Vase 1996; 21 (suppl A): 113–22 Theron J. Cerebral protection during carotid angioplasty. J Endovasc Surg 1996; 3: 484–6 Yadav JS, Roubin GS, King P et al. Angioplasty and stenting for restenosis after carotid endarterectomy. Initial experience. Stroke 1996; 27: 2075–9 Yadav JS, Roubin GS, Iyer S et al. Elective stenting of the extracranial carotid arteries. Circulation 1997; 95: 376–81 Rasmussen PA, Perl J, Barr JD et al. Stent-assisted angioplasty of intracranial vertebrobasilar atherosclerosis: an initial experience. J Neurosurg 2000; 92: 771–8 Phatouros CC, Higashida RT, Malek AM et al. Endovascular stenting of an acutely thrombosed basilar artery: technical case report and review of the literature. Neurosurgery 1999; 44: 667–74 Al-Mubarak N, Gomez CR, Vitek JJ, Roubin GS. Stenting of symptomatic stenosis of the intracranial internal carotid artery. AJNR Am J Neuroradiol 1998; 19: 1949–51 Gomez CR, Misra VK, Campbell MS, Soto RD. Elective stenting of symptomatic middle cerebral artery stenosis. AJNR Am J Neuroradiol 2000; 21: 971–4 Mori T, Kazita K, Chokyu K et al. Short-term arteriographic and clinical outcome after cerebral angioplasty and stenting for intracranial vertebrobasilar and carotid atherosclerotic occlusive disease. AJNR Am J Neuroradiol 2000; 21: 249–54 Gomez CR, Misra VK, Liu MW et al. Elective stenting of symptomatic basilar artery stenosis. Stroke 2000; 31: 95–9 Horowitz MB, Pride GL, Graybeal DF, Purdy PD. Percutaneous transluminal angioplasty and stenting of midbasilar stenoses: three technical case reports and literature review. Neurosurgery 1999; 45: 925–30 Mori T, Kazita K, Mori K. Cerebral angioplasty and stenting for intracranial vertebral atherosclerotic stenosis. AJNR Am J Neuroradiol 1999; 20: 787–9 Connors JJ III. Intracranial angioplasty. In: Connors JJ 111, Wojak JC, eds. Interventional Neuroradiology. Philadelphia: WB Saunders,1999. Mohr JR, Thompson JL, Lazar RM et al. A comparison of warfarin and aspirin for the prevention of recurrent ischemic stroke. N Engl J Med 2001; 345: 1444–51 Berger PB. Clopidogrel after coronary stenting. Curr Interv Cardiol Rep 1999; 1:263–9 Berger PB, Bell MR, Rihal CS et al. Clopidogrel versus ticlopidine after intracoronary stent placement. J Am Coll Cardiol 1999;34: 1891–4 Waksman R, Ajani AE, White RL et al. Prolonged antiplatelet therapy to prevent late thrombosis after intracoronary gammaradiation in patients with in-stent restenosis: Washington Radiation for In-Stent Restenosis Trial plus 6 months of clopidogrel (WRIST PLUS). Circulation 2001; 103: 2332–5 Petruk KC, West M, Mohr G et al. Nimodipine treatment in poor-grade aneurysm patients. Results of a multicenter
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double-blind placebo-controlled trial. J Neurosurg 1988; 68: 505–17 Joshi S, Meyers P, Wang M et al. Intraarterial verapamil decreases vascular resistance in conductance arteries of human subjects (Letter). 2002; Feng L, Fitzsimmons BF, Young WL et al. Intra-arterial verapamil as adjunct therapy for cerebral vasospasm: safety and two-year experience. AJNR Am J Neuroradiol 2002; in press. Herrick IA, Gelb AW. Occlusive cerebrovascular disease: anesthetic considerations. In: Cottrell JE, Smith DS, eds. Anesthesia and Neurosurgery. St Louis: Mosby 1999. Sumii T, Lo EH. Involvement of matrix metalloproteinase in thrombolysis-associated hemorrhagic transformation after embolic focal ischemia in rats. Stroke 2002; 33: 831–6 Gasche Y, Copin JC, Sugawara T et al. Matrix metalloproteinase inhibition prevents oxidative stress-associated blood-brain barrier disruption after transient focal cerebral ischemia. J Cereb Blood Flow Metab 2001; 21: 1393–400 Montaner J, Alvarez-Sabin J, Molina CA et al. Matrix metalloproteinase expression is related to hemorrhagic transformation after cardioembolic stroke. Stroke 2001; 32: 2762–7 del Zoppo GJ, Hallenbeck JM. Advances in the vascular pathophysiology of ischemic stroke. Thromb Res 2000; 98: 73–81 National Institute of Neurological Disorders rt-PA Stroke Study Group: Generalized efficacy of t-PA for acute stroke. Subgroup analysis of the NINDS t-PA Stroke Trial. Stroke 1997; 28: 2119–25 Wardlaw JM. Overview of Cochrane thrombolysis metaanalysis. Neurology 2001; 57(5 suppl 2): 69–76 del Zoppo GJ, Higashida RT, Furlan AJ et al. PROACT. a phase II randomized trial of recombinant pro-urokinase by direct arterial delivery in acute middle cerebral artery stroke. PROACT Investigators. Prolyse in Acute Cerebral Thromboembolism. Stroke 1998; 29: 4–11 Kase CS, Furlan AJ, Wechsler LR et al. Cerebral hemorrhage after intra-arterial thrombolysis for ischemic stroke: the PROACT II trial. Neurology 2001; 57: 1603–10 Topol EJ, Califf RM, Weisman HF et al. Randomised trial of coronary intervention with antibody against platelet llb/llla integrin for reduction of clinical restenosis: results at six months. The EPIC Investigators. Lancet 1994; 343: 881–6 Meyers PM, Higashida RT, Phatouros CC et al. Cerebral hyperperfusion syndrome after percutaneous transluminal stenting of the craniocervical arteries. Neurosurgery 2000; 47: 335–343 Gossetti B, Martinelli O, Guerricchio R et al. Transcranial Doppler in 178 patients before, during, and after carotid endarterectomy. J Neuroimaging 1997; 7: 213–16 Jorgensen LG, Schroeder TV. Defective cerebrovascular autoregulation after carotid endarterectomy. Eur J Vasc Surg 1993; 7: 370–9 Penn AA, Schomer DF, Steinberg GK. Imaging studies of cerebral hyperperfusion after carotid endarterectomy. Case report. J, Neurosurg 1995; 83: 133–7 Baker CJ, Mayer SA, Prestigiacomo CJ et al. Diagnosis and monitoring of cerebral hyperfusion after carotid endarterectomy with single photon emission computed tomography: case report. Neurosurgery 1998; 43: 157–60 Kidwell CS, Saver JL, Mattiello J et al. Diffusion–perfusion MRI characterization of post-recanalization hyperperfusion in humans. Neurology 2001; 57: 2015–21 Mori T, Fukuoka M, Kazita K, Mori K. Follow-up study after percutaneous transluminal cerebral angioplasty. Eur Radiol 1998; 8: 403–8 Mani RL, Eisenberg RL, McDonald EJ Jr et al. Complications of catheter cerebral arteriography: analysis of 5,000 procedures. I. Criteria and incidence. AJR Am J Roentgenol 1978; 131: 861–5
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SECTION IV Upper extremity arterial diseases
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Upper extremity arterial diseases J Laredo and BB Lee
Introduction Upper extremity arterial disease is rare compared to lower extremity arterial disease, and accounts for only 5% of all cases of extremity ischemia. Unlike lower extremity ischemia where atherosclerotic occlusive disease is by far the most common etiology, upper extremity ischemia is cause by a wide variety of diseases which include in addition to atherosclerosis, Raynaud’s syndrome, embolic disease, trauma, collagen vascular disease, and thromboangiitis obliterans (Buerger’s disease) (Table 42.1).1–3 Distal artery disease in the upper extremity accounts for 90–95% of patients presenting with upper extremity ischemia where symptoms are caused by vasospasm or obstruction of the palmar and digital arteries and arterioles.1–3 Treatment of distal upper extremity artery disease remains mainly pharmacologic. In contrast, proximal artery disease of the upper extremity accounts for less than 10% of patients presenting with upper extremity ischemia where symptoms are caused by atherosclerotic disease, both occlusive and embolic.1,2 Treatment of proximal upper extremity artery disease is primarily by revascularization, both endovascular and surgical. Endovascular intervention, namely angioplasty and stenting, is most often performed and has been most successful in the treatment of obstructive lesions of the subclavian artery.4 Revascularization of more distal lesions of the upper extremity arteries (i.e. distal to the axillary artery) is required much less because of the abundant collateral circulation around the shoulder, and when indicated, often requires surgical reconstruction.5 Treatment of the upper extremity arteries distal to the axillary artery (brachial, ulnar, and radial arteries) remains predominantly surgical, while treatment of the palmar and digital arteries and arterioles remains predominantly pharmacologic.1,6 This chapter will focus on the etiologies of upper extremity ischemia, including common presentations, diagnostic testing, indications for intervention, and available treatments.
Clinical presentation Patients with upper extremity ischemia typically present with symptoms ranging from chronic digital ischemia to global arm ischemia to subclavian steal syndrome.1–3 Hand ischemia symptoms include Raynaud’s syndrome, rest pain, digital ulcers and gangrene. Global arm ischemia symptoms include activity-related hand, forearm, arm, and shoulder fatigue analogous to claudication in the lower extremity. Subclavian steal
syndrome is specific for proximal obstruction of the subclavian artery where the patent vertebral artery supplies the affected upper extremity in a retrograde fashion, resulting in a syndrome of vertebrobasilar symptoms and ipsilateral upper extremity claudication. It is clinically useful to divide patients presenting with upper extremity ischemia into two groups: those with small artery involvement affecting the digital and palmar arteries and those with large artery involvement affecting the arteries proximal to the wrist.
Small artery disease Approximately 90–95% of patients with upper extremity ischemia have small artery disease where the most common symptom is Raynaud’s syndrome.1,2,6 Raynaud’s syndrome is caused by vasospasm of the digital arteries and arterioles and is characterized by episodic digital ischemia provoked by stimuli such as cold or emotional stress (Figure 42.1). The affected digits undergo tri-color changes in which they initially turn white, followed by blue and then red, usually resolving in 10–60 minutes after removal of the inciting stimulus. The digits are usually normal between attacks. Raynaud’s syndrome has a female-to-male ratio of 4:1 and its typical onset is during the second and third decades of life. It is estimated that 5–15% of the healthy population is affected with this disorder. The vast majority of patients (89%) with Raynaud’s syndrome have primary Raynaud’s syndrome, which is also known as Raynaud’s disease. Raynaud’s disease should not be confused with secondary Raynaud’s syndrome which is also known as Raynaud’s phenomenon.2,6 Patients with primary Raynaud’s syndrome do not have evidence of arterial occlusive disease or signs of other systemic disorders. Primary Raynaud’s syndrome is not life threatening and patients usually lead normal lives. To confirm the diagnosis of primary Raynaud’s syndrome or Raynaud’s disease, patients must have Raynaud’s syndrome for more than two years without evidence of systemic disease.1,2,6 In contrast, secondary Raynaud’s syndrome is due to an underlying condition (Table 42.2). Patients with secondary Raynaud’s syndrome due to collagen vascular diseases are more likely to have arterial obstruction resulting in digital ulceration and gangrene.1,6 In addition, Raynaud’s syndrome often precedes the underlying systemic disease by 10–20 years, therefore once a diagnosis of Raynaud’s syndrome is made, secondary Raynaud’s syndrome must be confirmed or excluded.6 The major differences between primary and secondary Raynaud’s syndrome are summarized in Table 42.3. 401
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Table 42.1
Etiology of upper extremity ischemia
Small artery diseases Raynaud’s syndrome Connective tissue disease Buerger’s disease Vibration injury Hypercoagulable states Neoplasms Frostbite Large artery diseases Atherosclerosis Aneurysmal disease Takayasu’s arteritis Giant cell arteritis Radiation arteritis Cardiac emboli Trauma Arterial thoracic outlet syndrome
Other causes of upper extremity ischemia due to small artery disease are listed in Table 42.1. These less common etiologies include Buerger’s disease, also known as thromboangiitis obliterans, which is a clinical syndrome characterized by segmental thrombotic occlusions of small- and medium-size arteries of the extremities. Approximately 10% of patients will have isolated upper extremity disease, 40–50% of patients have isolated lower extremity disease and 30–40% of patients have upper and lower extremity disease. This disease affects predominantly young, male smokers who present with distal limb ischemia and localized digital gangrene. Onset of symptoms is typically before age 45, in patients with a longstanding history of tobacco abuse. In the upper extremity, the ulnar
Table 42.2
Causes of secondary Raynaud’s syndrome
More common Collagen vascular diseases Scleroderma Systemic lupus erythematosus Mixed connective tissue disease Rheumatoid arthritis Sjogren syndrome Polymyositis CREST syndrome (calcinosis, Raynaud’s syndrome, esophageal involvement, sclerodactyly, telangectasia) Necrotizing vasculitis Less common Arterial occlusive disease Hyperviscosity syndromes Traumatic Drug-induced Miscellaneous
or radial arteries are commonly occluded with extensive digital and palmar artery occlusions.2 Long-term use of vibrating tools may lead to vibration injury of the digital and palmar arteries resulting in vasospasm which eventually leads to arterial obstruction. Hypothenar hammer syndrome occurs in patients with occupations where the hand is used as a hammer.1,2 Affected individuals include carpenters, mill workers, and machinists. These patients develop chronic traumatic aneurysm of the ulnar artery and present with digital and palmar ischemia due to thrombosis and embolization. Hypercoagulable conditions also contribute to the development of small artery upper extremity ischemia.1,2 These conditions include underlying cancer, protein S and protein C deficiencies, and antiphospholipid antibodies. Frostbite injury results in digital nerve injury leading to small artery upper extremity ischemia caused by vasospasm of the digital arteries.1,2
Large artery disease The causes of upper extremity ischemia due to large artery disease are similar to those found in the lower
Table 42.3 Characteristics of primary and secondary Raynaud’s syndrome
Figure 42.1 Raynaud’s syndrome in a 54-year-old man, demonstrating the characteristic palor of the distal digits in response to cold.
Etiology Tissue loss Collagen vascular disease Hands Clinical course Vasospasm Occlusive disease Physical exam Unilateral disease Angiogram needed
Primary Raynaud’s syndrome
Secondary Raynaud’s syndrome
Unknown No No
Many conditions Common Common
Not involved Often benign Yes No Often normal Never Rarely
Often involved Variable Yes Yes Abnormal Yes Often
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Upper extremity arterial diseases extremities (Table 42.1). These diseases account for less than 10% of all patients presenting with upper extremity ischemia. The most common etiologies are atherosclerosis and aneurysms, which result in arterial obstruction and embolization.1–3 Patients with atherosclerosis of the large arteries often present with upper extremity claudication, rest pain, and in severe cases digital gangrene.1–3 Intermittent ischemia is usually due to embolic disease. Subclavian steal syndrome results from subclavian artery lesions that develop proximal to the origin of the vertebral artery where the distal subclavian artery is supplied by the vertebral artery through retrograde filling (Figure 42.2). Patients with this syndrome often complain of vertebrobasilar symptoms which include dizziness, vertigo, unsteadiness or imbalance, drop attacks, light-headedness, and visual disturbances. Arm symptoms also include fatigue, coolness, and pain.1–3 Aneurysms of the great vessels and axillary arteries may produce upper extremity ischemia from thrombosis or emboli.2,7,8 Primary aneurysms of the innominate or subclavian arteries may lead to embolic disease of the digital and palmar arteries. Aneuryms of the subclavian artery due to arterial thoracic outlet syndrome also produce similar symptoms. Giant cell arteritis and Takayasu’s arteritis are autoimmune disorders involving the upper extremities characterized by long segment stenoses, occlusions, and aneurysms.1,2 Both diseases are associated with slow progressive occlusions of the large arteries of the upper extremities. Giant cell arteritis is most often found in elderly Caucasian women whereas Takayasu’s arteritis often presents in young Asian women.1,2
Clinical diagnosis After obtaining a careful history, physical examination must include measurement of bilateral upper extremity blood pressures, evaluation of the thoracic outlet, palpation of upper extremity pulses, and careful inspection of the hands and digits for evidence of fixed cyanosis, ulceration, or gangrene. Presence of a supraclavicular pulse or prominent subclavian
(a)
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pulse or axillary pulse, may indicate the presence of aneurysmal disease. Auscultation of the supraclavicular region may identify a bruit suggestive of a subclavian artery lesion. Loss of an upper extremity pulse indicates occlusive disease of the affected proximal artery. An Allen test should be included in the upper extremity examination to assess the patency of the palmar arch. Lastly, Doppler insonation of the palmar and digital arteries is often indicated. Several non-invasive tests provide comprehensive evaluation of the upper extremity arteries. Duplex ultrasound scanning provides excellent imaging of the upper extremity arteries. Pulse volume recording of the digits and digital blood pressure responses to cold temperatures are useful in the work up of Raynaud’s syndrome. Indications for intervention in patients with upper extremity ischemia include disabling claudication, embolic disease, rest pain, and tissue loss.
Treatment of upper extremity ischemia Small artery disease Treatment of upper extremity ischemia due to small artery disease is mainly pharmacologic.1,6,9 The treatment of Raynaud’s syndrome is summarized in Table 42.4 and consists of pharmacologic treatment of vasospasm in primary Raynaud’s syndrome, and treatment of the underlying systemic disease in patients with secondary Raynaud’s syndrome.6,9 Patients with secondary Raynaud’s syndrome also need treatment for vasospasm. The mainstay of treatment of patients with Buerger’s disease is smoking cessation, aggressive local wound care, and surgical therapy. Patients with small artery disease due to vibration injury are best managed by discontinuation of the use of the vibratory tools and pharmacologic treatment of vasospasm. Pharmacologic treatment of vasospasm is also useful in patients with frostbite injury.9 Anticoagulation is the mainstay of treatment in patients with hypercoagulable disorders.
(b)
Figure 42.2 Subclavian steal syndrome. The patient was a 63-year-old woman with left arm ischemia and vertebrobasilar insufficiency. (a) Prestenting of the left subclavian artery occlusion. Note filling of the distal left subclavian artery via the left vertebral artery consistent with a subclavian steal; (b) post-stenting of the left subclavian artery using a 6 x 40 mm Wallstent.
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Table 42.4
Treatment of Raynaud’s syndrome
Primary Raynaud’s syndrome Conservative therapy Mittens Cold avoidance Biofeedback Drug therapy Calcium entry blockers α-blockers Nitroglycerin Thyroid preparations Prostaglandins Secondary Raynaud’s syndrome Treat underlying cause Treatment of connective tissue diseases does not help vasospasm Need to treat vasospasm with primary Raynaud agents
Finally, patients with hypothenar hammer syndrome are best managed with surgical resection of the ulnar artery aneurysm and replacement of the artery with an autogenous vein graft.1 Large artery disease Proximal disease Symptomatic stenotic and occlusive lesions of the large arteries of the upper extremity have been successfully treated using both endovascular and surgical approaches.10 The most commonly performed endovascular procedures are angioplasty and stenting of the proximal large arteries.4,11–18 These procedures are often performed via a femoral artery or brachial artery approach. The most commonly performed surgical procedures are bypass grafting, endarterectomy, and aneurysm repair.7,8,19–23 Proximal subclavian artery lesions have long been treated surgically using a supraclavicular surgical approach.19,20
(a)
Both carotid–subclavian artery bypass and subclavian artery to carotid artery transposition procedures have been used successfully to treat upper extremity ischemia and subclavian steal syndrome. Recent reports have documented excellent patency rates with very low peri-operative morbidity.19,20 A review of a 20-year experience of carotid–subclavian artery bypass with prosthetic graft reported a peri-operative morbidity rate of 6% with a zero stroke and death rate in 51 patients undergoing the procedure.19 Hospital stay averaged 2 days and 10-year patency was 92%.19 Subclavian artery to carotid artery transposition is also associated with low peri-operative morbidity and excellent long-term patency rates.20 An analysis of the medical literature revealed cumulative 5-year patency rates of 84% for carotid–subclavian artery bypass and 99% for subclavian to carotid artery transposition.20 Subclavian artery angioplasty and stenting is also associated with low complication rates, high technical success, and acceptable long-term patency rates.4,11–14,16 A recent review of 110 patients who underwent angioplasty of proximal subclavian artery lesions reported a 93% technical success rate, a 1% stroke rate and a 7% minor complication rate.4 More than 50% of the patients required stent placement. The 5-year patency rate was excellent at 89%.4 Innominate artery lesions are more challenging in that in addition to contributing to upper extremity ischemia, these lesions are also important sources of emboli to the cerebral circulation. Innominate artery lesions also contribute to ischemic strokes and transient ischemic attacks. Similar to subclavian artery lesions, occlusive lesions of the innominate artery have long been treated surgically using both transthoracic and extrathoracic bypass procedures.21–23 Both surgical approaches have excellent peri-operative mortality and morbidity rates and excellent long-term patency rates. A recent review of these procedures revealed 10-year patency rates of 94.4% for transthoracic bypass procedures and 60.3% for extrathoracic bypass procedures.21
(b)
Figure 42.3 Innominate artery stenting via a retrograde approach. The patient was a 68-year-old man with right eye amaurosis fugax and right arm claudication. Access to the innominate artery was via a cut-down on the right common carotid artery. (a) Prestenting of the innominate artery lesion; (b) post-stenting of the innominate artery lesion using a 10 x 40 mm Wallstent. Note the bovine aortic arch where the left common carotid artery and innominate artery share a common origin.
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Upper extremity arterial diseases Reports of successful endovascular treatment of innominate artery lesions have appeared in the literature.11–18 Sixty-six subclavian artery and seven innominate artery lesions underwent angioplasty and stenting via both femoral and brachial artery approaches.12 Technical success was 93% with a procedural morbidity rate of 17.8%. The reported 3-year patency rate was 84%. Another study by a single operator reported 93% technical success in the treatment of 151 occlusive lesions of the proximal great vessels.11 Angioplasty alone was successful in 141 great vessel lesions which included 13 innominate artery lesions. Over 5 years, angioplasty failure (complete occlusion) occurred in previously occluded subclavian arteries (n = 5) treated with angioplasty alone.11 Peri-procedural complications were few and long-term patency was excellent in the subclavian and innominate lesions.11 Primary stenting of the subclavian and innominate arteries has been successful in the treatment of vertebrobasilar insufficiency and upper extremity ischemia in 48 patients at a single center.16 Technical success was 96%, mortality was 4.2% and morbidity was 8.3%. Two-year cumulative patency was 77%.16 Collectively, all of these studies demonstrate excellent technical success rates, low peri-procedural mortality and morbidity with acceptable long-term patency.11–18 Because of the risk of cerebral embolization associated with innominate artery stenting, we perform a combined open surgical and endovascular procedure to treat symptomatic innominate artery lesions causing cerebrovascular symptoms. This approach utilizes surgical exposure of the right common carotid artery, followed by clamping of the common carotid artery immediately before, and during the stenting procedure. Clamping of the right common carotid artery minimizes the risk of embolization to the cerebral circulation. Stenting of the innominate lesion is then performed in a retrograde fashion
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(Figure 42.3). Other clinicians have reported similar success with this approach.17,24 Technical improvements in selective catheters, guidewires, and low-profile balloon-expandable stents have made angioplasty and stenting of subclavian and innominate artery lesions first-line treatment. Extrathoracic surgical bypass or transposition is often reserved for subclavian and innominate artery lesions not amenable to endovascular angioplasty and stenting. Innominate artery lesions contributing to both cerebral embolization and to upper extremity ischemia will remain high-risk lesions requiring distal embolic protection. These high-risk innominate artery lesions are amenable to treatment utilizing a combined surgical and endovascular angioplasty and stenting procedure. Distal disease Upper extremity ischemia due to large artery occlusive disease distal to the axillary artery is relatively rare because of the abundance of collateral circulation around the shoulder. Occlusive lesions of the brachial, radial, and ulnar arteries are most often treated with surgical bypass (Figure 42.4). The efficacy of angioplasty and stenting of these large arteries has not been reported in the literature. Surgical bypass grafting of the upper extremity for treatment of ischemia accounts for approximately 4% of all vascular surgical procedures.5 A retrospective review of patients with upper extremity ischemia treated with surgical bypass, were compared with patients with lower extremity ischemia treated with surgical bypass grafting.5 Sixty-one upper extremity bypass procedures were performed in 56 patients over a 12-year period. Indications for surgical bypass were upper extremity claudication (n = 18, 30%), rest pain (n = 35,
(b)
(a)
(c)
Figure 42.4 Upper extremity ischemia treated with brachial artery to radial artery bypass grafting. The patient was a 68-year-old man with severe left hand rest pain. (a) An angiogram of the left upper extremity revealed patent brachial, radial, and ulnar arteries to the level of the wrist with subsequent occlusion of the radial and ulnar arteries; (b) angiogram at the wrist level reveals reconstitution of the distal left radial artery; (c) completion of the brachial artery to radial artery bypass procedure using left cephalic vein graft. The patient experienced complete resolution of his left hand rest pain.
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57%), and tissue loss (n = 8, 13%). Autogenous vein grafts (n = 51, 83%) and PTFE grafts (n = 10, 17%) were used for surgical reconstruction. Operative mortality was 1.8% and peri-operative morbidity was 1.8%. One-year patency was 87%. Patency of vein grafts was 90% and patency of PTFE grafts was 70%. Compared with patients undergoing lower extremity bypass, patients who underwent brachial bypass were more commonly younger (mean age 56 vs. 68), female gender (55.4 vs. 36.4%), non-diabetic (87 vs. 48%), and smokers (73 vs. 36%).5 Treatment of upper extremity ischemia due to occlusive lesions of the large arteries distal to the axillary artery remains predominantly surgical. Upper extremity surgical bypass grafting has been shown to be a durable procedure with minimal mortality and morbidity. Aneurysmal disease Aneurysms of the upper extremities are rare and account for less than 1% of all peripheral artery aneurysms.7,8 Subclavian artery aneurysms remain the most common upper extremity artery aneurysm.8 The majority of patients with subclavian
artery aneurysms are symptomatic at the time of diagnosis. Subclavian artery aneurysms are most commonly due to atherosclerosis and thoracic outlet compression. Thoracic outlet compression with post-stenotic dilatation is the most common cause of aneurysms of the distal subclavian and proximal axillary arteries, whereas atherosclerosis is the most common cause of proximal, intrathoracic subclavian artery aneurysms.8 Patients with proximal subclavian artery aneurysms most often present with symptoms related to the mass effect of the aneurysm with compression or inflammation of the adjacent thoracic structures. Distal embolization with hand ischemia is the next most common presentation. Treatment of subclavian artery aneurysms is mainly surgical,7,8 although reports of aneurysm exclusion using covered stents have appeared in the medical literature.25–27 In patients with subclavian artery aneurysms associated with thoracic outlet compression, treatment requires decompression of the thoracic outlet by first rib resection, aneurysm resection, and artery replacement using a bypass graft.8 Patients with proximal, intrathoracic subclavian artery aneurysms require aneurysm resection and artery replacement with a bypass graft (Figure 42.5).
(a)
(b)
(c)
(d)
Figure 42.5 Treatment of a left subclavian artery aneurysm causing distal embolization and left hand ischemia. The patient was a 66-year-old man who presented with left hand ischemia due to embolization from a 6-cm-diameter left subclavian artery aneurysm. Attempted endovascular repair was unsuccessful. (a) Computed tomography of the chest demonstrating the left subclavian artery aneurysm; (b) a 3-dimensional reconstruction of the aortic arch and great vessels demonstrating the left subclavian artery aneurysm; (c) intrathoracic exposure of the subclavian artery aneurysm and clamping of the proximal subclavian artery demonstrating an endoluminal dissection (arrow); (d) the subclavian artery was replaced using an 8-mm-diameter PTFE graft which was anastomosed to the proximal subclavian artery stump. The graft was then tunneled through the chest wall and the distal anastomosis was performed to the proximal axillary artery. (See Color plates.)
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REFERENCES 1. 2.
3. 4.
5. 6. 7. 8. 9. 10. 11. 12.
13. 14.
Greenfield LJ, Rajagopalan S, Olin JW. Upper extremity arterial disease. Cardiol Clin 2002; 20(4): 623–31 Abou-Zamzam AM, Edwards JM, Porter JM. Pathology of upper extremity arterial disease. In: Ernst CB and Stanley JC, eds. Current Therapy in Vascular Surgery, 4th edition. St. Louis: Mosby, 2001: 135–8 Yao JST. Revascularization of the upper extremity. In: Ernst CB and Stanley JC, eds. Current Therapy in Vascular Surgery, 4th edition. St. Louis: Mosby, 2001: 138–43 De Vries JP, Jager LC, Van den Berg JC et al. Durability of percutaneous transluminal angioplasty for obstructive lesions of proximal subclavian artery: long-term results. J Vasc Surg 2005; 41(1): 19–23 Roddy SP, Darling RC 3rd, Chang BB et al. Brachial artery reconstruction for occlusive disease: a 12-year experience. J Vasc Surg 2001; 33(4): 802–5 Landry GJ, Edwards JM, Porter JM. Current management of Raynaud’s syndrome. Adv Surg 1996; 30: 333–47 Davidovic LB, Markovic DM, Pejkic SD et al. Subclavian artery aneurysms. Asian J Surg 2003; 26(1): 7–11 Bower TC. Subclavian and axillary artery aneurysms. In: Ernst CB and Stanley JC, eds. Current Therapy in Vascular Surgery, 4th edition. St. Louis: Mosby, 2001: 190–5 Eberhardt RT, Coffman JD. Drug treatment of peripheral vascular disease. Heart Dis 2000; 2(1): 62–74 Greenberg RK, Waldman D. Endovascular and open surgical treatment of brachiocephalic arterial disease. Semin Vasc Surg 1998; 11(2): 77–90 Motarjeme A. Percutaneous transluminal angioplasty of supraaortic vessels. J Endovasc Surg 1996; 3(2): 171–81 Sullivan TM, Gray BH, Bacharach JM et al. Angioplasty and primary stenting of the subclavian, innominate, and common carotid arteries in 83 patients. J Vasc Surg 1998; 28(6): 1059–65 Korner M, Baumgartner I, Do DD, Mahler F, Schroth G. PTA of the subclavian and innominate arteries: long-term results. Vasa 1999; 28(2): 117–22 Gonzalez A, Gil-Peralta A, Gonzalez-Marcos JR, Mayol A. Angioplasty and stenting for total symptomatic atherosclerotic occlusion of the subclavian or innominate arteries. Cerebrovasc Dis 2002; 13(2): 107–13
15. 16. 17. 18. 19.
20. 21. 22. 23. 24. 25. 26.
27.
Huttl K, Nemes B, Simonffy A, Entz L, Berczi V. Angioplasty of the innominate artery in 89 patients: experience over 19 years. Cardiovasc Intervent Radiol 2002; 25(2): 109–14 Brountzos EN, Malagari K, Kelekis DA. Endovascular treatment of occlusive lesions of the subclavian and innominate arteries. Cardiovasc Intervent Radiol 2006; 29(4): 503–10 Peterson BG, Resnick SA, Morasch MD, Hassoun HT, Eskandari MK. Aortic arch vessel stenting: a single-center experience using cerebral protection. Arch Surg 2006; 141(6): 560–3 Woo EY, Fairman RM, Velazquez OC et al. Endovascular therapy of symptomatic innominate-subclavian arterial occlusive lesions. Vasc Endovascular Surg 2006; 40(1): 27–33 AbuRahma AF, Robinson PA, Jennings TG. Carotid–subclavian bypass grafting with polytetrafluoroethylene grafts for symptomatic subclavian artery stenosis or occlusion: a 20-year experience. J Vasc Surg 2000; 32(3): 411–8 Cina CS, Safar HA, Lagana A, Arena G, Clase CM. Subclavian carotid transposition and bypass grafting: consecutive cohort study and systematic review. J Vasc Surg 2002; 35(3): 422–9 Takach TJ, Reul GJ, Cooley DA et al. Brachiocephalic reconstruction I: operative and long-term results for complex disease. J Vasc Surg 2005; 42(1): 47–54 Takach TJ, Duncan JM, Livesay JJ et al. Brachiocephalic reconstruction II: operative and endovascular management of single-vessel disease. J Vasc Surg 2005; 42(1): 55–61 Modarai B, Ali T, Dourado R et al. Comparison of extra-anatomic bypass grafting with angioplasty for atherosclerotic disease of the supra-aortic trunks. Br J Surg 2004; 91(11): 1453–7 Payne DA, Hayes PD, Bolia A et al. Cerebral protection during open retrograde angioplasty/stenting of common carotid and innominate artery stenoses. Br J Surg 2006; 93(2): 187–90 Danzi GB, Sesana M, Bellosta R et al. Endovascular treatment of a symptomatic aneurysm of the left subclavian artery. Ital Heart J 2005; 6(1): 77–9 Veraldi GF, Furlan F, Tasselli S, Tomasi I, Firpo M. Endovascular repair of intrathoracic left subclavian artery aneurysm with stent grafts: report of a case and review of the literature. Chir Ital 2005; 57(3): 355–9 Chambers CM, Curci JA. Treatment of nonaortic aneurysms in the endograft era: aneurysms of the innominate and subclavian arteries. Semin Vasc Surg 2005; 18(4): 184–90
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Introduction
activity in men particularly for those whose work involves over the head movements.
JE Molina
In 1927 Adson and Coffey described clinically what they called “scalene anticus syndrome” where the subclavian artery vessel could be compressed by the anterior scalene muscle.1 In 1958, Rob and Standeven introduced the term “thoracic outlet compression syndrome.”2 However, the definition needs to be explained in order to address the syndromes that pertain to the upper opening of the chest cavity. The opening comprises the space between the manubrium of the sternum the first rib and the T1 vertebral body (Figure 43.1 and 43.2). “Outlet” means that some structures or organs come out of the chest cavity either to the arms or to the neck. The only structures exiting the chest cavity are the innominate and subclavian arteries. The subclavian veins, on the contrary, enter the thoracic cavity at the front of this space and therefore it is called the “thoracic inlet,” because the flow of blood goes from the outside to the inside of the chest cavity. The brachial plexus going to the arms originates in the cervical spine and only the last branch comes from between C7 and T1.3 Nevertheless, since these trunks run parallel to the subclavian artery the compression of both structures fall under the term “thoracic outlet syndrome.” The anterior scalene muscle separates these compartments. Compression at the inlet therefore entails obstruction or pinching of the subclavian vein only. Causes includes Paget–Schroetter syndrome, and obstruction by catheters or other endovascular devices. In summary, the anterior portion of the upper opening of the chest cavity is considered to be the inlet and the posterior area is considered the outlet separated by the anterior scalene muscle.
Thoracic outlet syndrome As per our definition above this syndrome entails compression of the brachial plexus and/or the subclavian artery. The causes of this syndrome are multiple. Some originate after trauma, particularly the backlash injury common in automobile accidents;4,5 congenital anomalies like cervical rib,6,7 occupational activities as in secretaries or people who work exclusively with keyboards and develop a slouch type of habit with the chest sunken and the shoulders advanced anteriorly. It can be associated with kyphosis or scoliosis and has been described in women with obesity and enlarged breasts. It may occur also associated with strenuous physical 408
Symptoms With the exception of the trauma cases, the majority of patients have a chronic, long history of numbness and tingling of the hands and fingers, particularly with abduction of the arms to the shoulder level or over the head. Some patients complain of painful paresthesias which often occur at night and awaken the patient, who complains of having the whole limb asleep and cold. Their limitations on having the arms above the shoulder or head level are quite restrictive. In others, the symptoms are present while typing or driving their cars. Diagnosis Evaluation by physical exam is of utmost importance. Several provoking maneuvers can be implemented which are outlined further down. Although multiple tests have been devised to make an objective diagnosis there is no valid laboratory test to diagnose neural compression. This remains so far essentially a clinical test, as stated by Leffert.8 Because compression of the brachial plexus can be associated with pinching of the subclavian artery, a positive test showing this mechanism helps to confirm the diagnosis. Compression of the artery occurs only in about 28% of the cases (Table 43.1) Therefore only a positive test has any value. At the time of the physical exam attention must be paid to the presence of atrophy of the interosseous muscles or of the thenar area of the hand, which is a sign of neural damage. Provoking maneuvers of abduction of the arm anteriorly and laterally to 90 º and to 180 º brings on the symptoms. The radial pulse must be checked to verify its disappearance or a pallor that is sometimes dramatically apparent in the hand and fingers. The numbness goes away within a few seconds by bringing the arm down. Provoking maneuvers as described by Wright,9 Adson,1 and Roos5 should be implemented as well. The Wright maneuver is particularly useful: the arm is abducted 90º with external rotation and turning of the head to the affected side at the same time the individual takes a deep breath and holds it. The symptoms usually appear immediately even though the radial pulse may remain present. If the patient cannot raise the arm there is obviously a problem of the shoulder joint or in the muscles in the base of the neck, but this should not be confused with thoracic outlet syndrome.
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Table 43.1 Neurogenic thoracic outlet syndrome concomitant findings in 119 patients Vascular Compression∗ Arterial 158 Total
mid scl mus
Both (28.5%)
∗
Assessed by duplex-ultrasound. 33 with no intrinsic abnormality. One with subclavian artery aneurysm and peripheral embolization.
cl
∗∗
ant
a ●
v 1 2
Figure 43.1 Normal anatomy of the superior aperture of the chest showing the various components. scl mus = subclavian muscle tendon, cl = Clavicle, ant = anterior scalene tendon, mid = middle scalene muscle, a = subclavian artery, v = Subclavian vein. 1 = first rib, 2 = second rib. Arrows around the vein point to the inlet tunnel through which the vein runs at the level where it is often constricted. Arrows in the thoracic outlet point to the tunnel between the anterior scalene muscle and fibers of the middle scalene muscle through which the subclavian artery and the brachial plexus run.
Work-up The only laboratory tests of any use to confirm the diagnosis of thoracic outlet syndrome are as follows. ●
Venous 11 34∗∗
Doppler ultrasound of the subclavian artery obtained at the time the patient abducts the arm (Figure 43.3) In a strong, positive case the velocity in the subclavian artery
Figure 43.2 The anatomy of the first rib with the arrows indicating the levels of transection for its removal. Areas of muscle insertions are indicated by the name of the various muscles.
increases significantly or the pulsation disappears altogether. The second test is the simple chest x-ray in order to confirm or rule out the presence of a cervical rib or any other rib abnormalities. Some patients may have fusion between the second and the first rib posteriorly and have a partial or complete cervical rib (Figure 43.4). Using the old Gruber classification,6 the rib being too short (class I or II of Gruber classification) is not a reason for not operating on these patients (surgery would normally be reserved for class III only) (Figure 43.5). Our recommendation is that as long as there is a cervical rib, even a short or small rib, and the patient is positive for symptoms, the operation should proceed and the cervical rib with its fibrous attachment removed in order to cure the patient. If the plain x-ray is not sufficient to clarify the anatomy, which may be very important, then a CT of the ribcage with 3-dimensional reconstruction should be obtained (Figure 42.4).
Unnecessary tests An arteriogram is almost never necessary unless the duplex ultrasound shows some abnormality of the vessel suspicious for aneurysm formation or thrombosis, particularly in older individuals. Non-contributory tests to make a diagnosis of thoracic outlet syndrome are MRI, arteriogram, CAT scans, and EMG. Although occasionally one of these tests may be necessary to clarify special situations none of these exams should be requested as a first-line approach. Treatments Since the description by Adson and Coffey1 of the scalene anticus syndrome many contributions have been made in this area. Among them McCleery,10 Ferguson et al.,10 and Clagett,11 should be mentioned, as well as the more recent contributions by Urshell,12 Roos,13 and the present authors.14 Decompression at the thoracic outlet has evolved from the simple scalenectomy proposed by McCleery, which is no longer used, to scalenectomy with first rib resection using either the supraclavicular approach, the posterior approach, the axillary route, or a combination of both. The posterior approach was the first standard operation proposed in 1962 for the removal of the first rib by Clagett.11 This operation however is a formidable procedure derived from the methods used for thoracoplasties,
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(a)
(b)
Figure 43.3 (a) Duplex ultrasound of the subclavian artery with the arm down showing the normal pulsatile pattern; (b) the same artery with the arm elevated to 135 degrees showing dampening of the pulsatile tracing indicating compression.
cutting through several muscle layers in the back. In 1968, Ferguson10 was the first one to propose to treat the thoracic outlet syndrome by always resecting the first rib along with the scalene muscles. The supraclavicular approach has been championed by Stoney and others, and involves an anterior route through the base of the neck resecting the first rib, scalene muscles, and fibrous tissue surrounding the brachial plexus.15–17 One disadvantage is that the entire rib can not be resected anteriorly. Usually a good portion of the subclavicular rib is not accessible. Another point is that it is not cosmetically appealing, particularly to women (who are the majority of
(a)
patients with this syndrome). There is also a risk of causing damage to some of the nerves if not identified properly, particularly the phrenic nerve running behind the anterior scalene muscle. The transaxillary approach proposed by Roos in 1966 became more popular.13 It is still the preferred route used by many surgeons at the present time. Among its disadvantages if used as a sole incision is that it has given origin to significant number of complications, many serious, entailing damage to the vessels and brachial plexus.18,19 The exposure is difficult because one has to work through a very small incision in the armpit and trying to reach a cervical rib without causing
(b)
Figure 43.4 (a) 3-dimensional CT scan image showing the fusion of the first and the second rib on the right side in a 12-year-old with severe thoracic outlet syndrome; (b) the same rib viewed from a posterolateral position.
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Figure 43.5 Specimen resected from a patient with cervical rib where the end of it inserts on the posterior aspect of the anterior scalene muscle tendon. At the far left is the level of transection of the rib from the sternum and the far right the level of resection from the spine.
damage to the structures in the vicinity is challenging. To avoid these problems, we developed a combined approach, done in one session but combining the advantages of the transaxillary approach with a limited posterior route to access the spinal end of the rib. The technique has been previously described in detail14 but briefly involves a mechanical arm holder which attaches to the operating table and suspends the affected arm at a 90º angle from the body (Figure 43.6). The height of the arm can be adjusted as desired with a mechanical crank that moves the holder up and down. First we carry out the transaxillary stage only to visualize the anterior portion of the rib dividing the subclavius tendon, the anterior scalene muscle, and part of the medial scalene muscle. The rib is dissected extrapleurally and divided at its sternal insertion. The arm is now brought alongside the body and a second incision is made
Figure 43.7 Posterior incision parallel to the trapezius ridge after the transaxillary stage has been completed.
behind and parallel to the trapezius ridge (Figure 43.7). Going through the fibers of the trapezius, the elevator of the scapula is visualized. This muscle is retracted towards the shoulder and immediately beneath is the first rib. The fibers of the medial scalene muscle are divided. The muscles connecting the inferior border of the rib to the second are divided and the rib is completely isolated in its entire circumference. At the joint to the transverse process of the spine the rib is divided (Figure 43.2). The results of a series of patients operated in this manner during the past 20 years are shown in Table 43.2. This approach prevents all trauma to the vessels or nerve trunks and leaves cosmetically acceptable incisions.
Compression syndromes of the thoracic inlet The thoracic inlet comprises the anterior portion of the superior opening of the chest in front of the anterior scalene muscle. The most prominent condition here is the so-called Paget–Schroetter syndrome or “effort” thrombosis of the subclavian vein, which is an acute obstruction of the vessel that rapidly propagates into the arm (Figure 43.8).
Table 43.2 results
Figure 43.6 The setup for the transaxillary stage of the operation. The arm holder supports the forearm at 90º from the arm allowing a steady exposure.
Neurogenic thoracic outlet syndrome
Cured Improved No improvement Complications Total
No.
%
108 6 2 3 119
91 5 1.4 2.6 100
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Figure 43.8 Typical venogram of a patient with an acute Paget–Schroetter syndrome with thrombosis extending from the axillary vein to the thoracic inlet showing the network of collateral circulation that develops within a few days.
Other conditions are: obstruction of the vein by intraluminal devices like pacemaker leads, central catheters for dialysis or for administration of medications, implant of intravenous defibrillator leads, or it may happen from intermittent recurring pinching of the vein by the surrounding structures. Paget–Schroetter syndrome Pinching of the vein occurs in the channel formed between the first rib, the subclavius muscle, and the anterior scalene muscle. This could occur as one single acute event or a chronic repetitive pinching of the vessel by these structures caused by the physical activity of the individual. As the vein is traumatized, the endothelium becomes damaged, leading to thrombosis followed by fibrosis and the development of anatomical structure at that level. Most of the time it follows a sudden effort done with the arm lifting or pushing heavy objects. The term “effort thrombosis of the subclavian vein” which is synonymous, is therefore a correct cause–effect type of name given to this entity. The syndrome effects mostly young people in their productive years and could be triggered also by a sporting activity like climbing, swimming, tennis, weight lifting, and others. It is also seen in workers who perform heavy physical exertion jobs like mechanics, railroad liners, loaders of heavy equipment or freight, or people doing repetitive movements with their arms above the shoulder level. There is no predisposition to this occurrence related to pre-existing hypercoagulable abnormalities.20,21 Diagnosis The patient is usually seen on an emergency basis. The arm is edematous with blue discoloration and painful. It affects usually its whole length from the shoulder down to the fingers. Because the thrombosis progresses distally toward the arm, the symptoms usually become worse with time. The laboratory work-up of choice to confirm the diagnosis is a duplex ultrasound of the subclavian vessels. This usually shows the extent of the thrombosis and complete lack of flow through the subclavian vein. With a diagnosimade in this manner, the patient needs to undergo a venogram (Figure 43.8), either antegrade or retrograde, to show the length
Treatment The adequate treatment has evolved during the past 20 years22,23 but in spite of many opinions,24 it is now very well established what should be done to attain re-establishment of the subclavian vein patency which in all cases requires surgical intervention and must be conducted within the first two weeks of the event. The syndrome should be treated as an emergency.22,25,26 At the time the venography is obtained an infusion catheter is placed within the clot and the thrombolytic therapy implemented immediately. This constitutes the first stage of the treatment. Several thrombolytic agents have been used: urokinase, tenecteplase (TNK, Genentech, South San Francisco, CA), and alteplase (Activase, Genentech). If urokinase is used, we usually infuse 2200 units per kg of weight as a base, followed by a continuous infusion through the catheter at the same rate (2200 U/kg/hour) until the clot is dissolved. This dose averages about 150,000 units per hour. If tenecteplase is chosen, the average infusion is 0.25 mg per hour (0.05 mg/kg/hour). If alteplase is chosen the dose is the same, namely 0.25 mg per hour, which is equivalent to 0.05 mg/kg/ hour. This continuous infusion of the thrombolytic agent is carried out until the total resolution of the thrombus is attained. In the majority of cases it takes from 8–12 hours for it to disappear. As soon as this is completed the operation is undertaken as soon as possible. Details of this treatment have been previously published and the reader is referred to those articles for the specific protocols at the various stages.22,26,27 The operation is conducted via a subclavicular approach.27 The anterior half of the first rib is removed along with the subclavius tendon and the anterior scalene muscle, and a vein patch laid over the structure. The patient is given anticoagulants, namely Coumadin and Plavix, for eight weeks, at the end of which time everything is discontinued and the patient is considered cured. Results We advocate a treatment of the Paget–Schroetter syndrome as an emergency because the vein suffers very rapid deterioration, fibrosis, and obstruction leading to total obliteration as early as 2 weeks after the original event. Our experience treating over 100 of these cases over a period of approximately 21 years shows that normal flow and caliber of the vein is reestablished in 100% of the cases. No other previous treatments have reported such successful results. The reader is referred to our publication.26 Chronic obstruction of the subclavian vein This condition comprises a wide variety of mechanisms leading to the obstruction of the subclavian vein (Figure 43.9). Many of them are due to implant of devices via the subclavian vein (pacemaker and defibrillator leads, central catheters for chemotherapy or drug administration, or as a chronic stage of a once-acute Paget–Schroetter syndrome.28 The treatments available to solve this condition are not readily successful because it depends on the status of the inflow coming from the axillary vein. Whatever device is in the lumen of the vein it must be removed as a first step, and then either a vein
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Figure 43.9 Long chronic obstruction of the subclavian vein that had previous stent implants, but is severely fibrosed with multiple levels of structure. The whole segment needed to be removed and replaced by vascular homograft.
patch plasty or the implant of a vascular homograft can be attempted.28,29 These cases usually involve very long gaps of fibrotic obliterated subclavian, and sometimes innominate vein. Therefore, the incision needs to be extended through the manubrium of the sternum to obtain adequate exposure. Extension of the incision into the manubrium of the sternum (Figure 43.10) avoids a high morbidity operation like a claviculectomy to reach this area. The details of this operation have been published and should be looked up for details.30,31 When total obliteration exists, there is no channel through which a radiologist can advance any guidewires and therefore
(a)
413
the whole segment has to be excised and substituted by a graft, or a very long vein patch should be laid connecting both ends of inflow and outflow followed by implant of a covered stent. Arterial homographs have been used for this operation using straight thoracic aortic grafts taken from infants or child donors.29 The grafts are pliable and easy to work with. The immediate success rate is high but they need periodic longterm follow-up because the grafts tend to become calcified and reobstructed. They need to be remanipulated with balloon plasty or even implant of stents.29 Other types of synthetic grafts like Goretex or Dacron grafts have failed completely when implanted in that position. During the past few years we have switched to the use of long segments of saphenous vein, taken from the thighs in order to give greater diameter, which are connected from the axillary vein to the innominate vein, and laid as a patch, not as a cylindrical conduit. At 24 hours post-operation, a venogram is obtained which always shows reocclusion of the graft but the advantage of this procedure is at this point a radiologist can easily pass a guidewire from the arm through the axillary vein and the vein patch into the innominate vein, balloon dilate that segment and implant a covered stent. In our experience we have eight patients treated in this manner and seven of them had remained open up to 2 years after the stent implant. However, in two patients the graft occluded and they required another intervention of balloon angioplasty of the stented segment with implant of a new stent at the proximate or the distal end where stenosis was detected. This procedure, although still experimental, is implemented
(b)
Figure 43.10 (a) Approach used when the obstructed segment of the subclavian vein extends into the innominate vein and cannot be reached or exposed through the standard subclavicular incision. The anterior half of the first rib has been removed. Blunt dissection is carried out behind the stump of the first rib behind the sternum and from the notch of the sternum down. Using a neuroairtome the manubrium of the sternum is divided in the direction shown by the arrows. (b) By retracting the upper portion of the manubrium the entire axillary subclavian and innominate vein complex is easily exposed in an extrapleural manner; Ax = axillary vein, Scl = subclavian vein, In = innominate vein.
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only when no other option is available, but has so far shown encouraging results. Because chronic obstruction of the subclavian vein is a very serious problem, our recommendation is that if any child is considered to be a candidate for an intravenous device like a pacemaker it is preferable to use the internal jugular vein using techniques previously described by us32 that will prevent occlusion of the subclavian vein. Recommendation for the adult population is to always perform a duplex ultrasound exam of the upper veins of the body before inserting either pacemakers, central catheters, or defibrillators, by which a serious problem that doesn’t have an easy solution can be avoided. Unfortunately, this advice is not followed most of the time. There are other options and routes on how to implant effective defibrillator systems and pacemaker devices avoiding the routine use of the subclavian veins.33 The reader is referred
to the multiple publications available in the recent literature to illustrate this point.
In summary The intravenous implant of devices in the subclavian veins should be avoided as much as possible. In children it is preferable to use the internal jugular veins following published techniques, or via other routes like a mediastonomy approach, or use of direct epicardial access to the heart. In adults, when more than one device is already in place in the subclavian vein ultrasound should be routinely done before doing any further implants of this nature. This will prevent the chronic severe problems that develop from occluded subclavian veins at the thoracic inlet.
REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16. 17.
Adson AW, Coffey JR. Cervical rib: A method of anterior approach for relief of symptoms by division of the scalenus anticus. Ann Surg 1927; 85: 839–43 Rob CG, Standeven A. Arterial occlusion complicating thoracic outlet compression syndrome. Brit Med J 1958; 2: 709–12 Rayan GM. Lower trunk brachial plexus compression neuropathy due to cervical rib in young athletes. Am J Sport Med 1988; 16: 77–9 Capistrant TD. Thoracic outlet syndrome in cervical strain injury. Minn Med 1986; 69: 13–7 Rosati LM, Lord JW. Neurovascular compression syndromes of the shoulder girdle. In: Modern Surgical Monographs. New York: Grune & Stratton, 1968 Murphy JB. The clinical significance of cervical ribs. SG&O 1906; 3: 514–20 Makhoul RG, Machleder HI. Developmental anomalies at the thoracic outlet: an analysis of 200 consecutive cases. J Vasc Surg 1992; 16: 534–45 Leffert RD. Thoracic outlet syndromes. Hand Clinics 1992; 8: 285–97 Wright IS. The neurovascular syndrome produced by hyperabduction of the arms. Am Heart 1945; 29: 1–5 Ferguson TB, Burford TH, Roper CL. Neurovascular compression at the superior thoracic aperture; surgical management. Ann Thorac Surg 1968; 167: 573–9 Clagett OT. Research and Prosearch. Presidential address. J. Thorac Cardiovasc Surg 1962; 44: 153–66 Urschel HC Jr, Paulson DL, McNamara JJ. Thoracic outlet syndrome. Ann Thorac Surg 1968; 6: 1–9 Roos DB. Transaxillary approach for 1st rib resection to relieve thoracic outlet syndrome. Ann Surg 1966; 163: 354–8 Molina JE. Combined posterior and transaxillary approach for neurogenic thoracic outlet syndrome. J Am Coll Surg 1998; 187: 39–45 Cheng SWK, Stoney RJ. Supraclavicular reoperations for neurogenic thoracic outlet syndrome. J Vasc Surg 1994; 19: 565–72 Reilly LM, Stoney RJ. Supraclavicular approach for thoracic outlet decompression. J Vasc Surg 1988; 8: 329–34 Falconer MA, Li FWP. Resections of the first rib in costoclavicular compression of the brachial plexus. Lancet 1962: 59–63
18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33.
Melliere D, Becquemin JP, Etienne G, Le Cheviller B. Severe injuries resulting from operation for thoracic outlet syndrome: can they be avoided? J Cardiovasc Surg 1991; 32: 599–603 Dale A. Thoracic outlet compression syndrome: critique in 1982. Arch Surg 1982; 117: 1437–45 Martinelli I, Battaglioli T, Bucciarelli P et al. Risk factors and recurrence rate of primary deep vein thrombosis of the upper extremities. Circulation 2004; 110: 566–70 Molina JE. Letter to editor. Circulation 2005; 111: e118 (web site) Molina JE. Surgery for effort thrombosis of the subclavian vein. J Thorac Cardiovasc Surg 1992; 103: 341–6 Kunkel JM, Machleder HI. Treatment of Paget–Schroetter syndrome. A staged multidisciplinary approach. Arch Surg 1989; 124: 1153–8 Rutherford RB, Hurlbert SN. Primary subclavian-axillary vein thrombosis: consensus and commentary. Cardiovasc Surg 1996; 4: 420–3 Molina JE. Need for emergency treatment in subclavian vein effort thrombosis. J Am Coll Surg 1995; 181: 414–20 Molina JE, Hunter DW, Dietz CA. Paget–Schroetter syndrome treated with thrombolytics and immediate surgery. J Vasc Surg 2007 (in press) Molina JE. Operative technique of first rib resection via subclavicular approach. Vasc Surg 1993; 27: 667–72 Molina JE. Treatment of chronic obstruction of the axillary subclavian and innominate veins. Int J Angiol 1999; 8: 87–90 Molina JE. Use of cryopreserved small aortic homografts for large veins replacement. J Vasc Surg 1999; 33: 545–9 Molina JE. A new surgical approach to the innominate and subclavian vein. J Vasc Surg 1998; 27: 576–81 Molina JE. Approach to the confluence of the subclavian and internal jugular veins without claviculectomy. Sem Vasc Surg 2000; 13: 10–9 Molina JE, Dunnigan AC, Crosson JE. Implantations of transvenous pacemakers in infants and small children. Ann Thorac Surg 1995; 59: 689–94 Molina JE. Surgical options for endocardial lead placement when upper veins are obstructed or non-usable. J Intervent Card Electrophys 2004; 11: 149–54
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SECTION V Thoracic aorta
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Thoracic aorta: epidemiology and pathophysiology EB Diethrich
Introduction The aorta is the major vascular conduit between the left ventricle and the systemic arterial bed. Over time, aging and the effects of atherosclerosis, infection, inflammation, increased protease activity, and mechanical and genetic factors may reduce the elasticity of the aorta, making it susceptible to injury and the development of aneurysms, which are focal enlargements involving all three layers of the arterial wall. An aneurysm may be fusiform, affecting the entire circumference of the artery, or it may be saccular, involving only part of the artery circumference. The most common definition of an aneurysm is that it represents a 50% increase over the normal diameter of the artery.1 Most aneurysms are found in the distal aorta. While dissection of an aneurysm may occur in any artery, it is more common in the proximal aorta.2 Patients with ascending or aortic arch aneurysms have been shown to be significantly younger at presentation than those with descending or thoracoabdominal aneurysms (60.1 years vs. 69.0 years; p < 0.0001); ascending/arch aneurysms were also smaller at initial presentation (5.0 cm vs. 6.0 cm, p < 0.0001).3 Indeed, the natural history of the thoracic aortic aneurysm (TAA) is related to size.3–5 Aneurysms are inclined to rupture as arterial pressure increases within the aneurysm and the radius of the aneurysm enlarges (Figure 44.1).6 Recent study indicates relative aortic size is more important than absolute aortic size in predicting complications. Although initial aortic size has been associated with an increased risk of aortic rupture (p = 0.0320), a stronger association has been seen as the aortic size index (ASI) increases (p = 0.0022). The ASI calculation (aortic diameter (cm) divided by body surface area (m2)) captures the interaction between body surface area and aortic size and also appears to be an important predictor of dissection and death.3 Indeed, TAA is potentially lethal, and prompt, effective therapeutic intervention is extremely important. Unfortunately, medical management options for TAAs are limited. While beta-blocker therapy may slow the rate of aortic dilatation and reduce morbidity and mortality in some patients, 5-year survival in patients with thoracic aneurysms who did not undergo surgery was only 54%.5 Other study results suggest surgical mortality over 50% following rupture, and a median length of hospital stay for surviving patients of 16 days.7
In this chapter, we examine the epidemiology, etiology, and pathophysiology of TAAs. It has been observed that while considerable literature regarding thoracic aortic procedures has become available in the last decade, relatively little information has been offered regarding the natural history of aortic aneurysms.8
Epidemiology Thoracic aortic aneurysms are less common than abdominal aortic aneurysms (AAAs) and may involve the ascending, arch, or descending thoracic aorta or a combination of these segments. The etiology of TAAs is quite varied, and a broad spectrum of causes has been proposed. Although infectious aneurysms resulted in a 2:1 ratio of thoracic to abdominal aortic aneurysms in early autopsy studies, TAA incidence later declined because of widespread antibiotic treatment of syphilitic aneurysms.9 At present, TAAs are likely to be atherosclerotic, resulting from arterial wall remodeling and dilatation; or degenerative, caused by abnormal metabolic processes such as those seen in Marfan syndrome, Ehlers–Danlos syndrome, and Takayasu’s disease.4 TAAs may also be caused by chronic aortic dissection (Figures 44.2 and 44.3), trauma,
Figure 44.1
Ruptured thoracic aortic aneurysm.
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Textbook of peripheral vascular interventions The incidence of TAA rupture has been described to be between 1 and 5 per 100,000 person-years.6,10,11 A more recent study,12 over a 15-year period among 177 patients with thoracic aortic disease, indicates there were 28 with TAA rupture (16%), and the annual age- and sex-adjusted incidence was 3.5 per 100,000 persons for TAA rupture (95% confidence interval, 2.2–4.9). Increases in TAA incidence as measured over the last several decades may be explained by enhanced emergency medical services, diagnostic modalities, and clinician awareness.12
Physiology and pathophysiology of the aorta
Figure 44.2 Angiogram of dissecting aneurysm of the ascending aorta.
and inflammation. Most TAAs are discovered incidentally during evaluation of other medical problems. Bickerstaff et al. report the estimated overall annual incidence of TAAs is ~6 cases per 100,000 person-years, with men affected 2–4 times more often than women.6 Other authors have noted more similarity between incidence rates in men and women, with elderly women representing “an increasing portion of clinically recognized thoracic aortic aneurysms and constituting the majority of patients whose aneurysm eventually ruptures.”10
Figure 44.3
CT of dissecting aneurysm in the ascending aorta.
The aorta is an elastic artery with three defined layers: the intima, media, and adventitia. The intima is a single layer of endothelial cells that rests on the basal lamina; the subendothelial tissue is comprised of collagen and elastin fibers, fibroblasts, and a mucoid ground substance. The intimal layer is separated from the media by the internal elastic lamina, which is mostly elastin, and has fenestrae that allow diffusion from the lumen into the aortic wall. The media contains vascular smooth muscle cells (VSMCs) within a matrix of elastin, collagen, and ground substance; its elastic fibers are arranged as circumferential lamellae, which give the media its structural integrity and maintain the forward flow of blood during diastole.4 Endothelial cells and VSMCs are the major cellular components of the vessel wall. In the normal aorta, endothelial cells cover the luminal surface of the wall and of the vasa-vasori originating from the adventitia, and they supply oxygen and nutrients to VSMCs in the media.13 Smooth muscle cells in the media provide vascular resistance. The histologic characteristics associated with an aortic aneurysm include loss of elastic fibers, and in AAAs a decreased numbers of VSMCs.4 It has been proposed that loss of structural integrity of the adventitia, not the media, is required for aneurysm formation.14 The adventitia incorporates loose connective tissue (with fibroblasts, collagen, elastin, and ground substance) and maintains maximal aortic outer diameter.15 Among factors that may be involved in the development of aneurysms are abnormal proteolysis, the presence of elastolytic serum enzymes, and deficiencies of collagen and elastin.9 Recently, Kirsch et al. have observed that the aortic media was significantly thinner in the maximal dilatation area than in the transition area, and that medial thinning tended to be compensated by a median increase of 20% of the adventitial width.13 As a result, there was similar overall aortic wall thickness in both areas. These investigators speculate that microvessel development with accumulation of macrophages in their close vicinity reflects an active destruction process, mostly in the media of the transition area. Ultimately, this appears to cause extracellular matrix destruction and VSMC loss, which may explain vessel wall weakening and subsequent dilatation. Kirsch et al. further suggest that microvessel density in the adventitia maximal dilatation area may reflect an increase in metabolic needs related to VSMC regeneration, perhaps related to a healing process that may be inadequate to compensate for vascular wall tension.13
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Thoracic aorta: epidemiology and pathophysiology Collagen and elastin are the major structural proteins of the aorta; the former is responsible for the tensile strength of the vessel, while the latter lends recoil capacity. Fibrillin is another protein integral to the microfibrillar organization of the extracellular matrix, which is essentially a ladder for elastogenesis. Other extracellular matrix proteins (laminin, glycosaminoglycans, proteoglycans, and fibronectin) may also be important in aneurysm formation.4 It has been known for some time that elastin, VSMC, collagen, and ground substance are modified with advancing age. Over time, even in the normal aorta, elastic fibers splinter, collagen predominates, and ground substance increases such that the aorta becomes less distensible, weaker, and more dilated.16 It has been proposed that interactions between mechanical and biological factors lead to pathological vascular remodeling of the arterial wall in aortic aneurysms. The major histopathological features associated with ascending thoracic aortic aneurysms are abnormalities of the cellular and matrix constituents of the media (VSMCs, elastin, collagen, and mucoid ground substance). Recent work by Tang et al. suggests that pathophysiology of ascending aortic aneurysms results in medial thinning and increasing aortic diameter, with the actual mass of media becoming greater. As such, the density of medial VSMCs is preserved in ascending thoracic aortic aneurysms.17 Although the findings of Kirsch et al.13 were similar, aneurysmal specimens in the study by Tang et al. were also characterized by a significantly thickened intima. Tang et al. speculate that the mechanisms for luminal enlargement in TAAs and AAAs are different with regard to the survival of VSMCs and atrophy of the media but share common pathophysiology involving degeneration of the matrix.17
Etiology Metabolic and genetic predictors of aneurysmal disease Marfan syndrome Marfan syndrome is one of the most prevalent hereditary connective tissue disorders and is inherited in an autosomal dominant manner with variable penetrance. Marfan syndrome is caused by mutations in the fibrillin 1 gene on chromosome 15. Roughly a quarter of cases are spontaneous and not associated with a family history. Approximately 90% of patients with Marfan syndrome will develop changes in the aorta and heart valves.2 It has been demonstrated that aneurysms in the ascending aorta are more common than in the aortic arch, descending, or thoracoabdominal regions. In a recent study, aneurysm characteristics including mean initial aortic size, aortic size index, and body surface area in patients with Marfan syndrome or a family history of aortic or aneurysmal disease were similar to those without. However, patients with Marfan syndrome were significantly younger (37.7 years vs. 62.6 and 63.1 years, p = 0.0001).3 Familial TAAs Although Marfan syndrome is a well-known cause of vascular pathologies, non-Marfan’s patients may also manifest familial clustering of thoracic aortic aneurysms and dissections. In one database, Elefteriades et al. have detailed family trees on 300 of 1,600 patients and shown 21% of aneurysm probands had a first-order relative with a known or likely aortic aneurysm.8
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They assert the true number is certainly much higher as these estimates are based only on family interviews and not imaging of relatives and suggest the most common pattern of inheritance is autosomal dominant with incomplete penetrance. The same group reports familial TAAs have a relatively early age of onset and tend to grow at a faster rate than non-familial or Marfan-associated lesions and recommends screening of firstorder relatives of probands with TAA.18 In this study, probands with ascending TAAs were significantly more likely to have kindred with ascending TAAs; those with descending TAAs were more likely to have kindred with AAAs. Such disparity may indicate that descending TAAs and AAAs have features in common that are different from those of ascending TAAs. Research indicates ascending TAAs leading to type A dissections are inherited in an autosomal dominant manner,18,19 with variable age of onset and decreased penetrance, primarily in women.19 Tran-Fadulu et al. have also suggested a novel unidentified loci may be responsible for the phenotype seen in the three affected families they studied; marked variability in the age of onset of aortic disease indicated genetic or environmental factors might be responsible for modifying the phenotype.19 Genome-wide screening of a large cohort of patients has been advocated as a means of identifying specific genetic mutations for this heterogeneous disorder.20 Ehlers–Danlos syndrome Ehlers–Danlos syndrome represents a group of connective tissue disorders. Increased risk of premature death occurs only in Ehlers–Danlos type IV, which is the vascular form of the syndrome caused by mutations in the type III procollagen gene.2 Vascular Ehlers–Danlos syndrome (IV) is inherited as an autosomal dominant trait with a variety of molecular mechanisms observed, most of which have been unique to a particular family with no correlation between genotype and phenotype.21 Vascular Ehlers–Danlos syndrome is of particular importance to surgeons because knowledge of the condition may help in the management of vascular complications. In one study, among symptomatic probands, the average age at presentation was 23 years with the first complication seen by age 50. Arterial rupture and dissection were the most common presentations.22 Takayasu’s disease In Takayasu’s disease (TD), which is a chronic inflammatory disease of the aorta and its branches, aneurysms of the aorta are relatively common, with an estimated frequency of at least 10%. Descending thoracic and thoracoabdominal aortic aneurysms are the most common aneurysms associated with TD. Most descending thoracic or thoracoabdominal aortic aneurysms occurring during TD are extensive. In Kieffer et al.’s series, 23 of the 33 cases (70%) involved the entire descending thoracic aorta and most of the thoracoabdominal aorta.23 Aneurysms were more often fusiform than sacciform and usually calcified. Corticosteroid therapy, often used in treating Takayasu’s disease, has been associated with TAA rupture.24 Physical and clinical factors associated with rupture Age The risk of TAA rupture increases dramatically with age,11,25 and the proportion of women with TAAs increases in the
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elderly as well.10,25 Juvonen et al. showed in a multivariate analysis of descending TAAs and thoracoabdominal aneurysms that the relative risk of rupture increased significantly with every decade of age.26 As such, many clinicians, including our group, have long supported offering elective surgery to younger patients, particularly with the advent of endovascular techniques.27–31 Indeed, pre-emptive surgical repair has been shown to restore life expectancy to normal in patients with TAAs.5 Size The Yale group has repeatedly shown that aortic size is a very strong predictor of rupture, dissection, and mortality.3–5 For aneurysms greater than 6 cm in diameter, the rupture rate has been shown to be 3.7% per year, with a combined rate of death, rupture, or dissection of 15.6% per year.5 In a more recent report, the aortic size increased at a mean of 0.10 cm per year, and the odds ratio for rupture was increased 27-fold for aneurysms > 6 cm (p = 0.0023).3 Hypertension The effects of hypertension may be described using Laplace’s law, which states that as a cylinder increases in diameter, wall tension increases; wall tension also varies directly with the pressure in the lumen.32 As such, it is not surprising that chronic hypertension is noted in most patients with aneurysms – diastolic hypertension, in particular, has been associated with the initial development of aneurysms.33 In a report by Juvonen et al., two of three patients with TAAs had a history of hypertension.26 Patients with aneurysms are often treated with betaadrenergic blocking agents and other antihypertensives, and the effectiveness of such treatment may have blunted the significance of hypertension as a risk factor for rupture in some studies.25 Recent work suggests underlying hypertension is frequently seen in patients with descending aneurysms and their kindred, but not those with ascending aneurysms. As such, it would appear that specific risk factors for lesions in different segments of the aorta may vary.18 Chronic obstructive pulmonary disease (COPD) Chronic obstructive pulmonary disease has been known to be a risk factor for aneurysm rupture for some time. Although many patients with TAA are smokers, some studies indicate COPD appears to be a more significant risk factor.25,33 Griep et al. have suggested this finding may be an “indicator of intolerance of connective tissue to smoking-related toxicity both in the lung and in the aorta.”25 Other investigators have also linked aortic aneurysms with COPD, reporting the proportion of patients with airway obstruction (defined as forced expiratory volume in 1 second/forced vital capacity of 70% or less) was higher in those with TAAs and AAAs (100/240; 42%) than in controls (51/223; 23%) or those with non-aneurysmal coronary artery disease (43/238; 18%).34 Other research, however, does not demonstrate a significant effect of pulmonary disease on rupture and dissection rates, perhaps because there are differing definitions of what constitutes significant pulmonary disease.3 Smoking In the abdominal aorta, fatal aneurysms were found to be increased in smokers in the Whitehall study.35 In patients with TAAs, more rapid expansion of aneurysms has been shown
when there is a history of smoking.26,36,37 In the study by Juvonen et al., there was an increase of 0.70 cm/year in smokers versus 0.35 cm/year in non-smokers.26 In this same report, half of all patients with TAAs were smokers. Other investigators have demonstrated smoking is associated with a greater aortic arch diameter.38 Renal failure Although renal failure has been identified as a risk factor for expansion and/or rupture of TAAs and AAAs by several groups of investigators,39–41 other researchers have not shown it to be a significant risk factor for aneurysm rupture.3,5,25 Arteriosclerosis Concepts regarding the relationship of arteriosclerosis and TAA development have been controversial. While early research indicated the majority of TAAs were arteriosclerotic in origin,42 aortic aneurysms were thought to represent a late degenerative stage of atherosclerotic disease,43 and the presence of intraluminal thrombus and atherosclerosis was linked to accelerated growth,37 other investigators suggest atherosclerosis risk factors and aortic atherosclerotic plaques are weakly associated with distal aortic dilatation and assert that atherosclerosis plays only a minor role in aortic dilatation in the general population.38 Certainly, it appears clear that aortic aneurysms are not solely a product of associated disease processes, but are likely to have primary genetic and molecular-based causes.4,17–19
Summary Although the natural history of TAAs has been more fully elucidated in the last several decades, much work remains in determining the etiology and pathophysiologic mechanisms associated with this inherently lethal disease. It is clear that interactions between mechanical and biological factors lead to pathological vascular remodeling of the arterial wall in aortic aneurysms. The major histopathological features associated with ascending thoracic aortic aneurysms are abnormalities of the cellular and matrix constituents of the media (VSMCs, elastin, collagen, and mucoid ground substance). At present, it appears a range of genetic and environmental influences are at play in the development of TAAs. Indeed, a variety of recognized metabolic alterations seen in diseases processes such as Marfan and Ehlers–Danlos syndrome, and Takayasu’s disease, clearly increase the likelihood of aneurysm formation, and the pathologic mechanisms have been described. In addition, familial clustering of TAAs has been shown, indicating the propensity for TAA development may be inherited. Less is known regarding the mechanisms responsible for these lesions. It has long been established that rupture of TAAs is more likely over time, with advanced age, as aneurysm size increases, and that it may also be influenced by other disease processes including COPD, and by lifestyle choices such as smoking. It seems likely that with recent advances in the understanding of genetics and molecular biology, the basic causes of vascular remodeling will be more fully described and that additional knowledge about prevention and treatment will be forthcoming.
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Johnston KW, Rutherford RB, Tilson MD et al. Suggested standards for reporting on arterial aneurysms. J Vasc Surg 1991; 13: 452–8 Baxter BT. Heritable diseases of the blood vessels. Cardiovasc Pathol 2005; 14: 185–88 Davies RR, Gallo A, Coady MA et al. Novel measurement of relative aortic size predicts rupture of thoracic aortic aneurysms. Ann Thorac Surg 2006; 81: 169–77 Coady MA, Rizzo JA, Goldstein LJ, Elefteriades JA. Natural history, pathogenesis, and etiology of thoracic aortic aneurysms and dissections. Cardiol Clin 1999; 17: 615–35 Davies RR, Goldstein LJ, Coady MA et al. Yearly rupture or dissection rates for thoracic aortic aneurysms: simple prediction based on size. Ann Thorac Surg 2002; 73: 17–27 Bickerstaff LK, Pairolero PC, Hollier LH et al. Thoracic aortic aneurysms: a population-based study. Surgery 1982; 92: 1103–8 Cowan JA Jr, Dimick JB, Wainess RM et al. Ruptured thoracoabdominal aortic aneurysm treatment in the United States: 1988 to 1998. J Vasc Surg 2003; 38(2): 319–22 Elefteriades JA. Natural history of thoracic aortic aneurysms: indications for surgery, and surgical versus nonsurgical risks. Ann Thorac Surg 2002; 74(5): S1877–80; discussion S1892–8 Kouchoukos Ni, Dougenis D. Surgery of the thoracic aorta. NEJM 1997; 336: 1876–88 Clouse WD, Hallett JW Jr, Schaff HV et al. Improved prognosis of thoracic aortic aneurysms: a population-based study. JAMA 1998; 280(22): 1926–9 Johansson G, Markström U, Swedenborg J. Ruptured thoracic aorticaneurysms: a study of incidence and mortality rates. J Vasc Surg 1995; 21: 985–88 Clouse WD, Hallett JW Jr, Schaff HV et al. Acute aortic dissection: population-based incidence compared with degenerative aortic aneurysm rupture. Mayo Clin Proc 2004; 79(2): 176–80 Kirsch EW, Radu NC, Gervais M, Allaire E, Loisance DY. Heterogeneity in the remodeling of aneurysms of the ascending aorta wit tricuspid aortic valves. J Thorac Cardiovasc Surg 2006; 132(5): 1010–6 White JV, Scovell SD. Etiology of abdominal aortic aneurysms: The structural basis for aneurysm formation. In: Calligaro KD, Dougherty MJ, Hollier LH, eds. Diagnosis and Treatment of Aortic and Peripheral Arterial Aneurysms. Philadelphia: WB Saunders, 1999: 3–12 White JV. Role of adventitial defects in the pathogenesis of aortic aneurysms. In: Veith F, ed. Current Critical Problems in Vascular Surgery, vol 5. St. Louis: Quality Medical Publishing, 1993: 293–301 Movat HZ, More RH, Haust MD. The diffuse internal thickening of the human aorta with aging. Am J Pathol 1958; 34: 1023–31 Tang PC, Coady MA, Lovoulos C et al. Hyperplastic cellular remodeling of the media in ascending thoracic aortic aneurysms. Circulation 2005; 112(8): 1098–105 Albornoz G, Coady MA, Roberts M et al. Familial thoracic aortic aneurysms and dissections – incidence, modes of inheritance, and phenotypic patterns. Ann Thorac Surg 2006; 82(4): 1400–5 Tran-Fadulu V, Chen JH, Lemuth D et al. Familial thoracic aortic aneurysms and dissections: three families with early-onset ascending and descending aortic dissections in women. Am J Med Genet A 2006; 140(11): 1196–202 Elefteriades JA. Beating a sudden killer. Sci Am 2005; 293: 6 –71 Germain DP, Herrera-Guzman Y. Vascular Ehlers–Danlos syndrome. Ann Genet 2004; 47(1): 1–9 Pepin M, Schwarze U, Superti-Furga A, Byers PH. Clinical and genetic features of Ehlers–Danlos syndrome type IV, the vascular type. N Engl J Med 2000; 342: 673– 80
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Kieffer E, Chiche L, Bertal A et al. Descending thoracic and thoracoabdominal aortic aneurysm in patients with Takayasu’s disease. Ann Vasc Surg 2004; 18(5): 505–13 Hall S, Barr W, Lie JT et al. Takayasu arteritis: a study of 32 North American patients. Medicine 1983; 64: 89–99 Griepp RB, Ergin MA, Galla JD et al. Natural history of descending thoracic and thoracoabdominal aneurysms. Ann Thorac Surg 1999; 67(6): 1927–30; discussion 1953–8 Juvonen T, Ergin MA, Galla JD et al. Prospective study of the natural history of thoracic aortic aneurysms. Ann Thorac Surg 1997; 63(6): 1533–45 Thompson CS, Rodriguez JA, Ramaiah VG et al. Acute traumatic rupture of the thoracic aorta treated with endoluminal stent grafts. J Trauma 2002; 52: 1173–7 Thompson CS, Gaxotte VD, Rodriguez JA et al. Endoluminal stent grafting of the thoracic aorta: initial experience with the Gore Excluder. J Vasc Surg 2002 35: 1163–70 Ramaiah V, Rodriguez-Lopez J, Diethrich EB. Endografting of the thoracic aorta. J Card Surg 2003; 18: 444–54 Diethrich EB. Thoracic aortic endografting. J Cardiovasc Surg (Torino) 2005; 46: 99–100 Wheatley GH 3rd, Gurbuz AT, Rodriguez-Lopez JA et al. Midterm outcome in 158 consecutive Gore TAG thoracic endoprostheses: single center experience. Ann Thorac Surg 2006; 81(5): 1570–7; discussion 1577 Li JK. Comparative cardiac mechanics: Laplace’s law. J Theor Biol 1986; 118(3): 339–43 Dapunt OE, Galla JD, Sadeghi AM et al. The natural history of thoracic aortic aneurysms. J Thorac Cardiovasc Surg 1994; 107: 1323–33 Sakamaki F, Oya H, Nagaya N, Kyotani S, Satoh T, Nakanishi N. Higher prevalence of obstructive airway disease in patients with thoracic or abdominal aortic aneurysm. J Vasc Surg 2002; 36(1): 35–40 Strachan DP. Predictors of death from aortic aneurysms among middle-aged men: the Whitehall study. Br J Surg 1991; 78: 401–4 Galla JD, Ergin MA, Lansman SL et al. Identification of risk factors in patients undergoing thoracoabdominal aneurysm repair. J Card Surg 1997; 12(2 suppl): 292–9 Bonser RS, Pagano D, Lewis ME et al. Clinical and patho-anatomical factors affecting expansion of thoracic aortic aneurysms. Heart 2000; 84(3): 277–83 Agmon Y, Khandheria BK, Meissner I et al. Is aortic dilatation an atherosclerosis-related process? Clinical, laboratory, and transesophageal echocardiographic correlates of thoracic aortic dimensions in the population with implications for thoracic aortic aneurysm formation. J Am Coll Cardiol 2003; 42(6): 1076–83 Cambria RA, Gloviczki P, Stanson AW et al. Outcome and expansion rate of 57 thoracoabdominal aortic aneurysms managed nonoperatively. Am J Surg 1995; 170(2): 213–7 Perko MJ, Norgaard M, Herzog TM, Olsen PS, Schroeder TV, Pettersson G. Unoperated aortic aneurysm: a survey of 170 patients. Ann Thorac Surg 1995; 59(5): 1204–9 Masuda Y, Takanashi K, Takasu J, Morooka N, Inagaki Y. Expansion rate of thoracic aortic aneurysms and influencing factors. Chest 1992; 102(2): 461–6 Joyce JW, Fairbairn JF 2nd, Kincaid OW, Juergen JL. Aneurysms of the thoracic aorta. A clinical study with special reference to prognosis. Circulation 1964; 29: 176–81 Reed D, Reed C, Stemmermann G, Hayashi T. Are aortic aneurysms caused by atherosclerosis. Circulation 1992; 85(1): 205–11
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Radiology and anatomy of the thoracic aorta AR Owen, GH Roditi, and AW Reid
Introduction A detailed knowledge of thoracic vascular anatomy is mandatory for planning surgical or endovascular intervention of the thoracic aorta and its branches. Vascular diseases follow typical anatomical patterns and familiarity with these is central to interpretation, diagnosis, and classification of pathology. This chapter deals with the applied anatomy and radiology of the most common diseases of the thoracic aorta.
Anatomy Radiologically the thoracic aorta may be divided into the root, ascending, arch, and descending parts. The root extends from the aortic valve to the upper limits of the coronary sinuses and is contained by pericardium. The three sinuses are focal dilatations (anterior, left, and right posterior sinuses), which correspond to the cusps of the aortic valve. The right coronary artery arises from the anterior sinus and the left coronary artery from the left posterior sinus, hence the left anterior sinus is also called the non-coronary sinus. The ascending aorta extends superiorly to the level of the manubrium angle, where it becomes the arch. The arch subsequently runs superoposteriorly from right to left, arching over the pulmonary trunk and left main bronchus to reach the left side of the fourth thoracic vertebra (Figure 45.1). The left main pulmonary artery is attached to the junction of the arch and the descending aorta (the “isthmus”) by the ligamentum arteriosum. The typical branch pattern of the aortic arch (in 65% of the population) commences with the brachiocephalic artery (BCA) which divides into the right subclavian (RSCA) and right common carotid arteries (RCCA). The left common carotid artery (LCCA) is the next branch and is followed by the left subclavian artery (LSCA). However, variations in arch branching are common. In the most common variant (27%) the LCCA arises from the BCA, the so-called “bovine” arch. The left vertebral artery arises directly from the aorta between the LCCA and the LSCA in 2.4 to 5.8% of the population.1 The descending aorta runs through the posterior medisatinum to the left of the vertebral column, becoming the abdominal aorta as it passes through the aortic hiatus in the diaphragm at the level of the twelfth thoracic vertebra. It gives rise to the following branches: ● ●
intercostal arteries (nine pairs); bronchial arteries;
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esophageal arteries (up to five pairs); spinal arteries; superior phrenic arteries; subcostal arteries.
The aorta is fixed at the aortic valve, major branching points, the aortic isthmus, the intercostal arteries, and at the diaphragmatic hiatus. Its fixation at the isthmus plays an important role in trauma, especially sudden deceleration injuries, where the aorta just beyond the origin of the LSCA is the site of partial/complete transection in 85% of cases.2
Imaging techniques Developments in multiplanar imaging such as multislice computerized tomography (CT), magnetic resonance imaging (MRI), transesophageal echocardiography (TOE), and intravascular ultrasound (IVUS) have furthered our understanding of aortic disease greatly. Contemporary multislice CT angiography protocols can capture the entire length of the
Figure 45.1 Reformatted coronal CT scan of the thorax showing the aortic arch (A) lying above pulmonary artery (arrow) and left main bronchus (arrowhead).
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Radiology and anatomy of the thoracic aorta thoracic aorta and its great vessel branches during the passage of a short and concentrated bolus of contrast medium with very thin slice thickness such that the acquired data is “isotropic” and can therefore be reviewed in any plane with the same image quality. Contrast medium should ideally be injected into a right antecubital vein as left-sided injections can lead to elongation of the bolus and delay in its arrival to the heart, due to compression of the left brachiocephalic vein (LBCV) against the sternum by an enlarged or unfolded aorta. Arterial phase imaging is essential for the detection of aortic pathology and is aided by bolus tracking, whereby imaging acquisition is triggered (manually or automatically) upon arrival of the contrast bolus in the aorta. Pulsation artifact may be reduced by ECG-gating. Multiplanar reformatted images of the aorta and great vessels (Figure 45.2) aid in understanding the anatomy and pathology of the aorta, particularly when it is elongated, unfolded, or aneurysmal. Workstation tools also facilitate planning of endovascular repair. Other 3D reconstructions, including maximum-intensity projection, curvilinear reformation, and volume rendering, are invaluable for assessment of complex 3D vascular anatomical relationships. CT software packages are now available which allow “virtual” deployment of the stent-graft, enabling accurate calculation of the dimensions of the prosthesis before insertion. Virtual intravascular endoscopy is a 3D tool that provides intraluminal information and which has the potential to assess the position of stentgraft wires relative to arterial branch ostia. Several types of MRI sequence are used to image the aorta, depending upon what information is sought. ECG-gating is typically required to limit movement artifact from cardiac and aortic pulsation. “Black blood” sequences are used to show the aortic wall elegantly, free of adjacent flowing blood. Flowing blood causes a “flow void,” leaving the vessel appearing
(a)
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“empty,” the wall and intima being shown to advantage (Figure 45.3). However, contrast-enhanced MR angiography is the mainstay of imaging using a peripheral intravenous injection of the paramagnetic agent gadolinium to delineate flowing blood. Conventionally imaged in the coronal or oblique plane, the MR angiogram can be reformatted into any axis to aid diagnostic power and anatomical understanding.
Anatomical considerations in aortic disease Embyrology and anatomical variants A clear understanding the developmental abnormalities of the thoracic aorta requires a knowledge of vascular embryology. The great vessels of the thorax develop from two dorsal aortae that communicate with the aortic sac via several pairs of branchial arch arteries. The aortic sac communicates with the heart via the truncus arteriosus, which subsequently divides to form the ascending aorta and pulmonary trunk. The development of normal adult anatomy requires the involution of particular vascular segments, and complete or partial failure of involution of these is responsible for the commonest developmental abnormalities. The commonest anomaly is the “bovine” arch, which occurs in 27% of cases and ranges from a common origin for the RBCA and LCCA through to the LCCA arising as the first branch of the RBCA artery. This is important to recognize in the planning of catheter-based interventions, especially left carotid stenting, where access to the LCCA may be hindered by this common anomaly. Similarly, the shortened distance between the LCCA and the RCCA may make stenting of a RBCA stenosis challenging (Figure 45.4).
(b)
Figure 45.2 Reformatted coronal (a) and sagittal (b) CT scan of the thoracic aorta illustrating 3D anatomical relationships. (SVC: superior vena cava; LV: left ventricle; AV: aortic valve; AA: ascending aorta; PA: pulmonary artery; LMB: left main bronchus; LA: left atrium).
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Figure 45.3 “Black blood” MRI of the ascending aorta, showing wall detail and an intimal flap (arrow) in a chronic dissection under surveillance.
Double aortic arch results when the most caudal part of the right dorsal aorta fails to involute. A vascular ring (encircling esophagus and trachea) is created, with the right arch typically being wider and more superior than the left. Double aortic arch is the commonest vascular ring and often results in compressive symptoms. The left arch is infrequently atretic (it may even be a fibrous band) making differentiation from a right aortic arch difficult. A right-sided aortic arch results from persistence of the right dorsal arch and involution of a segment of the left arch. The arch therefore lies to the right of the spine, but the aorta may descend on either side. Two variants are described: in right aortic arch with aberrant LSCA there are four branches of the arch, the aberrant LSCA being the final branch
(a)
(Figure 45.5). This configuration forms a true vascular ring that is completed by the ligamentum arteriosum. Approximately 40% of cases of right aortic arch are associated with an aberrant SCA originating from a diverticulum (Kommerell’s diverticulum) which is formed by a remnant of the left dorsal aorta.3 In right aortic arch with mirror image branching, the arch gives rise to three branches: a left BCA, a RCCA, and a RSCA – a “mirror image” of the normal anatomy. This variant is not a true vascular ring and therefore does not produce compressive symptoms but it is associated with a very high incidence of severe cyanotic congenital heart disease, typically tetralogy of Fallot or truncus arteriosus and is consequently typically identified in neonates. An aberrant RSCA is reported to occur in 0.1–0.5% of individuals and results when the right fourth aortic arch and the right dorsal aorta involute cranially to the seventh intersegmental artery. This vessel arises from the aorta distal to the LSCA (sometimes from the diverticulum of Kommerell) and courses posteriorly through the mediastinum behind the esophagus before reaching the right arm. As it does not produce a true vascular ring (there is no ligamentum arteriosum), compressive symptoms (e.g. dysphagia) are rare. Coarctation of the aorta results from partial involution of the left dorsal aortic arch. It may occur proximal (preductal) or distal (post-ductal) to the ligamentum arteriosum depending on whether the involution occurs cranial or distal to the left sixth arch artery. Upper body hypertension and collateral blood flow via intercostal arteries is associated with notching of the inferior surface of the third to eighth ribs (Figure 45.11b). This is bilateral in post-ductal coarctation, right-sided in preductal coarctation, and left-sided in coarctation associated with aberrant RSCA. Aneurysm Aortic dimensions vary with age, gender, and body surface area. At the annulus, mean diameters are 2.6 cm for men and
(b)
Figure 45.4 DSA of a bovine-type aortic arch. The LCCA (arrow) arises as the first branch of the RBCA. There is a tight stenosis at the RBCA origin (a) that was successfully stented; (b) despite only 3.5 cm of stentable vessel between the LCCA and RCCA origins. Knowledge of the anatomy enabled an optimally sized stent (3 cm) to be selected.
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Figure 45.5 Contrast-enhanced MRA of a right-sided aortic arch showing a LSCA arising as the last branch of the arch from the diverticulum of Kommerell (arrow).
2.3 cm for women, rising to 2.9 cm and 2.6 cm respectively in the proximal ascending aorta.4 A proximal aorta greater than 4 cm is considered aneurysmal whereas in the descending aorta, aneurysm is present when the diameter reaches 3 cm. Wall thickness should not exceed 4 mm.5 Normal dimensions increase over time at an approximate rate of 1–2 mm per 10 years.6 In contrast, aneurysms of the ascending aorta expand at a rate of 1.3 ± 1.2 mm per year.7 Repair is considered when the maximal sac diameter exceeds 5–6cm.8–10 All mechanisms that weaken the aortic wall, and the aortic laminated media in particular, lead to higher wall stress which can induce aortic dilatation and aneurysm formation, eventually resulting in aortic dissection or rupture. Aneurysms are principally atherosclerotic in origin, but a number of rare diseases predispose: either inherited (e.g. the connective tissue disorders, Marfan syndrome, familial aortic dissection and Ehler–Danlos syndrome type IV) inflammatory (mycotic/ infective) (Figure 45.6), or traumatic. Dissection Dissection is classically defined as a disruption of the aortic wall with formation of an intimal flap that separates the true from the false lumen. The Stanford classification separates dissection into types A and B. In type A, the intimal tear is proximal to the origin of the LSCA (Figure 45.7) and in type B it is distal. The dissection usually stops at an aortic branch vessel or at the level of an atherosclerotic plaque. Classification requires high-quality multiplanar imaging to identify the anatomical distribution of the dissection. Prompt diagnosis and treatment of dissection are essential. Untreated, 36–72% of patients die within 48 hours of diagnosis and 62–91% die within one week.11 The anatomical distribution of the dissection largely dictates the treatment. Type A dissection (75% of cases) should be surgically repaired to avoid the potentially fatal sequelae of extension into the pericardium, pleural space, coronary arteries, or aortic valvular ring. Type B dissections
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Figure 45.6 Contrast-enhanced MRA of the thoracic and abdominal aorta showing separate mycotic aneurysms (arrows) caused by systemic MRSA infection, contracted following coronary artery bypass surgery.
have been conventionally treated medically unless complications ensue (e.g. refractory pain or hypertension, extension, pseudoaneurysm, or symptomatic branch vessel involvement). Endovascular repair is emerging as an alternative treatment, and has a peri-procedural morbidity and mortality (less than 30% at 30 days in most series) that compares favorably with surgery, particularly in the emergency setting.12–15 The latest imaging techniques have furthered our understanding of dissection and produced a refinement in disease classification.16 Class 1 is the classic form of dissection, which results in the true and false lumen. Flow in the false lumen
Figure 45.7 Stanford type A dissection. Axial CT scan just superior to the level of the aortic valve showing ascending aortic aneurysm with dissection and intimal tear (arrow).
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may be bidirectional depending on the pressure gradient between the two lumina and consequently the dissection can spread in an antegrade or retrograde direction. There is high pressure and wall stress in the false lumen which explains the tendency of this lumen to expand over time. CT is now sufficiently accurate to demonstrate not only the intimal flap, but tears linking the true and false lumina. Surgery or stent-grafting is targeted towards occlusion of the intimal tear, so its identification on imaging is central to clinical decision making. If the tear cannot be located on the CT scan, the more invasive IVUS can be used for precise localization immediately prior to endoluminal treatment (Figure 45.8). Class 2 dissection is an intramural hemorrhage/hematoma possibly secondary to rupture of the vasa vasorum17 which causes wall thickening and may progress to class 1 dissection, rupture, or may heal.18 After several days, intramural hematoma may manifest on T1-weighted MRI as high signal intensity as a result of methemoglobin formation, but this sign may be absent in the acute phase.19 The MRI diagnosis and anatomical localization of intramural hematoma influences decision making. Imaging goals are to confirm the diagnosis, document the anatomical extent of dissection, delineate the location of the intimal tear, demonstrate extravasation, and assess any sidebranch involvement. The commonest and most important branches to be involved are the mesenteric and renal arteries, so it is imperative to image as far inferiorly as the pelvis. It is important to realize that exclusion of the intimal tear may induce ischemia in visceral vessels that are supplied by the false lumen. In this situation, therapeutic options include branch vessel stenting or false lumen fenestration. The presence of pericardial effusion, pleural effusion (usually leftsided) peri-aortic fluid or left atrial compression indicate a poor prognosis and a mortality of greater than 50%.20 Involvement of the coronary ostia is rare, but myocardial ischemia may result from true lumen collapse during diastole. If the false lumen is completely thrombosed, central displacement of the intimal flap, calcification, or separation of intimal
Figure 45.8 Axial IVUS demonstrating the intimal defect in a patient with aortic dissection.
layers can be regarded as definitive signs of dissection.21 While a chest radiograph will be abnormal in 60–90% of cases22,23 it is insufficient to exclude dissection.24 CT is the most widely used imaging modality for the diagnosis and anatomical classification of dissection with a sensitivity approaching 100%.25,26 In our protocol, an unenhanced examination is performed first, as contrast medium may obscure an intramural hematoma. CT is not, however, as sensitive as TOE for the detection of intimal tears and it cannot identify or quantify aortic valve regurgitation.4 A number of potential pitfalls in the diagnosis of dissection on CT are recognized,27 and a thorough knowledge of these is essential if one is to avoid misdiagnosis. Examples include technical errors (e.g. poor contrast enhancement), aortic wall/cardiac motion, and streak artifacts. The latter arise from high-attenuation structures such as calcification or surgical sutures. They typically only extend over 2–3 axial slices, appear as straight parallel lines, or radiate from a single point, and generally extend beyond the confines of the aorta. The most problematic streak artifacts originate from an enhanced LBCV and superior vena cava, projecting over the ascending thoracic aorta and simulating a Stanford type A dissection. Peri-aortic structures such as the superior pericardial recess, a lowlying LBCV, the left superior intercostal vein, pleural thickening/effusion, or atelectasis, may all mimic dissection. Aortic diverticulum at the isthmus may be confused with a dissection. These are typically smooth in contour and located on the anteromedial aspect of the aorta, but may cause confusion if they are atypically placed (e.g. anterolateral) or compressed against the aortic wall.28 Aortic aneurysm with intraluminal thrombus may be difficult to differentiate from dissection with a thrombosed false lumen. In such cases, medial displacement of intimal calcification or a high-attenuation thrombosed false lumen on unenhanced CT suggest dissection. Aneurysms typically demonstrate peripheral calcification and are more often focal, whereas in dissection a long segment of the aorta is typically involved and the thrombosed false lumen spirals around the true lumen.29 Confusion can arise if there is calcification on the intraluminal surface of thrombus within an aneurysm. MRI is a sensitive tool for the detection of dissection and can identify aortic regurgitation, but is not widely available out-of-hours and the safe transfer of critically ill patients into the MR scanner presents several logistical challenges. Its optimal role is in the surveillance of chronic dissection.30 On cine gradient echo imaging, the intimal tear is demonstrated as a dark line against the high signal intensity of flowing blood. Evaluation of the tear throughout the cardiac cycle allows identification of true lumen collapse, which may be associated with end-organ ischemia. If the intima is separated circumferentially from the media this poses the risk of fatal intimointimal intussusception. Penetrating aortic ulcer A penetrating atherosclerotic ulcer (PAU) is a focal atheromatous lesion that breaches the internal elastic lamina and extends into the media, resulting in a variable degree of intramural hemorrhage.31,32 PAU typically appears in the middle and distal third of the descending aorta as a contrastfilled “diverticulum” surrounded by intramural hematoma.
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Radiology and anatomy of the thoracic aorta The peripheral aortic wall may demonstrate thickening and contrast-enhancement and an intimal flap is not present.33 Hematoma is located beneath a frequently calcified and inwardly displaced intima. Yucel et al.34 demonstrated that MRI is superior to CT in differentiating acute intramural hematoma from atherosclerotic plaque and chronic intraluminal thrombus. TOE has also been used successfully and has been reported to be highly sensitive and specific in the differentiation of aortic disease.35 Atheromatous ulcers that are confined to the intimal layer can be difficult to differentiate from PAU. Caution is advised in making a diagnosis of penetrating an atherosclerotic ulcer, particularly if discovered incidentally. IVUS, which can accurately delineate the separate layers of the aortic wall, may be invaluable in the evaluation of penetration by atheromatous ulcers.36 The natural history of PAU is poorly understood and contentious. Some authors believe that because PAU breaches the intima it can progress to dissection, aneurysm formation, or spontaneous rupture.37 Indeed, it has been considered by several investigators to have a poorer prognosis than classic aortic dissection.31,32,38,39 Coady et al.39 reported that the risk of aortic rupture was higher in patients with PAU (40% of cases) than in patients with type A (7%) or type B dissection (3.6%). Consequently, it is believed that grafting of the affected area is the treatment of choice.31,32,38,39 In particular, persistent or recurrent pain, hemodynamic instability, and a rapidly expanding aortic diameter have been considered indications for intervention.31 However, others believe that intervention is not always necessary because the disease may have a benign course.33,40 In a study by Harris et al., few patients developed dissection or rupture during follow-up, and the authors emphasize that most patients with PAU are high risk for surgery because of advanced age and co-morbidity.40 Consequently, for those patients who require treatment, endovascular repair is advocated.41 In view of the uncertainty about outcome, close clinical surveillance and early serial imaging is advised to exclude ulcer/hematoma extension or the development of complications. Blunt trauma Traumatic aortic injury usually results from rapid deceleration during road traffic accidents. The tear is typically transverse and involves the three layers of the aorta to varying degrees and is most frequently found at the aortic isthmus (Figure 45.9). The vast majority of complete ruptures die at the scene or in the emergency room42–44 and one-third of survivors will die if they do not undergo repair within 24 hours.44 This data underpins the surgical philosophy of prompt aortic repair. However, surgical repair carries significant morbidity and mortality, partly due to co-morbidity.42,43,45 Recently, Rousseau et al. reported their experience of traumatic aortic injury and concluded that those patients who survive to reach hospital may not necessarily have a uniformly bad prognosis. They suggest that delayed treatment while other injuries are treated may be justified, surmising that survivors have preserved aortic integrity because the adventitia and surrounding mediastinal structures are intact.46 A review of chest radiographs in 49 cases of aortic rupture revealed that a widened mediastinum, indistinct aortic shadow, a left apical cap, and right tracheal deviation were the
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most frequent abnormalities, but these features are non-specific47 and no patient in this cohort had a normal chest radiograph. CT is highly sensitive and has a high negative predictive value for aortic injury, but specificity is lower. Understandably, direct radiological signs (e.g. intimal tear, contour abnormality) are more specific than indirect signs (e.g. mediastinal or periaortic hematoma).48 A common radiological challenge is differentiation of an acute traumatic aortic isthmus pseudoaneurysm from a normal ductus diverticulum. Unfortunately, both the aortic isthmus and the ductus diverticulum are located anteromedially, just distal to the origin of the LSCA. Diagnostic confusion can result, but a smooth anteromedial outpouching should allow a confident identification of the normal ductus diverticulum. Angiography is reported to have very high sensitivity (100%) and specificity (97%) for the diagnosis of traumatic injury (Figure 45.10b) and may still be required in equivocal cases.49 Angiography also allows immediate progression to endovascular repair when diagnosis and anatomical location have been confirmed. The minority who survive traumatic aortic injury are at significant risk of pseudoaneurysm formation (Figure 45.9). These progressively expand over time and may be mistaken for a mediastinal mass on a chest radiograph. CT, MR, or angiography will demonstrate their true nature. Coarctation Aortic coarctation is a highly variable entity, both in its severity and morphology, ranging from a focal peri-ductal stenosis (the so-called “adult type,” and comprising the great majority of cases) to a tubular hypoplasia of the transverse aorta (the “infantile” type). However, the lesion may be positioned anywhere from the transverse arch to the iliac bifurcation. The infantile type is associated with major cardiac abnormalities, including hypoplastic left heart and transposition of the great arteries. Without early intervention, patients develop an extensive collateral circulation, principally from the branches of the subclavian, the superior intercostal, and the internal mammary arteries (Figure 45.11) to allow arterial blood to bypass the area of coarctation. An enlarged LSCA may produce a prominent opacity in the superior mediastinum on the chest radiograph. The most useful radiographic sign is an abnormal contour of the aortic arch, the “figure 3 sign.” The superior contour of the “3” represents the dilated arch proximal to the coarctation and/or a dilated LSCA. The inferior contour represents post-stenotic dilatation and the “waist.” Between the two is the coarctation itself. MRI is the imaging modality of choice for evaluation and surveillance of patients with aortic coarctation. After intervention, imaging is essential to exclude residual stenosis or complications (e.g. aneurysm). In addition to delineating the entire aorta, it is also able to quantify the collateral circulation, left ventricular and aortic valve function. MRI is the most accurate imaging modality for the assessment of left ventricular volume and mass50 and velocity mapping can be used to quantify the degree of stenosis and/or regurgitation of the frequently co-existant bicuspid aortic valve.51 Pseudocoarctation is a rare anomaly that is also characterized by stenosis of the thoracic aorta just distal to the LSCA. This appearance is produced by elongation and “kinking” of the aorta and while there is no accompanying hemodynamic
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(a)
(b)
(c) Figure 45.9
Sagittal MRI demonstrating post-traumatic pseudoaneurysm (arrow).
obstruction, the condition may still be complicated by aneurysm formation and surveillance is suggested.52,53 Takayasu’s arteritis Takayasu’s arteritis is a rare, chronic granulomatous arteritis with a possible autoimmune origin that causes obliterative disease of the aorta and its major branches.54 It carries significant morbidity and mortality as a result of progressive ischemia of the affected vessels. Stenoses are typically segmental and the coronary and pulmonary arteries may also be involved.54–56 The clinical presentation and laboratory tests at the onset of the disease are typically non-specific and prompt
diagnosis is therefore highly dependant upon accurate imaging.56 This usually demonstrates the classical anatomical distribution of great vessel origin stenosis, but the aorta itself can be narrowed.54 The disease has historically been evaluated with conventional angiography, but this technique is only able to demonstrate the vessel lumen. Contrast-enhanced MRI is not only able to demonstrate thickening of the vessel wall, but may reveal the mural edema and increased mural vascularity that reflects disease activity and occurs prior to the development of stenoses.54,57 These features are best demonstrated on delayed fat-suppressed T1-weighted imaging which depicts progressive accumulation and delayed washout of gadolinium.57
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Figure 45.10 Aortic transection: (a) axial CT scan demonstrating mediastinal hematoma and intimal tear (arrows); (b) DSA of aortic transection with contained rupture at the aortic isthmus; and (c) successful treatment by endovascular stentgraft. (Images courtesy of Dr DHA McCarter, Glasgow Royal Infirmary).
repair, particularly in the emergency setting.12,58–61 A detailed preoperative knowledge of the radiological anatomy and size is potentially more essential for endoluminal stent-grafting than for open surgery. Prerequisites for endovascular repair include a neck suitable for proximal fixation and adequate arterial access. The LSCA can usually be covered without vertebrobasilar or left arm ischemia, but occasionally a carotidosubclavian shunt or transposition is necessary. Similarly, disease extending as far as the celiac axis may require its occlusion and subsequent aortoceliac bypass. Complex cases involving the ascending and arch of the aorta have been successfully treated with hybrid surgical–radiological techniques. Optimal fixation is achieved by over-sizing the device relative to the proximal neck by 15–20%. If the common femoral arteries are of small caliber and will not allow passage of the stent-graft delivery system, surgical conduits may be attached to the iliac artery or abdominal aorta to facilitate access.62 Preprocedural CT or MRI are both reported to accurately identify the artery of Adamkiewicz in the majority of cases (this is the most important arterial supply to the thoracolumbar spinal cord and arises from the ninth to twelfth intercostal artery in the majority of cases).63–65 In doing so, these imaging modalities may help guide positioning of the stentgraft in order to preserve spinal cord perfusion and prevent paraplegia.
Aortic stent-grafting Aortic diseases that are potentially suitable for endovascular repair include: aneurysm, dissection, traumatic rupture and pseudoaneurysm, intramural hematoma, and PAU. Morbidity and mortality are lower than following open
Post-operative imaging The objectives of post-operative imaging are to exclude complications and record baseline appearances for future reference. Patients who have undergone thoracic aneurysm repair are at risk of a subsequent non-contiguous aneurysm, and therefore warrant surveillance of the entire aorta.66 Image
(a)
(b)
Figure 45.11 Aortic coarctation: (a) CT angiography demonstrating coarctation at the aortic isthmus with enlarged subclavian and internal mammary arteries (arrows) forming collateral bypass via the chest and abdominal wall; (b) bilateral enlarged, tortuous intercostal arteries provide collateral flow back into the descending aorta. (See Color plates.)
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interpretation can be confusing; variations in post-operative anatomy can mimic complications and it is therefore mandatory that the radiologist is familiar with both the spectrum of aortic surgery and the individual patient’s surgical anatomy. Close clinico-radiological liaison is essential. Following repair of a Stanford type A dissection, a persistent intimal flap is seen distal to the graft site in up to 75–100% of cases67 (Figure 45.12) and after communicating dissection up to 25% of patients develop aneurysm distal to the graft site.68 There is an additional risk of pseudoaneurysm formation at the anastamotic site resulting from partial dehiscence of the suture line.69 This is the usual explanation for the presence of flowing blood in a perigraft space, but this situation is sometimes deliberately created surgically.67,69 Abnormal soft tissue is occasionally seen surrounding a graft or anastomosis, but this appearance can usually be explained once the operative details have been reviewed. Soft tissue may have been intentionally wrapped around anastomoses to aid hemostasis or is seen when an inclusion graft technique has been used.67 The length of the graft does not always match the extent of the aneurysm and residual dilatation of the remaining native abdominal aorta may be seen. The appearances of the descending aorta will be abnormal if an inclusion graft technique has been used and this may suggest further aneurysm formation.
Summary Radiology now has a pivotal role not only in the diagnosis and classification, but also in the treatment of diseases of the thoracic aorta. A comprehensive knowledge of thoracic vascular anatomy (including normal variants and post-operative
Figure 45.12 Axial CT scan following type A aortic dissection repair showing a persistent dissection flap in the aortic arch.
appearances) is a prerequisite for the vascular radiologist, interventionalist, or surgeon in the interpretation of pathology and the planning of treatment. Imaging techniques that already demonstrate anatomy and pathology in exquisite detail will continue to evolve in parallel with advances in technology and will undoubtedly further our understanding of aortic disease.
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Kang SG, Lee DY, Maeda M et al. Aortic dissection: percutaneous management with a separating stent-graft – preliminary results. Radiology 2001; 220(2): 533–39 Nienaber CA, Fattori R, Lund G et al. Nonsurgical reconstruction of thoracic aortic dissection by stent-graft placement. N Engl J Med 1999; 340(20): 1539–45 Lee JT, White RA. Current status of thoracic aortic endograft repair. Surg Clin North Am 2004; 84(5): 1295–1vii Czermak BV, Waldenberger P, Fraedrich G et al. Treatment of Stanford type B aortic dissection with stent-grafts: preliminary results. Radiology 2000; 217(2): 544–50 Herold U, Piotrowski J, Baumgart D et al. Endoluminal stent graft repair for acute and chronic type B aortic dissection and atherosclerotic aneurysm of the thoracic aorta: an interdisciplinary task. Eur J Cardiothorac Surg 2002; 22(6): 891–7 Svensson LG, Labib SB, Eisenhauer AC, Butterly JR. Intimal tear without hematoma: an important variant of aortic dissection that can elude current imaging techniques. Circulation 1999; 99(10): 1331–6 Stefanadis CI, Karayannacos PE, Boudoulas HK, Stratos CG, Vlachopoulos CV, Dontas IA et al. Medial necrosis and acute alterations in aortic distensibility following removal of the vasa vasorum of canine ascending aorta. Cardiovasc Res 1993; 27(6): 951–6 Maraj R, Rerkpattanapipat P, Jacobs LE, Makornwattana P, Kotler MN. Meta-analysis of 143 reported cases of aortic intramural hematoma. Am J Cardiol 2000; 86(6): 664–8 Wolff KA, Herold CJ, Tempany CM, Parravano JG, Zerhouni EA. Aortic dissection: atypical patterns seen at MR imaging. Radiology 1991; 181(2): 489–95 Erbel R, Oelert H, Meyer J et al. Effect of medical and surgical therapy on aortic dissection evaluated by transesophageal echocardiography.
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Implications for prognosis and therapy. The European Cooperative Study Group on Echocardiography. Circulation 1993; 87(5): 1604–15 Erbel R, Engberding R, Daniel W et al. Echocardiography in diagnosis of aortic dissection. Lancet 1989; 1(8636): 457–61 Hagan PG, Nienaber CA, Isselbacher EM et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA 2000; 283(7): 897–903 Slater EE, DeSanctis RW. The clinical recognition of dissecting aortic aneurysm. Am J Med 1976; 60(5): 625–33 Hartnell GG, Wakeley CJ, Tottle A, Papouchado M, Wilde RP. Limitations of chest radiography in discriminating between aortic dissection and myocardial infarction: implications for thrombolysis. J Thorac Imaging 1993; 8(2): 152–5 Sebastia C, Pallisa E, Quiroga S et al. Aortic dissection: diagnosis and follow-up with helical CT. Radiographics 1999; 19(1): 45–60 Nienaber CA, von Kodolitsch Y, Nicolas V et al. The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl J Med 1993; 328(1): 1–9 Batra P, Bigoni B, Manning J et al. Pitfalls in the diagnosis of thoracic aortic dissection at CT angiography. Radiographics 2000; 20(2): 309–20 Morse SS, Glickman MG, Greenwood LH et al. Traumatic aortic rupture: false-positive aortographic diagnosis due to atypical ductus diverticulum. AJR Am J Roentgenol 1988; 150(4): 793–6 Heiberg E, Wolverson MK, Sundaram M, Shields JB. CT characteristics of aortic atherosclerotic aneurysm versus aortic dissection. J Comput Assist Tomogr 1985; 9(1): 78–83 Erbel R, Alfonso F, Boileau C et al. Diagnosis and management of aortic dissection. Eur Heart J 2001; 22(18): 1642–81 Stanson AW, Kazmier FJ, Hollier LH, Edwards WD, Pairolero PC, Sheedy PF et al. Penetrating atherosclerotic ulcers of the thoracic aorta: natural history and clinicopathologic correlations. Ann Vasc Surg 1986; 1(1): 15–23 Welch TJ, Stanson AW, Sheedy PF, Johnson CM, McKusick MA. Radiologic evaluation of penetrating aortic atherosclerotic ulcer. Radiographics 1990; 10(4): 675–85 Kazerooni EA, Bree RL, Williams DM. Penetrating atherosclerotic ulcers of the descending thoracic aorta: evaluation with CT and distinction from aortic dissection. Radiology 1992; 183(3): 759–65 Yucel EK, Steinberg FL, Egglin TK et al. Penetrating aortic ulcers: diagnosis with MR imaging. Radiology 1990; 177(3): 779–81 Sommer T, Fehske W, Holzknecht N et al. Aortic dissection: a comparative study of diagnosis with spiral CT, multiplanar transesophageal echocardiography, and MR imaging. Radiology 1996; 199(2): 347–52 Waller BF, Pinkerton CA, Slack JD. Intravascular ultrasound: a histological study of vessels during life. The new ‘gold standard’ for vascular imaging. Circulation 1992; 85(6): 2305–10 Hayashi H, Matsuoka Y, Sakamoto I et al. Penetrating atherosclerotic ulcer of the aorta: imaging features and disease concept. Radiographics 2000; 20(4): 995–1005 Benitez RM, Gurbel PA, Chong H, Rajasingh MC. Penetrating atherosclerotic ulcer of the aortic arch resulting in extensive and fatal dissection. Am Heart J 1995; 129(4): 821–3 Coady MA, Rizzo JA, Hammond GL et al. Penetrating ulcer of the thoracic aorta: what is it? How do we recognize it? How do we manage it? J Vasc Surg 1998; 27(6): 1006–15 Harris JA, Bis KG, Glover JL et al. Penetrating atherosclerotic ulcers of the aorta. J Vasc Surg 1994; 19(1): 90–8 Murgo S, Dussaussois L, Golzarian J et al. Penetrating atherosclerotic ulcer of the descending thoracic aorta: treatment by endovascular stent-graft. Cardiovasc Intervent Radiol 1998; 21(6): 454–8 Lamme B, de Jonge IC, Reekers JA, de Mol BA, Balm R. Endovascular treatment of thoracic aortic pathology: feasibility and mid-term results. Eur J Vasc Endovasc Surg 2003; 25(6): 532–9 Kato N, Dake MD, Miller DC et al. Traumatic thoracic aortic aneurysm: treatment with endovascular stent-grafts. Radiology 1997; 205(3): 657–62 Borsa JJ, Hoffer EK, Karmy-Jones R et al. Angiographic description of blunt traumatic injuries to the thoracic aorta with specific relevance to endograft repair. J Endovasc Ther 2002; 9 Suppl 2: II84–II91 Kasirajan K, Heffernan D, Langsfeld M. Acute thoracic aortic trauma: a comparison of endoluminal stent grafts with open repair
46. 47. 48.
49. 50. 51. 52. 53. 54. 55. 56. 57. 58. 59.
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and nonoperative management. Ann Vasc Surg 2003; 17(6): 589–95 Rousseau H, Dambrin C, Marcheix B et al. Acute traumatic aortic rupture: a comparison of surgical and stent-graft repair. J Thorac Cardiovasc Surg 2005; 129(5): 1050–55 Stark P, Cook M, Vincent A, Smith DC. Traumatic rupture of the thoracic aorta. A review of 49 cases. Radiologe 1987; 27(9): 402–6 Mirvis SE, Shanmuganathan K, Miller BH, White CS, Turney SZ. Traumatic aortic injury: diagnosis with contrast-enhanced thoracic CT – five-year experience at a major trauma center. Radiology 1996; 200(2): 413–22 Fabian TC, Davis KA, Gavant ML et al. Prospective study of blunt aortic injury: helical CT is diagnostic and antihypertensive therapy reduces rupture. Ann Surg 1998; 227(5): 666–76 Bottini PB, Carr AA, Prisant LM et al. Magnetic resonance imaging compared to echocardiography to assess left ventricular mass in the hypertensive patient. Am J Hypertens 1995; 8(3): 221–8 Vriend JW, Oosterhof T, Mulder B. Noninvasive imaging for the postoperative assessment of aortic coarctation patients. Chest 2005; 127(6): 2295 Sebastia C, Quiroga S, Boye R et al. Aortic stenosis: spectrum of diseases depicted at multisection CT. Radiographics 2003; 23 Spec No: S79–S91 Kessler RM, Miller KB, Pett S, Wernly JA. Pseudocoarctation of the aorta presenting as a mediastinal mass with dysphagia. Ann Thorac Surg 1993; 55(4): 1003–5 Nastri MV, Baptista LP, Baroni RH et al. Gadolinium-enhanced three-dimensional MR angiography of Takayasu arteritis. Radiographics 2004; 24(3): 773–86 Numano F, Okawara M, Inomata H, Kobayashi Y. Takayasu’s arteritis. Lancet 2000; 356(9234): 1023–5 Johnston SL, Lock RJ, Gompels MM. Takayasu arteritis: a review. J Clin Pathol 2002; 55(7): 481–6 Choe YH, Han BK, Koh EM et al. Takayasu’s arteritis: assessment of disease activity with contrast-enhanced MR imaging. AJR Am J Roentgenol 2000; 175(2): 505–11 Ishida M, Kato N, Hirano T et al. Endovascular stent-graft treatment for thoracic aortic aneurysms: short- to midterm results. J Vasc Interv Radiol 2004; 15(4): 361–7 Czermak BV, Waldenberger P, Perkmann R et al. Placement of endovascular stent-grafts for emergency treatment of acute disease of the descending thoracic aorta. AJR Am J Roentgenol 2002; 179(2): 337–45 Dake MD, Kato N, Mitchell RS et al. Endovascular stent-graft placement for the treatment of acute aortic dissection. N Engl J Med 1999; 340(20): 1546–52 Neuhauser B, Perkmann R, Greiner A, Steingruber I, Tauscher T, Jaschke W et al. Mid-term results after endovascular repair of the atherosclerotic descending thoracic aortic aneurysm. Eur J Vasc Endovasc Surg 2004; 28(2): 146–53 Garzon G, Fernandez-Velilla M, Marti M et al. Endovascular stentgraft treatment of thoracic aortic disease. Radiographics 2005; 25 Suppl 1: S229–S244 Hyodoh H, Kawaharada N, Akiba H et al. Usefulness of preoperative detection of artery of Adamkiewicz with dynamic contrastenhanced MR angiography. Radiology 2005; 236(3): 1004–9 Yoshioka K, Niinuma H, Ohira A et al. MR angiography and CT angiography of the artery of Adamkiewicz: noninvasive preoperative assessment of thoracoabdominal aortic aneurysm. Radiographics 2003; 23(5): 1215–25 Takase K, Sawamura Y, Igarashi K et al. Demonstration of the artery of Adamkiewicz at multi-detector row helical CT. Radiology 2002; 223(1): 39–45 Pressler V, McNamara JJ. Aneurysm of the thoracic aorta. Review of 260 cases. J Thorac Cardiovasc Surg 1985; 89(1): 50–4 Riley P, Rooney S, Bonser R, Guest P. Imaging the post-operative thoracic aorta: normal anatomy and pitfalls. Br J Radiol 2001; 74(888): 1150–8 Gaubert JY, Moulin G, Mesana T et al. Type A dissection of the thoracic aorta: use of MR imaging for long-term follow-up. Radiology 1995; 196(2): 363–9 Krinsky G, Reuss PM. MR angiography of the thoracic aorta. Magn Reson Imaging Clin N Am 1998; 6(2): 293–320
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Introduction Lesions in the thoracic aorta are often life-threatening, and traditional open repair carries the risks of significant morbidity and mortality. As yet, the number of endoprostheses available for treating thoracic aortic pathologies is smaller than that for repairing abdominal aortic aneurysms (AAAs), likely because the reported prevalence of thoracic aortic aneurysms (TAAs) is lower. Still, the investigative work for descending thoracic aneurysms treated with endografts has advanced to the point of Food and Drug Administration (FDA) approval of the Gore TAG device (WL Gore & Associates, Flagstaff, AZ) for that specific pathology. It is the only such device approved in the US. Mounting experience with thoracic endograft procedures suggest they may be a viable means of treating a variety of problems in the thoracic vascular territory, including chronic atherosclerotic aneurysms, dissecting aneurysms, penetrating ulcers, aortobronchial fistulas, acute transections, and lesions caused by complications of previous aortic repair such as coarctations.1–19 Endovascular intervention avoids sternotomy or thoracotomy, chest tubes, respirators, general anesthesia, and blood loss is limited. Complications such as paraplegia, renal failure, and cardiac and pulmonary difficulties are minimized. Selection of patients on the basis of favorable anatomy and pathology for a specific device is critical to procedural success. The results of medical management for thoracic aortic aneurysms compare poorly with endovascular treatment10 or surgical intervention. In one study, for example, beta-blocker therapy was associated with 5-year survival of only 54% in patients with thoracic aneurysms who did not undergo surgery.20 When a thoracic aneurysm ruptures, emergent open surgical intervention is linked with a mortality rate of more than 50%, and renal failure and cardiac complications are common.21 Even under the best of circumstances, conventional surgical repair is generally associated with prolonged hospitalization, post-operative monitoring in an intensive care unit (ICU), and a recuperation period of 3–6 months. Discussions continue regarding the role of endografting in asymptomatic type B dissecting aneurysms. Recent data from the INSTEAD (INvestigation of STEnt grafts in patients with type B Aortic Dissection trial) indicate there is not a significant advantage in treating these lesions with endografts. Clearly, these data will be subjected to further scrutiny in additional studies. A recent report indicates: “Contemporary follow-up mortality in patients who survive to hospital 432
discharge with acute type B aortic dissection is high, approaching 1 in every 4 patients at 3 years, despite access to and availability of modern therapeutic strategies.”22 My sentiments regarding thoracic aortic endografting and endovascular intervention, in general, have long been the same – in selected patients, endografting shows evident benefit in the treatment of a variety of pathologies. When we consider the complications associated with open thoracic aortic repair – even when skilled operators are involved – the need for a minimally invasive approach that reduces the likelihood of complications and improves the odds of a more rapid recovery has always been great. Indeed, successful intervention that minimizes complications is extremely important in any medical or surgical setting. At present, a number of innovative techniques addressing thoracic aortic pathologies that incorporate endovascular repair alone or with surgical methods have been described.1–19,23,24 In this chapter, the indications for endovascular intervention of TAAs are described, a review of the Gore TAG device is presented and compared with our institutional experience.
Thoracic aortic aneurysms Background Aneurysms are focal enlargements involving all three layers of the arterial wall; they may be fusiform – affecting the entire circumference of the artery, or saccular – involving only part of the artery circumference. The most common definition of an aneurysm is that it represents a 50% increase over the normal diameter of the artery. Aneurysms are inclined to rupture as arterial pressure increases within the aneurysm and the radius of the aneurysm enlarges.25 The risk of TAA rupture increases dramatically with age, and the proportion of women with TAAs increases in the elderly as well.26 Aortic size is a very strong predictor of rupture, dissection, and mortality.27–29 For aneurysms greater than 6 cm in diameter, the rupture rate has been shown to be 3.7% per year, with a combined rate of death, rupture, or dissection of 15.6% per year.28 Hypertension is noted in most patients with aneurysms. Diastolic hypertension, in particular, has been associated with the initial development of aneurysms.30 Chronic obstructive pulmonary disease (COPD) is also a risk factor for aneurysm rupture. Although many patients with TAA are smokers, some studies indicate COPD appears to be a more significant risk factor.30 Renal failure has been identified as a risk factor for expansion and/or rupture of TAAs and AAAs in some
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Thoracic aorta: thoracic aortic aneurysms research,31 but other researchers have not shown it to be a significant risk factor for aneurysm rupture.26–28 Concepts regarding the relationship of arteriosclerosis and aneurysm development have been controversial; it seems that aortic aneurysms are likely to have primary genetic and molecularbased causes. Marfan syndrome is one of the most prevalent hereditary connective tissue disorders and commonly causes aneurysms in the ascending aorta.32 Similarly, Ehlers–Danlos syndrome is another connective tissue disorder known to cause early vascular complications; arterial rupture and dissection are familiar presentations.33 Takayasu’s disease, a chronic inflammatory disease of the aorta and its branches, is associated with extensive aneurysms of the aorta.34 Familial predisposition for TAAs has also been identified; these aneurysms tend to occur relatively early in life and grow at a faster rate than non-familial or Marfan-associated lesions.35
Endovascular intervention Technical considerations Complex and difficult-to-treat aneurysms are often found in the descending thoracic aorta. Selection of patients for endovascular procedures on the basis of favorable anatomy and pathology for a specific device is key to the success of the procedure, and endovascular technology may be used only in patients who are willing to adhere to a lifetime of surveillance. The proximal and distal landing zones are extremely critical, and the iliac and femoral arteries must be suited to large-bore sheath delivery. Intravascular ultrasound is very helpful in determining graft size and optimal landing areas. At present, the profile of thoracic endografts is considerably larger than that of its abdominal aortic counterparts, and endovascular intervention requires careful planning to be a success. Although graft manufacturers are directing more attention now to developing low-profile devices, until these are available, operators must be experienced in the use of conduits from either the common iliac artery or even the lower abdominal aorta itself (Figure 46.1). The conduit provides a smooth entry for the endograft and the conduit can either be ligated or used as a bypass to the common femoral artery. Hopefully, these techniques will be obviated when low-profile devices are available.
Figure 46.1 Photograph illustrating technique for incorporating a conduit for endograft delivery when the femoral and iliac arteries are small or diseased.
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In some cases, the proximal aorta is relatively small and the distal landing zone much larger. Since tapered grafts are not yet available, it is necessary to “customize” the device (Figure 46.2), a process that will also be obviated when manufacturers expand their graft product lines. Recent approaches to thoracoabdominal aneurysm repair include rerouting the visceral branches surgically with grafting of the aneurysm (Figure 46.3)24; this technique will surely expand the indications for endografts. Considerable investigation is being directed toward endovascular treatment of thoracoabdominal aneurysms using fenestrated and branched grafts (Figure 46.4). At present, these procedures require fairly extensive preprocedural planning and, in some cases, a long operative time. The progressive development of imaging modalities has enabled significant advancement in the numbers of pathologies that may be treated favorably. Imaging There are a number of modalities used to image the thoracic aorta. The determination regarding whether a patient is a candidate for an endograft is usually made on the basis of computed axial tomography (CT) and aortography. In addition, intravascular ultrasound (IVUS) and transesophageal echo (TEE) imaging can be useful in appreciating the complex pathology of the thoracic aorta. We have not found magnetic resonance imaging (MRI) and angiography (MRA) are very helpful in preoperative planning. When the new 64-slice CT scanner is used in conjunction with 3D reformation software (General Electric, Phoenix,
Figure 46.2 Example of graft customization to accommodate varying diameters in the arch and descending thoracic aorta. Commercial devices are not yet available.
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(a)
(b)
Figure 46.3 Rerouting of visceral branches allows endoluminal grafting in thoracoabdominal aneurysms. Similar concepts are being applied to aortic arch aneurysms.
AZ), the diseased aorta may be visualized in every plane. The previous limitations of transaxial tomographic images were related to not being able to properly assess the length and appreciate the tortuosity of the aorta. The new 64-slice technology permits us to distinguish calcium, thrombus, and true aortic lumen size and are able to take true perpendicular measurements of the aorta to determine which graft(s) will be
Figure 46.4 Fenestrated and branched grafts are being investigated and will be available commercially in the future.
best suited to the procedure. In addition, with the 3D reformation software, we are able to determine center-line lengths and the ideal tube angulations needed to open the thoracic arch. This information allows image-intensified positioning at the time of graft placement. The primary imaging modality used during implantation of the thoracic endoluminal graft is fluoroscopic aortography. In our institution, to acquire these images, a fixed ceilingmounted fluoroscopic C-arm is used. Most facilities have used portable C-arms, though leading facilities are now choosing fixed imaging systems. The clinician may need to learn a new method for these procedures; with a fixed C-arm, the patient is mobile and the C-arm becomes static. We have opted for a hybrid C-arm, the Fischer SPX (Fischer, Denver, CO) that pans around a stationary patient (Figure 46.5). This allows the physician to focus on one site, instead of having to follow the operative site. The fixed table we use is a radiolucent, pedestaltype table. It has a full range of motions including Trendelenberg, reverse Trendelenberg, and side-to-side tilt capabilities. We have been instrumental in the development of this equipment to enhance performance of these procedures. The fluoroscopic equipment is used in conjunction with a contrast pressure injector. The combination of these produces angiographic and digitally subtracted angiographic (DSA) images. These images are used to determine and mark the desired landing zone. To acquire these images, the tube is angled (using the predetermined ideal tube angle) for proximal grafts (Figure 46.6). Fluoroscopy provides real-time imaging during catheter and guidewire manipulation; continuous fluoroscopy is used when optimal image quality is required (i.e. selective catheterization). Pulsed fluoroscopy is used when less detail is required, such as is positioning an OmniFlush (Angiodynamics, Queensbury, NY) or pigtail catheter.
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Figure 46.5 Ceiling-mounted C-arms are ideal for imaging complex aneurysmal disease before and during intervention. This carbon fiber table, developed at the Arizona Heart Institute, permits complete, unobstructed imaging during endovascular procedures.
(a) Figure 46.6
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Most systems today also have a second monitor to transfer a reference image used for guidance “roadmapping.” Another imaging technique is digital subtraction arteriography, which is generally obtained as one station (or field of view) at a time. A mask is created for later subtraction, contrast is injected, and the image intensifier and the object are held in a constant position as motion artifact is detrimental to the accuracy of digital images. Contrast injectors are very useful during fluoroscopy and DSA imaging. The main considerations include the total volume of contrast to be delivered, and the injection rate (ml/second); together, these determine the duration of the bolus. Also important are the maximum pressure in pounds per square inch (psi), which is the peak pressure the pump will generate during injection, and the pressure rate rise, which is the time to peak pressure. In practice, the latter is generally 0.4 seconds. Other features that some contrast injectors also offer are inject delays and x-ray delays. The former delays the injection of contrast to allow mask images to be acquired, while the latter delays x-ray exposure, preventing unnecessary images prior to the contrast arriving at the area of interest. When using IVUS in the thoracic aorta, a large probe is required (8.4 French) with more penetration (10 MHz) and compatibility with a large guidewire (0.035 inch). IVUS is useful in assessing and measuring the neck of a thoracic aneurysm being treated by endoluminal grafting. The exact origin of the subclavian artery can also be identified. IVUS also defines the extent of thoracic dissection and greatly assists treatment of coarctation of the aorta (Figure 46.7).36
(b) Drawing illustrating the importance of proper positioning of the radiographic equipment at the time of graft deployment.
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Figure 46.7 Intravascular ultrasound is an important imaging modality, particularly in dealing with complex aortic dissections.
The Gore TAG device The TAG device is approved for endovascular repair of aneurysms of the descending thoracic aorta in patients who have appropriate anatomy, including adequate iliac/femoral access, aortic inner diameter in the range 23–37 mm, and ≥ 2-cm non-aneurysmal aorta proximal and distal to the aneurysm. The TAG device is a flexible, self-expanding endoprosthesis constrained on the leading edge of a delivery catheter (Figure 46.8). The endoprosthesis comprises an expanded PTFE tube with a nitinol support structure. The delivery catheter is inserted into the femoral artery, and the endoprosthesis is deployed to exclude the aneurysm from circulation. The procedure is generally performed in a catheterization
Figure 46.8 The Gore TAG device is the only commercial graft approved in the US for deployment in the thoracic aorta.
laboratory or operating room by a vascular surgeon and interventional radiologist, although this varies from institution to institution. The TAG device is available in diameters of 26 to 40 mm and in 10-, 15-, and 20-cm lengths. The profile of the device depends on the diameter of the TAG device and requires a 20-French, 22-French, or 24-French introducer sheath (Figure 46.9). The TAG device has a unique self-expanding deployment mechanism, which allows graft expansion to begin centrally and propagate simultaneously in both antegrade and retrograde directions. This type of deployment allows rapid intraluminal expansion of the device and minimizes the displacing forces relating to high arterial blood flow. An overlap of at least 3 cm is recommended when more than one TAG device is deployed (when diameters are different); if the deployed devices are of the same diameter, a 5-cm overlap is suggested. Intraluminal profiling and expansion of the deployed TAG device can be enhanced in some cases by use of the Gore Tri-lobed Balloon (Figure 46.10), which permits intraluminal blood flow to continue distally during balloon inflation. Other non-compliant balloons are available that do not require multiple inflations to ensure complete circumferential apposition. Although some investigators have noted occasional difficulties in deflating the balloon that necessitated surgical removal of the balloon, we have not experienced this problem. Clinical results We reviewed our consecutive clinical experience with the TAG device endoprosthesis for the endovascular exclusion of assorted descending thoracic aortic pathologies in 158 highrisk surgical patients (mean age 72 ± 12.1 years).37 Indications for study enrollment were atherosclerotic aneurysm (n = 76), aortic dissection (n = 36), penetrating aortic ulcer (n = 15), contained rupture (n = 11), pseudoaneurysm (n = 10), traumatic aortic injury (n = 5), aortobronchial fistula (n = 4), and aortic coarctation (n = 1). Although patients were enrolled prospectively in this study, they were not randomized. Many would not have been candidates for open surgical therapy; thus, a randomized study using this same patient population
Figure 46.9 The Gore TAG device is delivered through a sheath available in 20–24-French sizes.
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nearly identical to results outside the IDE. We required an iliac conduit in 10.1% of our other cases versus 15% in the IDE study, and we delivered 8.9% of the devices without a sheath, something not done in the IDE study. Twenty percent of patients in the IDE study underwent carotid–subclavian bypass associated with the endografting. We do not employ this except as indicated except in situation where the internal mammary artery must be protected or the vertebral circulation might be compromised. The mortality rate in our cases outside the IDE was 3.8%, which is somewhat higher than the 1.5% rate seen within the IDE, likely because complex pathologies such as dissections and ruptures were excluded in the IDE.
Summary
Figure 46.10 Gore provides a tri-lobed balloon for postdeployment expansion of the endograft. The theoretic advantage is that it allows partial blood flow during ballooning, which may decrease blood pressure changes and graft movement.
would have had to compare endovascular therapy against medical therapy, even though the natural history of patients with thoracic aneurysms > 6 cm is poor.38 Technical success was 98.7% (156 of 158 patients). Three (1.9%) patients developed transient paraparesis after graft deployment, and one (0.6%) patient developed paraplegia. Post-implantation endoleaks were observed in 18 (11.5%) patients, and 12 patients required reintervention. At 30 days, mortality was 3.8% (6 of 156) and, at a mean follow-up of 21.5 ± 18.8 months, overall mortality was 17.3% (27 of 156). The 2.6% rate of spinal cord ischemia in this study compares favorably with results from the pivotal trial. Only one patient was left with a serious permanent deficit, and this patient was at high risk for neurologic injury secondary to acute type B dissection. We used cerebrospinal fluid (CSF) drainage selectively and believe this adjunctive therapy is important when treating high-risk candidates, such as those with a history of previous abdominal aortic aneurysm repair. Overall, endoluminal grafting of descending TAAs and other pathologies with the TAG device was feasible and safe in highrisk surgical patients in a series we performed under an investigator device exemption (IDE). Interestingly, the results of the IDE study, in which the restrictions were more stringent, were
Following FDA approval of the Gore TAG thoracic endograft for endovascular treatment of thoracic aneurysmal disease, a new era in management of these life-threatening lesions has begun. Data from single-center trials indicate endograft implantation appears an effective option for TAAs and treatment of a variety of other pathologies as well. Treating aortic arch and high descending aneurysmal disease is a challenge with current technology. Considerable advances have been made in the design and manufacture of branched and fenestrated grafts in this region as in the abdomen. Testing of devices in the aortic arch has been initiated in Japan and Australia. Unfortunately, the high incidences of embolization and stroke bear evidence of the precarious nature of grafting in the arch. We have observed atherosclerotic debris at the origins of the brachiocephalic and left common carotid arteries. Passing fenestrated and branched devices across such areas must be done with techniques that prevent embolization. Some investigators have even suggested the use of embolic protection devices; however, this may be somewhat cumbersome. The challenge remains to develop a flexible, low-profile device that causes a minimum of trauma to the vessels. Mid-term results in the descending thoracic aorta are better with endovascular intervention than medical therapy alone. Ultimately, with proof-of-principle established in upcoming studies, there will be explorations into the treatment of aneursymal disease in the ascending aorta and the aortic arch for both atherosclerosis and dissecting aneurysms. Our institution already has established research protocols to initiate these investigations based on our extensive experience with endografting in the thoracic aorta. While it is early in our efforts, it is already apparent that, in spite of significant challenges, this anatomic area will be amenable to endografting for treatment of a variety of pathologic conditions.
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24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35.
36. 37. 38.
Diethrich EB, Ghazoul M, Wheatley GH et al. Surgical correction of an ascending type A dissection: simultaneous endoluminal exclusion of the arch and distal aorta. J Endovasc Ther 2005; 12: 660–66 Diethrich EB, Ghazoul M, Wheatley GH et al. Great vessel transposition for antegrade delivery of the TAG endoprosthesis in the proximal aortic arch. J Endovasc Ther 2005; 12: 583–87 Bickerstaff LK, Pairolero PC, Hollier LH et al. Thoracic aortic aneurysms: a population-based study. Surgery 1982; 92: 1103–8 Griepp RB, Ergin MA, Galla JD et al. Natural history of descending thoracic and thoracoabdominal aneurysms. Ann Thorac Surg 1999; 67(6): 1927–30; discussion 1953–8 Davies RR, Gallo A, Coady MA et al. Novel measurement of relative aortic size predicts rupture of thoracic aortic aneurysms. Ann Thorac Surg 2006; 81: 169–77 Davies RR, Goldstein LJ, Coady MA et al. Yearly rupture or dissection rates for thoracic aortic aneurysms: simple prediction based on size. Ann Thorac Surg 2002; 73: 17–27 Coady MA, Rizzo JA, Goldstein LJ, Elefteriades JA. Natural history, pathogenesis, and etiology of thoracic aortic aneurysms and dissections. Cardiol Clin 1999; 17: 615–35 Dapunt OE, Galla JD, Sadeghi AM et al. The natural history of thoracic aortic aneurysms. J Thorac Cardiovasc Surg 1994; 107: 1323–33 Cambria RA, Gloviczki P, Stanson AW et al. Outcome and expansion rate of 57 thoracoabdominal aortic aneurysms managed nonoperatively. Am J Surg 1995; 170(2): 213–7 Baxter BT. Heritable diseases of the blood vessels. Cardiovasc Pathol 2005; 14: 185–88 Pepin M, Schwarze U, Superti-Furga A, Byers PH. Clinical and genetic features of Ehlers–Danlos syndrome type IV, the vascular type. N Engl J Med 2000; 342: 673–80 Kieffer E, Chiche L, Bertal A et al. Descending thoracic and thoracoabdominal aortic aneurysm in patients with Takayasu’s disease. Ann Vasc Surg 2004; 18(5): 505–13 Albornoz G, Coady MA, Roberts M et al. Familial thoracic aortic aneurysms and dissections – incidence, modes of inheritance, and phenotypic patterns. Ann Thorac Surg 2006; 82(4): 1400–5 Irshad K, Miller PH, McKendrick M et al. The role of IVUS for stentgraft repair in TAA and TAD. In: Amor M, Bergeron P, eds. Thoracic Aorta Endografting. Marseille: Com & Co, 2004: 73–7 Wheatley GH, Gurbuz AT, Rodriguez-Lopez JA et al. Midterm outcome in 158 consecutive Gore TAG thoracic endoprostheses: single center experience. Ann Thorac Surg 2006; 81: 1570–7 Pitt MP, Bonser RS. The natural history of thoracic aortic aneurysm disease: an overview. J Card Surg 1997; 12(suppl. 2): 270–8
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Thoracic aortic dissection J May, GH White, and JP Harris
Introduction Acute aortic dissection is a life-threatening emergency with an overall in-hospital mortality of 27% reported by the International Registry of Acute Aortic Dissection (IRAD).1 If the condition is left untreated, 36–72% of patients die within 48 hours of diagnosis, and 62–91% die within one week.2 The incidence of acute dissection has been reported to be greater than that of ruptured abdominal aortic aneurysm.3 This chapter will deal with the classification, pathological features, clinical presentation, and related conditions in the thoracic aorta. The epidemiology and imaging of the thoracic aorta are covered in Chapters 44 and 45. We will focus on recent advances in endovascular management, which have superseded earlier methods.
Classification Aortic dissection begins with a tear in the aortic intima, allowing blood from the lumen to force its way through the media, thus creating a false lumen, which is limited by the adventitia. The false lumen usually extends longitudinally in an antegrade direction, but may extend in a retrograde direction in some cases. Antegrade dissection usually advances down the lateral aspect of the descending thoracic aorta. If it continues into the abdominal aorta, the celiac, superior mesenteric, and right renal arteries usually arise from the true lumen and the left renal artery from the false lumen. Aortic dissection is arbitrarily classified as acute if it occurs within 2 weeks of the onset of symptoms and chronic if it occurs after this time. Three classification systems, based on the entry point of the dissection and proximal or distal extension have been suggested, (Figure 47.1). The DeBakey classification4 designates type I as dissection originating in the ascending aorta and extending through the arch to the descending thoracic aorta with or without involvement of the abdominal aorta. Type II is dissection originating in and confined to the ascending aorta. Type III is dissection originating in the descending thoracic aorta and limited to it (type IIIA) or dissection originating in the descending thoracic aorta extending into the abdominal aorta (type IIIB). The Stanford classification5 divides aortic dissections into Stanford type A, with dissection in the ascending aorta irrespective of the site origin, and Stanford type B with dissection originating in and confined to the descending thoracic aorta. Aortic dissection may also be classified as proximal and distal equating with Stanford type A and B respectively. IRAD has reported that 65% of intimal tears occur in the ascending aorta, 10% in the
aortic arch, 20% in the descending aorta, and 5% in the abdominal aorta.1
Clinical features Of the 464 patients analysed by IRAD investigators,1 two out of three were male. The mean age for all patients was 63 years. Twothirds of the patients were classified type A and one-third type B. The commonest symptom was acute pain of sudden onset which occurred in 84% of patients. The site of the pain tended to be in the anterior chest in type A and in the back and abdomen in type B. Although described as characteristic, migratory pain was present in only 16% of IRAD patients. Hypertension was present in 70% of patients with type B dissection compared with 35% in type A. It should be noted, however, that dissection involving the brachiocephalic trunk or left subclavian artery may result in misleadingly low recording of blood pressure. Almost 10% of patients in the IRAD study who presented with syncopy were more likely to have type A dissection than type B dissection and were more likely to have cardiac tamponade. They were also more likely to have a stroke and more likely to die in hospital. Pulse deficits are common in patients with aortic dissection, being present in 18% of type A dissection and 9% of type B dissection in the IRAD study (Table 47.1).1 A pulse deficit has been reported in 30–50% of patients in whom the aortic arch or
Figure 47.1 Three classification schemes for acute aortic dissection. Adapted from Atkins et al.6
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Table 47.1 Pulse deficits in acute aortic dissections arranged according to classification and anatomical site. Derived from IRAD study1
tends to be a more localized process, progressing to aortic dissection in only 16% of cases.6
Immediate treatment
By classification Type A Type B
18.7% 9.2%
By anatomical site Brachiocephalic trunk Left common carotid artery Left subclavian artery Femoral arteries
14.5% 6.0% 14.5% 13–14%
thoracoabdominal aorta, or both, are involved.6 Spinal cord ischemia is more common with type B than type A aortic dissections. Despite the interruption of intercostal arteries the incidence is relatively low (2–3%).6
Related conditions of the thoracic aorta Intramural hematoma and penetrating atheromatous ulcer are two forms of degenerative aortic pathology which are considered to be closely related to dissection of the thoracic aorta. Intramural hematoma differs from dissection in that there is no overlying intimal defect communicating with the collection of blood in the media. The etiology of intramural hematoma is unclear. Rupture of vasa vasorum has been implicated. More recently, penetrating atheromatous ulcer has been thought to be responsible despite the inability to image the overlying ulcer in all cases of intramural hematoma.6 The IRAD investigators, in a paper aptly titled “Acute intramural hematoma of the aorta: a mystery in evolution,” have pointed out that although there is agreement on the definition and management of aortic dissection, the treatment of intramural hematoma remains controversial due to our incomplete knowledge of its natural history.7 Table 47.2 compares these two components of the acute aortic syndrome. Since intramural hematoma involves the descending thoracic aorta in 60% of cases, in contrast to aortic dissection which involves the ascending aorta in 65% of cases, it is less frequently associated with aortic insufficiency and pulse deficit. Intramural hematoma
The first objective is to reduce the systolic blood pressure by the use of intravenous antihypertensive medications and beta-blockers to stabilize the dissection and reduce the risk of rupture.
Traditional management Due to potential complications of tamponade, acute aortic valve insufficiency, and obstruction to the coronary arteries, graft repair of the ascending aorta with or without valve repair is the preferred treatment for type A dissection, unless other complications of the dissection such as visceral ischemia are considered to be a greater threat to the patient’s life. This approach has been based on the superior 30-day mortality rate of 23% for surgical repair compared with > 50% for medical management (Figure 47.2). The reverse is true for type B dissection which does not have the catastrophic cardiac complications nor high risk of rupture associated with type A dissection. Uncomplicated type B dissection has traditionally been treated by medical therapy with surgical intervention reserved for complications. This management plan is based on the superior 30-day mortality rate for medical therapy of 10% compared with that of 30% for surgical graft replacement of descending aortic dissection (Figure 47.3). It is also supported by a recently published Swedish study8 of 66 consecutive patients with type B dissection who were recruited over an 11-year period, treated conservatively and followed for a minimum of 2 years and a maximum of 15 years. Ten patients (15%) developed a dissecting aneurysm exceeding 6 cm in diameter. Three of these died from rupture. Actuarial survival was 82% at 5 years and 69% at 10 years.
Table 47.2 A comparison of components of the acute aortic syndrome. Derived from IRAD study1
Patients Age (mean years) Site Type A Type B Overall mortality
Intramural hematoma
Acute dissection
58 (57%) 68.7
952 (94.3%) 61.7
40% 60% 20.7%
65% 35% 23.9%
Figure 47.2 Thirty-day mortality following type A aortic dissection for medical versus surgical management. Adapted from IRAD study.1
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retrospective comparison of 80 patients with chronic type B aortic dissection treated with endovascular repair by the senior author and 80 patients treated medically. Survival at 2 years of 94.9% in the endovascular group was superior to 67.5% in the medically treated group. The INSTEAD trial, however, resulted in a slightly but not significantly higher 1-year mortality in the stent graft group. Seven patients (11%) in the best medical therapy group required crossover to the stent graft group, two for malperfusion and four for false lumen expansion. The authors conclude that medical therapy with close observation is the preferred treatment while stent grafts are indicated for complications.
Figure 47.3 Thirty-day mortality following type B aortic dissection for medical versus surgical management. Adapted from IRAD study.1
Progression of dissection may lead to aortic branch obstruction and malperfusion syndrome which may affect the cerebral, visceral, renal, or extremities arterial supply. Atkins et al.6 have emphasized, however, that aortic branch compromise and malperfusion syndromes are not synonymous as branch vessel obstruction is often incomplete and variable in severity. They have also reported that subclavian and lower extremity obstructions are better tolerated than mesenteric obstruction. Aortic branch obstruction was also found by these authors to be associated with an increase in early mortality.
Endovascular treatment of acute aortic dissection The traditional treatment referred to above was challenged by two papers in the New England Journal of Medicine in 1999.2,9 Dake and his colleagues2 from Stanford reported 19 patients with acute aortic dissection, 15 type B and 4 type A. By deploying an endograft across the primary entry tear they achieved complete thrombosis of the false lumen in 15 patients and partial thrombosis in the remaining 4 patients. Nienaber et al.9 reported 12 consecutive patients with acute type B aortic dissection and compared the result with surgery in 12 matched controls. Three patients in each group previously had surgery for type A dissection. There were no deaths in the endovascular group in the first 12 months. By contrast, 4 of the surgically treated patients died in the same period (1 peri-operatively). At 3 months MRI documented complete thrombosis of the false lumen in all 12 patients in the endovascular group. By sealing off the primary entry tear and inducing false lumen thrombosis, endovascular repair has the potential to prevent progression of dissection and aneurysmal dilatation of the false lumen. Although promising in concept, subsequent reports have lacked long-term follow up data. The first randomized control trial comparing endovascular treatment with best medical therapy in the treatment of uncomplicated chronic type B aortic dissection is the INvestigation of STEnt graft in patients with type B Aortic Dissection (INSTEAD) trial.10 The impetus for this trial was a
Recent advances in endovascular treatment of acute aortic dissection Improved imaging in aortic dissection (see Chapters 48 and 49) has demonstrated the mobility of the intimal flap in acute dissection compared to that in chronic dissection. It has also become apparent that compromised blood flow to arterial beds is dynamic rather than static in a majority of instances. This has led to the realization that expansion of, and restoration of flow in, the proximal true lumen by means of an endovascular graft, is capable of favorably influencing pressures in the true and false lumen. This may result in restoration of flow in previously compromised branch arteries without the need for distal stenting or fenestration procedures. The treatment of uncomplicated acute type B dissection remains essentially medical. The clinical pathway followed by the Cleveland Clinic for this group is very sound (Dr. Daniel Clair, personal communication). Asymptomatic patients are scanned twice in hospital and at 4–6 weeks after discharge to pick up early expansion of the false lumen. Since the New England Journal of Medicine papers in 1999, the treatment for complicated acute type B dissection has been largely endovascular. Experience since then has refined endovascular treatment in a number of respects. Treating the entire descending thoracic aorta The original concept of covering the entry tear only was based on the fear of paraplegia if the entire extent of the dissection was treated by endografting. Since the incidence of paraplegia has been universally and surprisingly low (less than 2%) there is now a tendency to treat the descending thoracic aorta from the left subclavian artery to the diaphragm. This may be achieved with covered stents alone, or in combination with uncovered stents. Mossop et al.11 have reported favorable results using purposebuilt self-expanding bare metal stents in 25 patients over a 4-year period. With this procedure together with adjunctive covered stents and coil embolization, they achieved stabilization of the true lumen and thrombosis in the false lumen in 85% of patients. Interestingly they reported no instances of aortic wall trauma resulting from deployment of bare stents. This is contrary to anecdotal experience of bare stents cutting through the fragile intimal flap. Design modification Endograft design and technique has been modified following reports of aortic wall perforation from uncovered proximal
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stents.12 Problems have also resulted from open stents crossing the ostium of the left common carotid artery. Case 1 This 72-year-old male patient underwent endovascular repair of a type B dissection in the proximal descending thoracic aorta in 2000. The endograft was deployed adjacent to the left common carotid artery to maximize the length and quality of the proximal anchor zone. This resulted in the struts of the proximal bare stent crossing the ostium of the left common carotid artery (Figure 47.4). The patient was asymptomatic on discharge but was readmitted three weeks later following a right-sided TIA. He had no further problems following ligation of the left common carotid artery and revascularization of the distal common carotid artery via the left subclavian artery, using a cervical approach. As a result of these complications there are now a number of thoracic endografts available which do not have an open stent or open web at the proximal end. Technique modifications For many vascular interventionalists, experience has shown that in cases of aortic dissection it is safer to refrain from the use of balloon dilatation. Similarly there is an awareness that oversizing the endograft can be dangerous. This should be related to the diameter of the normal aorta proximal to the dissection and not to the combined diameter of the true and false lumens. Modification of indications The indications for intervention have been modified to anticipate problems rather than waiting for them to occur. For instance, patients exhibiting significant reduction in diameter of the true lumen in the proximal descending thoracic aorta (Figure 47.5a) are best treated promptly (Figure 47.5b) rather
(a)
Figure 47.4 Arch aortogram demonstrating struts of the proximal uncovered stent of a thoracic endograft crossing the ostium of the left common carotid artery. The aortogram was performed via the left common carotid artery at open operation following a TIA.
than delaying until elevation of lactate, creatinine, and other markers of distal ischemia appear. Adjunctive procedures There are some adjunctive procedures that we have found to be useful in selected patients. Deployment of an uncovered stent for end-organ ischemia in the visceral segment of the abdominal aorta Case 2: This 34-year-old male patient presented in 2006 with a type B dissection. Although the true lumen was not reduced in the
(b)
Figure 47.5 (a) Aortogram demonstrating marked reduction in diameter of the true lumen of dissected proximal descending thoracic aorta; (b) thoracic aortogram demonstrating thoracic endograft deployed in proximal descending thoracic aorta which has expanded as a result of this. The mid descending thoracic aorta has improved but remains reduced in size. Flow is no longer visible in the false lumen.
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Figure 47.6 Thoracic aortogram demonstrating no reduction in true lumen.
thoracic aorta (Figure 47.6), it was reduced to a slit in the visceral portion of the abdominal aorta (Figure 47.7). This resulted in loss of perfusion to the right kidney. A bare stent was deployed in the visceral portion of the aorta to expand the true lumen (Figure 47.8). This resulted in reperfusion of the right kidney (Figure 47.9). Use of occluding endograft Deployment of an occluding endograft to encourage thrombosis in patients with residual flow in the false lumen (Figure 47.10).
Figure 47.7
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Figure 47.8 Aortogram demonstrating a bare stent deployed in visceral segment of abdominal aorta, resulting in reperfusion of the right renal artery.
Deployment of a covered stent in the iliac arteries to close the re-entry point in patients with retrograde filling of the false lumen. Case 3: This 59-year-old male patient presented in 2002 with acute type B dissection. The compromised false lumen (Figure 47.5a) was treated by deploying a thoracic endograft in the proximal descending thoracic aorta (Figure 47.5b). This resulted in thrombosis of the false lumen in the proximal
Contrast CT demonstrating true lumen reduced to a slit. Note no perfusion of right kidney.
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Figure 47.10 Contrast CT of distal descending thoracic aorta demonstrating thoracic endograft deployed within the true lumen and a blind endograft deployed within the false lumen to encourage thrombosis of this channel.
Figure 47.9 Contrast CT demonstrating stent in true lumen which has resulted in expansion of this channel and reperfusion of right renal artery. Contrast can now be seen in both kidneys.
two-thirds of the descending thoracic aorta. The distal thoracic and abdominal false lumen remained patent and continued to expand over time. The false lumen in the abdominal aorta was filled by a large communication with the true lumen at the left common iliac level (Figure 47.11). In 2006, three endovascular procedure were undertaken during the one operation as follows: ●
●
●
A purpose-built bare thoracic stent (Cook Inc., Figure 47.12a) was deployed in the descending thoracic
(a)
aorta between the primary (covered) endograft and the diaphragm to expand the true lumen (Figure 47.12b). Two blind endovascular occluders were deployed in the false lumen of the distal thoracic aorta to encourage thrombosis (Figure 47.12b). A bifurcated endovascular AAA graft (Cook Inc.,) was deployed in the true lumen of the infrarenal aorta. The left limb of this endograft closed the large communication between the true and false channels at the left common iliac artery level (Figure 47.13).
(b)
Figure 47.11 Aortogram demonstrating the true lumen (narrow) and the false lumen (wide) being filled via a large communication at the left common iliac level (arrow): (a) early; (b) late.
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(b)
Figure 47.12 (a) Bare dissection stent (Cook Inc.,); (b) aortogram demonstrating a bare thoracic stent deployed in the true lumen of the descending thoracic aorta between the primary (covered) thoracic endograft proximally (broad arrow) and the diaphragm distally. Two occluding blind endografts can also be seen in the false lumen adjacent to the bare stent (narrow arrows).
Deployment of fenestrated abdominal aortic endografts and covered stents to exclude the false lumen in patients in which these have become aneurysmal and involved a communication with the true lumen at the renal level Case 4: This 40-year-old female patient presented with a type B dissection in 1989 which was treated medically. In 2004 she required an urgent Bentall operation. By 2005 the false lumen in the abdominal portion of her dissected aorta had reached 6 cm in diameter and involved the renal arteries (Figure 47.14).
A fenestrated AAA was performed using covered stents bilaterally for the renal arteries. Investigation, prompted by further expansion of the dissecting aneurysm, revealed that the covered stent in the left renal artery had migrated partially into the aortic lumen (Figure 47.15) resulting in an endoleak into the false lumen. This was corrected by deployment of a second covered stent in the left renal artery (Figure 47.16). The latter was achieved only after a difficult cannulation of the primary covered stent which was projecting well into the aortic lumen.
Figure 47.13 Contrast CT following endovascular AAA repair. Note the left ipsilateral limb of the endograft has sealed the re-entry point at the left common iliac level. Flow is no longer demonstrated in the false lumen (arrow).
Figure 47.14 Coronal section contrast CT of 6-cm aneurysm in the dissected abdominal aorta 16 years after original presentation of type B dissection, which was treated conservatively. An urgent Bentall operation was performed 1 year before this scan.
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Figure 47.16 Post-procedure aortogram following deployment of a secondary covered stent in the left renal artery resulting in restoration of an isolated false lumen. Figure 47.15 Plain x-ray demonstrating metallic framework of fenestrated AAA endograft and bilateral covered renal stents. The left renal stent has migrated partially into the lumen of the aorta creating a communication between the true and false lumens at this site.
REFERENCES 1. 2. 3. 4. 5. 6. 7.
Hagan PG, Nienaber CA, Isselbacher EM et al. The International Registry of Acute Aortic Dissection (IRAD): new insights into an old disease. JAMA 2000; 283: 897–903 Dake MD, Kato N, Mitchel RS, Semba CP et al. Endovascular stentgraft placement for the treatment of acute aortic dissection N Eng J Med. 1999; 340(20): 1546 –52 Kouchoukos NT, Dougenis D. Surgery of the thoracic aorta. N Engl J Med 1997; 336: 1876–88 DeBakey ME, Henly WS, Cooley DA. Surgical management of dissecting aneurysms of the aorta. Thorac Cardiovasc Surg 1965; 49: 130–48 Dailey PO, Trueblood H, Stinson EB. Management of acute aortic dissection. Ann Thorac Surg 1970; 10: 237–46 Atkins MD, Black JH, Cambria RP. Aortic dissection: Perspectives in the era of stent graft repair. J Vasc Surg 2006; 43A: 30A–43A (suppl.) Evangelista A, Mukherjee D, Mehta R et al., for the IRAD Investigators. Acute intramural hematoma of the aorta: A mystery in evolution. Circulation 2005; 111(8): 1063–70
8. 9. 10.
11. 12.
Winnerkvist A, Lockowandt U, Rassmussen E, Radegran K. A prospective study of medically treated acute type B aortic dissection. Eur J Vasc Endovasc Surg 2006; 32: 349–55 Nienaber CA. Nonsurgical reconstruction of thoracic aortic dissection by stent-grant placement. New Eng J Med 1999; 340: 1539–45 Nienaber C, Zannetti S, Barbieri B et al., INSTEAD study collaborators. Investigation of stent grafts in patients with type B aortic dissection: Design of the INSTEAD trial – a prospective, multicenter, European randomised trial. Am Heart J 2005; 149: 592–9 Mossop P, McLachlan C, Amukotuwa S, Noxon I. Staged endovascular treatment for complicated type B aortic dissection. Nat Clin Pract Cardiovasc Med 2005; 2: 316–21 Malina M, Brunkwall J, Ivancev K et al. Late Aortic arch perforation by graft-anchoring stent: Complication of endovascular thoracic aneurysm exclusion. J Endovasc Surg 1998; 5: 274–7
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SECTION VI Abdominal aorta
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Abdominal aortic aneurysm treatment by endoluminal exclusion: a historical perspective JC Parodi, CJ Schönholz, and RR Heuser
Introduction Endoluminal treatment of aneurysms has emerged as a potential therapeutic alternative since its introduction in 1991.1 Although initial and mid-term results of endoluminal aneurysm exclusion are very encouraging, late adverse events still represent a big limitation for the widespread use of the technique.2–7 To obtain information about the long-term results, we retrospectively reviewed the available data on 30 consecutive patients followed for more than 5 years after the endoluminal treatment of abdominal aortic aneurysms (AAA) using the home-made Parodi endograft (PE). In addition, prospectively gathered information on 136 consecutive patients treated using the Vanguard endograft (Boston Scientific Corp., Natick, MA) was analyzed. Only mid-term results (mean 28 months, range 7–53 months) were available for evaluation in the latter group (VE). The information served as a basis of comparison with the results of the PE group.
Materials and methods We collected information on the outcome of 30 consecutive patients whose AAA was excluded using the initial endograft design created by Parodi. All patients had at least a contrastenhanced computed tomography (CT) scan, complete medical examination, and color duplex studies before treatment. The PE essentially consisted of a tubular or tapered fabric graft (aortoaortic or aortouni-iliac configurations) attached at both ends by large Palmaz stents (Figure 48.1). Also, the aortouni-iliac exclusion was completed by performing a femorofemoral bypass and occluding the contralateral common iliac artery with a stent plug, as described in detail previously.8 Mean follow-up in this group of patients was 59 months (range 32–119 months). All patients were males; the average age was 71.3 years. The average size of the AAA was 59 mm in diameter at the time of treatment. All patients had at least one CT scan with contrast enhancement after the fifth year of the procedure. One hundred and thirty-six patients were treated using the Vanguard device in its three versions (I, II, and III). Of these patients, 100 consecutive patients with a complete follow-up were included in this study. The Vanguard endograft
was a thin-walled Dacron (polyethylene terephthalate) graft fully supported over its entire length by a diamond-shaped nitinol stent, which provides radial and longitudinal force to maintain its conformability. The final length of the endograft can be tailored, adding or omitting extensions. Mean follow-up was 28 months (range 7–53 months). Eighty-seven percent of the patients were males, the average age was 70.4 years, and the average size of the AAA was 56 mm. Patients were followed every 6 months with clinical examination, plain x-ray of the abdomen, color duplex, and contrast-enhanced CT. Additional conventional 5-mm-thick sections through the device were obtained with a 3-min delay to detect endoleaks.
Results Parodi endograft (PE) Of 103 patients treated from September 1990 to March 1996 in our institution, 51 patients underwent aortic tube graft replacement, with 8 patients having only one proximal stent, and 45 aortoiliac stent grafting. However, the following description refers to the results after 5 years of implantation. Patients with acute and mid-term failures were not included. This limitation produced a case selection. Only the survivors are analyzed; even patients whose cause of death was related to the treatment were not considered if the episode occurred within the first 5 years after the treatment. The aortoaortic endograft design failed in 12 patients out of 15 (80% failure rate). All failures were due to the development of a distal endoleak (Figure 48.2). The aneurysm increased in size in eight patients (43.7 ± 6.3 mm vs. 52.8 ± 11.9 mm, p = 0.08); the aneurysm sac remained the same size in 3 and decreased in another 4 patients (44.3 ± 8.6 mm vs. 36.7 ± 6.1 mm, p = 0.2). Two patients with aneurysm shrinkage presented distal endoleaks, whereas 3 patients (20%) had a successful durable exclusion: the size of the aneurysm decreased in 2 of them and the other patient did not register any diameter change. The aortoaortic design was abandoned in 1994. The aortouni-iliac design of the PE was successful in 10 out of 15 patients in the long term. The size of the aneurysm decreased in size in all 10 cases and no endoleak developed (46.6 ± 5.9 mm vs. 40.3 ± 5.1 mm, p = 0.02). Five patients developed late endoleaks. There were type I endoleaks, one a 449
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(a)
(b)
Figure 48.1 (a) Aortoaortic stent graft. (b) aortouni-iliac configuration. The procedure is completed by performing a femorofemoral bypass. The contralateral common iliac artery is occluded by a covered stent.
proximal and the others distal (iliac) endoleaks, and 2 patients had persistent type II endoleaks. All 5 patients with endoleaks had their aneurysms enlarged (70.6 ± 12.3 mm vs. 80.2 ± 14.3 mm). Careful measurement of the proximal neck indicated that neck dilatation did not take place using the PE, regardless of the final outcome. In the 15 patients who had the aortoaortic design, excluding their aneurysm, the initial neck diameter was 23.9 ± 2.4 mm and after 78 months 24.2 ± 2.9 mm (p = 0.7). In the aortouni-iliac design, the initial neck diameter was 25.3 ± 2.2 mm and after 78 months was 25.7 ± 2.6 mm (p = 0.6). Vanguard endograft Twenty two percent of the 100 patients developed adverse events during a mean follow-up of 28 months. No proximal or distal type I endoleaks were registered. Four of the five causes of failures were device-related. The only non-device-related failure was the development of a type II endoleak (25%) that caused enlargement of the aneurysm in five patients (5%) and infection of the endograft (2%). Device-related failures were: ● ● ● ●
occlusion of one limb: 8%; dislocation of segments: 3%; wearing of the graft: 3%; fracture plus migration: 3%.
The three aneurysm ruptures were related to the development of acute type III endoleaks: one of the patients suffered a dislocation of segments and in the other two patients wearing of the graft ended in aneurysm rupture. Infection occurred in two patients, the first after 2 years of implantation related to a surgical drainage of a kidney abscess. The second patient
Figure 48.2 CT (computed tomography) reconstruction of a type I distal endoleak (arrow).
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Abdominal aortic aneurysm treatment by endoluminal exclusion: a historical perspective had an inflammatory aneurysm. Six months after a successful exclusion, the patient developed an abscess involving the right psoas muscle. The endograft was removed. The proximal and distal necks were suture ligated and an axillobifemoral bypass was constructed. Streptococcus bovis was isolated from the surgical samples. The patient is still alive 10 months after the endograft explantation. The aneurysm increased in size in 13 patients (3.9 ± 1.9 mm). In all of them, an endoleak was detected. The aneurysm sac remained the same size in 14 patients and decreased in another 73 patients (6.97 ± 5.94 mm.). Eleven patients with aneurysm shrinkage presented a type II endoleak (6.33 ± 4.5 mm). Fifty-three patients were evaluated with plain abdominal radiographs: thirteen endografts demonstrated increased distance between stents struts, indicating broken sutures. In six patients we found broken sutures, leading to separation of the first two rows of nitinol. In three patients significant separation occurred between the first two rows of nitinol and the rest of the device. The distal segment migrated caudally, resulting in a type III endoleak.
Discussion Interesting data emerged from the present study that deserves comment and elaboration. Several findings will be discussed.
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Neck dilatation Neck dilatation is the main concern of several investigators in the field.9,10 No neck dilatation was found in the initial group of patients (PE). Only one case (3.33%) of proximal endoleak resulted in the long term, in a patient in whom the proximal stent was placed far from the renal arteries and in contact with the mural thrombus. Lack of neck dilatation was also found by May in a recently published study.11–15 In two of our long-term cases, even a reduction of the diameter of the proximal neck was evident (Figure 48.3). Encapsulation of the proximal bare segment of the proximal stent was seen in the two patients in whom we performed a post-mortem examination (Figure 48.4). It seems reasonable to think that balloon-expandable stents behave in a different way to selfexpandable stents. Balloon-expandable stents stretch the wall from the beginning but no further increase of the diameter of the stent takes place over time. By contrast, self-expandable stents continue to expand until the nominal diameter is reached unless tissue resistance limits its expansion. When the expandable force is concentrated in reduced surfaces, dilatation takes place very rapidly, producing migration of devices; an example of this was the initial experience using the Anaconda device in Europe (Benedetti Valentini, personal communication). The anchoring mechanism in the Anaconda device is a single ring with a shape that resembles the mouth of an anaconda snake. In spite of the lack of conclusive evidence, the limited data available indicate that the bare
Figure 48.3 No changes in the aorta at the level of the renal arteries were registered in this patient. However, reduction of the diameter of the proximal neck was evident after 10 years.
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Figure 48.4 Encapsulation of the proximal bare segment of the proximal stent was seen in the two patients in whom we performed a post-mortem examination.
stent segment (balloon and self-expandable) when it is embedded in the vessel wall is regularly covered by a layer of myointimal hyperplasia. Stents actually become part of the architecture of the arterial wall. The distal neck of an abdominal aortic aneurysm had a quite different behavior when an endograft was fixed to it: almost regularly, the distal neck of the aorta dilated over time. Eighty percent of the aortoaortic endografts failed by this mechanism, resulting in distal endoleak. The difference in behavior of the proximal and distal neck is most probably due to the different composition of the wall. The proximal neck is richer in elastic fibers and seldom calcified. Mural thrombus in the proximal neck exists in a small proportion of patients and apparently does not have a significant impact in results.16 In addition, strong intercrossing fibers in the adventitia coming from the visceral branches give strength and stability to the proximal neck adjacent to the renal arteries’ ostia. The data mentioned above refers to cases of the PE group. Results using the Vanguard device are somewhat different, but (at least in the mean term) no significant neck dilatation resulted. During the first 12 months the neck had the tendency to dilate in a very discrete manner (24.1 ± 2.9 mm vs. 24.4 ± 2.9 mm); subsequently, the neck stabilized (24.2 ± 2.9 mm vs. 24.3 ± 2.8 mm). The late caudal migration of the separated distal segment of the device in the VE group (three patients) was produced by fracture of the metal skeleton of the endograft. As the mean follow-up in this group is just 28 months, no further conclusions can be drawn in terms of long-term neck dilatation. Our policy of deploying the proximal end of the endograft crossing the renal arteries’ ostium or flush to them is probably responsible for the secure fixation of the endograft. With regard to the iliac arteries as landing zones for endograft fixation, 13% of the PE cases showed late type I endoleak after 5 years. Those iliac arteries were dilated (more than 15 mm in diameter) before the treatment. In the two cases of late endoleak from the iliac arteries after 5 years, only the proximal iliac artery was covered by the endograft. The region of the iliac bifurcation, which has the maximum strength, was not reached by the endografts. We adopted a policy of covering the whole common iliac artery in 1992. No other iliac dilatation was registered.
Shrinkage of aneurysms and endoleaks Shrinkage of aneurysm was constant during follow-up when the aneurysm was effectively excluded with the PE (47 ± 5.5 mm vs. 40.3 ± 4.7 mm, p = 0.004). The presence of type I endoleaks resulted in aneurysmal growth in two-thirds of cases (49.7 ± 13.1 mm vs. 59.5 ± 17.5mm, p = 0.1). Only 2 out of 30 patients of the PE group had persistent type II endoleaks, seen in the follow-up CT scans. These patients suffered aneurysmal growth (78 ± 5.6 mm vs. 84 ± 8.5mm, p = 0.4). The fact that one-third of the patients with type I endoleaks had no aneurysmal growth is intriguing. The probable explanation for this finding is the following: small-flow type I endoleaks with an appropriate outflow (several lumbar arteries) have a low pressure inside the sac; conversely, highflow endoleaks with no outflow result in rapid aneurysmal growth and rupture.17–21 There were three ruptures of the aneurysm in the Vanguard endograft group. Interestingly, those patients were free of endoleaks for more than 2 years, and the development of an acute type III endoleak resulted in aneurysmal rupture within the following 48 hours. The cause of an acute type III endoleak was a dislocation of the contralateral limb in one patient and perforation of the fabric graft in the other two patients. Those patients had no type II endoleaks and the size of the aneurysm had decreased before the late complication. Post-mortem study in one patient disclosed an atrophic wall of the remnant aneurysm. Speculation can be made in terms that if a late endoleak occurs it will find an atrophic wall to contain it. Resistance to dilatation would be decreased, as well as the strength of the wall. One could conclude that a late-onset endoleak in a free of endoleak sac represents a great risk for rupture. Thus, durable, material fatigue-free, reliable endografts are mandatory. Type II endoleaks Type II endoleaks were present in 6.6% of the aneurysms after 5 years in the PE group. The two cases of long-term type II endoleaks resulted in a very discrete increase in the size of the aneurysm. In 11 of the 100 cases of VE, type II endoleaks provoked aneurysmal growth. Of those patients, five were successfully treated by embolization or clipping of the offending branches after aneurysm enlargement more than 4 mm. Persistent type II endoleak and infection were the only causes of long-term failure that were not device-related in the Vanguard group. Long-term type II endoleaks can, in theory, induce or facilitate device failure. We demonstrated in a model that hemodynamic changes inside the aneurysmal sac in the presence of type II endoleaks could be the following. Systolic pressure is always lower inside the aneurysmal sac. In the presence of an endoleak, diastolic and mean pressure are higher inside the sac in comparison to the systemic pressure. As an explanation, we can speculate that the blind end of the aneurysm sac has an inappropriate outflow for the blood that enters the sac during systole. This explanation seems reasonable, since the diastolic and mean pressures dropped as the outflow of the aneurysm increased. These pressure changes produced extra stress on the endograft, which expanded during systole and collapsed during diastole.22
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Abdominal aortic aneurysm treatment by endoluminal exclusion: a historical perspective It is gaining general acceptance that a large inferior mesenteric artery (IMA) should be coil embolized during the initial treatment, providing that the superior mesenteric artery (SMA) and at least one hypogastric artery are wide open. Opinion on what to do with open lumbar arteries is divided. The most common approach is to leave them alone and treat those patients that after 6 months still have backflow from the arteries which results in aneurysmal growth. Our empiric approach is to coil embolize the IMA and fill the sac with Spongostan when the IMA and several lumbar arteries are open (Figure 48.5).23 Long-term outcome of patients treated in this way is still unknown. Alternatives to treating type II endoleaks after 6 months when the aneurysm increases its size are laparoscopic clipping of the branches (Figure 48.6), coil embolization of the IMA through microcatheters introduced through the SMA, and coil embolization of lumbar arteries through the iliolumbar branch. Direct puncture of the aneurysm with coil and thrombin injection is also an alternative.24 Conversion to an open procedure is the last alternative to be considered. Occlusion of one limb of the endograft No limb occlusion resulted in the long-term follow-up in the 15 cases of aortouni-iliac endografting (PE). Occlusion of one of the limbs of the VE group occurred in eight patients, being the main cause of failure. Occlusion of the limbs in the VE group mostly occurred after 18 months of implantation. Remodeling of the aneurysm and angulation of the limbs was evident in most. Dislocation of segments In three cases, dislocation of segments occurred in the VE group, all after 2 years of the initial treatment. One case ended with rupture of the aneurysm. Dislocation was the result of extreme angulation of the device after remodeling. Fracture of wires and sutures In 24.5% of the VE cases, we visualized separation of segments or fracture of metal components. In spite of this, only three
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Lumbar artery
Figure 48.6
Video-assisted clipping of the collateral branches.
patients suffered the consequences of this loss of integrity of the endograft. Fracture and separation of the two initial rows of the endograft produced migration of the device caudally with the occurrence of an endoleak. These findings are evidence that preclinical testing of the devices performed by the medical industry was incomplete and insufficient. The complexity and multiplicity of vectors of forces acting permanently and dynamically inside the aneurysmal sac, in addition to the foreign body reaction of the recipient of the endograft, may explain the loss of integrity of the devices. Pulsation and external forces acting on the endograft produce complex movement of the endograft component as a whole and also motion and micro motion among components. Friction among metals removes the protective oxide layer covering the endograft, facilitating corrosion, and fracture. Wearing of the fabric graft The most vulnerable spot in endografts is where the metal component interacts with the fabric graft. Wearing results from friction and is aggravated when a metal component protrudes, concentrating the friction on a small area of the fabric graft. Angulation and fracture of the metal skeleton further facilitate wearing of the fabric graft. In the VE group three cases of wearing of the fabric graft were detected. Two patients suffered an aneurysm rupture.
coils IMA
Spongistatin into the sac
Figure 48.5 Coil embolization of the inferior mesenteric artery (IMA) and sac filling with Spongostan.
Migration of the endograft Migration of the endograft is a subject very often seen in the surgical literature, mostly related to neck dilatation.25–28 There are obvious variables related to migration: radial force of the device, length of the proximal neck, angulation of the neck, area in which the proximal end is positioned (crossing the renal arteries, flush or far from them), utilization of hooks and barbs, and angulation of the endograft. Traction force from the proximal end was calculated to be about 10 newtons (1 kg). In the PE group no migration was observed. In the VE group, three endografts migrated caudally when the first two rows of the metal skeleton separated.
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Summary of the analysis of long- and mid-term failures in both groups Adverse events in the Parodi endograft group (PE) were related to: ● ● ●
●
dilatation of the distal aortic neck; persistent type II endoleak; late type I endoleak probably due to implantation of the endograft far from the renal artery take-off; dilatation of a previously ectatic iliac artery.
There were no device-related failures in the long term in the PE group Adverse events in the VE group were mostly related to device failure: occlusion of one limb (8%), dislocation of a segment (3%), wearing of the fabric graft (3%), and proximal migration (3%). Non-device-related failures were persistent type II endoleak with enlargement of the aneurysm (5%) and infection (2%). Four of the five causes of adverse events in the Vanguard endograft group were related to device failure. Persistent type II endoleak and infection were the only non-device-related complications. Redesign of the Vanguard device is mandatory and should take into account the lessons learned in the clinical setting. There are potential solutions to offer to a new design of a totally supported endograft: ●
●
●
●
occlusion of the limbs, the most common cause of late failure, can be solved using kink-resistant limbs (like the Wallgraft); dislocations of segments: reliable locking mechanisms can be included in the design; fractures: stronger structures resistant to fatigue and carefully tested using appropriate testing models could eventually solve the problems; wearing of the fabric graft: stronger graft and metal skeleton designed and incorporated into the system in such a way that friction with the fabric graft becomes less critical. A non-totally supported system such as the PE or the Ancure device should be considered as a valid alternative.
Conclusion 1. Aortoaortic endografts have a high failure rate due to distal neck dilatation. 2. The aortouni-iliac configuration using the Parodi endograft had acceptable results in the long term. A few conditions
should be fulfilled, however, to achieve good results: the proximal stent should be crossing or flush to the renal arteries ostia and the common iliac arteries should be completely covered by the endograft. As this is our current practice, it is reasonable to assume that this endograft could be extremely useful in the treatment of aneurysms. Further studies are necessary to confirm our observation. 3. Type II endoleaks produce aneurysmal growth in a small proportion of patients of both groups analyzed. 4. The totally supported Vanguard device had a high rate of failure in the mid-term: 22% of the patients needed a secondary procedure after a mean follow-up of 28 months. Four of the five causes of failures were device-related. 5. It is clear that the endoluminal treatment of aneurysms is a complex matter and further developments are needed before its widespread use is recommended.
Perspectives for the future of endoluminal treatment of aneurysms Analysis of failures is providing valuable information, suggesting new directions or resuming old directions abandoned in the past. Application of existing technology is still in its infancy, and application of future technology is warranted. Going back to the initial concept when the first endograft was created is extremely useful. The first design resembled the proven surgical aortic replacement with a fabric graft using surgical sutures. Instead of suture, a stent attached and sealed the fabric graft. Simplifying the concept, all we have to achieve is the replacement of the surgical suture by a mechanical device as reliable, or perhaps more reliable. Totally supported devices have several advantages over the non-supported systems but also many drawbacks. Both ways should be explored, perhaps using them in different situations and anatomic conditions. In the mean time, application of endografts should be limited to centers with large experience and just offering treatment to high-risk patients with a short life expectancy, harboring a large (more than 5.5 cm) or symptomatic aneurysm. Encouraging experiences treating endoluminally ruptured aneurysms are being reported and will probably represent a good indication in the future.29,30 Aortic dissections and thoracic aneurysms are emerging as indications for endoluminal treatment, accounting for their high complication and mortality rates resulting from standard surgical treatment.
REFERENCES 1. 2. 3.
4.
Parodi JC, Palmaz JC, Barone HD. Transfemoral intraluminal graft implantation for abdominal aortic aneurysms. Ann Vasc Surg 1991; 5: 491–9 Parodi JC. Endoluminal stent grafts: overview. J Invasive Cardiol 1997; 9: 227–9 May J, White GH, Waugh R et al. Improved survival after endoluminal repair with second-generation prostheses compared with open repair in the treatment of abdominal aortic aneurysms: a 5-year concurrent comparison using life table method. J Vasc Surg 2001; 33(2 suppl.): S21–6 Greenberg RK, Lawrence-Brown M, Bhandari G et al. An update of the Zenith endovascular graft for abdominal aortic aneurysms:
5.
6. 7.
initial implantation and mid-term follow-up data. J Vasc Surg 2001; 33(2 suppl.): S157–64 White RA. Clinical and design update on the development and testing of a one-piece, bifurcated, polytetra-fluoroethylene endovascular graft for abdominal aortic aneurysm exclusion: the Endologix device. J Vasc Surg 2001; 33(2 suppl.): S154–6 Matsumura JS, Katzen BT, Hollier LH, Dake MD. Update on the bifurcated EXCLUDER endoprosthesis: phase I results. J Vasc Surg 2001; 33(2 suppl.): S150–3 Zarins CK, White RA, Moll FL et al. The AneuRx stent graft: fouryear results and worldwide experience 2000. J Vasc Surg 2001; 33(2 suppl.): S135–45. [Review]
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13.
14. 15. 16. 17.
18. 19.
Parodi JC, Criado FJ, Barone HD, Schonholz C, Queral LA. Endoluminal aortic aneurysm repair using a balloon expandable stent-graft device: a progress report. Ann Vasc Surg 1994; 8: 523–9 May J. Symposium on distortion and structural deterioration of endovascular grafts used to repair abdominal aortic aneurysms. Introduction. J Endovasc Surg 1999; 6: 1–3 Harris P, Brennan J, Martin et al. Longitudinal aneurysm shrinkage following endovascular aortic aneurysm repair: a source of intermediate and late complications. J Endovasc Surg 1999; 6: 11–6 Chaikof EL, Matsumura JS. Endovascular repair of abdominal aortic aneurysms: problems and progress. Semin Vasc Surg 1999; 12: 163–4 Albertini J, Kalliafas S, Travis S et al. Anatomical risk factors for proximal perigraft endoleak and graft migration following endovascular repair of abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 2000; 19: 308–12 Walker SR, Macierewicz J, Elmarasy NM et al. A prospective study to assess changes in proximal aortic neck dimensions after endovascular repair of abdominal aortic aneurysms. J Vasc Surg 1999; 29: 625–30 Sonesson B, Malina M, Ivancev K et al. Dilatation of the infrarenal aneurysm neck after endovascular exclusion of abdominal aortic aneurysm. J Endovasc Surg 1998; 5: 195–200 May J. The outcome of endoluminal repair of AAA with short proximal necks. Cardiovasc Surg 2000; 8: 329–30 Gitlitz DB, Ramaswami G, Kaplan D, Hollier LH, Marin ML. Endovascular stent grafting in the presence of aortic neck filling defects: early clinical experience. J Vasc Surg 2001; 33: 340–4 May J, White GH, Waugh R et al. Rupture of abdominal aortic aneurysms: a concurrent comparison of outcome of those occurring after endoluminal repair versus those occurring de novo. Eur J Vasc Endovasc Surg 1999; 18: 344–8 White RA, Donayre C, Wallot I et al. Abdominal aortic aneurysm rupture following endoluminal graft deployment. J Endovasc Ther 2000; 7: 257–62 Lumsden AB, Allen RC, Chaikot EL et al. Delayed rupture of aortic aneurysms following endovascular stent grafting. Am J Surg 1995; 170: 174–8
20. 21. 22. 23. 24.
25. 26.
27.
28. 29. 30.
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Torsello GB, Klenk E, Kasprzak B et al. Rupture of abdominal aortic aneurysm previously treated by endograft stent-graft. J Vasc Surg 1998; 28: 184–7 Umscheid T, Stelter WJ. Time-related alterations in shape, position, and structure of self-expanding, modular aortic stent–grafts: a 4year single-center follow-up. J Endovasc Surg 1999; 6: 17–32 Parodi JC, Berguer R, Ferreira LM, La Mura R, Schermerhorn ML. Intra-aneurysmal pressure after incomplete endovascular exclusion. J Vasc Surg 2001; 34: 909–14 Lehmann JM, Macierewicz JA, Davidson IR et al. Prevention of side branch endoleaks with thrombogenic sponge: one-year follow-up. J Endovasc Ther 2000; 7: 431–3 van den Berg JC, Nolthenius RP, Casparie JW, Moll FL. CT-guided thrombin injection into aneurysm sac in a patient with endoleak after endovascular abdominal aortic aneurysm repair. AJR Am J Roentgenol 2000; 175: 1649–51 Makaroun MS, Deaton DH. Is proximal aortic neck dilatation after endovascular aneurysm exclusion a cause for concern? J Vasc Surg 2001; 33(2 suppl.): S39–45 Albertini J, Kalliafas S, Travis S et al. Anatomical risk factors for proximal perigraft endoleak and graft migration following endovascular repair of abdominal aortic aneurysms. Eur J Vasc Endovasc Surg 2000; 19: 308–12 Harris PL, Vallabhaneni SR, Desgranges P et al. Incidence and risk factors of late rupture, conversion, and death after endovascular repair of infrarenal aortic aneurysms: the EUROSTAR experience. European Collaborators on stent/graft techniques for aortic aneurysm repair. J Vasc Surg 2000; 32: 739–49 Broeders IA, Blankensteijn JD, Wever JJ, Eikelboom BC. Midterm fixation stability of the EndoVascular Technologies endograft. EVT Investigators. Eur J Vasc Endovasc Surg 1999; 18: 300–7 Ohki T, Veith FJ. Patient selection for endovascular repair of abdominal aortic aneurysms: changing the threshold for intervention. Semin Vasc Surg 1999; 12:226–34 Armon MP, Wenham PW, Hopkinson BR. Suitability for endovascular aneurysm repair in an unselected population (Br J Surg 2001; 88: 77–81). Br J Surg 2001; 88: 889–90
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Role of Doppler ultrasound in the assessment of peripheral vascular disease K Irshad, M Ali, AW Reid, A Sinha, and DB Reid
Introduction Peripheral arterial disease is a common disorder with a prevalence of about 5–9% in the general population. Arteriography has been the standard technique for nearly a century to diagnose and plan treatment.1 During the last two decades there have been significant developments in minimally invasive endovascular techniques and also an increasing use of non-invasive investigations. For the evaluation of peripheral vascular occlusive and aneurysmal disorders duplex ultrasonography has become the first-line investigation, particularly in the limb and carotid arteries. The combination of conventional 2D imaging, Doppler waveform, and color flow provides “triplex” imaging. Such detailed ultrasonography can now be confidently used to diagnose and characterize peripheral arterial lesions and is a less invasive method than either magnetic resonance angiogram (MRA) or digital subtraction angiogram (DSA). Doppler ultrasound not only provides a diagnostic ability to assess and measure the severity of disease prior to treatment but is also a reliable method for subsequent monitoring of open and endovascular interventions.
penetration of ultrasound for deeper placed vessels such as the aorta and iliac vessels a lower frequency transducer is used. In color flow Doppler imaging, the velocity measured is displayed as a waveform image. Furthermore color Doppler computes and converts the measurements into an array of colors (Figure 49.1). Blood flow pattern can then be visualized in real time with long segments of vessels being assessed rapidly and accurately.3–5 Power Doppler uses a color map to show the distribution of the power or amplitude of the Doppler signal. Flow direction and velocity information are not provided in power mode Doppler display.6 The normal arterial Doppler flow pattern in peripheral vessels is a “high resistance” type. Typically the flow profile is triphasic because forward flow is strong in systole and a short reversal of flow in early diastole is then followed by forward flow of low amplitude. The normal high-resistance flow pattern becomes low resistance if a stenosis is present proximally. At the level of stenosis there is a localized increase in velocity proportional to the degree of stenosis and Doppler flow pattern becomes biphasic or monophasic.7
Technical aspects in evaluation of peripheral vascular interventions Doppler technology is based on the Doppler shift principal first described by Christian Doppler, an Austrian physicist in 1842.2 When ultrasound is transmitted towards a stationary reflector, the reflected waves are the same frequency as those from the transmitter. If the reflector is moving towards the transmitter the reflected frequency is higher than the transmitted frequency. If the reflector is moving away, the frequency will be lower than the transmitted frequency. The difference between the transmitted and received frequency is proportional to the speed that the reflector is moving. This phenomenon is called the Doppler effect and in vascular imaging it is used to determine the speed of the blood flow and calculate the degree of arterial narrowing. High-frequency transducers are used for the assessment of smaller caliber vessels obtaining high-quality resolution, for example 15–20-MHz transducers. In order to achieve a greater 456
Figure 49.1 Longitudinal scan of abdominal aorta with and without color flow imaging. The section of the superior mesenteric artery (SMA) is shown anteriorly. (See Color plates.)
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Contrast-enhanced ultrasound imaging Contrast agents like galactose (Levovist) produce micronsized bubbles which make blood more reflective by color flow Doppler ultrasound and further improve the quality of imaging. The effect of a contrast agent is to “raise” the signal from small vessels to a point at which they are detectable on color imaging. These agents were initially used for areas of subtle flow like neovascularity around tumors.8,9 A recent novel application for contrast enhanced duplex is the detection of endoleak following endovascular repair of abdominal aortic aneurysm.10–12
Duplex ultrasound in different anatomical situations Abdominal aorta Doppler ultrasonography provides an accurate measurement of aortic size and is therefore invaluable in serial assessment of small abdominal aortic aneurysms. Indications for abdominal aortic scanning includes a pulsatile abdominal mass, hemodynamic compromise in the lower extremities, abdominal pain, and a bruit. At sonography the aorta is visualized as a hypoechoic tubular structure with an echogenic wall (Figure 49.2). In the aorta flow is typically a high resistance type.
Figure 49.3 Longitudinal ultrasound of a peri-vascular swelling showing swirling blood using color flow, hence distinguishing between a pseudoaneurysm and hematoma. (See Color plates.)
mono or biphasic Doppler waveform with a reduced peak systolic and an increased end diastolic velocity.
Iliac arteries The proximal segment of the iliac arteries and the distal external iliac arteries can be visualized in most cases. The middle part of the iliac arteries are tortuous and deeply placed in the abdomen and pelvis. This part can be difficult to visualize, particularly in the presence of adipose tissue. The aorta and proximal iliac segments can be visualized with a low-frequency 2–3-MHz transducer. In case of poor visualization a proximal stenosis can also be diagnosed by the presence of
Arteries of upper and lower limbs Arteries of the upper and lower extremities can easily be accessed by using ultrasound imaging as unlike abdominal and thoracic vessels there is not an acoustic interface. A higher frequency transducer can be used because the depth of arteries is usually less than 6 cm from the skin. Doppler waveform analysis and color flow imaging allow the distinction between a stenosis and an occlusion. It is also useful for the assessment of a peri-vascular mass like a pseudoaneurysm or hematoma13 (Figure 49.3). Atherosclerotic narrowing is displayed on Doppler analysis as increased pulsatility proximal to the stenosis, increased systolic and diastolic pressure at the stenosis and turbulence just distal to the stenosis and dampening of flow distal to the stenosis (Figure 49.4).
Figure 49.2 Transaxial image of an abdominal aortic aneurysm containing a large amount of layered thrombus.
Figure 49.4 Femoral thromboembolic occlusion in a critically ischemic leg. The curser in on a small residual proximal lumen.
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Figure 49.5 Color flow Doppler ultrasound showing the left common carotid artery with a peak systolic velocity of 103 cm/second and an end diastolic velocity of 12.7 cm/second, which is predictive of a distal stenosis. (See Color plates.)
Carotid arteries Duplex ultrasound is the first-line investigation for suspected carotid artery disease (Figure 49.5). A tight stenosis can be accurately assessed by measuring peak systolic velocity measurements or velocity ratios of the internal carotid and common carotid arteries.14,15 Carotid artery Doppler examination can reliably differentiate between internal and external carotid arteries where the waveform has a characteristic shape. The location, size, and presence of branches are also useful markers for distinction. Doppler waveform in the normal internal carotid artery is a low-resistance profile as it supplies the brain which has low vascular resistance. There are broad systolic peaks, gradual systolic decelerations, and prolonged diastolic flow throughout the cardiac cycle. In contrast there is high resistance to blood flow in the external carotid artery as it supplies mainly muscles, bones, and cutaneous tissue where
Figure 49.6 Longitudinal carotid ultrasound of a patient with a carotid stent with and without color flow imaging. There is a normal color flow pattern throughout the stented portion. Color flow is also shown in the vertebral artery. (See Color plates.)
Figure 49.7 Longitudinal color flow Doppler ultrasound of the right common carotid artery showing a pseudoaneurysm following a stab wound to the neck. (See Color plates.)
resistance is high for blood flow. The waveform in the external carotid artery has narrow systolic peaks. Because of highly reliable and reproducible Doppler results there is a growing trend to performing carotid endarterectomy without invasive angiography.16,17 Doppler can also be used for follow up after stenting (Figure 49.6). Pseudoaneurysms The use of duplex and color flow Doppler is helpful in differentiating between a peri-vascular mass and a pseudoaneurysm. The presence of flow and the typical swirling motion confirms the diagnosis of a false aneurysm. In traumatic and iatrogenic aneurysms there is often a small communicating channel between the artery and the pseudoaneurysm (Figure 49.7). To-and-fro movement during systole and diastole is detected by Doppler as blood moves in and out of the communicating channel.18
Figure 49.8 Color flow Doppler ultrasound in the left cephalic vein showing turbulence of the color flow pattern in a patient with traumatic arteriovenous fistula at the wrist. (See Color plates.)
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Figure 49.9 Longitudinal abdominal ultrasound of the upper inferior vena cava filled with tumor/ thrombus. (See Color plates.)
AV fistula Color flow Doppler or is also useful in establishing the diagnosis of an abnormal communication between an artery and vein. Turbulence and arterialized signals are seen in the veins on Doppler spectrum (Figure 49.8).19,20
Peripheral veins It is difficult to evaluate the venous system accurately using only clinical examination. Doppler ultrasound is the most reliable non-invasive imaging method which is best done in conjunction with clinical examination. It provides accurate information of venous anatomy and hemodynamics. Doppler has an important role in the assessment of varicose veins (Figure 49.9) and deep venous thrombosis (Figure 49.10). Most of the patients for femoropopliteal and subclavian segment evaluation can be assessed by 5-MHz transducer. For assessment of iliac and caval segments a 3.5MHz transducer may be needed for deeper penetration. Higher frequency transducers can be used for visualization of superficial veins.
Conclusion and future developments
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Figure 49.10 Transverse color flow Doppler ultrasound showing an incompetent saphenofemoral junction.
but also on proper assessment of the peripheral vascular tree. Doppler ultrasound is a valuable non-invasive method of choice to reliably evaluate peripheral vascular lesions. Superficial vessels like the carotid and femoral arteries can be easily assessed for vessel wall morphology and flow dynamics using high-frequency transducers. Doppler results are so good in these segments that surgery can be carried out without angiography. Ultrasound is of particular importance when assessing carotid artery disease and some advances in plaque morphological evaluation have made interventions safer.21 The ICAROS registry confirmed that echolucent plaque is high risk for cerebral complications and indicates that these patients are better treated by endarterectomy.22,23 Furthermore, recent developments have made it possible to examine the artery from within the vessel using intravascular ultrasound during interventional procedures.24 A high-frequency 20-MHz probe can be passed over a 0.014-inch guidewire to show 360° histological detail of the vessel wall. Virtual histology intravascular ultrasound produces a color-coded map of the plaque and is currently being evaluated to see if it will predict how the carotid plaque will behave at the moment of angioplasty and stenting.24,25
A satisfactory clinical outcome in peripheral vascular disorders is not only dependent upon the adequate surgical technique
REFERENCES 1. 2. 3.
Dos Santos, Lamas A, Pereira CJ. L’arteriographie des members de l’aorte et ses branches abdominales. Bull Soc Nat Chir 1929; 55: 587–601 Currie GR, White DN. Color coded ultrasonic differential velocity arterial scanner (echoflow). Ultrasound Med Biol 1978; 14: 27–35 Polak JF, Karmel MI, Mannic JA et al. Determination of the extent of peripheral arterial disease with colour assisted
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duplex sonography; comparison with angiography. AJR 1990; 155: 1085–9 De Vires S, Hunink M, Polak JF. Summary receiver operating characteristic curves as a technique for meta analysis for the diagnostic performance of duplex ultrasonography in peripheral arterial disease. Acad Radiol 1996; 3: 361–9 Robert A Bucek et al. Three dimensional colour Doppler sonography in carotid artery stenosis. AJNR Am J Neuroradiol 2003; 24: 1294–9
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Textbook of peripheral vascular interventions Merritt CRB, Hykes DL, Hedrick WR et al. Medical diagnostic ultrasound instrumentation and clinical interpretation. Topics in radiology council report. JAMA 1991; 265: 1155–9 Polak JF, Dobkin GR, O’Leary DH et al. Internal carotid artery stenosis; accuracy and reproducibility of colour Doppler assisted duplex imaging. Radiology 1989; 173: 793–8 Leen E, Horgan P. Ultrasound contrast agent for hepatic imaging with non- linear modes. Current Probl Diagnostic Radiol 2003; 32: 66–87 Tschammler A, Viesr G, Schindler R, Schuermann R, Wolf K. Ultrasound contrast media: in vitro studies. J Ultrasound Med 1993; 12: S33 Henao et al. Contrast enhanced Duplex surveillance after endovascular abdominal aortic aneurysm repair: Improved efficacy using a continuous infusion technique. J Vasc Surg 2006; 43(2): 259–63 Giannoni MF, Palombo G, Sbarigia E et al. Contrast enhanced ultrasound imaging for aortic stent graft surveillance. J Endovasc Ther 2003; 10: 208–17 Reid AW, Reid DB, Roditi GH. Vascular imaging: an unparalleled decade. J Endovasc Ther 2004; II (suppl. II): II.163–79 Gooding GA, Effeny DJ. Ultrasound of femoral artery aneurysms. AJR 1980; 134: 477–80 Moneta GL, Edward JM, Chitwood RW et al. Correlation of North American Symptomatic Carotid Endarterectomy Trial (NASCET) angiographic definition of 70% to 99% internal carotid artery stenosis with duplex scanning. J Vasc Surg 1993; 17: 152–9 Suwanwela N, Can U, Furie KL et al. Carotid Doppler Ultrasound Criteria for internal carotid artery stenosis based on residual lumen diameter calculated from en-bloc carotid end-arterectomy specimens Stroke 1996; 27: 1965–9
16. 17. 18. 19. 20. 21. 22.
23. 24. 25.
Chen JC, Salvain AJ, Taylor DC et al. Predictive ability of duplex ultrasonography for internal carotid artery stenosis of 70–99%: a comparative study. Ann Vasc Surg 1998; 12: 244–7 Bendick PJ, Brown W, Hernandez D, Glover JL, Bove PG. Threedimensional vascular imaging using Doppler ultrasound. Am J Surg 1998; 176: 183–7 Abu Yousaf MM, Wierse JA, Shamma AR. The “to and fro” sign: duplex Doppler evidence of femoral Pseudo aneurysm. AJR 1988; 150: 632–4 Roubidoux MA, Hertberg BS, Carrol BA et al. Color flow and image directed Doppler ultrasound evaluation of iatrogenic arteriovenous fistula in the groin. J Clin Ultrasound 1990; 18: 463–9 Altin RS, Flicker S, Naideck HJ. Pseudoaneurysm and arteriovenous fistula after femoral artery catherization: association with low femoral punctures. AJR 1989; 152: 629–31 Reid DB. Carotid plaque characterization: helpful to endarterectomy and endovascular surgeons[Commentary]. J Endovasc Surg 1998; 5: 247–50 Biasi GM, Mingazzini PM, Baronio L et al. Carotid plaque characterization using digital imaging processing and its potential in future studies of carotid endarterectomy and angioplasty. J Endovasc Surg 1998; 5: 240–6 Biasi GM, Ferrari SA, Nicolaides AM et al. The ICAROS registry of carotid artery stenting. J Endovasc Ther 2001; 8: 46–53 Irshad K, Reid DB, Miller PH et al. Early clinical experience with colour three-dimensional intravascular ultrasound in peripheral interventions. J Endovasc Ther 2001: 8: 329–38 Diethrich EB, Irshad K, Reid DB. Virtual histology and color flow intravascular ultrasound in peripheral interventions. Semin Vasc Surg 19: 155–162
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Abdominal aortic dissections OC Morcos, JC Pereda, and ML Marin
Introduction Acute aortic dissection can be a life-threatening catastrophe and can affect all segments of the aorta with different implications on treatment as well as mortality. Insight into the lethality of acute dissection can be gained from the International Registry of Acute Aortic Dissection (IRAD) study.1 Overall mortality in this study was 27.4% with a 31.4% mortality when intervention was necessary for distal dissections. Isolated abdominal dissections are a rare manifestation of this disease with abdominal pain being the most common symptom in this subset.2,3 A review of the world literature by Graham et al.3 resulted in only 47 patients with isolated abdominal dissections. Presentation is acute in 70–80% of circumstances.2,3 The presentation spectrum includes abdominal pain (with or without visceral ischemia), lower extremity ischemia, refractory hypertension, aortic rupture, aortic aneurysm formation, or dissections may be completely asymptomatic. The relative rarity of this entity makes the natural history and long-term outcomes of different treatment modalities comparative as most information is derived from the treatment of thoracic dissections. The peak incidence of this disease is between 60 and 65 years old and 60–67% of patients are male.2,3 It has no classification system of its own and is often grouped in with descending thoracic anuerysms with distal extension (DeBakey type IIIb).4 The diagnosis and treatment of isolated abdominal aortic dissection is likely to change with the introduction of advanced diagnostic and therapeutic (namely endovascular) management of this disease. This chapter will focus on the pathogenesis, diagnosis, and current treatment strategies of aortic dissections as they relate to the abdominal aorta and its branches.
Pathogenesis The inciting event in aortic dissection is a rupture or tear in the aortic intima and then media. It can occur in a histologically normal aorta but often reveals an abnormal degradation of the medial collagen and elastin fibers. The primary factor is a loss of vascular smooth muscle cells and increased elasticity of the media.5 Advanced age and hypertension are probably the most important reasons for this.6 Typically, the tear does not involve the entire circumference around the aorta. This space created by the intimal rupture fills with blood, propagates in either longitudinal or transverse direction, and becomes the false lumen of the dissection. The flow of blood is generally antegrade but retrograde
dissection and flow may occur. The location of the tear occurs in the abdominal aorta in 1–5% of all aortic dissections.7,8 These intimal disruptions occur in areas of the aorta subjected to the greatest change in pressure dynamics and wall tension.9 This is greatest in the ascending aorta and aortic arch, which perhaps is the reason for the low incidence of spontaneous tears occurring in the abdominal aorta, where arterial hemodynamics are different. LaPlace’s law dictates that wall tension is inversely proportional to the absolute thickness of an object. The false lumen, with its relatively thinned out adventitial wall, becomes prone to rupture and aneurysmal degeneration because of this and its increased luminal radius. Fenestrations in the flap created, usually at aortic branch points, allow for re-entry into the true lumen and false lumen patency. The intimal flap may cause intermittent or permanent obstruction of the aorta and its branches depending on location and the presence of fenestrations.
Clinical presentation and diagnosis As stated earlier, a wide variety of clinical signs and symptoms may be present in patients with dissection. A clinician must be open to the idea of aortic dissection as a differential diagnosis in a wide variety of presentations. An acute presentation denotes the onset of symptoms and diagnosis of less than 2 weeks with any period longer than that being chronic. Historically, hypertension accompanies a large percentage of patients with acute aortic dissection. When isolated to the abdominal aorta, this occurs with a frequency of 40–70%.2,10 When hypotension is present, a suspicion of aortic rupture or more extensive dissection is warranted. The presence of hypotension with abdominal aortic dissection is a potent risk factor for mortality and may complicate up to 15% of dissections.3 The most common presentation of those people symptomatic with aortic abdominal dissection is abdominal pain and is present in up to 70% of patients.2 In these patients a high index of suspicion for mesenteric vascular involvement is of utmost importance, as mortality in these patients is high. Infrequently, aortic dissection accompanies an atherosclerotic aneurysm, occurring with a frequency between 2 and 12%.1 Aortic rupture generally occurs when there is a pre-existing degenerative abdominal aortic aneurysm. Cambria et al.,11 in their review of 325 patients with aortic dissection, reported that rupture only occurred when a concomitant aneurysm was already present. Rupture is a deadly complication of aortic dissection, with mortality rates approaching 70%.12 461
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Rupture can occur in 10–28% of patients with isolated abdominal aortic dissections and mortality rates of 90% have been reported.2,3 Branch vessel involvement is a common indication for intervention and is termed malperfusion syndrome when resultant end-organ ischemia occurs. Aortic branch compromise is associated with an increase in early mortality.11 Morbid outcomes depend on the particular branch or branches affected. Renal, visceral, and lower extremity ischemia has traditionally been reported in 30–50% of patients with all types of dissection.13 Its frequency related to isolated abdominal aortic dissections is unknown because only case series are available for review. Dynamic and static obstruction describe two mechanisms by which this occurs.14 In static obstruction, organ perfusion can become static causing obstruction or thrombosis if the dissection extends into branch ostia. Because the dissection process often shears the wall around the branch vessel, the vessel often doesn’t suffer ill effects of malperfusion. Restoration of the true lumen is unlikely to resolve this alone and intervention is generally needed to restore branch vessel flow. With dynamic obstruction, the dissection plane does not extend into the branch ostia but rather compresses the true lumen, causing vessel compromise. Deficits are not fixed but in a dynamic state of flux. The circumferential percentage of aorta dissected can determine the amount of true lumen collapse. Prompt relief of malperfusion states with interventional or surgical means can be life saving. Lower extremity ischemia is an indication for intervention and may reveal a hint as to the extensiveness of dissection and is historically associated with higher morbidity rates.11,15 Lower extremity pulse deficits occurred in roughly 14% of all IRAD patients.1 However, mortality stemming from this is uncommon but may be accompanied by other branch vessel compromise.16 On the other hand, Henke et al. found that independent risk factors associated with death included increased age, presence of shock, acute renal failure, and acute limb ischemia.17 There is significant association of acute limb ischemia with both mesenteric ischemia and infarction and renal ischemia.17 Overall amputation rates reach around 2%.17 Most institutional series have shown a relatively infrequent presentation of peripheral ischemia ranging from 7 to 12%.2,3,10,11,13 Mesenteric ischemia is a feared and often lethal complication of aortic dissection. In the IRAD study,1 20% of those patients with a descending thoracic or abdominal dissection underwent surgical therapy. Visceral ischemia was the cause of death in 15.4% of patients with descending aortic dissections.1 The presence of perfusion on imaging studies can be misleading, as suggested by Neri et al.,18 who reported difficulty in diagnosis and a high mortality in those patients with non-occlusive intestinal ischemia. Mortality rates are as high as 87% in patients with mesenteric ischemia.11 The frequency of asymptomatic presentation and incidental discovery is about 17–20%.2,3
Radiologic diagnosis Because the presentation of acute aortic dissection can vary widely, radiologic assistance is necessary. It can possibly delineate
diagnosis, causes, potential for complications, and provide operative planning in those cases requiring intervention. Physical examination is non-specific and cannot be relied upon to guide management. High clinical suspicion, however, is paramount in selecting appropriate adjunctive studies. Aortography (see Figure 50.1) was long considered the gold-standard examination for diagnosis of an acute aortic dissection. Because of the time necessary to perform the examination and its invasiveness, it cannot be considered a first-line diagnostic study. Furthermore, it cannot show the presence of intramural hematoma or thrombosis of a false lumen and, in those circumstances, may result in a false negative reading of the examination.19 Its use in diagnosis has been supplanted by other, more accurate imaging studies and its role has been relegated to therapeutic modalities.20 Transesophageal echocardiography has been an excellent modality in diagnosing ascending and proximal descending dissections but has no role in diagnosing isolated abdominal aortic dissection because of its inability to examine the aorta beyond the diaphragm. Magnetic resonance imaging (MRI) is extremely accurate in diagnosing aortic dissection and has an overall sensitivity and specificity of greater than 95%.20 Its usefulness in the acute setting is limited, however, because of its infrequent availability, time to test, and patient issues (precluded by claustrophobia or metallic implants). Patients presenting with suspicion of isolated abdominal aortic dissection should be evaluated by contrast-enhanced computed tomography (CT). Since the level of dissection cannot be ascertained on history and physical examination alone, CT of the chest, abdomen, and pelvis should initially be done. It was the most common diagnostic study used in IRAD.1 It is widely available, non-invasive, and (in most circumstances) quick to attain. It can be used for follow-up comparisons and is less user-dependent than other modalities. The true lumen can be differentiated from the false lumen by its continuity with a normal segment of aorta and the false lumen is generally larger than the true lumen for reasons described above.21 In addition to those reasons, CT can aid in both operative and endovascular planning. In Figure 50.1, note the orientation of the dissection. This has important therapeutic implications for the treatment of various scenarios.
Medical therapy Institution of prompt medical therapy in those patients presenting with dissection cannot be stressed enough and is often the only treatment necessary for descending thoracic and abdominal aortic dissections. As mentioned earlier, hypertension is present in 40–70% of all patients presenting with an isolated abdominal aortic dissection.2,3,10 The presence of hypotension, however, is ominous and often associated with an extensive ascending dissection or aortic rupture. Patients admitted with this diagnosis should be admitted to an intensive care monitoring unit in addition to undergoing appropriate diagnostic studies. Intravenous antihypertensive medications should be administered expeditiously to those patients who arrive with a diagnosis of dissection and are hypertensive. The first antihypertensive
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Figure 50.1 This computed tomography scan is of a 56-year-old male presenting with abdominal pain. Series (a) demonstrates preoperative findings of an isolated infrarenal aortic dissection on computed tomography, angiography, and three-dimensional CT reconstructions; series (b) demonstrates intraoperative images of placement of a bifurcated endovascular stent-graft proximal to the intimal tear. To preserve flow to the internal iliac arteries, they were not embolized and thus the distal end of the false lumen was coil embolized to prevent retrograde flow. Continued
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Figure 50.1—cont’d Series (c) depicts the post-operative appearance, with false lumen thrombosis and shrinkage. Artifact appears secondary to the platinum coils.
used should be a beta-blocker (metoprolol, esmolol, labetalol) often in conjunction with morphine sulfate for the pain or direct vasodilating drugs such as sodium nitroprusside. The beta-blocker should be administered prior to direct vasodilators to avoid a reflex sympathetic stimulation.14 If beta-blockade is contraindicated, calcium channel blockers such as verapamil or diltiazem should be used.
Surgical therapy Current surgical and endovascular treatments are indicated in isolated abdominal aortic dissections in the presence of intractable pain or hypertension, aortic rupture, visceral or mesenteric ischemia, lower extremity ischemia, associated aortic aneurysm, or to prevent future aneurysmal degeneration.2 Farber et al. recommended elective repair if an abdominal dissection was present in conjunction with an aneurysm of 3 cm or greater in diameter because of rupture in one patient with an aneurysm of 3.5 cm.2 The potential for future aneurysmal degeneration of the weakened false lumen is further an indication for repair. Although beta-blockers have been shown to retard the growth of aneurysms associated with abdominal aortic aneurysms,22 close surveillance is warranted in the case of medically treated dissections. The natural history of isolated abdominal aortic dissections is unknown and cannot be correlated from the natural history of “garden variety” abdominal aortic aneurysms. The etiology and pathophysiology are different and therefore outcomes can be expected to be different. The surgical treatment for aortic dissection has been changing since the advent of aortic endovascular stent-grafts in the early 90s (see Figure 50.1).23,24 The application of stentgrafting for non-aneurysmal lesions was advocated soon thereafter and is currently used to treat a wide variety of
arterial pathologies.25,26 Less invasive therapies are rapidly replacing traditional open repairs, particularly in patients who are unstable or with severe underlying co-morbid medical conditions. Patients with isolated abdominal aortic dissection often present in extremis. Treatment of its complications were traditionally approached via open surgical means by fenestration or aortic replacement and bypass. This offers the advantage of direct inspection of affected organs and their arterial supply. More recently percutaneous techniques have gained favor and are an excellent alternative to open surgical procedures. Endovascular stent-grafts can be used to line the entry tear and divert blood flow into the lumen proximal to major aortic branches. Alternatively, the device can be positioned in the standard method of aneurysm exclusion if the dissection begins more distally. This isolates the false lumen and causes thrombosis within it thus ensuring a better prognosis.27 The aorta undergoes remodeling and the false lumen can disappear with time.28 Dake et al. showed thrombosis in 15 of 19 patients (79%) who underwent stent-grafting.29 This has good application in the descending thoracic aorta but can be prohibitive if the dissection begins in the abdominal aorta cephalad to the visceral arteries. The celiac, superior mesenteric, and renal arteries limit the area available for landing the device. Many dissections, however, begin infrarenally and are good candidates for a stent-graft. This therapy has the advantage of theoretically reducing the risk of aneurysmal degeneration of the false lumen. Bare metal stents are not advocated for use in sealing a proximal tear. Injury to the intima can cause further disruption and deviation of flow through the stent interstices. Placement of the device includes percutaneous or open access to the femoral artery. Preoperative imaging should guide the side of puncture, as this should be done with the goal in mind of entering the true lumen. Often a brachial artery approach may be necessary and the access site of choice,
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Abdominal aortic dissections particularly if there is doubt about the accessibility of the true lumen from a distal approach. Under fluoroscopic guidance, a soft wire followed by a pigtail catheter for imaging followed by a stiff wire should be navigated into the descending thoracic aorta. A device with dimensions selected based on preoperative CT should be advanced over the wire. Ideal positioning of the stent-graft should be as close to the renal artery orifices as possible. Angiography to attain the proper obliquities should be done just prior to deployment. Inflation of a compliant 33mm balloon should be performed to provide optimal apposition to the aorta. Completion angiography is performed to confirm device position, determine if leaks are present, and ensure filling of proximal branch aortic vessels as well as peripheral arteries. CT angiography may be used for comparison and follow-up (see Figure 50.1). In order to adequately treat patients with malperfusion syndrome, the true and false lumen access must be established either transfemorally or transbrachially.Angiography and intravascular ultrasound can assist with anatomical identification of branch vessels. Pressure gradients are measured in both the true and false lumen and a determination of therapy is made. If flow can be restored to an aortic branch with stenting, this should be performed after wire access into this vessel is established. It may become necessary to fenestrate the dissection wall to provide improved flow to a compromised vessel. This technique30 culminates in increased flow in both the true and false lumen. The direction of fenestration should be performed from the smaller (usually true) to the larger (usually false) lumen using an endovascular needle or the stiff end of a 0.014-inch wire. Angiography confirms placement in the opposite lumen. A wire is advanced into the lumen and over it a balloon creates a fenestration in the dissection wall. Intravascular ultrasound or a targeting balloon can be used for precise puncture of the wall. Hemodynamics may become unpredictable after fenestration and stenting and thus warrant careful intra and post-procedural surveillance.
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Figure 50.2 Proposed algorithm to managing isolated abdominal dissection. Note that “complications” refers to the development of a malperfusion state, rupture, dissection propagation, aneurysm formation, or endoleak (if done endovascularly). Surveillance includes periodic history and physical examinations and serial imaging. ∗Appropriately selected patients who are generally healthy may benefit form prophylactic endovascular stent-grafting to prevent late complications.
Serial imaging should be performed at regular intervals and should be lifelong. A European Task Force32 recommended surveillance at 1, 3, 6, and 12 months after an acute event and yearly thereafter. Their method of choice was MRI because of lack of ionizing radiation and use of nephrotoxic agents but CT angiography is a valuable and reliable method if those risks are kept in mind.
Conclusion Follow-up The long-term follow-up of asymptomatic patients or those treated by intervention for isolated abdominal aortic dissections should be stringent (see Figure 50.2). This includes aggressive treatment of hypertension, office visits, and surveillance diagnostic imaging. The highest risk of complications occurs within the first few months after initial presentation. Only 17–20% of patients present with incidental diagnostic imaging and are asymptomatic.2,3 Asymptomatic patients may develop aneurysms of the false lumen or dissection extension and may become symptomatic with signs of visceral or peripheral ischemia. Persistent patency of the false lumen has been reported in a large percentage of patients treated for dissection without endovascular stent-graft as has an increase in luminal diameter of the false channel.31 The development of false lumen aneurysmal degeneration is an indication for repair as rupture has an exceedingly high mortality rate.3 Treatment with antihypertensives, particularly beta-blockade, is important in both the asymptomatic and treated patients. From aortic aneurysm literature, beta-blockers have been shown to slow the rate of expansion and thus may slow false channel widening.22
The development of an acute aortic dissection is often a catastrophic event that has historically had poor mortality rates. Overall mortality rates approach 30%.1 Little is known about isolated abdominal aortic dissections because of their rarity. In fact the largest case series in the literature is of ten patients.2 The data, therefore, are surmised from the descending thoracic dissection literature. Adequate follow-up is paramount to both medical and operative outcomes. Newer management techniques and advances have improved survival with the incorporation of endovascular methods to achieve similar but less invasive therapy. Because of this, previously untreated dissections now can be prophylactically repaired to prevent future complications. The use of endografts in the face of dissections has been performed for many years but has yet to be studied in a prospective manner.33 The INSTEAD trial (INvestigation of STEnt grafts in patients with distal Aortic Dissection) is now underway in Europe and will address the outcome of treatment of endovascular stent-grafting versus conventional antihypertensive therapy in descending thoracic dissections in a randomized, prospective manner.34 As newer treatments emerge and trials are completed, our understanding of the disease may improve with a resultant improvement in morbidity and mortality rates.
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REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14.
15. 16.
17. 18.
Hagan PG, Nienaber CA, Isselbacher EM et al. The International Registry of Acute Aortic Dissection (IRAD): New insights into an old disease. JAMA 2000; 283: 897–903 Farber A, Wagner WH, Cossman DV et al. Isolated dissection of the abdominal aorta: clinical presentation and therapeutic options. J Vasc Surg 2002; 36: 205–10 Graham D, Alexander JJ, Franceshi D, Rashad F. The management of localized abdominal aortic dissections. J Vasc Surg 1988; 8: 582–91 DeBakey ME, Henly WS, Cooley DA. Surgical management of dissecting aneurysms of the aorta. J Thorac Cardiovasc Surg 1965; 49: 130–48 Marsalese DL, Moodie DS, Lytle BW et al. Cystic medial necrosis of the aorta in patients without Marfan’s syndrome: Surgical outcome and long-term follow-up. J Am Coll Cardiol 16: 68–73 Mehta RH, Manfredi R, Hassan F et al. Chronobiological patterns of acute aortic dissection. Circulation 2002; 106: 1110–5 Hirst, A, Johns V, Kime W. Dissecting aneurysms of the aorta. Medicine 1958; 37: 217–79 Roberts, CS, Roberts WC. Aortic dissection with the entrance tear in abdominal aorta. Am Heart J 1991; 121: 1834–5 Wheat MW. Acute dissection of the aorta. Cardiovasc Clin 17: 241–62 Becquemin J-P, Deleuze P, Watelet J, Testard J, Melliere D. Acute and chronic dissections of the abdominal aorta: clinical features and treatment. J Vasc Surg 1990; 11: 397–402 Cambria RP, Brewster DC, Gertler JP et al. Vascular complications associated with spontaneous aortic dissection. J Vasc Surg 1988; 7: 199–209 Mozes G, Gloviczki P, Park WM, Schultz HL. Spontaneous dissection of the infrarenal aorta. Semin Vasc Surg 2002; 15: 128–36 Borst HG. Organ ischemia. In: Borst HG, Heinemann MK, Stone CD, eds. Surgical Treatment of Aortic Dissection, first edition. New York: Churchill Livingstone, 1996: 249–64 Black J, Cambria RP. Aortic dissection: perspectives for the vascular/endovascular surgeon. In: Rutherford RB, ed. Vascular Surgery, sixth edition. St. Louis: Elsevier Saunders, 2005 1512–33 Lauterbach SR, Cambria RP, Brewster DC et al. Contemporary management of aortic branch compromise resulting from acute aortic dissection. J Vasc Surg 2001; 33: 1185–92 DeBakey ME, Henly WS, Cooley DA, Morris GC, Crawford ES. Dissection and dissecting aneurysms of the aorta: twenty-year follow-up of five hundred twenty seven patients treated surgically. Surgery 1982; 92: 1118–34 Henke PK, Williams DM, Upchurch Jr. GR et al. Acute limb ischemia associated with type B aortic dissection: Clinical relevance and therapy. Surgery 2006; 140: 532–40 Neri E, Sassi C, Massetti M et al. Nonocclussive intestinal ischemia in patients with acute aortic dissection. J Vasc Surg 2002; 36: 738–45
19.
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21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33. 34.
Mugge A, Daniel WG, Laas J et al. False negative diagnosis of proximal aortic dissection by computed tomography or angiography and possible explanations based on transesophageal echocardiographic findings. Am J Cardiol 1990; 65: 527–9, 1990 Moore AG, Eagle KA, Bruckman D et al. Choice of computed tomography, transesophageal echocardiography, magnetic resonance imaging, and aortography in acute aortic dissection: International Registry of Acute Aortic Dissection (IRAD). Am J Cardiol 2002; 89: 1235–8 LePage MA, Quint LE, Sonnad SS et al. Aortic dissection: CT features that distinguish true lumen from false lumen. AJR Am J Roentgenol 2001; 177: 207–11 Nienaber CA, von Kodolitsch Y. Therapeutic management of patients with Marfan syndrome: focus on cardiovascular involvement. Cardiology in Review 1999; 7: 332–41 Parodi JC, Palmaz JC, Barone HD. Transfemoral intraluminal graft implantation for abdominal aortic aneurysms. Ann Vasc Surg 1991; 5: 491–9 Marin ML, Veith FJ. Transfemoral repair of abdominal aortic aneurysms. New Engl J Med 1994; 331: 1751 Marin ML, Veith FJ, Cynamon J et al. Initial experience with transluminally placed endovascular grafts for the treatment of complex vascular lesions. Ann Surg 1995; 222: 449–69 Ohki T, Marin ML, Veith FJ. Use of endovascular grafts to treat nonaneurysmal arterial disease. Ann Vasc Surg 1997; 11: 200–5 Bernard Y, Zimmermann H, Chocron S et al. False lumen patency as a predictor of late outcome in aortic dissection. Am J Cardiol 2001; 87: 1378–82 Nienaber CA, Fattori R, Lund G et al. Nonsurgical reconstruction of thoracic aortic dissection by stent-graft placement. N Engl J Med 1999; 340: 1539–45 Dake MD, Kato N, Mitchell RS et al. Endovascular stent-graft placement for the treatment of acute aortic dissections. N Engl J Med 1999; 340: 1546–52 Nienaber CA, Eagle KA. Aortic dissection: New frontiers in diagnosis and management: Part II: Therapeutic management and follow-up. Circulation 2003; 108: 772–8 Beregi JP, Haulon S, Otal P et al. Endovascular treatment of acute complications associated with aortic dissection: Midterm results from a multicenter study. J Endovasc Ther 2003; 10: 486–93 Erbel R, Alfonso F, Boileau C et al. Diagnosis and management of aortic dissection: task force report of the European Society of Cardiology. Eur Heart J 2001; 22: 1642–81 Marin ML, Lyon RT, Hollier LH, Kaplan DB. Experience with endovascular grafts in the treatment of infrarenal aortic aneurysms associated with proximal aortic dissection. Am J Surg 1999; 177: 102–6 Nienaber CA, Zannetti S, Barbieri B et al. Investigation of stent-grafts in patients with type B aortic dissection: Design of the INSTEAD trial-a prospective, multicenter, European randomized trial. Am Heart J 2005; 149: 592–9
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Endovascular treatment of abdominal aortic occlusive disease C Klonaris and A Katsargyris
Introduction The distal abdominal aorta is commonly affected by atherosclerosis in patients with ischemic peripheral atherosclerotic disease.1 Two different patterns of atherosclerotic disease affect the infrarenal aorta including: (1) localized disease of the aortic bifurcation involving the lower part of the abdominal aorta and the common iliac arteries, whether symmetric or not; and (2) isolated lesions of the infrarenal abdominal aorta without involvement of the aortic bifurcation. This latter pattern of focal stenosis or occlusion of the infrarenal aorta above the aortic bifurcation is relatively rarely observed. Interestingly, it is more frequently documented in women aged 30–50 years, in contrast to chronic multilevel atherosclerotic disease that has a male predominance (male–female ratio, approximately 6:1).2 Heavy smoking as well as elevated blood lipid concentrations are among the most important risk factors,3,4 while the hypoplastic aorta syndrome has also been reported to play a significant role in this aortic pathology.5 Embolic occlusion of the distal aorta is much less frequent, but may occur in patients with mitral valve disease. Other rare causes of aortic obstruction include fibromuscular dysplasia, Takayasu’s arteritis, and retroperitoneal fibrosis. Clinical symptoms of chronic aortic obstruction include bilateral upper thigh and buttock claudication, along with erectile dysfunction in males. These symptoms should be differentiated from those arising from spinal stenosis. In cases of acute occlusion in a previously non-stenotic aorta, patients present with acute bilateral limb ischemia, since usually there are not enough collateral pathways.
Treatment options Surgical intervention Aortic endarterectomy (Figure 51.1) and bypass have been traditionally the treatments of choice for infrarenal aortic occlusive disease with well-documented long-term results.6–13 In carefully selected patients the 11-year cumulative patency rate after localized endarterectomy of the abdominal aorta is 86%,14 while long-term patency after aortofemoral bypass is reported to be 85–90% and 70–75% at 5 and 10 years respectively. However, these procedures are associated with significant morbidity and mortality,5 while they may also lead to sexual dysfunction in male patients.15,16 Complications of aortic endarterectomy
include hemorrhage, early limb ischemia due to embolization or dissection at the distal endarterectomy endpoint, as well as late aneurysmal dilation of the endarterectomized segment, while aortobifemoral bypass may be complicated among others with renal dysfunction and colon or lower extremity ischemia. Percutaneous transluminal angioplasty (PTA) Percutaneous transluminal angioplasty (PTA) has been proposed as an alternative to surgery in aortic lesions and was initially described in 1980 by Grollmann et al.,17 Velasquez et al.,18 and Tegtmeyer et al.19 Since then, several series have been published demonstrating successful results of PTA with low complication rates in localized stenoses of the distal infrarenal aorta20–28 as well as in lesions involving the aortic bifurcation and common iliac arteries.20–22,25,29 Aortic PTA has an excellent reported outcome compared with PTA at other sites with initial technical success up to 98%, and 5-year primary and secondary patency of 75 and 97% respectively.5 Stenting The development of intravascular stents has added another useful weapon in the vascular surgeon’s armamentarium for the treatment of abdominal aortic occlusive disease. In the late 1980s, stents began to demonstrate their efficacy especially in reducing significant recoil after PTA, as well as in the treatment of specific lesions such as total occlusions or dissections.28,30–43 Particularly in the iliac arteries, stenting was shown to reduce the incidence of restenosis in comparison with balloon angioplasty.44 Based on these data, Diethrich et al.45 began in 1990 to offer stent therapy to patients with abdominal aortic lesions that were considered to be at high risk for conventional surgery. In a total of 24 patients, they reported a 100% cumulative primary patency at 5 years. Additional studies have shown that stent placement in the infrarenal aorta is feasible, safe, and successful.45–52 Recently, Simons et al.53 in a series of 17 patients who underwent primary stenting at the infrarenal aorta, reported a 3-year primary and secondary aortic hemodynamic patency of 83% and 100% respectively. Stoeckelhuber et al.54 reported primary clinical patency rate of 100% for primary aortic stenting during a mean follow-up of 110 months. In our department, 11 patients (6 men, median age 68, range 62–73) with abdominal aortic occlusive disease have been treated percutaneously within a 4-year period. Seven patients 467
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(b)
(a)
(c) Figure 51.1 Endarterectomy of the abdominal aorta: (a) surgical exposure of the abdominal aorta; (b) patch aortoplasty with Dacron following endarterectomy; and (c) macroscopic view of thrombotic material removed from the distal abdominal aorta.
had symptomatic infrarenal aortic stenosis and 4 had aortic occlusion (2 acute and 2 chronic). In 3 patients the occlusion was extending to both iliac arteries. Successful recanalization was achieved in all patients using a hydrophilic wire (Terumo), catheter coaxial technique, and subsequent stenting of the distal aorta and iliac arteries (Figure 51.2 and 51.3). No thrombolysis was performed in these cases. All patients were managed exclusively via a percutaneous route except one with concomitant total chronic occlusion of the right common and external iliac artery who required an additional femorofemoral bypass graft after successful aortic stenting. During the follow-up period (median 18 months, range 6–36 months) all arteries were patent except a patient who presented with acute aortobi-iliac occlusion in whom the left iliac artery was thrombosed 4 months after the procedure. Cumulative results reported in the literature, regarding endovascular therapy of occlusive aortic disease are shown in Table 51.1.
Technical considerations In the presence of an isolated lesion in the infrarenal aorta, angioplasty and stenting can be performed through only one femoral access site. Balloon diameter is chosen according to the stenosis characteristics; for non-calcified lesions, balloon diameter should be equal to that of the aorta. However, in case of a significantly calcified aorta the dilation should initially be
performed with a lower diameter balloon in order to minimize the risk of aortic rupture. Subsequently, the procedure may continue with a larger diameter balloon depending on initial results and the aortic tolerance. For lesions that are located near the aortic bifurcation, the use of a large-diameter balloon should be avoided due to inherent risks of common iliac artery injury. In such cases, the “kissing angioplasty” technique should be preferentially applied, through bilateral common femoral arteries punctures. In total occlusion of the infrarenal aorta, recanalization with a hydrophilic guidewire via the femoral or brachial approach may be attempted. Alternatively, fibrinolysis through the brachial artery may be performed particularly for relatively recent occlusions that do not seem to be older than 6 months. In the latter case, the fibrinolysis catheter has to be advanced down to the center of the thrombotic material. Once the recanalization is achieved, the procedure continues as it is usually performed for a stenosis. In cases of initial brachial approach, the guidewire can be snared using the femoral access to facilitate dilation of the aorta with appropriate balloon sizes or/and stent deployment Pressure gradients should be routinely measured before and after angioplasty. Additionally, angiography is performed to obtain images of the mesenteric arteries and celiac trunk. If the result obtained with PTA is satisfactory (disappearance of pressure gradients, absence of angiographically estimated residual stenosis or dissection), stent implantation is not
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(b)
Figure 51.2 (a) Digital subtraction angiography demonstrating total aortobi-iliac occlusion; (b) control angiogram demonstrating optimal results obtained after stenting in the infrarenal aorta and both common iliac arteries.
considered to be necessary. Otherwise, the procedure should continue with placement of either a balloon-expandable or a self-expanding stent. However, there are reports suggesting that surface irregularities after balloon angioplasty tend to correlate with early thrombus formation, acute occlusion, and late myointimal replacement. Therefore some authors suggest routine primary stenting after predilation in all cases61,62 in order to provide a smooth cylindrical lumen that favors nonturbulent flow, less thrombus formation, and consequently a larger aortic lumen. For ulcerated lesions with high embolic potential, primary stenting with a covered stent should be considered.
(a)
Finally, for lesions that involve the lower part of the abdominal aorta and the proximal part of one or both common iliac arteries, angioplasty and stenting should be performed with the “kissing” technique through bilateral femoral access.
Complications of percutaneous treatment Although complications that may occur after aortic dilation are the same with those in other vascular territories, they
(b)
Figure 51.3 (a) Digital subtraction angiography demonstrating an atherosclerotic lesion of the distal aorta near the aortic bifurcation; (b) angiogram showing successful treatment with placement of kissing iliac stents.
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Table 51.1
Mid-term results of endovascular treatment of occlusive lesions of the distal aorta
Author
Year
Cases
Tegtmeyer et al.20 Morag et al.29 Belli et al.55 Long et al.47 Diethrich et al.45 Hedeman-Joosten et al.56 Mendelsohn et al.57 Scheinert et al.58 Rosset et al.59 De Vries et al.5 Stoeckelhuber et al.54 Laxdal et al.60
1985 1987 1989 1993 1993 1996 1998 1999 2000 2004 2006 2007
32 13 13 7 24 38 20 48 31 69 9 25
∗
Mean follow-up (months) 14 36 27 15 10 34 10 24 24 57 110 40
Survival rate (%)
Secondary patency (%)
100 100 100 100 100 100 95 100 97.5 100 88.8 100
93.7 85.7 92.3 85.7 100 89.5 100 100 98.3 97 100 83∗
Good functional result (%) 90.6 85.7 92.3 85.7 100 100 95 100 83.9 – 100 –
Primary assisted patency at 5 years
can potentially be of greater clinical impact. While dissection, recollapse, or residual stenosis can be simply treated by additional stenting, aortic rupture, although not common, is a potentially life-threatening complication and therefore may require immediate surgical management. To eliminate exsanguination in such circumstances, a large-occlusion latex balloon should be advanced and inflated into the aorta, covering the site of rupture and left inflated until the patient is ready for surgery. Alternatively, an aortic stent-graft can be deployed across the rupture. A computerized tomography (CT) scan prior to the intervention may be useful in avoiding this complication, by excluding complete or near-complete circular calcification of the aorta (Figure 51.4), which is considered to be a risk factor for aortic rupture during dilation. Distal embolization is reported in less than 1% of aortic stenoses treated percutaneously. Subacute thrombosis after aortic dilation or stenting has never been reported in isolated aortic lesions, but it may occur after remodeling of the
Figure 51.4
aortic bifurcation. Finally, due to their large diameter, aortic stents are rarely re-obstructed.
Conclusion Although further randomized studies are necessary in order to definite conclusions regarding the role of percutaneous techniques for the treatment of distal aortic occlusive disease, it seems that endovascular treatment of atherosclerotic lesions in the infrarenal aorta is feasible, safe, and effective. Endoluminal techniques can be used either for short focal stenoses or for complex lesions including total aortobi-iliac occlusions, depending on the extent and degree of calcification. Based on preliminary short- and mid-term results, we consider this modality to be a true alternative to open surgery for initial treatment of these lesions. Its use is expected to increase in the near future limiting thus the number of patients that will require conventional open surgery.
Abdominal CT scan showing complete circular calcification of the abdominal aorta.
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Hallisey MJ, Meranze SG, Parker BC, Rholl KS, Miller WJ, Katzen BT, van Breda A: Percutaneous transluminal angioplasty of the abdominal aorta. J Vasc Interv Radiol 1994; 5(5):679–87 Sigwart U, Puel J, Mirkovitch V, Joffre F, Kappenberger L: Intravascular stents to prevent occlusion and restenosis after transluminal angioplasty. N Engl J Med 1987; 316(12):701–06 Morag B, Rubinstein Z, Kessler A, Schneiderman J, Levinkopf M, Bass A: Percutaneous transluminal angioplasty of the distal abdominal aorta and its bifurcation. Cardiovasc Intervent Radiol 1987; 10(3):129–33 Becker GJ, Palmaz JC, Rees CR, Ehrman KO, Lalka SG, Dalsing MC, Cikrit DF, McLean GK, Burke DR, Richter GM et al.: Angioplasty-induced dissections in human iliac arteries: management with Palmaz balloon-expandable intraluminal stents. Radiology 1990; 176(1):31–8 Gunther RW, Vorwerk D, Bohndorf K, Peters I, el-Din A, Messmer B: Iliac and femoral artery stenoses and occlusions: treatment with intravascular stents. Radiology 1989; 172(3):725–30 Gunther RW, Vorwerk D, Antonucci F, Beyssen B, Essinger A, Gaux JC, Joffre F, Raynaud A, Rousseau H, Zollikofer CL: Iliac artery stenosis or obstruction after unsuccessful balloon angioplasty: treatment with a self-expandable stent. AJR Am J Roentgenol 1991; 156(2):389–93 Long AL, Page PE, Raynaud AC, Beyssen BM, Fiessinger JN, Ducimetiere P, Relland JY, Gaux JC: Percutaneous iliac artery stent: angiographic long-term follow-up. Radiology 1991; 180(3):771–78 Palmaz JC, Garcia OJ, Schatz RA, Rees CR, Roeren T, Richter GM, Noeldge G, Gardiner GA, Jr., Becker GJ, Walker C et al: Placement of balloon-expandable intraluminal stents in iliac arteries: first 171 procedures. Radiology 1990; 174(3 Pt 2):969–75 Strecker EP, Liermann D, Barth KH, Wolf HR, Freudenberg N, Berg G, Westphal M, Tsikuras P, Savin M, Schneider B: Expandable tubular stents for treatment of arterial occlusive diseases: experimental and clinical results. Work in progress. Radiology 1990; 175(1):97–102 Cikrit DF, Becker GJ, Dalsing MC, Ehrman KO, Lalka SG, Sawchuk AP: Early experience with the Palmaz expandable intraluminal stent in iliac artery stenosis. Ann Vasc Surg 1991; 5(2):150–55 Martin EC, Katzen BT, Benenati JF, Diethrich EB, Dorros G, Graor RA, Horton KM, Iannone LA, Isner JM, Ramee SR et al: Multicenter trial of the wallstent in the iliac and femoral arteries. J Vasc Interv Radiol 1995; 6(6):843–49 Sapoval MR, Chatellier G, Long AL, Rovani C, Pagny JY, Raynaud AC, Beyssen BM, Gaux JC: Self-expandable stents for the treatment of iliac artery obstructive lesions: long-term success and prognostic factors. AJR Am J Roentgenol 1996; 166(5):1173–79 Palmaz JC, Laborde JC, Rivera FJ, Encarnacion CE, Lutz JD, Moss JG: Stenting of the iliac arteries with the Palmaz stent: experience from a multicenter trial. Cardiovasc Intervent Radiol 1992; 15(5):291–97 Henry M, Amor M, Ethevenot G, Henry I, Amicabile C, Beron R, Mentre B, Allaoui M, Touchot N: Palmaz stent placement in iliac and femoropopliteal arteries: primary and secondary patency in 310 patients with 2-4-year follow-up. Radiology 1995; 197(1):167–74 Murphy TP, Webb MS, Lambiase RE, Haas RA, Dorfman GS, Carney WI, Jr., Morin CJ: Percutaneous revascularization of complex iliac artery stenoses and occlusions with use of Wallstents: three-year experience. J Vasc Interv Radiol 1996; 7(1):21–7 Colapinto RF, Stronell RD, Johnston WK: Transluminal angioplasty of complete iliac obstructions. AJR Am J Roentgenol 1986; 146(4):859–62 Sullivan TM, Childs MB, Bacharach JM, Gray BH, Piedmonte MR: Percutaneous transluminal angioplasty and primary stenting of the iliac arteries in 288 patients. J Vasc Surg 1997; 25(5):829-838; discussion 838–29 Richter GM, Roeren T, Noeldge G, Landwehr P, Allenberg JR, Kauffmann GW, Palmaz JC: [Initial long-term results of a randomized 5-year study: iliac stent implantation versus PTA]. Vasa Suppl 1992; 35:192–93 Diethrich EB, Santiago O, Gustafson G, Heuser RR: Preliminary observations on the use of the Palmaz stent in the distal portion of the abdominal aorta. Am Heart J 1993; 125(2 Pt 1):490–501 Lim MC, Choo M, Tan HC: Stenting of stenosis of the abdominal aorta. Singapore Med J 1995; 36(5):562–65 Long AL, Gaux JC, Raynaud AC, Faintuch JM, Pagny JY, Lacombe P, Fiessinger JN, Relland JY, Beyssen BM: Infrarenal aortic stents: initial clinical experience and angiographic follow-up. Cardiovasc Intervent Radiol 1993; 16(4):203–08
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Hedeman Joosten PP, Ho GH, Breuking FA, Jr., Overtoom TT, Moll FL: Percutaneous transluminal angioplasty of the infrarenal aorta: initial outcome and long-term clinical and angiographic results. Eur J Vasc Endovasc Surg 1996; 12(2):201–06 Mendelsohn FO, Santos RM, Crowley JJ, Lederman RJ, Cobb FR, Phillips HR, Weissman NJ, Stack RS: Kissing stents in the aortic bifurcation. Am Heart J 1998; 136(4 Pt 1):600–05 Scheinert D, Schroder M, Balzer JO, Steinkamp H, Biamino G: Stent-supported reconstruction of the aortoiliac bifurcation with the kissing balloon technique. Circulation 1999; 100(19 Suppl):II295–300 Rosset E, Malikov S, Magnan PE, Poirier M, Valerio N, Ede B, Branchereau A: Endovascular treatment of occlusive lesions in the distal aorta: mid-term results in a series of 31 consecutive patients. Ann Vasc Surg 2001; 15(2):140–47 Laxdal E, Wirsching J, Jenssen GL, Pedersen G, Aune S, Daryapeyma A: Endovascular treatment of isolated atherosclerotic lesions of the infrarenal aorta is technically feasible with acceptable long-term results. Eur J Radiol 2007; 61(3):541–44 Tetteroo E, van der Graaf Y, Bosch JL, van Engelen AD, Hunink MG, Eikelboom BC, Mali WP: Randomised comparison of primary stent placement versus primary angioplasty followed by selective stent placement in patients with iliac-artery occlusive disease. Dutch Iliac Stent Trial Study Group. Lancet 1998; 351(9110): 1153–59 Palmaz JC: Intravascular stenting: from basic research to clinical application. Cardiovasc Intervent Radiol 1992; 15(5):279–84
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SECTION VII Thoracoabdominal aneurysms and dissections
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Thoracoabdominal aneurysms and dissections: current indications and management JF Dowdall, Q Lu, and RK Greenberg
Introduction The introduction of endovascular repair in 1991 revolutionized aneurysm treatment. Endovascular abdominal aortic aneurysm (AAA) repair has been associated with acceptable early and mid-term results in appropriately selected patients. This technique is proven to reduce acute mortality by two-thirds for infrarenal aneurysms greater than 5.5 cm.1,2 However, they require more intensive follow-up and their durability is unproven in the long term.3–5 Given the success of the technique in the abdominal aorta and the relatively high morbidity of open aortic procedures in the thoracoabdominal and thoracic regions there is increasing interest in the use of fenestrated technology in this area.
Interventional treatment for thoracoabdominal aneurysms Up to 50% of abdominal aortic aneurysms are not suitable for conventional endoluminal grafting, often for anatomical reasons6 including compromised proximal neck anatomy. If aneurysms in proximity to or involving important branches are to be treated, clearly the branch vessels have to be preserved. Options include open repair with bypass or reimplantation of involved branches, hybrid procedures with preliminary extraanatomic bypasses to involved branches followed by endovascular stent-graft placement,7 or the use of fenestrated or branched endografts to preserve the involved branches by endovascular stenting (Figure 52.1). Thoracoabdominal aneurysms provide a considerable surgical challenge to the patient as well as presenting the surgeon with a multitude of technical and cognitive challenges that extend through the peri-operative period. Although results of surgical repair of thoracoabdominal aortic aneurysms (TAAA) continue to improve, there remains a high incidence of post-operative renal and neurologic complications, often culminating in death. Paraplegia and paraparesis remain a major cause of morbidity and mortality after extensive TAAA repair. Cross-clamping the proximal descending aorta can contribute to the development of spinal cord ischemia by several mechanisms including distal hypoperfusion and increased CSF pressure.8
Renal failure after TAAA continues to be a significant and potentially lethal complication. Reduced kidney temperature may be associated with renal protection.9 The mortality associated with the conventional open treatment of thoracoabdominal aneurysms ranges from 5 to 34%.10–13 Although some centers have reported consistently low peri-operative mortalities, the mortality in many centers remains discouraging. Given this high mortality, the mortality reduction achieved with endovascular repair thoracoabdominal aneurysms has the potential to be considerably greater than that for large or small infrarenal aneurysms treated in an analogous manner. Aortic aneurysms involving side branches are complex in terms of operative strategies, peri-operative management, and judgment about the appropriateness of intervention. Patients with complex or extensive aneurysms are frequently treated medically and are not offered surgical therapy owing to extreme morbidity and mortality expectations, yet many of these patients ultimately die from rupture. Strategies to preserve the visceral and renal vessels are required if thoracoabdominal endovascular repair is to be possible. Commercially available devices designed to treat infrarenal aortic aneurysms rely upon a stable proximal neck in excess of 15 mm to establish a seal and, with some grafts, fixation. A shorter proximal neck, or one that appears irregular or unhealthy, may be associated with a higher risk of further aortic degeneration, increased incidences of device migration, or late proximal endoleaks.14 The transition to devices that transcend the renal segment with uncovered stents (fenestrated devices) can offer some fixation advantages, but still rely upon the infrarenal neck for a seal. Analysis of fenestrated devices have ensured at least intermediate-term stability with respect to a lack of device migration, allowing safe progression of similar devices into the thoracoabdominal aorta without undue fear of migration inciting late visceral vessel loss.15 The concept of fenestrations is to create holes in a stent-graft and line these up with branch vessels thus allowing the proximal fixation site of the graft to be moved upwards into a more healthy section of the aorta. This improves security of attachment and hemostatic sealing while maintaining perfusion of the branch vessels. Fenestration allows the technology of endovascular grafting to be applied to juxtarenal aneurysms, an area previously only amenable to open surgery which often involved significant risk of renal failure and mesenteric ischemia.16 475
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Figure 52.1 Four-vessel branch graft with branches to celiac, superior mesenteric, and both renal arteries.
The first reports of fenestrated endografting emerged in 1999 and were in animal models using home-made devices.17,18 Most of the centers performing appreciable numbers of fenestrated grafts have now reported their intermediate-term results.15,19,20 The only commercially available fenestrated endograft at present is the Zenith device (Cook, Bloomington, IN). Currently in the US, the device is limited to investigational use but is now available as a commercial device for sale in the European Union, Canada, Australia, and New Zealand. The design is similar to the standard Zenith device with stainless steel Gianturco stents sewn on to a woven polyester graft. There are two main components: a tubular component which contains the fenestrations and a bifurcate component which is similar to the standard Zenith device, with a variety of limb extensions (Figure 52.2). The device comes loaded in the familiar H&L-B introducer system (Figure 52.3) with some significant modifications. On initial unsheathing of the stentgraft it remains constrained by posterior diameter-reducing ties (Figure 52.4), which allows the device to be manipulated partially deployed in the aorta so that the fenestrations can be accurately placed and cannulated. There are also anterior and posterior gold markers as well as gold markers around the fenestrations and scallops to aid in orientation of the device (Figure 52.5). Imaging One of the most important aspects of endovascular repair of any aortic pathology is preoperative planning. This becomes even more important in complex repairs where inaccuracies are less likely to be tolerated. Multidetector row CT scanning technology is now widely available and provides resolution in many cases of down to 1 mm. With such detailed CT scanning the clinician is provided with an extremely large dataset (often images numbering into the thousands), which can be unwieldy. It is therefore vital to have some form of post-processing to deal with these data so that it can be effectively used to
Figure 52.2
Fenestrated device.
determine pathology and plan endografts. This is why a workstation is practically compulsory when it comes to planning complex endografts. The use of a workstation with the availability of centerline of flow analysis (e.g. AquariusWS; Terarecon, San Francisco, CA) has simplified the planning stage of endografting considerably in our practice. Follow-up with high-quality CT and a workstation allows problems to be identified early. The use of surface rendered images in particular with templates designed to identify metal stents allows component relations to be followed and separation to be identified with ease (Figure 52.6).
Figure 52.3
H&L-B introducer system.
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Figure 52.4
longitudinal orientations. One novel concept is to preload the branch with a wire and catheter, thus giving relatively easy access to the branch by simply snaring the preloaded wire. Branch device implantation can be made more difficult by tortuosity and limited space around branches. Forces at branch points, analogous to the situation at bifurcations, result in displacement forces on the entire graft with possibility for migration and failure. Helical branches (Figure 52.8) were developed at the Cleveland Clinic in an attempt to negate some of these factors. The helical design has a larger orifice (similar to a standard vascular end-side anastomosis) and a gentle curve, both of which contribute to reducing the forces on the device. The helical design was created to provide a long overlap zone between the device and the self-expanding stent-graft, as well as alter the direction of the branch in an effort to diminish the tortuosity and risk of kinking. In other respects it performs the same function as other types of directional branch. Endograft technology has the potential to even eliminate the majority of complex open procedures thus limiting mortality and providing a treatment option to patients who have long been deemed “inoperable.” However, designing and implanting a device that will accommodate the visceral vessels of the aorta is an intricate task, and requires that the interventionist is facile with visceral and renal cannulation and intervention. The prosthesis must be able to accommodate branches to the visceral segment of the aorta and maintain the perfusion of critical end organs. These will be dependent on accurate design and precise deployment of the device. Thus, device-related complications that can occur following infrarenal aneurysm repair, such as migration or component separation, will have catastrophic implications if encountered following
Posterior diameter-reducing ties.
Branched grafts Fenestrated grafting requires that the branches to be stented are situated in undiseased segments of aorta so that the fenestrations can be brought into apposition with the aortic wall to prevent leakage. Necks shorter than 3 mm are not suitable for treatment with fenestrated grafts. In a thoracoabdominal aneurysm, by definition the branch vessels are emerging from aneurysmal aorta. In this case formal branch grafts are clearly required. There are two types of branch: reinforced fenestrations and directional branches. In reinforced fenestrations, a fenestration is reinforced with a nitinol ring such that a covered stent-graft can be used to traverse the gap between the device and the branch. Here, the seal is between the nitinol ring and the mating stent-graft and is conceptually similar to fenestrated grafting (Figure 52.7). Generally reinforced branches are used where the aortic lumen is small. Directional branches are used to provide more favorable flow dynamics in aneurysms with large lumens, particularly when the aortic prosthesis will be situated a significant distance from the branch ostia (> 10 mm). These can emerge from the body of the graft in a variety of configurations and at transverse and
(a) Figure 52.5
477
(b)
(a) Anterior gold markers; (b) posterior gold markers.
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Figure 52.6 Surface rendered CT of branch endograft demonstrating stents. Note the four-stent overlap between proximal and distal components.
a repair that incorporates critical aortic branches.21–24 Therefore, treatment of aneurysms of the more proximal aorta is optimally performed with a device that has proven to be stable in the infrarenal segment and will require proficiency on the part of the interventionist in planning and sizing, and in technical issues with implantation of aortic endografts. Despite the obstacles for development of such technologies, successful early- and intermediate-term results have been achieved in a number of centers using endovascular means to treat aneurysms of juxtarenal and thoracoabdominal aorta. In our experience in the Cleveland Clinic branch vessel technology has made it technically feasible to preserve critical end-organ perfusion in the setting of thoracoabdominal (TAA) aneurysms.25 Seventy-three patients with TAAA were treated. Peri-operative mortality was 5% (4/73). One resulted from a myocardial infarction after a planned conduit and iliac endarterectomy required for device access. Two died from cardiovascular complications prior to discharge and one from worsening biventricular failure 7 days post-operatively. Overall survival and freedom from aneurysm-related mortality were 94, 85, and 81%; and 94, 89, and 89% respectively. There were eight endoleaks in total (three type 1 and five type 3, 11%) requiring three early secondary interventions and four after 30 days.26 Device durability issues coupled with an increased incidence of secondary interventions have thwarted the application of endovascular repair in patients who may be candidates for open surgery. It has also been suggested that the follow-up paradigms after endovascular repair are more involved and costly in contrast to open surgery. However, despite the increased requirement for secondary interventions, most of these procedures can be performed with minimal morbidity,27,28 and the simplest procedures have been shown to be superior to open surgery with respect to mortality.1 More complex pathologies (Figure 52.9), including proximal anastomotic aneurysm in
Figure 52.7
Reinforced fenestration.
patients with previous infrarenal repairs (Figure 52.10), have a higher risk associated with open surgery, thus there is a great potential benefit in applying endovascular procedures to these patients. It is likely that the mortality risk-reduction benefit achieved with endovascular repair of large aneurysms (approximately 3% absolute risk reduction in “fit” patients1) will pale in comparison to the potential risk reduction were more proximal aortic aneurysms treated in an analogous manner. This is likely to be the principle reason for the endurance of thoracoabdominal endovascular repair. Secondary interventions and their minimal associated morbidity are unlikely to eclipse the benefits. This technique has the potential for wide dissemination but is has taken quite some time. There are several reasons why this may be so. First, as the devices are not yet FDA approved, each patient must be part of an investigational device exemption in the US. There is also a perception that the technical aspect of inserting a branched endovascular graft is very complex. Available data today suggest that fenestrated and branched endovascular grafting is relatively safe and feasible with a low morbidity and mortality. It is clearly an option for the high-risk patient with compromised proximal neck morphology, and particularly in high-risk patients who undoubtedly have high morbidity and mortality associated with complex aortic repair. The relative proportion of aneurysms involving the renal arteries is small, yet up to 40% of all AAA are precluded from conventional endovascular repair. It is likely that fenestrated techniques will allow for endovascular repair to be conducted in these patients. It is likely that improvements in the technology will go a long way to simplifying the planning and deployment process. Assiduous follow-up is vital as late complications, such as component separation can occur.
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(a)
Figure 52.9 Type 3 thoracoabdominal aneurysm repaired with a four-vessel branch device.
redirected through the tear in the intima into the false lumen. Though commonly quoted, the link between abnormality in the media or cystic medial necrosis and dissection, has been suggested to only occur in a minority of dissections.30 Other theories cite a role for aortic intramural hematoma and penetrating aortic ulcers in the genesis of aortic dissection.31 Frequently histopathology within this area of the aortic wall may reveal deterioration of medial collagen and elastin fibers,
(b) Figure 52.8 (a) Helical branch; (b) surface rendered CT image depicting helical branch in implanted device. White arrow indicates origin of helical branch; red arrow indicates junction with mating graft and green arrow demonstrates end of mating graft. (See Color plates.)
Interventional treatment for thoracic aortic dissections Acute aortic dissection is the most common catastrophe affecting the aorta (occurring three times more commonly than ruptured abdominal aortic aneurysm).29 The mortality for Stanford type B aortic dissections annually is in excess of that reported for ruptured aneurysms. Aortic dissection begins with a tear in the aortic intima, allowing access for the blood column to the aortic intramural space. Blood flow is
Figure 52.10 Type 4 thoracoabdominal repair in a patient with previous infrarenal open repair.
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although clearly aortic dissection can occur in a histologically normal aorta. The tear is usually transverse and does not involve the entire circumference of the aorta. The intimomedial layer is cleaved both longitudinally and circumferentially for a variable distance. The flow of blood through the dissection is usually antegrade within the aortic wall although retrograde dissection can occur. The false lumen is the blood-filled space between the dissected layers of the aortic wall. Depending on the circumference involved, dilation of the false lumen may compress the true lumen. Fenestrations within the intimal flap downstream, often occurring where branch ostia are cleaved off by the dissecting process, lead to sites of re-entry for flow into the true lumen, thus maintaining false lumen patency. The usual pattern for the dissection plane in descending aortic dissection is down the left posterolateral aspect of the aorta. As a result the celiac, superior mesenteric, and right renal arteries typically emerge from the true lumen and the left renal artery arises from the false lumen, but variations in this pattern are often seen. The dissection, through a variety of mechanisms, may obstruct distal perfusion to the aorta or a branch vessel either partially or completely. Classification based on time is: acute dissection (less than 2 weeks), chronic dissection (greater than 2 months), or an intermediate category termed subacute. More commonly, aortic dissection is classified anatomically using one of two systems – DeBakey or Stanford. In the Stanford classification all dissections that involve the ascending aorta are grouped together as type A regardless of where the primary tear occurs. Proponents of this simpler system contend that the clinical behavior of patients with aortic dissection is essentially determined by involvement of the ascending aorta. Critics suggest that individual patients in the type A classification may be quite different from one another and that this often depends upon the distal extent of dissection. The Stanford classification, apart from being the simplest, is also the most clinically relevant. Proximal dissections (type A) usually require emergent graft replacement of the ascending aorta owing to the high risk of cardioaortic complications (aortic rupture, cardiac tamponade, acute aortic insufficiency, or coronary artery ostial occlusion). Distal dissections (type B) should be managed medically unless specific complications such as ongoing pain (presumed to indicate increased risk of acute rupture) or malperfusion syndrome complicate the dissection. Malperfusion syndrome, in which vascular beds are critically compromised, may occur in aortic dissection through different mechanisms. Branch vessel obstruction is often subtotal, waxing and waning in severity after symptom onset. Virtually any aortic branch can be affected and the clinical events will vary depending on the vascular territory involved. Mesenteric vessel involvement is associated with intestinal infarction, whereas subclavian or lower-extremity occlusive events may be better tolerated. Identifying the mechanisms of branch compromise is crucial to formulating effective treatment modalities. Different pathophysiologic mechanisms of ischemia have been proposed.32–35 Immediately after an aortic dissection, the true lumen collapses to a variable degree and the false lumen expands. The first mechanism involves compression of the true lumen within the descending thoracic aorta. This process occurs, most commonly, in the setting of a deep proximal tear with an absence of a large distal fenestration. The mean false lumen pressure increases rapidly, as a result of poor outflow, which in turn results in true lumen
compression that ultimately inhibits flow to the viscera and lower extremities. If a large distal fenestration is present, the false lumen acts in a manner similar to that of a shunt, thus distal ischemia is rarely noted because flow is not compromised. If the dissection plane propagates into a visceral or lower extremity branch, individual branch ischemia may be noted. Although many branch vessel dissections are without sequellae, two types of symptomatic branch vessel obstructions can develop. The obstruction can result from a false lumen that has occluded where thrombus resides at the ostium of the branch vessel (static obstruction), or the flow impingement can occur if the dissection flap functions similar to a mechanical valve oscillating with the pulsatile aortic flow, occluding the visceral vessel ostium during systole, and allowing flow during diastole.34 In this form (dynamic obstruction), the compressed true lumen is unable to provide adequate flow volume or the dissection flap may prolapse into the vessel ostium, which remains anatomically intact. This is the more common mechanism of branch compromise. Despite the plethora of treatments that have been advocated, the consequences of this disease remain devastating. Death occurs as a result of end organ ischemia or aortic rupture. Acute mortality has been most closely associated with ischemic complications, while long-term mortality is traditionally linked to aortic degeneration and late rupture. Ischemic complications have been reported to occur in up to 30% of all cases of distal dissections.36–40 Rupture, on the other hand is less common in the acute setting but still occurs in up to 20% of patients over their lifespan. Although a great deal of progress has been made, reports still reveal exceptionally high mortality rates in the subset of patients that suffer ischemic complications (16–25%).38,40,41 Diagnosis Non-invasive imaging studies will provide the necessary information to select appropriate methods that can be performed safely. Angiography and intravascular ultrasound are valuable tools for determining the extent of dissections, specific luminal characteristics, and branch vessel relationships. Cross-sectional imaging studies including computed tomography (CT) or magnetic resonance imaging (MRI) and transesophageal echocardiography are extremely accurate in terms of locating the proximal fenestration of aortic dissections. Multislice CT scanning has allowed us to obtain neck to pelvis imaging with an accurately timed contrast bolus. Although MR can provide additional physiological data, the loss of resolution in the axial plane diminishes its usefulness for device design. The addition of time as a further dimension to CT scanning allows dynamic images to be viewed gated to certain phases of the cardiac cycle. Dynamic CT scans give clear images of the movement of the aortic wall and septum and may aid in decision making in the future. Imaging studies should be carefully evaluated to determine the extent of the dissection, noting potential sites for proximal and distal fixation of a stent-graft if an endovascular option is entertained. Treatment As many as 40% of patients suffering acute aortic dissection die immediately, most of these from proximal dissection where a mortality of approximately 1% per hour has been
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Thoracoabdominal aneurysms and dissections: current indications and management quoted for untreated patients.42 Therefore the treatment is invariably surgical. Classically, the decision to intervene on a patient suffering from an acute distal aortic dissection is based upon the presence of rupture, ischemia, or radiographic evidence of rapid aortic growth. Otherwise the treatment is usually medical. The lack of ability to define parameters that will predict acute or long-term complications of dissection has frustrated our ability to treat patients prior to the development of extreme physiologic duress. Medical The natural history of untreated distal dissection is less well established but is certainly more benign than proximal ones with a reported initial hospital mortality of up to 10%.43 The target systolic blood pressure typically ranges between 90 and 110 mmHg, primarily relating to both pain control and anti-impulse therapy. In general, there are two goals of blood pressure management in acute dissection. First, aortic wall stress is lowered by decreasing the systolic blood pressure, which reduces the possibility of rupture. Second, shear stress on the aorta needs to be decreased. This is to minimize the rate of rise of aortic pressure to decrease the likelihood of dissection propagation (sometimes called “anti-impulse” therapy). The drugs most commonly used for these purposes are betablockers. Sodium nitroprusside is a direct arterial vasodilator and may be used to rapidly reduce blood pressure but it should be combined with a beta-blocker to reduce the shear stress on the aortic wall. The rate of rise of aortic pressure is increased when sodium nitroprusside is used alone. Betablockers decrease the inotropic state of the myocardium and the heart rate, thus drop the rate of rise of aortic pressure (dP/dt, or change in pressure over change in time). Optimal agents are beta-1-selective blocking agents with a short half-life that can easily be titrated to achieve the target blood pressure. Caution must be exercised when reaching extreme doses of antihypertensive regimens because they may be indicative of significant proximal true lumen compression with impending ventricular failure. Open surgery Proximal dissections Urgent surgical repair of proximal dissection is the treatment of choice for all patients unless major neurologic deficits or peripheral vascular complications of the dissection pose greater overall risk (i.e. visceral ischemia) than the threat of proximal rupture. Immediate surgery is required and there are presently no viable endovascular options. In this review, therefore, we principally concentrate on dissections distal to the left subclavian artery and their management. Distal dissection Threatened or actual rupture is the main indication for acute graft replacement in distal dissection. Unless an extensive aneurysm is present, resection should be confined to the proximal descending aorta, as mortality and spinal cord ischemia risk increase with extensive aortic replacement, particularly in the setting of acute dissection. Open repair of acute distal aortic dissection is a morbid procedure with mortalities ranging in different series from 644 to 69%45 in several large series. Aortic graft replacement may not cure malperfusion
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syndromes depending on the pathophysiology of the ischemic insult. Open surgical techniques include central or focal descending thoracic aortic replacement, diffuse aortic replacement, and for dynamic obstruction (the commonest mode of malperfusion syndrome) fenestration techniques may be appropriate. This involves wide resection of the dissected septum to relieve aortic obstruction by equalizing flow between the true and false lumens. When visceral flow is affected this may have to be extended into the visceral aortic segment, often involving a throacoabdominal approach. Endovascular treatment Interventional techniques include visceral vessel stenting, aortic fenestration, and the use of covered or uncovered stents in the aorta. Although many therapies have attempted to address the acute circumstances the disease creates, the underlying pathophysiology of the disease remains complex and sometimes confusing, which complicates outcome analysis. Most treatments are viewed as partially effective, and leave clinicians with several questions regarding the appropriate management in the acute and chronic settings. Prior to any endovascular intervention, the access site must be chosen. True lumen access is usually preferred and can be obtained from either a brachial or a femoral approach. If the true lumen is significantly compromised, access is best achieved via the femoral vessel with a diminished pulse. Alternatively, access to the true lumen can be established from within the aortic arch using selective catheterization techniques. Regardless of the technique utilized to gain access, specific characteristics of the true and false lumen must be obtained in an effort to demonstrate the proximal entry tear of the dissection, respective true-to-false lumen diameters or area ratios, detectable fenestrations sites, branch vessel involvement, and an assessment of luminal flow for each end organ and the lower extremities. In our experience, the only radiographic factor that was found to be predictive of an ischemic syndrome was the absolute diameter and relative sizes of the true lumen with respect to the false lumen. True-to-false lumen ratios of < 0.4 were more significantly associated with a visceral ischemic syndrome, while ratios > 0.8 were never observed in the setting of ischemia.46 It must be emphasized that this calculation pertains only to acute dissections; chronic dissection ratio calculations were not predictive of ischemia. The confirmation of position within the true or false lumen is facilitated by IVUS scans. Angiography should be performed in the proximal, undissected aorta to fully appreciate intimal flap mobility and any dynamic aortic obstruction, and may be assured by brachial artery cannulation in most cases. If branch vessel compromise is noted than wire access to its true lumen should be obtained. This will allow stent placement. Stent grafting The hemodynamics of aortic dissections must be viewed in the context of cardiovascular physiology and the material properties of the aorta. Uncovered stents do not direct flow away from the false lumen and therefore any benefit of such a stent is related purely to the presence of radial force. The amount of radial force required to collapse the false lumen (which typically has a mean arterial pressure in excess of the
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true lumen) may be greater than the aortic wall strength. It is also difficult to distribute the force equally along the aortic adventitia in the setting of a dissection with irregular flap morphology or tortuosity. Animal studies,47–49 as well as early clinical experiences have reinforced this concept. The aim of aortic stent grafting for aortic dissection, whether acute or chronic, is to cover the entry tear and thereby direct flow into the true lumen thereby depressurizing the false lumen and inducing thrombosis without exposing the patient to the morbidity and mortality of conventional open repair. Proponents of endovascular management cite low rates of paraplegia associated with endovascular repair. In the Cleveland Clinic from 2001 to 2006, paraplegia occurred in 12 of 111 open repairs for chronic distal dissection and none of 41 endovascular repairs. Although the difference reached statistical significance, the comparison may not be accurate owing to differences in the extent of the repair. The endovascular group were also older (mean age 71 vs. 62) and had more extensive co-morbidity with a significantly higher incidence of coronary artery disease and respiratory co-morbidity and a significantly lower GFR. However these are selected nonrandomized patients and it is therefore difficult to make any inferences. Paraplegia can certainly occur after multiple stents but, as in open surgery, may be a less common phenomenon when the stented segment is kept short.50 Endovascular therapy for aortic dissection should ideally be divided into that required in the acute versus the chronic phase. In the acute phase treatment may be required for branch vessel occlusion or impending rupture. There is currently no evidence to support “prophylactic” stenting of uncomplicated aortic dissections in the acute phase. The choice of therapy must center on the degree of true lumen compression and the patency of the false lumen. In the setting of true lumen compression with dissection into branch vessels, critical branches may be protected by the placement of self-expanding stents within them to ensure true lumen supply of blood to the end organ. This is followed by the placement of an endovascular stent graft proximally over the major fenestration to block false lumen inflow, allowing for passive contraction of the false lumen, resulting in true lumen expansion. In the absence of branch vessel dissection, placement of the aortic prosthesis usually suffices. These techniques have the potential to provide the majority of end organs with flow derived from the true lumen. We do not stent the entire dissected aorta in these patients, just the area of the entry tear. There are indications that stent-graft treatment is broadening the indications for repair, particularly in the acute phase. The latest report from the EUROSTAR and UK Thoracic Endograft registry,51 demonstrated that 43% of distal aortic dissection patients were asymptomatic and treated with stentgrafts to prevent late aneurysm formation, an indication that may or may not be validated by future trials. There is currently no evidence to suggest that endovascular repair should be applied to uncomplicated distal dissection. It is difficult, however, to extract meaningful data from the literature as much of the endovascular treatment of dissections is occurring on an ad-hoc basis on selected patients. The INvestigation of STEnt grafts in patients with distal Aortic Dissection (INSTEAD) trial52 is currently following patients treated in European centers. It is the first randomized trial to investigate the role of stent-graft treatment in patients without acute complications
following a distal dissection in comparison to medical therapy alone. Inclusion criteria are patients with distal subacute and chronic dissections without evidence of malperfusion syndrome, and the outcomes, primarily mortality during follow-up, will ascertain whether there is a benefit from early stent-grafting. Secondary, endpoints, such as the late development of thoracoabdominal aneurysms, will also be interesting and the subject of extended follow-up. Endovascular fenestrations Aortic fenestration techniques have a role in select cases. This method of therapy functions by equalizing blood pressure differentials between the true and false lumen, allowing passive equalization of flow channels. Short-term success with observed resolution of ischemia of the mesentery or lower extremities has been reported.38,53 However, it is unlikely that this technique will aid in the prevention of long-term aortic degeneration, given the persistence of flow within both lumens and the obligatory diminished wall thickness of each portion of the aorta. Fenestration of the intimal flap may be performed by several techniques. The goal of fenestration of the dissected intima is to decompress the false lumen, allowing for unrestricted flow in both the true and false lumens. Fenestration is most commonly performed from the smaller (usually true) to the larger (usually false) lumen. One technique uses an endovascular puncture needle to access the false lumen. After contrast injection confirms placement in the opposite lumen, an angioplasty balloon of at least 12–15 mm in diameter and 20–40 mm in length is used to create a fenestration tear. In light of the dramatic and unpredictable alterations in intimal flap anatomy and flow dynamics incurred by overly aggressive fenestration in the visceral aorta, those investigators with the largest series of patients currently recommend that percutaneous fenestration be limited to the distal aorta. Chronic dissections Unlike the emergent situation encountered when intervening on acute dissections, the indication for intervention in chronic dissection generally allows for a well-planned, elective approach. It is carried out principally for aneurysmal degeneration of the dissected aorta and is the reason why patients with aortic dissection should have ongoing surveillance after the acute phase. It is likely that this occurs in at least 20% of cases.30,54 Aneurysms that are the sequelae of chronic dissection tend to be more extensive and occur in younger patients compared with degenerative aneurysms. Given the mortality associated with the open thoracoabdominal repair resulting from chronic dissections, there is a strong desire to develop other treatment methods. However, the dissected aorta often does not have anatomy that allows for a proximal and distal seal with an endovascular prosthesis. Commonly, the dissection extends into the visceral aortic segment where multiple fenestrations between the two lumens exist. These preclude complete exclusion of the false lumen with a conventional endovascular approach and it seems unlikely that partial exclusion of the false lumen will affect aortic growth or rupture in a beneficial fashion. Branched stent-graft technologies are likely to have an important role in the future management
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Conclusion The interventional treatment of thoracoabdominal aneurysms and dissections has changed considerably in the last few years.
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There is now array of potential treatment modalities available to the interventionist. The exact place for some of these remains to be finally determined but it seems likely that given the extensive co-morbidity in many of these patients an interventional strategy will have many advantages. Clear understanding of the pathophysiology of these conditions and the effects of intervention is vital to prevent inappropriate treatment strategies with potential for morbidity.
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Greenhalgh RM, Brown LC, Kwong GP, Powell JT, Thompson SG. Comparison of endovascular aneurysm repair with open repair in patients with abdominal aortic aneurysm (EVAR trial 1), 30-day operative mortality results: randomised controlled trial. Lancet 2004; 364: 843–8 Prinssen M et al. A randomized trial comparing conventional and endovascular repair of abdominal aortic aneurysms. N Engl J Med 2004; 351: 1607–18 Ohki T et al. Increasing incidence of midterm and long-term complications after endovascular graft repair of abdominal aortic aneurysms: a note of caution based on a 9-year experience. Ann Surg 2001; 234: 323–34 Buth J, Harris PL, van Marrewijk C. Causes and outcomes of open conversion and aneurysm rupture after endovascular abdominal aortic aneurysm repair: can type II endoleaks be dangerous? J Am Coll Surg 2002; 194: S98–S102 Zarins CK, White RA, Fogarty TJ. Aneurysm rupture after endovascular repair using the AneuRx stent graft. J Vasc Surg 2000; 31: 960–70 Greenberg RK et al. Endovascular management of juxtarenal aneurysms with fenestrated endovascular grafting. J Vasc Surg 2004; 39: 279–87 Black SA et al. Complex thoracoabdominal aortic aneurysms: endovascular exclusion with visceral revascularization. J Vasc Surg 2006; 43: 1081–9 Coselli JS, LeMaire SA, Conklin LD, Koksoy C, Schmittling ZC. Morbidity and mortality after extent II thoracoabdominal aortic aneurysm repair. Ann Thorac Surg 2002; 73: 1107–15 Coselli JS, Conklin LD, LeMaire SA. Thoracoabdominal aortic aneurysm repair: review and update of current strategies. Ann Thorac Surg 2002; 74: S1881–S1884 Cambria RP et al. Thoracoabdominal aneurysm repair: results with 337 operations performed over a 15-year interval. Ann Surg 2002; 236: 471–9 Coselli JS. Thoracoabdominal aortic aneurysms: experience with 372 patients. J Card Surg 1994; 9: 638–47 Hines GL, Busutil S. Thoraco-abdominal aneurysm resection. Determinants of survival in a community hospital. J Cardiovasc Surg (Torino) 1994; 35: 243–6 Cox GS et al. Thoracoabdominal aneurysm repair: a representative experience. J Vasc Surg 1992; 15: 780–7 Greenberg RK et al. Stent-graft migration: a reappraisal of analysis methods and proposed revised definition. J Endovasc Ther 2004; 11: 353–63 O’Neill S et al. A prospective analysis of fenestrated endovascular grafting: intermediate-term outcomes. Eur J Vasc Endovasc Surg 2006; 32: 115–23 West CA et al. Factors affecting outcomes of open surgical repair of pararenal aortic aneurysms: a 10-year experience. J Vasc Surg 2006; 43: 921–7 Browne TF et al. A fenestrated covered suprarenal aortic stent. Eur J Vasc Endovasc Surg 1999; 18: 445–9 Faruqi RM et al. Endovascular repair of abdominal aortic aneurysm using a pararenal fenestrated stent-graft. J Endovasc Surg 1999; 6: 354–8 Anderson JL, Adam DJ, Berce M, Hartley DE. Repair of thoracoabdominal aortic aneurysms with fenestrated and branched endovascular stent grafts. J Vasc Surg 2005; 42: 600–7 Muhs BE et al. Mid-term results of endovascular aneurysm repair with branched and fenestrated endografts. J Vasc Surg 2006; 44: 9–15 Cao P et al. Device migration after endoluminal abdominal aortic aneurysm repair: analysis of 113 cases with a minimum follow-up period of 2 years. J Vasc Surg 2002; 35: 229–35
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Conners MS III et al. Endograft migration one to four years after endovascular abdominal aortic aneurysm repair with the AneuRx device: a cautionary note. J Vasc Surg 2002; 36: 476–84 Lee JT et al. Stent-graft migration following endovascular repair of aneurysms with large proximal necks: anatomical risk factors and long-term sequelae. J Endovasc Ther 2002; 9: 652–64 Greenberg RK et al. Stent-graft migration: a reappraisal of analysis methods and proposed revised definition. J Endovasc Ther 2004; 11: 353–63 Greenberg RK et al. Beyond the aortic bifurcation: branched endovascular grafts for thoracoabdominal and aortoiliac aneurysms. J Vasc Surg 2006; 43: 879–86 Roselli EE, Greenberg RK, Kathryn Pfaff K. Endovascular treatment of thoracoabdominal aortic aneurysms. J Thorac Cardiovasc Surg 2007; 133(6): 1474–82 Becquemin JP et al. Outcomes of secondary interventions after abdominal aortic aneurysm endovascular repair. J Vasc Surg 2004; 39: 298–305 Verhoeven EL et al. Frequency and outcome of re-interventions after endovascular repair for abdominal aortic aneurysm: a prospective cohort study. Eur J Vasc Endovasc Surg 2004; 28: 357–64 Coady MA, Rizzo JA, Goldstein LJ, Elefteriades JA. Natural history, pathogenesis, and etiology of thoracic aortic aneurysms and dissections. Cardiol Clin 1999; 17: 615–35 Larson EW, Edwards WD. Risk factors for aortic dissection: a necropsy study of 161 cases. Am J Cardiol 1984; 53: 849–55 Coady MA, Rizzo JA, Elefteriades JA. Pathologic variants of thoracic aortic dissections. Penetrating atherosclerotic ulcers and intramural hematomas. Cardiol Clin 1999; 17: 637–57 Chung JW et al. True-lumen collapse in aortic dissection: part II. Evaluation of treatment methods in phantoms with pulsatile flow. Radiology 2000; 214: 99–106 Chung JW et al. True–lumen collapse in aortic dissection: part I. Evaluation of causative factors in phantoms with pulsatile flow. Radiology 2000; 214: 87–98 Williams DM et al. The dissected aorta: part III. Anatomy and radiologic diagnosis of branch-vessel compromise. Radiology 1997; 203: 37–44 Williams DM, LePage MA, Lee DY. The dissected aorta: part I. Early anatomic changes in an in vitro model. Radiology 1997; 203: 23–31 Fann JI et al. Surgical management of aortic dissection during a 30-year period. Circulation 1995; 92: II113–II121 Fann JI et al. Treatment of patients with aortic dissection presenting with peripheral vascular complications. Ann Surg 1990; 212: 705–13 Slonim SM et al. Percutaneous balloon fenestration and stenting for life-threatening ischemic complications in patients with acute aortic dissection. J Thorac Cardiovasc Surg 1999; 117: 1118–26 Slonim SM et al. Aortic dissection: percutaneous management of ischemic complications with endovascular stents and balloon fenestration. J Vasc Surg 1996; 23: 241–51 Cambria RP et al. Vascular complications associated with spontaneous aortic dissection. J Vasc Surg 1988; 7: 199–209 Slonim SM et al. Aortic dissection: percutaneous management of ischemic complications with endovascular stents and balloon fenestration. J Vasc Surg 1996; 23: 241–51 Anagnostopoulos CE, Prabhakar MJ, Kittle CF. Aortic dissections and dissecting aneurysms. Am J Cardiol 1972; 30: 263–73 Elefteriades JA et al. Management of descending aortic dissection. Ann Thorac Surg 1999; 67: 2002–5
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Nienaber CA, Rehders TC, Ince H. Interventional strategies for treatment of aortic dissection. J Cardiovasc Surg (Torino) 2006; 47: 487–96 Leurs LJ et al. Endovascular treatment of thoracic aortic diseases: combined experience from the EUROSTAR and United Kingdom Thoracic Endograft registries. J Vasc Surg 2004; 40: 670–9 Nienaber CA et al. INvestigation of STEnt grafts in patients with type B Aortic Dissection: design of the INSTEAD trial––a prospective, multicenter, European randomized trial. Am Heart J 2005; 149: 592–9 Williams DM, Brothers TE, Messina LM. Relief of mesenteric ischemia in type III aortic dissection with percutaneous fenestration of the aortic septum. Radiology 1990; 174: 450–2 Hollier LH et al. Thoracoabdominal aortic aneurysm repair. Analysis of postoperative morbidity. Arch Surg 1988; 123: 871–5
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SECTION VIII Atherosclerotic renal artery stenosis
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Atherosclerotic renal artery stenosis: epidemiology and pathophysiology KI Paraskevas, DP Mikhailidis, and G Hamilton
Introduction The clinical significance of atherosclerotic renal artery stenosis (ARAS) is its association with hypertension, progressive renal dysfunction, and increased risk for cardiovascular events. ARAS-associated hypertension is often severe, refractory to anti-hypertensive medication, and poorly controlled.1,2 ARAS most often occurs at the ostium or the proximal 2 cm of the renal artery.3 Distal arterial or branch involvement is distinctly uncommon. ARAS usually progresses over time, leading to renal artery occlusion, loss of renal mass, deteriorating renal function, and possibly end-stage renal disease (ESRD).1,2 Regardless of how renal disease is classified (degree of albuminuria or proteinuria, estimated glomerular filtration rate (eGFR), or presence of ESRD, the 10-year mortality associated with severe renal abnormalities is high (107 deaths per 1000 person-years).4 Patients with ESRD requiring dialysis treatment not only have increased morbidity and mortality, but also a decreased quality of life.5 In a study assessing primary causes of ESRD in patients starting dialysis treatment during the period 1991–1997, ARAS was estimated to increase from 1.4% in 1991 to 2.1% in 1997 for all new cases of ESRD.6 Although these numbers are small, one should bear in mind that most ESRD cases are not screened for the presence of renal artery stenoses. Therefore, the presence of atherosclerotic renal disease is likely to be more frequent. A more recent study sought to determine the prevalence of ARAS in patients 45 years of age or older starting renal replacement therapy.7 ARAS was the underlying pathology in 20 of 49 patients (41%) entering a dialysis program. In 13 patients with ARAS, the registered diagnosis of ESRD was hypertension or renovascular disease, or was unknown. These results support other evidence8 suggesting that the incidence of ARAS is under-reported and may also be an important cause of ESRD. Prompt recognition of this disease and application of the proper treatment is therefore crucial to preserve renal function and decrease the risk of progression to ESRD.9
Epidemiology of ARAS Due to the fact that ARAS and ARAS-associated renovascular disease (RVD) may be asymptomatic, their precise epidemiology is not known. Ethnic differences in ARAS epidemiology
have been reported; compared with white patients, black individuals are less likely to have ARAS.6 A number of post-mortem studies attempted to provide an estimate of the prevalence of the disease (Table 53.1). Although a higher incidence of ARAS is reported in early compared with most recent studies, all of them tend to agree that the incidence of ARAS increases with age. An incidence of 74% in autopsy subjects aged > 70 years at the time of death was reported in an early study.10 In another study, the incidence of ARAS almost doubled when autopsy subjects < 55 years were compared with an older (55–64 years) age group (31 vs. 59%, respectively). The incidence became even higher with increased age (73% for adults aged 65–74 years and 86% for aged > 75 years at the time of death).11 These results were verified in a study that determined the prevalence of hemodynamically significant (> 50%) ARAS as a cause of chronic renal failure leading to ESRD.12 Based on echo-color Doppler investigation, percentage positivity for > 50% ARAS was 3.2% in the 50- to 59-year-old group, 20% in the 60- to 69-year-old group and 25% in the > 70-year age group. More recent studies similarly support the concept that the incidence of ARAS increases with age.13–18 ARAS was reported in 11.1%, 18%, and 23% of patients aged 50–59, 60–69, and > 70 years, respectively.17 In another study,18 patients with ARAS (42 of 202) were significantly older than those (160 of 202) without (67.7 ± 10.8 vs. 60.2 ± 10.8 years old for ARAS and non-ARAS patients, respectively, p < 0.001). These results indicate that age is an important predisposing factor for the development of ARAS. In order to determine the incidence of ARAS, claims data from a 5% random sample of the US Medicare population were used to select patients without ARAS (n = 1,085,250).19 These patients were then followed-up for 2 years. The overall incidence of ARAS was 3.7 per 1000 patient-years. The prevalence of clinically manifest ARAS in the US Medicare population was approximately 0.5% overall and 5.5% in those with chronic kidney disease. However, as the authors themselves admitted, this study is likely to have underestimated the true prevalence of the disease because ARAS is often asymptomatic and only patients with symptomatic disease were included. Those with asymptomatic disease and those who died soon after reaching symptomatic stages were not considered. A population-based study of 834 free-living subjects > 65 years old (mean age 77.2 years) living in North Carolina without prior documented kidney disease, indicated that > 60% lumen occlusion (as identified by Doppler ultrasound measurement) 487
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Incidence of ARAS at autopsy
Study
Year
Number of autopsies/characteristic or cause of death of autopsy population
Incidence of ARAS
Holley et al.10 Schwartz et al.11 Sawicki et al.13 Uzu et al.14 Kuroda et al.15 Fujii et al.16
1964 1964 1991 1997 2000 2006
295/unselected 154/unselected 5,194/DM and non-DM 297/MI 346/stroke 346/stroke
53% 24% 4.3% 12% 10.4% 10.4%
DM: diabetes mellitus; MI: myocardial infarction.
was present in 6.8% (57 patients).20 Significant ARAS was unilateral in 50 and bilateral in 7 patients. Of the 64 renal arteries with significant stenosis, 57 kidneys had hemodynamically significant ARAS, while 7 arteries were occluded. ARAS was more common in men than in women (9.1 vs. 5.5%; p = 0.053), and its prevalence did not differ between black and white participants. However, a significant and independent association was demonstrated with increasing age, decreased high-density lipoprotein (HDL) cholesterol and increased systolic blood pressure. The same group recently reported results from a new prospective, population-based study.21 The aim was to estimate the incidence of new, as well as the progression of established ARAS among participants in the Cardiovascular Health Study (CHS). The CHS is a longitudinal, observational, populationbased study of risk factors for coronary heart disease (CHD) and stroke in adults > 65 years of age.22 Of the initial 834 patients, 610 surviving CHS participants were invited for a follow-up assessment. Of these, 119 responded. New hemodynamically significant ARAS was identified in 9 kidneys (incident disease: 8 new renal artery stenosis, 1 new renal artery occlusion). No significant change of prevalent ARAS was found compared with the first examination (mean study interval 8.0 ± 0.8 years). Additionally, no ≥ 60% renal artery stenosis at the first examination progressed to occlusion during this time. Anatomic progression to hemodynamically significant ARAS was observed in 4% of participants during a mean follow-up of 8 years, an annualized progression rate of 0.5% per year. An important limitation of this study is the small number of patients participating in the first study (n = 834)20 and the even smaller number of patients attending the 8-year follow-up (n = 119, or 14.3% of the original cohort). Unfortunately, to date there are no similar studies to verify these results. Thus, there is a need for large-scale trials so that more reliable results are derived before definite conclusions regarding the incidence and rate of progression of ARAS can be drawn. In a series of consecutive reports from the University of Washington,23–26 the rate of ARAS progression to > 60% stenosis during a 3-year follow-up period was recorded. The rate of progression to > 60% stenosis during the follow-up period was 8% for renal arteries that were initially classified as normal and 43% for arteries initially classified as having < 60% stenosis. Incident renal artery occlusions were observed only in arteries previously classified as having > 60% stenosis. The 3-year risk for occlusion among the group was 7%.
In another series,27 the rate of progression varied between 36 and 71%. Only 16% (14 of 85 arteries) progressed to total occlusion over a mean follow-up period of 52 months. However, the rate of progression to total occlusion occurred more frequently (39%) when there was a > 75% ARAS on the initial renal arteriogram. In a study reviewing the causes of ESRD in 683 patients over a 20-year period, 83 patients (12%) had documented ARAS as a cause of ESRD.28 Patients receiving dialysis due to ARAS and RVD had a much poorer prognosis than patients with ESRD due to other causes (median survival: 25 months, 2-, 5-, 10-, and 15-year survival: 56, 18, 5, and 0%, respectively). These results strongly suggest that ARAS should not be considered a benign disorder, but instead a condition associated with increased mortality and morbidity rates. The major problem with ARAS is the widespread atherosclerosis affecting many organs, a fact which makes this condition difficult to treat.29
ARAS, vascular co-morbidity, and risk factors ARAS often coexists with atherosclerotic disease in another arterial bed (Table 53.2).18,29–42 An early study including 395 patients showed that significant (> 50%) ARAS coexisted with abdominal aortic aneurysmal and occlusive disease in 38% and 33% of the patients, respectively.30 Valentine et al.31 verified this high incidence of ARAS in patients with abdominal aortic aneurysms (AAAs) or aorto-occlusive disease. After examining a total of 346 patients with AAA or aortic occlusive disease, they found that almost one third had concomitant significant (> 50%) ARAS. A more recent report produced even more striking results.37 In this study, four of ten patients with aortoiliac aneurysmal or occlusive disease had > 60% unilateral or bilateral ARAS. In addition, several studies support a high incidence of ARAS in patients with peripheral arterial disease (PAD). An early report showed that almost four of ten patients with PAD had concomitant ARAS.30 Another early report documented an even higher incidence; almost one in two patients with PAD had significant ARAS.41 A highly significant correlation between PAD and ARAS has also been reported in other studies.32,38,43 Statin therapy in PAD patients can improve renal function (as assessed by serum creatinine, cystatin C, and
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Studies showing an association between ARAS and vascular disease in other arterial beds
Study
Year
Outcome
Olin et al.30
1990
Swartbol et al.41 Valentine et al.31
1992 1993
Missouris et al.32
1994
Zierler et al.36
1998
Miralles et al.37
1998
Metcalfe et al.38 Weber-Mzell et al.34
1999 2002
Horita et al.35
2002
Reynolds et al.39
2004
Rigatelli40 Park et al.42
2004 2004
Tanemoto et al.18
2005
Tumelero et al.33
2006
Significant (> 50%) ARAS coexisted with AAAs, aorto-occlusive disease, and PAD in 38, 33, and 39% of the cases. ARAS was found in 221 of the 450 patients (49.1%) with PAD. Significant (> 50%) ARAS was detected in 98 of 346 patients (28%) with abdominal aortic aneurysmal or occlusive disease. There was a significant positive association between the presence of ARAS and the severity of PAD (p = 0.00015). Of 127 patients with PAD, 57 (44.9%) had RVD. Severe carotid artery disease and PAD was present in 19% and 21% of 149 ARAS patients. Greater than 50% asymptomatic stenosis in at least one of the internal carotid arteries and > 60% monolateral or bilateral ARAS was detected in 47 (28, 95% CI: 21.2–34.8%) and 67 (39.9, 95% CI: 32.5–47.3%) of 168 patients with aortoiliac aneurysmal or occlusive disease, respectively. ARAS was present in 36.2% (79 of 218) of PAD patients. Significant (> 50%) ARAS was found in 19 of 177 (10.8%) patients with CHD Carotid intima media thickness was significantly greater in patients with than in patients without ARAS (1.07 ± 0.10 vs. 0.84 ± 0.12 mm, p < 0.01). ARAS was found in 8 of 43 (19%) patients with significant thoracic aorta atherosclerotic plaque. There was a strong association between the presence of ARAS and thoracic atherosclerotic plaque (p = 0.02). ARAS was present in 12.5% of CHD patients (14 of 112 patients). ARAS was found in 158 of 1,459 patients (10.8%). Significant CHD was found in 994 of 1,459 patients (68.1%) A total of 134 of 994 CHD patients (13.5%) had concomitant ARAS. Incidence of CHD was significantly higher in patients with vs. patients without > 50% ARAS (19.0 vs. 6.3%, respectively, p = 0.01). The prevalence of CHD in patients with > 70% ARAS compared with those without was 75.9 vs. 45.3%, respectively (p < 0.01).
ARAS: atherosclerotic renal artery stenosis; AAA: abdominal aortic aneurysm; PAD: peripheral arterial disease; RVD: renovascular disease; CI: confidence interval; CHD: coronary heart disease.
calculated creatinine clearance)44,45 but not renal blood flow (as evaluated by duplex indices).45 A significant association between ARAS and CHD has also been reported. The incidence of concomitant ARAS in CHD patients varies between 10.8%34 and 13.5%.46 This correlation also applies to ARAS patients; individuals with significant (> 50%21 or > 70%33) ARAS are at increased risk of having CHD. A retrospective study including 1459 patients investigated the association between ARAS and concomitant vascular disease in other arterial beds.42 All patients undergoing coronary angiography for various indications were routinely screened for ARAS by abdominal aortography. Out of 1459 patients undergoing abdominal aortography, 158 (10.8%) had significant ARAS; 24 of these patients had bilateral stenosis. Significant CHD was found in 994 of the 1459 study population (68.1%). Of these 994 patients, a total of 134 (13.5%) had concomitant ARAS. Multivariate logistic regression showed that extracranial carotid artery stenosis (odds ratio (OR) = 4.89, 95% confidence interval (CI) = 2.57–9.33), p < 0.001), PAD (OR = 4.64, 95% CI = 2.65–9.33, p < 0.001), renal insufficiency (OR = 2.68, 95%
CI = 1.43–5.02, p = 0.002), significant CHD (OR = 2.01, 95% CI = 1.12–3.59, p = 0.019), hypercholesterolemia (OR = 1.92, 95% CI = 1.07–3.43, p = 0.028), hypertension (OR = 1.85, 95% CI = 1.16–2.95), p = 0.01), and age > 60 years (OR = 1.64, 95% CI = 1.01–2.64, p = 0.044) were significant clinical predictors of RVD. An association between ARAS and type 2 diabetes mellitus (T2DM) has also been reported.33,34,46 In an early study based on 5194 autopsies, the incidence of ARAS in the whole study group was 4.3%, but this almost doubled in those with T2DM.15 In addition, T2DM subjects showed a higher frequency of bilateral ARAS than those without T2DM (45 vs. 30%, respectively). Valabhji et al.46 reported that the incidence of ARAS in the 117 patients with T2DM and coexistent hypertension included in their study was 17% thus supporting the association between T2DM and ARAS. Weber-Mzell et al. investigated 177 patients for the presence of ARAS.34 In the majority of the 19 subjects with ARAS, concomitant T2DM was also noted (69 vs. 31%, p = 0.004). The results of a recent study support this interpretation.33 A significant higher
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percentage of patients with > 50% ARAS had concomitant T2DM compared with non-ARAS individuals (16.0% vs. 9.2%, respectively, p < 0.01). Current evidence shows that DM has become the single most important cause of ESRD.47 Approximately 30–40% of all patients with DM will develop nephropathy, and many will progress to ESRD. Given the progressive increase in the incidence of T2DM worldwide, the incidence of ARAS and ESRD will also rise. A number of diseases and conditions therefore appear to predispose to, or co-exist with, ARAS. The Dutch Renal Artery Stenosis Intervention Cooperative (DRASTIC) study developed a scoring system to predict the presence of ARAS.48 The authors analyzed the clinical characteristics of 477 patients with drug-resistant hypertension or an increase in serum creatinine concentration during therapy with angiotensin-converting enzyme (ACE) inhibitors. They then developed a clinical prediction rule to estimate the preangiographic probability of finding such a lesion with accuracy at least equal to radionuclide angiography. Age, symptomatic vascular disease, elevated cholesterol, and the presence of an abdominal bruit appeared as the most powerful predictors of detecting lesions of at least 50% vessel occlusion. The probability of stenosis according to this prediction rule can be used to select patients for renal angiography and assist the identification of patients most likely to have ARAS. In a large study including > 1,000,000 patients, multiple regression analysis showed that the following conditions were significantly (p < 0.05) associated with an OR for ARAS > 1: chronic kidney disease (adjusted OR = 4.61), hypertension (adjusted OR = 4.31), PAD (adjusted OR = 3.96), AAA (adjusted OR = 3.38), CHD (adjusted OR = 2.45), mesenteric ischemia (adjusted OR = 2.38), acute renal failure (adjusted OR = 1.59), cerebrovascular accident or transient ischemic attack (adjusted OR = 1.58), anemia (adjusted OR = 1.19), and cancer (adjusted OR = 1.09). The conclusions reached were that ARAS patients are at a much greater risk of atherosclerotic vascular disease and death than they are of progressing to renal replacement therapy. It also suggested that cardioprotective medication should receive at least as much attention as prevention of renal replacement therapy in affected patients. Overall, ARAS mirrors the extent and severity of atherosclerosis elsewhere. Mortality in patients with ARAS and RVD is related to cardiovascular events, including myocardial infarction, stroke, and CHD. Taken together, these data establish that ARAS is highly prevalent, particularly in diabetics and older patients with hypertension and other atherosclerotic disease, although in many patients it is an incidental finding.
Pathophysiology of ARAS and “ischemic nephropathy” A number of pathophysiological mechanisms may explain the clinical events accompanying ARAS, namely hypertension, progressive renal dysfunction, and ESRD.49 Due to the atherosclerosis-caused reduction of the arterial lumen, blood flow is impaired. This leads to altered pressure gradients and diminished blood flow to the renal parenchyma. These pressure gradients and changes in blood flow have been shown in hemodynamic studies across stenotic lesions to occur when
lumen occlusion exceeds 50%50 (or 70% according to an earlier study51) of the luminal area (“critical” stenosis). As a result of stenosis, hypoperfusion to the distal arterial segment results in inadequate blood supply to the kidneys. This is sometimes below the required levels for autoregulation of blood flow. Reduction of perfusion pressure to the kidney triggers pressor mechanisms to restore renal perfusion, including activation of the renin–angiotensin system and adrenergic stimuli. Further occlusion again reduces perfusion to the renal circulation initiating a repeat cycle of elevation of systemic pressures. Unless interrupted, this sequence can ultimately produce malignant-phase hypertension.52 A study on a porcine model demonstrated that experimental renovascular hypertension due to unilateral renal artery stenosis is accompanied by a progressive increase in systemic oxidative stress.53 As a result of placing an irritating copper stent in the renal artery progressive hyperplasia was stimulated leading to lumen obstruction. Hypertension develops with transient activation of the renin–angiotensin system, followed by a transition to pressor mechanisms that are dependent on oxidative stress. This was shown by measuring systemic plasma levels of prostaglandin F2a (PGF2a)-isoprostanes, an oxidative stress marker, the potential effects of which include a decrease in renal blood flow, sodium retention, and vasoconstriction.54 As experimental renal artery stenosis progressed, renal blood flow was significantly (p < 0.05) reduced, while systemic plasma levels of PGF2 significantly (p = 0.04) increased, in parallel with the increase (29%) in mean arterial pressure (p = 0.005). This was associated with decreased endogenous radical-scavenger levels in both stenotic and contralateral kidneys. The results of this study indicated a role for increased systemic oxidative stress in the pathogenesis of renovascular hypertension and for enhanced renal oxidation-sensitive mechanisms in the pathogenesis of ischemic and hypertensive renal injury. It has been hypothesized that controlling oxidative stress and inflammation may interrupt this cycle of atherosclerosis-induced renal injury in ARAS patients.47 When hypercholesterolemia is combined with ARAS, further magnification of oxidative stress pathways develops. Hypercholesterolemia induces renal endothelial dysfunction, upregulates intrarenal endothelin production and tissue inhibitor of metalloproteinase (TIMP)-1, TIMP-2, and TGF-β systems, and blunts matrix metalloproteinases.55 The overall result favors renal scarring by facilitating extracellular matrix deposition and blunting matrix degradation. The finding that reversal of the hypercholesterolemic diet in a pig model attenuated renal inflammation, normalized the expression of most fibrogenic factors, and regressed vascular and renal fibrosis,55 may provide rationale for the use of lipid-lowering strategies (i.e. statins) to preserve the kidney in hypercholesterolemia. A number of preliminary reports of statin use on renal function have shown promising results.44,45,56–59 An additional effect of hypercholesterolemia includes upregulation of angiotensin-converting enzyme and angiotensin II in the wall of atherosclerotic arteries. This upregulation activates tissue fibrogenic cytokines in the kidney (reflected by increased transforming growth factor-β (TGF-β), nuclear factor κB (NF-κB) pathways, endothelin-1 or adhesion molecules), thereby inducing vascular growth, cell migration, and inflammation.60,61 Furthermore, angiotensin II is a potent stimulus for preoxidant enzymes such as the nicotinamide
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Atherosclerotic renal artery stenosis: epidemiology and pathophysiology adenine dinucleotide phosphate (NAD(P)H) oxidase, leading to an increase in reactive oxygen species (ROS) production (e.g. superoxide anions) and consequently increased oxidative stress.47 ROS can induce vasoconstriction directly, as well as by decreasing nitric oxide (NO) bioavailability, resulting in endothelial dysfunction. In addition, hypertension downregulates endothelial NO synthase activity.56 The decreased bioavailability of NO and increased ROS in hypertension can also activate other mechanisms (e.g. low-density lipoprotein (LDL) oxidation, monocyte, and macrophage chemotaxis, smooth muscle cell proliferation) that can further contribute to the pathogenesis of atherosclerosis. Dietary intervention with antioxidant vitamins E and C in experimental hypercholesterolemic pigs was shown to normalize endothelium-dependent relaxation of the renal artery in vitro and improve the abnormal renal vascular smooth muscle response to exogenous NO.62 Another study showed that genetic variations in cytokine production, a family of important mediators of inflammatory and proliferative response in various disease states including atherosclerosis, could potentially influence the development and course of ARAS.63 Taken together, these studies indicate that multiple pathways, some of which depend on activation of the renin–angiotensin system and oxidative stress, participate in renal parenchymal scarring. Experimental studies on rat kidney demonstrated that repetitive acute insults can produce acute tubular injury capable of recovery after each episode. Nevertheless, these repeated insults are capable of provoking fibrogenic mechanisms that produce tubulointerstitial fibrosis much later, which is no longer reversible.64 Transient episodes of pressure reduction to the post-stenotic kidney may induce long-term, cumulative activation of profibrotic mechanisms. Determinants of the time course for progressive renal injury in ischemic nephropathy are not adequately understood. In principle, the more severe and prolonged the vascular injury, the less likely the kidney is to recover after restoration of blood supply. In most cases, ARAS develops in a setting of pre-existing vascular changes affecting the kidney as a result of aging, and other age-related conditions, such as hypertension, diabetes, dyslipidemia, and so on. Furthermore, due to the widespread nature of the disease, many other organs and systems are also affected.29 In these settings,
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restoration of normal renal function following ARAS-related ischemic injuries is difficult. Indeed, as the SMART (Second Manifestations of ARTerial disease) study indicated,65 nonobstructive atherosclerosis accelerates the decrease of renal size and the increase of serum creatinine with age, implying that deterioration of renal function is likely the result of direct parenchymal compromise, probably provoked by atherogenic factors. This extensive parenchymal disease may not be improved after revascularization thus limiting the benefit accrued from such a procedure. This limitation provides an incentive for early recognition of ARAS and the initiation of measures to help preserve renal function. It is also relevant that any atheroembolism during revascularization may further aggravate renal parenchymal disease. Besides atherosclerosis in the renal artery per se, as well as atherosclerotic disease in other arterial beds (PAD, CHD, AAA, aortic occlusive, and carotid artery disease), a number of emerging vascular risk factors appear to be associated with the development of ARAS. These include homocysteine,66 fibrinogen,67 C-reactive protein,68 uric acid,18,69 and creatinine.70 Finally, smoking is an important risk factor implicated in the development of ARAS.71
Conclusion ARAS is a clinically silent entity that may remain undetected. Besides its association with increased risk for future cardiovascular events,19 ARAS is coupled with grave consequences, namely malignant hypertension, progressive renal dysfunction and possibly ESRD. Although largely under-reported, the incidence of ARAS should progressively increase because of the aging population, as well as the increase in the incidence of T2DM and dyslipidemia. Ischemia-induced oxidative stress and inflammatory pathways cause repetitive insults to the renal arteries and the renal parenchyma. As a result, a vicious cycle develops where the increase in ARAS leads to further ischemic injury to the kidneys and loss of renal mass and vice versa. Hypercholesterolemia is a component of this cycle. Therefore, lipid-lowering therapy (e.g. statins) may interrupt this cycle of renal injury. Blood pressure lowering may also decrease the deterioration in renal function.
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Rigatelli G. Aortoiliac angiography during coronary artery angiography detects significant occult aortoiliac and renal artery atherosclerosis in patients with coronary atherosclerosis. Int J Cardiovasc Imaging 2004; 20: 299–303 Swartbol P, Thorvinger BO, Parsson H et al. Renal artery stenosis in patients with peripheral vascular disease and its correlation to hypertension. A retrospective study. Int Angiol 1992; 11: 195–9 Park S, Jung JH, Seo HS et al. The prevalence and clinical predictors of atherosclerotic renal artery stenosis in patients undergoing coronary angiography. Heart Vessels 2004; 19: 275–9 Rashid ST, Salman M, Agarwal S et al. Occult renal impairment is common in patients with peripheral vascular disease and normal serum creatinine. Eur J Vasc Endovasc Surg 2006; 32: 294–9 Youssef F, Gupta P, Seifalian AM et al. The effect of short-term treatment with simvastatin on renal function in patients with peripheral arterial disease. Angiology 2004; 55: 53–62 Alnaeb ME, Youssef F, Mikhailidis DP et al. Short-term lipid-lowering treatment with atorvastatin improves renal function but not renal blood flow indices in patients with peripheral arterial disease. Angiology 2006; 57: 65–71 Valabhji J, Robinson S, Poulter C et al. Prevalence of renal artery stenosis in subjects with type 2 diabetes and coexistent hypertension. Diabetes Care 2000; 23: 539–43 Chade AR, Lerman A, Lerman LO. Kidney in early atherosclerosis. Hypertension 2005; 45: 1042–9 Krijnen P, van Jaarsveld BC, Steyerberg EW et al. A clinical prediction rule for renal artery stenosis. Ann Intern Med 1998; 129: 705–11 Textor SC, Smith-Powell L. Pathophysiology of renal failure in ischemic renal disease. In: Novick A, Scoble J, Hamilton G, eds. Renal Vascular Disease. London: HBJ College & School Division, 1996: 289–302 Gross CM, Kramer J, Weingartner O et al. Determination of renal artery stenosis severity: comparison of pressure gradient and vessel diameter. Radiology 2001; 220: 751–6 Textor SC, Novick A, Tarazi RC et al. Critical perfusion pressure for renal function in patients with bilateral atherosclerotic renal vascular disease. Ann Intern Med 1985; 102: 309–14 Dzau VJ, Siwek LG, Rosen S et al. Sequential renal hemodynamics in experimental benign and malignant hypertension. Hypertension 1981; 3: I63–8 Lerman LO, Nath KA, Rodriguez-Porcel M et al. Increased oxidative stress in experimental renovascular hypertension. Hypertension 2001; 37: 541–6 Roberts LJ 2nd, Morrow JD. Isoprostanes. Novel markers of endogenous lipid peroxidation and potential mediators of oxidant injury. Ann N Y Acad Sci 1994; 744: 237–42 Chade AR, Mushin OP, Zhu X et al. Pathways of renal fibrosis and modulation of matrix turnover in experimental hypercholesterolemia. Hypertension 2005; 46: 772–9 Zhou MS, Jaimes EA, Raij L. Atorvastatin prevents end-organ injury in salt-sensitive hypertension: role of eNOS and oxidant stress. Hypertension 2004; 44: 182–90 Athyros VG, Mikhailidis DP, Papageorgiou AA et al. The effect of statins versus untreated dyslipidaemia on renal function in patients with coronary heart disease. A subgroup analysis of the GREek Atorvastatin and Coronary heart disease Evaluation (GREACE) study. J Clin Pathol 2004; 57: 728–34 Collins R, Armitage J, Parish S et al. MRC/BHF Heart Protection Study of cholesterol-lowering with simvastatin in 5963 people with diabetes: a randomised placebo-controlled trial. Lancet 2003; 361: 2005–16 Tonelli M, Isles C, Craven T et al. Effect of pravastatin on rate of kidney function loss in people with or at risk of coronary disease. Circulation 2005; 112: 171–8 Chade AR, Rodriguez-Porcel M, Grande JP et al. Mechanisms of renal structural alterations in combined hypercholesterolemia and renal artery stenosis. Arterioscler Thromb Vasc Biol 2003; 23: 1295–301 Chade AR, Rodriguez-Porcel M, Grande JP et al. Distinct renal injury in early atherosclerosis and renovascular disease. Circulation 2002; 106: 1165–71 Stulak JM, Lerman A, Porcel MR et al. Renal vascular function in hypercholesterolemia is preserved by chronic antioxidant supplementations. J Am Soc Nephrol 2001; 12: 1882–91 George S, Ruan XZ, Navarrete C et al. Renovascular disease is associated with low producer genotypes of the anti-inflammatory cytokine interleukin-10. Tissue Antigens 2004; 63: 470–5 Nath KA, Croatt AJ, Haggard JJ et al. Renal response to repetitive exposure to heme proteins: chronic injury induced by an acute insult. Kidney Int 2000; 57: 2423–33
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Bax L, van der Graaf Y, Rabelink AJ et al. Influence of atherosclerosis on age-related changes in renal size and function. Eur J Clin Invest 2003; 33: 34–40 Olivieri O, Friso S, Trabetti E et al. Homocysteine and atheromatous renal artery stenosis. Clin Exp Med 2001; 1: 211–8 Park JS, Park JH, Kang JY et al. Hyperfibrinogenemia is an independent risk factor for atherosclerotic renal artery stenosis. Am J Nephrol 1999; 19: 649–54 Homels MJ, van der Ven AJ, Kroon AA et al. C-reactive protein, atherosclerosis and kidney function in hypertensive patients. J Hum Hypertens 2005; 19: 521–6
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Athyros VG, Elisaf M, Papageorgiou AA et al. Effect of statins versus untreated dyslipidemia on serum uric acid levels in patients with coronary heart disease: a subgroup analysis of the GREek Atorvastatin and Coronary-heart-disease Evaluation (GREACE) study. Am J Kidney Dis 2004; 43: 589–99 Song HY, Hwang JH, Noh H et al. The prevalence and associated risk factors of renal artery stenosis in patients undergoing cardiac catheterization. Yonsei Med J 2000; 41: 219–25 Tobe SW, Burgess E, Lebel M. Atherosclerotic renovascular disease. Can J Cardiol 2006; 22: 623–8
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Radiological assessment of the renal arteries A Al-Kutoubi
Introduction The role of renal artery stenosis (RAS) in the development of hypertension is now well established. The prevalence of the disease ranges between 3 and 5% in hypertensive patients1,2 and is mostly due to ostial stenosis secondary to atherosclerosis in older patients. The incidence of RAS in patients with coronary and peripheral vascular disease is estimated at 20–50%.3–6 Fibromuscular dysplasia (FMD) which affects the different layers of the renal artery accounts for approximately 10–30% of RAS in hypertensive patients7,8 and is generally seen in younger patients, more commonly in females. Other rare causes such as Takayasu’s arteritis and neurofibromatosis are associated with RAS in the pediatric and young age groups. Imaging of renal artery stenosis has seen rapid development over the last two decades with refinement of some of the more advanced imaging methods. It is now possible to achieve a reasonable level of accuracy in screening for RAS by noninvasive methods.
Anatomy The renal arteries arise from the aorta at the level of L1/2. The orientation of the left artery is directly lateral whereas the right artery arises slightly more anterior to the equator of the aorta. This anatomical arrangement influences the angiographic imaging of the arteries and a left anterior oblique projection of 10–15º is often necessary to profile the origin of the right renal artery. The usual diameter of a healthy renal artery is 5–6 mm. Multiple renal arteries exist in up to 30% of people.9 The level of the accessory arteries may start as high as the celiac axis and be as low as the common iliac artery and they tend to have a smaller diameter. Multiple arteries are common in horseshoe kidneys and other cases of ectopia and frequently arise from the anterior aspect of the aorta or iliac arteries. The pattern of division of the renal arteries has been the subject of detailed angiographic studies10 but is probably of little importance in the context of RAS except when the division is very proximal and close to, or affected by, the stenosis in which case the approach for management may be modified. The orientation of the renal arteries is generally either horizontal or slightly inclined inferiorly and is affected by respiratory movement. However occasionally the renal arteries are sloped inferiorly, particularly on the right side, or may change their orientation 494
due to tortuousity or aneurysmal dilatation of the aorta. In cases where surgical bypass or renal transplantation is used the origin of the vessel varies depending on the technique used. In cadaveric renal transplantation the transplant artery is commonly anastomosed end-to-side to the external iliac artery whereas in live-related transplantation the artery is frequently anastomosed end-to-end to the internal iliac artery of the recipient. Many of these issues can now be clarified through the use of cross-sectional imaging prior to intervention and the appropriate approach may then be planned to avoid difficulties. Consequently the choice of the diagnostic or guiding catheter depends on the orientation of the artery, the site and type of stenosis, and also on the planned approach either from the femoral or brachial route.
Imaging methods The ideal imaging modality should be widely available, inexpensive, non-invasive, highly accurate, and reproducible, and can detect and quantify the location, type, and degree of stenosis. It should also provide information on the anatomical arrangements of the major vessels and the presence of disease in the aorta and approach vessels. All available imaging methods have some advantages and disadvantages and none provide all the information required but the combination of duplex ultrasound (US) and magnetic resonance angiography (MRA) provides most of the required information. Reduction in the luminal diameter of the renal artery by 50% is considered by most practitioners as a significant RAS.11 Duplex ultrasound (US) Ultrasound has been traditionally used for assessment of renal size and parenchymal disease and the availability of color Doppler provides a non-invasive method for the evaluation of blood flow without the need of contrast media. The initial emphasis was on detection of stenoses in the main renal arteries. This requires the patient to be fasting for 8 hours prior to the examination to optimize the study. A detailed study typically takes 60–80 minutes. A peak systolic velocity (PSV) of 180–200 cm/second at the point of maximum stenosis is used as the cut-off point to establish an RAS of at least 50%.12 The sensitivity is improved by comparing the velocity to that in the aorta. A ratio of PSV in the renal artery to PSV in the aorta of 3.3 or more is considered indicative of a significant RAS.
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Radiological assessment of the renal arteries The presence of anatomical variants and disadvantageous body habitus influence the results and prevent a successful study in up to 20% of patients.12 The indirect method of assessing the severity of RAS by measuring intrarenal blood flow distal to the stenosis by the “tardus parvus” waveform is easier and quicker to perform, more reproducible, and is now the preferred method. “Tardus” refers to delayed or prolonged early systolic acceleration (acceleration time AT is defined as the elapsed time in seconds from the beginning of the systole to the early systolic peak ESP and is normally more than 0.07 seconds);13,14 and “parvus” to diminished amplitude and rounding of the systolic peak (acceleration index AI indicates the slope of the line from the start of the systole to the ESP in m/second2 and is normally less than 3 m/s2).15 This method may be repeated after intervention to establish a new baseline and functional recovery. Collateral supply in cases of severe stenoses or occlusion and the presence of multiple renal arteries may produce false negative or false positive measurements. The other weaknesses of ultrasound are the interobserver variation and operator dependence. The combination of all the above-mentioned factors reduces the sensitivity of the test in detecting RAS to around 80–90%16 below that of MRA or contrast-enhanced computed tomography angiography (CECTA).11,17 Ultrasound however provides a useful method of assessing the functional significance of RAS in the form of measurement of the resistance index (RI) which is calculated from the Doppler spectrum using the formula: RI = (PSV – EDV)/PSV where is EDV is end diastolic velocity. Measurements are made in different parts of the kidney to ensure full assessment of the perfusion. An RI of more than 80 in patients with RAS is highly sensitive in identifying patients who will not benefit from intervention18 (Figure 54.1). Intravascular ultrasound (IVUS) is thought to provide the most accurate assessment of the pathology in the renal arteries.19,20 However, this test is expensive and not widely available, and suffers from complications related to the catheterization of the artery which are similar to those of angiography. The need to cross the lesion in order to quantify the stenosis adds to the risk. It is a useful adjunct during intervention but certainly not a screening test. Contrast-enhanced computed tomography angiography (CECTA) The advent of multidetector CT scanners (MDCT) has had a significant impact on the imaging of the vascular tree in general and renal arteries in particular. Sixty-four-row MDCTs are becoming commonplace in many countries and scanners with more rapid acquisition have been developed and are becoming commercially available. Even at 16 rows MDCT the imaging of renal arteries is frequently sufficient. Required contrast volumes are affected by the density of the contrast used and speed of acquisition and may be as low as 85 ml of 350 mgI/ml injected at 4–6 ml/second in 64-row MDCT.21 The spatial resolution of CECTA is higher than that of MRA. The typical resolution is 0.6 × 0.6 × 1.0 mm3 which is improved further with the increase of the number of detectors. The diagnostic accuracy of the two methods of atherosclerotic RAS is fairly similar and equally high however.11 The detection of FMD remains a problem particularly in branch stenoses although two published studies
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(a)
(b) Figure 54.1 Segmental renal artery Doppler waveform: (a) normal waveform; (b) tardus parvus waveform. Note the rounded peak and the delay from the start of the upwards stroke to the peak compared to the normal waveform.
indicate equal rate of detection by CECTA to that of angiography in patients who are known to have FMD.22,23 CECTA provides good information about the anatomical issues related to the renal arteries and also the degree of disease in the aorta and the presence of calcification. The images are usually post-processed and presented either as surface-shaded (SSD) or maximum intensity projections (MIP).24 It is possible with modern post-processing methods to measure the cross-sectional diameter of the renal artery at the point of maximum narrowing and compare it with the normal segment to estimate the degree of stenosis (Figure 54.2). The cortical thickness of the kidneys may be used as an indicator of significant RAS. Mounier-Vehier et al.25 found that a cortical thickness threshold of 8 mm identified significant RAS with a sensitivity of 73% and specificity of 93%. The major disadvantages of CECTA are the radiation dose and the nephrotoxicity of contrast. Kemerink et al.26 reported an effective dose of 5.2 mSv in four-row MDCT. The nephrotoxic effect is observed in 3.3% of normal population and is significantly increased in patients with compromised renal function.27 Measures to minimize the nephrotoxic effect include sufficient hydration and the use of low or iso-osmolar non-ionic contrast media.
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Figure 54.2 CECTA of RAS rendered in 3D. The diameter of the artery is measured at three different locations: at the origin, at the stenosis, and distal to the stenosis.
Magnetic resonance angiography (MRA) The ability to image vessels without contrast injection is one of the main advantages of MRA when there is no contraindication to the use of this modality. MRA uses two- and threedimensional time-of-flight (ToF), in which an image is created reflecting the difference in magnetization strength between flowing and stationary spins within the volume of interest; and phase contrast (PC), in which two interleaved acquisitions are applied with different sensitivity to flow velocity. Subtraction of one data set from the other produces an image of only the flowing spins, and these are used to image different parts of the vascular tree. PC studies provide information about the hemodynamics of flow within the artery and loss of signal due to dephasing artifact associated with turbulence generally indicates that the stenosis is significant28–31 whereas ToF sequences provide anatomical information. These sequences require a rather long acquisition time, typically 10 minutes, and are therefore significantly affected by respiratory movement. The sensitivity of MRA is greatly enhanced through faster gradient sequences coupled with the use of contrast injection of gadolinium-based contrast (0.1–0.2 mmol/kg body weight at 2–3ml/second) and timing the examination to the maximum concentration of contrast in the area of interest in the aorta to avoid venous filling. The single-plane breath-hold study takes typically about 20 seconds and provides a resolution of 1.5 × 1.5 × 2 mm3. The images are displayed in MIP format and can be rotated in any axis to improve assessment. Contrast-enhanced MRA (CEMRA) performed on a 1.5 Tesla scanner is now considered the most sensitive non-invasive test for the detection of RAS.32–34 Correlation with the gold standard of digital subtraction angiography (DSA) indicates that CEMRA detects all the stenoses that are diagnosed by angiography11,35,36 and has the added advantage of detecting some others that reduce the lumen in the anteroposterior
Figure 54.3 CEMRA rendered in MIP. There is an infrarenal abdominal aortic aneurysm with significant tortuousity of the aorta. Note FMD of the right renal artery.
Figure 54.4 CEMRA rendered in MIP. There are two arteries to the left kidney and one artery to the right kidney. All three arteries exhibit significant stenoses at their ostia. Mild atheromatous change is noted in the aorta.
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Figure 54.7 DSA of the aorta. Bilateral RAS: The stenosis on the right is eccentric and is probably better approached from the femoral artery as the lumen is superior. The stenosis on the left is irregular with a shelf-like appearance. The curve could be easily negotiated from the femoral approach.
plane which is difficult to detect on the usual angiographic views, because of the possibility of viewing the MRA data in the axial plane. CEMRA provides good imaging of the renal arteries and the aorta and can detect accessory arteries but it does not detect calcification like CECTA. There is a slight tendency to overestimate moderate ostial stenoses on CEMRA35,36 but combining the study with a PC sequence
Figure 54.5 CEMRA rendered in MIP. Severe tapered stenoses of the renal arteries on both sides in a case of Takayasu’s arteritis. Note the enlarged inferior mesenteric artery secondary to stenosis of the superior mesenteric artery.
Figure 54.6 CEMRA rendered in MIP. Oblique view of the pelvic arteries showing a severe stenosis at the origin of the renal transplant artery which is anastomosed end-to-side to the right external iliac artery.
Figure 54.8 Selective DSA of the left renal artery showing a severe bifurcation stenosis. The “kissing balloon” technique was used in this case.
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Figure 54.9 DSA showing total occlusion of the aorta and an irregular tight stenosis of the left renal artery. The right kidney was non-functional. This could only be approached from the brachial or radial routes.
improves the specificity. It is possible to detect FMD in the main arteries but assessment of branch disease is difficult because of respiratory movement37 (Figures 54.3–54.6). It is possible to get an idea about the size of the kidney and renal excretion from the associated image data set. Multiple functional parameters including renal perfusion, GFR, tubular concentration, and transit can be assessed by MRI38 and it is also possible to measure the differential pressure across the stenosis using flow dynamics38,39 but these criteria remain at present research tools and are not routinely used in the clinical context. Another criterion is the time between cortical and medullary perfusion after
Figure 54.10 Aortogram showing an ectopic pelvic kidney with a severe stenosis at the origin of the main artery just above the aortic bifurcation. A brachial or radial approach is preferable in this configuration.
Figure 54.11 Selective DSA of the left renal artery showing severe changes of FMD in the main artery with aneurysm formation. Note the tight focal stenosis in one of the lower pole branches.
Figure 54.12 DSA of the aorta showing a severe stenosis at the origin of an aorto-right renal vascular Y graft. The lateral limb of the graft is patent and anastomosed end-to-side to the distal renal artery which supplies the upper pole. The proximal limb fills but the artery at the point of anastomosis is occluded.
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observed in patients who are in renal failure43 and the decision to use gadolinium in this group of patients should be taken with caution.
Figure 54.13 Captopril renogram (posterior view). The upper half of the picture depicts a renogram showing a slight delay in excretion and washout in the right kidney. The lower half obtained after Captopril shows persistent nephrogram of the right kidney and no excretion confirming significant RAS on the right side.
angiotensin-converting enzyme (ACE) inhibitors, which is prolonged in patients with significant RAS particularly in the setting of normal creatinine.40,41 The use of MRA to evaluate post-intervention results is greatly hampered by artifacts from metal stents that result in loss of signal and make assessment of the site of treatment almost impossible by MRA. Indirect assessment through the measurement of corticomedullary perfusion time may still be possible however, particularly if a baseline study is performed after successful intervention. Gadolinium-based contrast media in the doses used for CEMRA do not have any significant nephrotoxic effect.42 However, nephrotic sclerosing fibrosis (NSF) has been
Digital subtraction angiography (DSA) Angiography remains the gold standard for the diagnosis of RAS but is no longer used for screening of patients with this disease. The only exception is in the context of FMD where finer changes or branch disease may be missed on other imaging modalities and may still be responsible for the patient’s hypertension. Other area where angiography may be required is post-stenting where restenosis is suspected clinically but is not assessable by US or CECTA. In cases where surgical clips interfere with MRA such as transplant artery stenosis. Angiography is invasive and associated with a reported incidence of puncture site and contrast related complications of about 2%.44 The approach for angiography may be femoral or alternatively through the brachial or radial routes. Four- or five-French catheters are routinely used and the shape of the selective catheter is chosen based on the flush aortogram that is done first to identify the anatomy, the normal variants, and associated pathology (Figures 54.7–54.12). Angiographic studies are now reserved for cases where intervention is planned based on non-invasive imaging, particularly CEMRA which provides most of the information that is required. Nephrotoxicity related to contrast media is higher when intra-arterial injections are made.27 Gadolinium-based contrast media45 and CO2 have been used to minimize the risk but it is worth mentioning that the dose of gadolinium that is necessary for good imaging in DSA exceeds that used in CEMRA and reaches nephrotoxic levels. Good images after CO2 require positioning of the patient to take advantage of the buoyancy of the gas which may be difficult because of the location of the renal arteries towards the equator of the aorta.
Suspected atherosclerotic renovascular hypertension Contra–indication to MRA
CECTA
Normal
CEMRA
Duplex US
Normal
Abnormal Abnormal
Abnormal
Normal (Consider CEMRA if strong clinical suspicion)
DSA + intervention
Figure 54.14 Suggested algorithm for investigation of atherosclerotic RAS. Use of different modalities depends on local availability and expertise. CECTA: contrast-enhanced computed tomography angiography; CEMRA: contrast-enhanced magnetic resonance angiography; US: ultrasound; DSA: digital subtraction angiography.
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Table 54.1
Summary of the advantages and disadvantages of the different imaging modalities
Duplex US CEMRA CECTA DSA Captopril renography
Detection of RAS
Calcification
Accessory arteries
Functional assessment
Other pathology
Likelihood of contrast nephrotoxicity
√√ √√√ √√√ √√√ √√
√ × √√√ √√ ×
√ √√√ √√√ √√√ ×
√√ √ √ × √√
√ √√ √√√ √ ×
None Low High High None
Key: ×: not useful; √: fair; √√: good; √√√: very good; US: ultrasound; CEMRA: contrast-enhanced magnetic resonance angiography; CECTA: contrast enhanced computed tomography angiography; DSA: digital subtraction angiograph.
Radionuclide captopril renography Radionuclide quantitative assessment of renal function is a non-invasive method that is commonly used. When an ACE inhibitor such as Captopril is added, the glomerular filtration rate (GFR) of the kidney that has a significant RAS falls by approximately 30% and the contralateral kidney by contrast shows an increase in urine output and GFR. The resultant asymmetry forms the basis for this modality (Figure 54.13). Sensitivity and specificity figures of 85–90% have been published in the literature46 but there are many difficulties associated with the interpretation of these studies in the presence of reduced renal function or bilateral RAS and in patients who are already on ACE inhibitors for treatment of their hypertension. The value of this test is probably more in excluding RAS when the study is totally normal. The improvement in other imaging modalities has relegated this test to the bottom of the list.
Renal vein renin This test is not useful in screening for RAS and does not provide any useful information as to who will benefit from intervention.47 Its value is probably limited to cases where an atrophic kidney is associated with hypertension where nephrectomy is being considered.
Conclusion A suggested algorithm for imaging in atherosclerotic RAS is given in Figure 54.14 and the pros and cons of different imaging modalities are given in Table 54.1.
Acknowledgment I would like to thank Mrs. Lilian Rizk Nabhan for secretarial assistance.
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Leund DA, Hagspiel KD, Angle JF et al. MR angiography of the renal arteries. Radiol Clin N Am 2002; 40: 847–65 Schoenberg SO, Prince MR, Knopp MV et al. Renal MR angiography. Magn Reson Imaging Clin N Am 2001; 6: 351–70 Leiner T, de Haan MW, van Engelshoven JMA et al. Contemporary imaging techniques for the diagnosis of renal artery stenosis. Eur Radiol 2005; 15: 2219–29 Tan KT, Van Beek EJR, Brown PWG et al. Magnetic resonance angiography for the diagnosis of renal artery stenosis: a meta-analysis. Clin Radiol 2002; 57: 617–24 Schoenberg SO, Reiger J, Weber C et al. High-spatial-resolution MR angiography of renal arteries with integrated parallel acquisitions: Comparison with digital subtraction angiography and US. Radiology 2005; 235: 687–98 Vasbinder GB, Nelemans PJ, Kessels AG et al. Accuracy of computed tomographic angiography and magnetic resonance angiography for diagnosing renal artery stenosis. Ann Intern Med 2004; 141: 674–82 Vasbinder GB, Maki JH, Nijenhuis RJ et al. Motion of the distal renal artery during three-dimensional contrast-enhanced breath-hold MRA. J Magn Reson Imaging 1996; 16: 685–96 Grenier N, Basseau F, Ries M et al. Functional MRI of the kidney. Abdom Imaging 2003; 28: 164–75 Schoenberg SO, Knopp MV, Londy F et al. Morphologic and functional magnetic resonance imaging of renal artery stenosis: a multireader tricenter study. J Am Soc Nephrol 2002; 13: 158–69 Niendoorf H, Haustein J, Cornelius I et al. Tolerance data of Gd-DTPA: A review. Eur J Radiol 1991; 13: 15–20 Thomsen HS. Nephrogenic systemic fibrosis: a serious late adverse reaction to gadodiamide. Eur Radiol 2006; 16: 2619–21 Hessel SJ. Complications of angiography and other catheter procedures. In: Abrams HL, ed. Abrams Angiography, third edition. Boston: Little Brown & Co., 1983: 1041–55 Kaufman JA, Geller SC, Waltman AC. Renal insufficiency: gadopentetate dimeglumine as a radiographic contrast agent during peripheral vascular interventional procedures. Radiology 1996; 198: 579–81 Lee VS, Rusinek H, Johnson G et al. MR renography with low-dose gadopentetate dimeglumine: feasibility. Radiology 2001; 221: 371–9 Nally JV, Clarke HS, Grecos GP et al. Effect of Captopril on 99mTCDiethylenetriaminepentaacetic acid renograms in two-kidney, one clip hypertension. Hypertension 1986; 8: 685–93 Vaughn ED Jr, Bubler FR, Laragh JH et al. Renovascular hypertension: renin measurements to indicate hypersecretion and contralateral suppression, estimate renal plasma flow, and score for surgical curability. Am J Med 1973; 55: 402–14
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Endovascular treatment of a renal artery stenosis: techniques, indications, and results M Henry, I Henry, A Polydorou, Ad Polydorou, and M Hugel
Introduction Renal artery stenosis (RAS) occurs frequently and is increasingly recognized thanks to technical improvements in duplex ultrasound, magnetic resonance angiography, CT scans, and systematic angiography during catheterization. RAS are most of the time atheromatous (80% of cases and over 40 years) but can also be due to fibromuscular dysplasia, which may be diagnosed in < 10% of cases, more often in young patients and women, and produces hyperplasia and fibrosis of the intima, the media, or the adventitia. Dysplasia of the media accounts for over two-thirds of cases and produces the typical “string of beads” appearance of the renal artery. Other causes of RAS can be recognized: arteritis (Takayasu’s disease), neurofibromatosis, and radiation. It can also be diagnosed in a renal transplant or a renal bypass graft. The prevalence of RAS is high. Rihal et al.1 found RAS greater than 50% in 19.2% of patients during cardiac catheterization of 297 hypertensive patients. The prevalence of RAS is 35–45% in patients with peripheral vascular disease, 14–24% in patients with cerebrovascular disease, and 7–30% in patients with coronary heart disease.2–4 In patients with renal insufficiency, the incidence of unsuspected RAS is as high as 24%.5 RAS greater than 60% has been reported to be 6.8% in patients older than 65 years of age.6 RAS can result in renovascular hypertension but can also lead to renal insufficiency, cardiac failure with pulmonary edema, and unstable angina. Renovascular hypertension occurs in response to a significant hemodynamic obstruction to renal blood flow. The resultant stimulation of renin and angiotensin production causes systematic hypertension and fluid retention. Atherosclerotic RAS, the most common cause of secondary hyperten-sion, affects fewer than 5% of the general hypertensive population.7 Renovascular disease leads to malignant hypertension in 10–45% of patients. In patients older than 50 years, it is responsible for 5–15% of the renal failure and dialysis-dependent population. Atherosclerotic renovascular disease represents an important public health problem. It has been demonstrated that it increases cardiovascular and all-cause mortality.8–12 There are however several clinical “high-risk” subsets of 502
patients in which atherosclerotic RAS is much more common:13 ● ● ● ● ●
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patients with abdominal bruit (systolic and diastolic); patients with onset of hypertension < 20 years or > 55 years; patients with malignant hypertension; patients with refractory or difficult to control hypertension; patients with azotenia with angiotensin converting enzyme inhibitor (ACE); patients with atrophic kidney; patients with hypertension and associated atherosclerotic disease; elderly patients with renal insufficiency.
The natural history of RAS is to progress over time resulting in renal artery occlusion, loss of renal mass, and a subsequent decrease in renal function. The incidence of progression in angiographic studies ranges from 39 to 49%. Vessels with the most severe stenoses result in total occlusion in 16% of the patients.14–17 In a prospective study of patients with RAS treated medically, progression occurred in 42% (11% progressed to occlusion). Of the patients over a 2-year period16 of particular importance is the realization that progression of RAS and loss of renal function are independent of the ability to medically control blood pressure.18 The treatment of RAS includes medical therapy, endovascular procedure, and surgery. Surgery remains high risk with a 2–7% peri-operative mortality rate, a 17–31% morbidity, deterioration in renal function rate of 11–31%, and reocclusion and restenosis in 5–18%.19–21 Indications for surgery are limited: failed percutaneous approach, hostile aorta infrarenal total occlusion and in association with aortic surgery. Percutaneous transluminal renal angioplasty (PTRA) has become the cornerstone for the therapeutic strategy for addressing RAS and is now the first treatment to be proposed. Balloon angioplasty alone was first proposed but several series reported the successful use of endovascular stents for treating suboptimal angioplasty results and as a primary intervention for atherosclerotic lesions (and particularly ostial lesions) with better immediate and long-term results than with PTA alone.22–27 Primary stenting is now the procedure of choice in most cases of atherosclerotic RAS.
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Endovascular treatment of a renal artery stenosis: techniques, indications, and results Renal angioplasty stenting can be performed by the femoral approach in the majority of the cases. The brachial or radial approach can be used as well. The technique benefits from the improvements of coronary technique: monorail systems for balloons and stents, low-profile devices, and 0.014- or 0.018-inch guidewires allowing direct stenting in 80–90% of the procedures. The procedural success is excellent (98–100%) with a low complication rate, a low restenosis rate, and a long-term patency rate of 85–98%.23–28 Numerous studies reported PTRA with or without stenting as beneficial to blood pressure control and on renal function.18–24,29–54 Renal artery stent placement can significantly slow the progression of renal failure.33 Indications for treatment of RAS are debated but a consensus is now developing that patients with significant RAS (≥ 70% diameter stenosis and/or ≥ 15 mmHg pressure gradients) in the setting of uncontrolled hypertension or renal insufficiency are appropriate candidates for PTRA. Other indications include patients with congestive heart failure (flash pulmonary edema) and unstable angina. Patients on hemodialysis whose parenchyma is supplied by stenotic renal arteries may also be considered candidates for PTRA.13,55–61 The treatment of RAS without hypertension or renal insufficiency is discussed but could be envisaged to preserve the renal function and the renal artery patency, to delay aggravation of the stenosis and the possible manifestation of renal insufficiency.
RAS: diagnosis Screening tests for RAS and associated renovascular hypertension are designed to either image the anatomic obstruction to blood flow in the renal arteries or to assess the physiologic significance of the obstruction. Screening tests designed to detect differences between the kidneys suffer from decreased sensitivity due to the high incidence (approximately 30%) of bilateral RAS. Historically, screening tests for RAS and renovascular hypertension consisted of intravenous urography and random or stimulated measurements of plasma renin activity. While a normal plasma renin level in an untreated patient is useful to rule out the presence of renovascular hypertension, the sensitivity and specificity of an elevated plasma renin level are too low to be useful as a screening test.62 Captopril renal scintigraphy has been proposed to diagnose RAS.63 Initial studies reported sensitivities and specificities as high as 90% for this test in a highly selected population of patients. However, more recent studies have demonstrated a wide variation in the test’s accuracy. The high incidence of bilateral RAS and the difficulty in interpreting the test in patients with renal insufficiency are problematic. This, combined with the high cost and the duration of the examination, makes this test unattractive for routine patient screening.13 Selective renal vein renin measurements have been shown to correlate with reduction in hypertension following revascularization of RAS.64 However, the requirement to perform these tests under controlled circumstances, withdrawing confounding medications, and its insensitivity in
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the presence of bilateral RAS makes it unattractive for routine screening. Multislice, contrast-enhanced spiral CT scans provide three-dimensional reconstructions of the aorta and renal arteries and give reliable data on the status of these arteries, provided that there has been no previous stenting. The presence of a stent in the renal artery may procedure artifacts and errors in the evaluation of residual and in-stent stenosis. While it may be useful in detecting RAS it requires a high volume of contrast media. It has therefore not gained acceptance as a standard screening test, but may be useful in selected patients such as those with suspected aneurysmal disease of the abdominal aorta.12,65,66 Magnetic resonance angiography (MRA) is a promising technique for imaging the abdominal aorta and renal arteries without the use of contrast media.67–69 Artifactual drop out of images at sites of increased turbulence (ostia of the renal arteries) and its relatively high cost continue to be problems in its general application as a screening tool. Renal duplex ultrasound imaging has become the non-invasive diagnostic test of choice over the past several years.70 It does not require any contrast agent, and is relatively inexpensive and easy to perform. Sensitivities and specificities are about 90%. The major drawback to this test is that it requires a skilled technician and good images may be difficult to obtain in some cases (e.g. in obese patients). Renal arteriography remains the gold standard for the diagnosis of RAS. This test can be performed in an outpatient setting. The risk is very low with a good technique. In a nontortuous aorta, the origins of the right and left renal arteries are identified best in a 20º LAO projection. Multiangle angiograms in AP, LAO, and RAO should be done to find the optimal projection and to identify the ostium of both renal arteries very clearly. Conventional angiography sometimes allows better visualization of the lesion and the pathoanatomy compared to DSA techniques. Patients suspected of RAS may undergo diagnostic angiography with intervention at the same time, which is both costeffective and efficient for the management of these patients. It is sometimes difficult to evaluate the exact severity of RAS even with good angiography and different views. The measure of the pressure gradient is useful in this case. Translesional pressure gradients are often measured using end-hole catheters, which can overestimate the gradient secondary to pressure damping.71 A 0.014-inch pressure wire seems better. This pressure wire may also be used in combination with papaverine to evaluate renal artery fractional flow reserve (FFR) in arteries with moderate stenosis. Subramanian72 demonstrated that maximal hyperemia can be achieved with papaverine, and that baseline pressure gradients correlated with FFR. They found a poor correlation between the visual angiographic estimation and hemodynamic measures of lesion severity. Furthermore, the visually estimated lesion severity was 74.9 ± 11.5% while the quantitative vascular angiographic lesion severity was 56.6 ± 10.8%. These techniques allow us to avoid interventions on hemodynamically insignificant stenoses. Percutaneous renal artery revascularization should be reserved for patients with RAS of 70% or greater and a translesional gradient of greater than 15 mmHg.
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Indications and contraindications for endovascular therapy Indications The clinical indications for PTRA are similar to those for surgical revascularization. ●
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Patients with uni or bilateral RAS ≥ 70% and poorly controlled hypertension. For aorto-ostial lesions, restenosis lesions following a suboptimal balloon angioplasty (≥ 30% residual diameter stenosis or dissection) the use of endovascular stents is preferred.38 For patients with fibromuscular dysplasia or renal branch artery lesions, balloon angioplasty with provisional stenting for unsatisfactory results is preferred.73,74 Patients with uni or bilateral RAS ≥ 70% and mild or moderately impaired renal function. Traditional teaching requires that both renal arteries be compromised to cause renal failure, but in the setting of patients with hypertensive renal insufficiency, a unilateral stenosis may serve to protect the affected kidney from hypertensive damage. This kidney might be expected to respond with improved function if the offending RAS is treated.55,56 Patients with uni or bilateral RAS ≥ 70% and recurrent pulmonary edema. Patients with uni or bilateral RAS ≥ 70% and unstable angina. Patients with acute or subacute renal failure or anuria due to total occlusion or subtotal stenosis of one or both renal arteries. Patients with RAS ≥ 70% with a single functioning kidney. Patients on hemodialysis whose parenchyma is supplied by stenotic renal arteries. Indications for patients with isolated RAS without hypertension or renal insufficiency have been debated as a means to preserve renal function. The natural history of atherosclerotic RAS is to progress with time. Timely intervention and correction of these lesions may prevent progressive narrowing of the vessel and loss of renal function.
Contraindications Contraindications to renal angioplasty and stenting are relative and not absolute. The risks versus benefit of the procedure must be weighted. We have to exclude: ●
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Patients with limited life expectancy due to concomitant non-cardiovascular or incurable diseases. Impossible access due to untreatable iliac and subclavian artery occlusion. Surgery is indicated. Patients with atheroembolism disease or a “shaggy” aorta are at increased risk of cholesterol emboli. These patients can now be treated with protection devices. Patients with renal artery aneurysms are at risk of rupture and could be better treated by surgery.
Severe contrast medium intolerance is not a contraindication because alternative contrast media such as carbon dioxide
or gadolinium using the digital subtraction technique exists. Nephrosclerosis is not a contraindication for intervention, as recently demonstrated by Zeller et al.40 PTRA may be proposed even for patients with a resistance index > 0.8.
Renal angioplasty and stenting: techniques Patient preparation, medications, and surveillance A baseline examination is mandatory before the procedure and before discharge. ●
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urea, serum creatinine, creatinine clearance and if possible GFR; blood pressure (BP) evaluation and if possible, ambulatory 24-hour blood pressure monitoring; evaluation of drug history; duplex-scan examination with renal–aortic flow velocity ratio, intrarenal resistance index.
Patients are pretreated with aspirin (100 mg /day), clopidogrel (75 mg/day), or ticlopidine (250 mg/twice a day) beginning with a loading dose the day before the intervention. Generally 5000 IU heparin are administered after placement of the sheath. Although unstudied with PTRA, some operators utilize bivalirudin based on its reliable anticoagulation and decreased bleeding events. The procedural use of glycoprotein II–IIIa inhibitors is currently under investigation. There is currently no indication for their routine use. After the procedure, medication should consist of 100 mg aspirin indefinitively, clopidogrel (75 mg) once a day or ticlopidine (250 mg) twice a day for one month. BP is carefully controlled because of the possibility of subacute BP decrease after renal revascularization and BP medications must be well adjusted. Depending on the patient’s cardiac status, we recommend 2 litres of saline infusion over a 24-hour period for patients with creatinine up to 3 mg/dl in order to work out the contrast medium. In cases of severe renal dysfunction with a serum creatinine greater than 3 mg/dl, we can perform the procedure with gadolinium or carbon dioxide. A careful monitoring of the renal function is mandatory before discharge. Renal duplex scanning is scheduled the day after the procedure, at 6 and 12 months and then annually. Angiography is performed when a restenosis is suspected on the basis of positive clinical and duplex scan finding. We recommend to measure serum creatinine value, and better creatinine clearance at 1 and 6 months, and biannually thereafter. Equipment and operating room This procedure can be performed in any catheterization laboratory. Digital subtraction is not mandatory except for the use of gadolinium or carbon dioxide. During the procedure, we need a careful monitoring of the BP via the access sheath or the guiding catheter using a Y connector. A continuous perfusion of this sheath or guiding catheter is also recommended.
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Endovascular treatment of a renal artery stenosis: techniques, indications, and results Procedure performance Access Femoral approach The femoral access is the easiest access and can be used in the majority of the cases, except in the case of: ●
● ●
Occlusion of pelvic arteries or abdominal aorta. A severe stenosis of pelvic arteries may be dilated before the procedure to facilitate the access. Severe tortuosities of iliac arteries in elderly patients. Acute angle of the renal artery. The brachial approach could be easier but the femoral access is not a contraindication and may be used with the coaxial technique (as described later in this chapter).
We recommend taking the right femoral artery for a right RAS and the left femoral artery for a left RAS. Four techniques may be proposed to perform a PTRA by this way: 1. Technique 1: guidewire technique (Figure 55.1). It is the first technique ever used, and is still used by radiologists but necessitates two puncture sites: (i) one for a pigtail catheter positioned in the abdominal aorta to inject contrast medium and visualize the position of both balloon and stent; (ii) one for catheterization of the renal artery. A 5-French diagnostic catheter (e.g. RDC, Cobra, Sidewinder) is used and the lesion is crossed with a 0.014-to 0.035-inch guidewire, depending on the balloon or on the stent. The diagnostic
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catheter is withdrawn and over the guidewire we advance the balloon stent to treat the lesion. Each step is checked by injection of contrast medium via the pigtail catheter. We do not recommend this technique because of the risks of local complications (two puncture sites), as well as because of the poor guidance of the balloon or stent, and a higher risk of stent-loss or stent malposition. 2. Technique 2: guiding catheter technique (Figure 55.2). This is the present authors’ favorite technique, and is easiest and quickest. Using the Seldinger technique the femoral artery is punctured and a 6- or 7-French sheath, generally 11 cm long, is introduced over a short introducer guidewire. In case of tortuous iliac arteries, a longer sheath (23 cm) is used for a better guidance of catheters and devices. A selective catheterization of the renal artery is then performed through the guiding catheter using a steerable 0.014-, 0.018-, or 0.035-inch guidewire with a flexible tip. The Renal Double Curve (RDC) guiding catheters are the most commonly used (Cordis, Miami, FL; Guidant Advanced Cardiovascular System Inc., Temecula, C; Boston Scientific, Natik, MA). Other guiding catheters could also be proposed: Hockey Stick, Right Judkins, IMA, Amplatz 1, and so on. 3. Technique 3: coaxial technique (Figures 55.3 and 55.4). This technique is used in case of an acutely angled course of the renal artery. A 5-French Simmons or Sidewinder type 1 or 2 diagnostic catheter is placed inside a 7-French
(a)
(b)
(c)
(d)
Figure 55.1 Technique 1: (a) 0.014–0.035-inch guidewire in a diagnostic catheter, and pigtail catheter insertion; (b) diagnostic catheter is withdrawn; (c) predilatation of the stenosis; and (d) stent implantation.
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(a)
(PROTECTED ANGIOPLASTY/STENTING)
(c)
(b)
(d)
Figure 55.2 Techniques 2 and 4: (a) guiding catheter or guiding sheath at the ostium; (b) predilatation of the stenosis; (c) optional guiding catheter or guiding sheath is advanced into the renal artery over the deflated balloon in place; and (d) stent implantation.
RDC guiding catheter. The ostium of the renal artery is cannulated by the diagnostic catheter. A stiff guidewire is placed inside the renal artery after crossing the RAS and the guiding catheter is slowly advanced over the guidewire and the diagnostic catheter and placed at the orifice of the renal artery. The diagnostic catheter is then withdrawn. 4. Technique 4: guiding sheath technique (Figure 55.2). A 6-French device (VISTA BRITE TIP IG, Cordis), available in RDC and hockeystick configuration, combines the traditional sheath with a guiding catheter and is introduced in the artery after placement of a 0.035-inch guidewire with the Seldinger technique. This device allows cannulation of the ostium of the renal artery and the intervention can be performed as with the guiding catheter technique. It is not recommended in case of calcified access arteries because of its smooth tip. Whatever the technique used, we recommend not using hydrophilic guidewires (except to recanalize an occlusion) because of the risk of perforation of the parenchyma and of significant hematoma. The low profile of new renal stent devices (e.g. GENESIS, Cordis; Express, Boston Scientific; RX Herculink Plus, Guidant ACS; Radix, Sorin Biomedica) allows intervention via a 6-French guiding catheter but it is sometimes difficult to inject contrast medium and to have good images to place the stent, so we recommend a 7-French guiding catheter.
The goal of renal artery intervention is to achieve an optimal angiographic and hemodynamic result with minimal manipulation of the renal artery to reduce atheroembolic complications. The “no touch” technique was proposed to minimize atheroembolization. In this technique, a 0.035-inch guidewire is advanced in the abdominal aorta superior to the renal arteries. Over the wire the guide catheter is advanced in proximity to the renal artery. The 0.035-inch wire is then retracted to the soft portion of the wire so that the guide catheter begins to assume its shape and approach the ostium of the renal artery. From this position, a 0.014-inch wire is directed through the guide and into the distal renal artery. The 0.035-inch wire is then removed and the guide catheter is then allowed to gently engage the ostium of the renal artery.71 Brachial approach Both left and right brachial approach can be used. According to the Seldinger technique, a 6- or 7-French sheath is introduced into the brachial artery and the descending aorta is reached with a 5- or 6-French right Judkins, or a multipurpose or Amplatz 1 catheter over a 0.035-inch Terumo stiff J-wire (Terum, Leuven, Belgium). In difficult cases with acute angulation between the subclavian and the aorta, a 5-French Simmons or Sidewinder catheter may be used. The catheter is placed in the abdominal aorta over the Terumo wire, then withdrawn, the Glidewire left in place and over this wire a 6- or 7-French guiding catheter is advanced and placed at the ostium of the renal artery. In some difficult cases and to have a better support, the Terumo wire can be exchanged for a 0.035-inch stiff Amplatz wire. It is important
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(a)
(b)
(c)
(d)
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Figure 55.3 Technique 3: (a) cannulation of renal artery with a Simmons/Sidewinder diagnostic catheter through the guiding catheter, and placement of a 0.018 stiff guidewire into the renal artery; (b) lesion crossed with the diagnostic catheter; (c) guiding catheter advanced over diagnostic catheter and guidewire as the diagnostic catheter is slowly withdrawn; and (d) guiding catheter placed at ostium with a 0.018-inch guidewire – next steps as described for technique 2.
not to cross the lesion and to advance the Glidewire inside the renal artery because of the risk of perforation (same risk as with the femoral approach). Alternatively, a multipurpose shaped guiding-sheath (VISTA BRITE TIPS IG) can be used and placed at the ostium of the renal artery. A long 6-French sheath (90 cm, e.g. Cook, Bjaeverskon, Denmark) can be positioned near the origin of the renal artery after placing a 0.014-inch or 0.018-inch guidewire into the renal artery by a 5-French diagnosis catheter. The technique reduces the sheath size but we do not recommend it because the guidance of the balloon or of the stent device is not as good as with a guiding catheter. Radial Approach Some interventionists recommend this approach.75 This technique is safe and is the same as for coronary procedure. We use a 6-French introducer and a 6-French guiding catheter and long devices (120 cm). Angioplasty technique Lesion crossing RAS is crossed with a 0.014- to 0.035-inch guidewire depending on the stent / balloon device used.
With the new generation of balloons and stents, we prefer to use 0.014- or 0.018-inch stiff guidewires. The stiffness of the 0.018-inch wire enables an optimal guidance of the low profile PTA balloon (3.7-French shaft) like Bypass Speedy, Gazelle Balloons (Boston Scientific), SAVY (Cordis), Submarine Rapido (Invatec Corp., Concessio Brexa, Italy). It is better to use the new monorail balloons and to abandon the old peripheral balloons with their large shafts and necessitating 0.035-inch guidewires. After lesion crossing, the pressure gradient can be measured as mentioned before. Pressure gradient measurements are justified in cases of stenosis, which seems borderline on angiography and to know if the RAS is really significant, or after the procedure to evaluate the residual stenosis. Intravascular ultrasound can also be used but is not indispensable in routine, and is time consuming and expansive. It could also be helpful for borderline stenosis and to know if a residual stenosis is significant or not, as well as to evaluate dissections. Lesion dilatation Two types of lesion should be discussed: ostial and non-ostial lesions.
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Figure 55.4
An example of coaxial technique.
Ostial lesions. It is now well known that all ostial lesions must be stented. A primary direct stenting can be attempted in the majority of the cases (90% of the lesions). However, we recommend to predilate a very tight stenosis (> 90%), as well as tight calcified lesions). We can use either a coronary balloon (3–4 mm in diameter) or a low-profile balloon with a diameter equal to that of the renal artery. We recommend never to overdilate a renal artery because of the risk of renal artery and aortic dissection and the risk of arterial rupture. Standard balloon length is 20 mm. For a short lesion, a balloon of only 10 mm in length can be used (OPTA LP, Cordis). The pressure needed for predilatation depends on the calcification of the lesion. Dilatation time is 10–30 seconds. During the dilatation, it is important to ask the patient whether he suffers from
(a) Figure 55.5
back pain. Pain could mean arterial dissection and risk of renal artery rupture. If the patient feels pain, stop the inflation, deflate the balloon and check quickly the artery with contrast medium. Dissection and rupture of the renal artery may be observed. Non-ostial lesions. We can try to treat these stenoses only by balloon angioplasty and do a provisional stenting in case of residual stenosis, dissection, and so on. We use the same technique as previously described with a balloon diameter equal to that of the renal artery. Stent implantation (Figures 55.5–55.7) Stents are mandatory for atherosclerotic ostial RAS because of better acute and long-term results compared to balloon angioplasty alone. For non-ostial lesions, distal trunk or side-branch stenosis,
(b)
Left ostial renal artery stenosis, angioplasty and stenting: (a) before angioplasty; (b) after stenting.
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(a) Figure 55.6
(b)
Right ostial renal artery stenosis, angioplasty, and stenting.
stent indications depend on the initial balloon/angioplasty results. In fibro dysplastic stenosis, balloon angioplasty alone is sufficient in almost all cases. At the beginning of our experience, we used rigid stents like Palmaz Stents (P 104, P 204). Now we recommend the use of the new generation of balloon-premounted, flexible, low-profile stents, available in diameters from 4 to 7 mm (Genesis, Cordis; Express, Boston; Nir, Boston; Herculink, Guidant; Radix, Sorin). These closed-cell stent designs are preferred, as they provide more radial strength at the renal ostium. Most of the stents allow a monorail technique. If guiding catheter is limited to 6-French, most stent devices can be used up to a balloon diameter of 6 mm. For larger balloon sizes, a 7-French guiding catheter has to be used. After predilatation of the lesions or when we suspect some
Figure 55.7
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difficulties to cross the stenosis with the stent, the technique of “stent protection” or “protected stenting” can be used (Figure 55.8). To this purpose, after predilatation, the guiding catheter tips are pushed carefully over the deflated balloon catheter into the trunk of the renal artery before retrieval of the balloon catheter. This later protects the stent when crossing the lesion but this technique may favor distal embolization. With the new low-profile renal artery stent devices, this technique of stent protection is not indispensable. The tip of the guiding catheter remains at the ostium and the stent is carefully and slowly advanced over the wire, crosses the lesion, and is correctly positioned to cover the stenosis and the ostium. With the intention that the proximal part of the stent should protrude by 1 or 2 mm into the aorta, the guiding catheter is carefully pulled back into the aorta, and the correct
Right ostial renal artery stenosis, angioplasty, and stenting, IVUS.
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Figure 55.8
“Protected renal stenting” with guiding catheter.
stent position checked by contrast injection. Orthogonal views should be employed to confirm proper stent placement. Improper placement of the stent with the ostium uncovered may contribute to restenosis or even stent embolization. If the position of the stent is correct, the stent is deployed. The ostium of the renal artery can subsequently be enlarged with a 1-mm larger balloon catheter but in most of the cases it is sufficient after stent deployment to pull back half of the length of the balloon and to inflate the balloon at higher pressure at the ostium to flare the ostium of the stent in the aorta. Once the stent is well deployed and in good location, the guide catheter can be advanced over the deflating balloon within the lumen of the stent for final angiography. Drug-eluting stents could be implanted in renal arteries with the same technique but their indications are not yet defined and discussed.76,77 In the GREAT study, a sirolimus-eluting Palmaz Genesis stent (Cordis) was compared to a bare Palmaz
Genesis stent. At 6-months follow-up there was a non-significant difference in the restenosis rate: 6.7 versus 14.3%. A decrease in the target lesion revascularization (TLR) rate was reported: 3.8 versus 7.7%. So we can say that there is a trend to a better outcome with drug-eluting stents and could propose the use of these stents for stenting of small renal arteries (= 5 mm in diameter). In these cases we could expect a lower restenosis rate as in coronary circulation. Final result In each case, selective and semi-selective angiograms of the lesion, the adjacent part of the aorta, and the intrarenal arteries should be performed to document the final result and eliminate some complications, such as peripheral embolism, perforation, dissection, and so on, which could require some specific treatments. Since several studies have shown a high incidence of restenosis in the presence of insufficient dilatation78 residual stenosis should not exceed 15%. Weilbull et al.79 suggests that the initial
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Endovascular treatment of a renal artery stenosis: techniques, indications, and results stenosis must be totally eliminated in order for the procedure to be deemed a complete success. Special cases Stenosis at a bifurcation When dealing with stenosis at the bifurcation and short common renal artery, guidewires should be placed in both branches and simple dilatation performed using the kissing balloon technique. If the result is unsatisfactory, then the guide from the minor branch previously dilated should be removed and the major branch stented. The stent mesh should then be crossed by a guidewire to reach the minor branch, the ostium of which should be redilated. When a significant residual stenosis in this branch is observed, or when both branches appear to be of significant diameter, then one may consider inserting a second stent through the neck of the first one to cover both ostia. This angioplasty can be performed with coronary balloons and stent devices via 8- or 9-French guiding catheters or by two approach ways, the brachial and femoral simultaneously. Another technique could be proposed to treat these lesions. A cutting balloon could be used to treat both arteries as we did in some cases with good success. This technique allows stenting to be avoided. The new peripheral cutting balloons have diameters up to 8 mm, which allows treatment of these arteries (Figure 55.9). Multiple stenoses (Figure 55.10) In cases of bilateral RAS, or stenoses of the main renal artery and accessory renal arteries at one side, all lesions can be treated simultaneously if the renal function is not too deteriorated. We have to limit contrast medium injections and to dilute this contrast medium. Heavily calcified ostial lesions In tight, heavily calcified ostial lesions, the Rotablator (Boston Scientific) can be helpful to debulk the ostium. We can use a burr up to 3 mm in diameter, which requires a 9-French guiding catheter. We have performed 17 cases without any significant complications, though the risk of embolization remains. A cutting balloon could also be proposed to treat these lesions. We recommend to never perform a direct stenting, because some lesions are impossible to dilate without previous debulking or pretreatment with a cutting balloon. Restenosis (Figure 55.11) In cases of restenosis, a simple balloon angioplasty can be efficient. Some other techniques could be proposed: ● ●
● ● ● ● ●
cutting balloon; debulking with excimer laser and balloon angioplasty thereafter; balloon angioplasty and new stent implantation; covered stent after new angioplasty; brachytherapy; in the future, drug-eluting stents may be another alternative; surgery could be an option.
Inflammatory disease The lesion is very fibrous, difficult, and sometimes impossible to dilate with a plain balloon. We recommend treating these lesions with a cutting balloon and if the result is unsatisfactory, a stent could be implanted. Before using a cutting balloon, we have treated some lesions with Rotablator and then used balloon angioplasty alone or with stent implantation. We do not recommend practicing
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a direct stenting in these lesions because some of them are undilatable with a balloon alone. Fibromuscular dysplasia (FMD) (Figure 55.12) Fibromuscular dysplasia is generally treated by simple balloon dilatation without stenting. Primary direct stenting should always be avoided. Stenting of FMD lesions is reserved for “bail out” situations and in case of unsatisfactory results. A cutting balloon is also a good option for these lesions. Aneurysms Complex renal aneurysms involving a bifurcation require surgery. Even large neck aneurysms can be thrombosed with a balloon-assisted coil embolization.80 Aneurysms can be excluded with PTFE covered stents or even with stents covered with autologous saphenous vein.81 Renal artery occlusion Recanalization of a renal artery occlusion is generally difficult and challenging and requires very experienced operators. Coronary or peripheral hydrophilic guidewires are used. The risk of arterial perforations and complications is high. Distal protection Techniques and results of RAS under protection will be described in detail in a later chapter. The use of distal protection devices (filters, protection balloons) is a new approach to treat RAS because of the risk of embolization during the procedure, which can lead to renal function deterioration, as we will discuss later in this chapter. The technique has been previously described.82–84 Two types of protection devices can be used: ●
●
Occlusion balloon. The Guardwire system (Medtronic, Minneapolis, MN) is the same as that used for carotid protection (Figures 55.13 and 55.14). Different filters can also be placed in a renal artery, the same filters used for carotid angioplasty.
With the guiding catheter is appropriately positioned, the protection device is carefully advanced across the lesions and positioned 2 or 3 cm beyond the target site. In the majority of the cases crossing the lesion with a protection device is easy and is the same technique as with any guidewire. In a few cases (angulated artery, tight, calcified stenosis) it could be helpful to first place a more supportive “buddy wire” in the renal artery before attempting to cross the lesion with the protection device. In cases of very tight stenosis a predilatation of the lesion with a coronary balloon may also be indispensable before crossing the lesion. With a Percusurge device, the Microseal adapter is attached and the occlusion balloon inflated to occlude the renal artery. On detaching the adapter, the occlusion balloon remains inflated. With a filter it is deployed by carefully removing the delivery sheath. Contrast injection confirms the accurate positioning of the protection device. Angioplasty and stenting of the renal artery can be performed under protection as previously described. After completion of the renal stenting the protection device has to be retrieved. If a Percusurge device is used, after stent deployment the aspiration catheter is advanced over the wire to the level of the lesion and positioned adjacent to the protection balloon. Any debris are removed using a 20-ml syringe connected to the proximal end of this catheter. At least two aspirations are performed. After removing the aspiration catheter, the Microseal adapter is reattached to the GuardWire and the occlusion
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Figure 55.9
Left renal artery stenosis at a bifurcation and angioplasty with cutting balloon.
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Figure 55.10
Bilateral renal angioplasty and stenting.
(a)
(b) Figure 55.11
(a) Bilateral renal artery restenosis; (b) post-redilatation final result.
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Figure 55.12
Fibromuscular dysplasia and angioplasty alone.
Figure 55.13
Bilateral renal artery stenosis.
Figure 55.14
Left renal artery stenosis treated under protection with the Percusurge device.
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Figure 55.15
FiberNet 3D filter.
balloon deflated allowing normal vessel flow. If the angiographic result is satisfactory, the device is removed. With filters, angiographic control is performed after stent deployment. If the result is satisfactory, the filter is withdrawn with the removal sheath. To facilitate protection device withdrawal and prevent it from getting caught on the stent, the guiding catheter is routinely advanced into the stent up its distal end. The aspirated blood or the filters are sent to the laboratory for analysis. In some cases with filters we can observe a slow or zero flow after stent deployment due to a clogged filter. In these cases, there is a stagnant column of blood proximal to the filter. Simply recapturing the filter will result in embolization to the kidney. It is indispensable to do an aspiration proximal to the filter prior to recapture of the device, either with an aspiration catheter or simply with the guiding catheter we can advance close to the filter. Aspiration catheters that can be used include: the Export Catheter (Medtronic), Pronto (Vascular Solutions Inc., Minneapolis, MN), or the Diver (Invatec, Roncadello, Italy). This technique of distal protection has some limitations: ●
●
●
●
●
●
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The distal protection device does not prevent emboli from reaching the kidney during initial catheter manipulation or angiography and during crossing the lesion. The use of distal embolic protection devices may be limited by the renal anatomy and the lack of devices currently available on the market and dedicated for this application. In cases involving large vessels, we have to select carefully the device and to choose one device with a diameter at least equal to the diameter of the renal artery. In cases of early renal artery bifurcation, it is not possible to protect all arteries. The protection device should be placed in the main branch. To place the protection device we need a landing zone after the stenosis of at least 1.5–2.0 mm. One of the major limitations of the filters is the pore size, which in general is greater than 100 µm and allows small particles to go to the kidney.
To overcome some problems encountered with current filters a new filter was recently proposed and is in experiment.
This filter the FiberNet (Lumen Biomedical Inc, Plymouth, MN) consists primarily of polyester fibers located coaxially around the distal tip of a guidewire assembly (Figure 55.15). This filter is soft and conformable. When actuated, it expands radially to fill the vessel providing excellent apposition to the vessel wall. Contained and captured emboli are recovered/ removed both by aspiration through the retrieval catheter and also by retention within the filter fibers when the filter is closed and retracted into the retrieval catheter. Aspiration is achieved through the retrieval catheter using the vacuum syringes to provide suctions. This filter enables the capture of emboli as small as 30/40 µm without compromising the flow through the filter and in our study the number of particles removed appears to be much higher than with other filters. The possibility of suction through the retrieval catheter during device removal is probably one of the major improvements with this device allowing cleaning of the dilated area and of the inner part of the stent. This technique allows aspiration of the debris, which can protrude through the struts of the stents after stent placement and dilatation and which could embolize after the procedure. The maximum diameter of this device is 7 mm, which is enough in most of the cases. The landing zone required to place this filter is shorter than with other devices (about 1 cm). We began the first human study with this new protection device, which seems very promising. Complications Several complications are described as follows. Renal function deterioration ● Transcient contrast nephropathy, which resolves without the need for dialysis. ● Severe deterioration of the renal function. ● Renal failure may be due to an excessive contrast medium injection. A temporary dialysis can solve this problem. The use of diluted, limited amounts of contrast helps limiting the incidences of this type of complication. CO2-assisted PTRA and the use of gadolinum in patients with baseline renal insufficiency prevents this complication from occurring. ● Atheroembolism may lead to renal failure. This could appear rapidly after the procedure but in general appears
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Figure 55.16
Left renal artery rupture after angioplasty in a patient suffering from aortoarteritis and treatment with a covered stent.
3–4 weeks later. This complication may be detected in patients with baseline renal insufficiency, but in patients with normal renal function as well. The use of protection devices should limit these complications.84,85 Renal rupture and perforation (Figure 55.16) The incidence of arterial perforation and rupture is < 1%19,45,86 but delayed rupture can occur up to 24 hours after the procedure. It is important to quickly recognize a renal rupture during the procedure. With simple balloon inflation we may obtain sealing, but it is better to quickly implant a covered stent. Where failure occurs, surgery is mandatory. Hematoma of the kidney may be the consequence of placing a guide in too distal a position, or by using rigid 0.035-inch or slippery hydrophilic guidewires. These wires may easily penetrate the parenchyma. Some hematomas remain asymptomatic and require a strict surveillance associated with several postprocedural echos or CT scan. They usually stabilize after reversal of heparin. Some hematomas are symptomatic, painful, and may occasionally require surgery and even nephrectomy.
In a series of 857 procedures, we had 4 arterial ruptures (0.5%), 3 successfully treated with covered stents, and one treated surgically (no covered stent available at that time). This patient died from myocardial infarction. We also had 2 arterial perforations, 1 due to a hydrophilic guidewire and necessitating surgery (success), 1 due to a normal guidewire leading to a parenchyma perforation, with perinephric hematoma. Coil embolization solved this problem. Pseudoaneurysms These have been reported and have been successfully treated with covered stents. McWilliams87 reported a pseudoaneurysm of the distal renal artery following PTA for ostial stenosis, which was treated with bench surgery and autotransplantation. Dissection Dissection distal to the stent may happen and should be fixed with a second stent. These dissections can lead to occlusions of side branches. Dissections may also appear after balloon
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Figure 55.16, cont’d.
angioplasty and could lead to vessel thrombosis if stents are not implanted (Figures 55.17).
distal embolization. It rarely requires treatment, unless it is very extensive.
Long retrograde dissection Long retrograde dissection of the descending aorta has been described.85 An overdilatation of the ostium can be responsible for this complication.
Stent misplacement and dislodgement These have been described, generally without complications but sometimes with necessary implantation of other stents. A careful positioning of the stent at the ostium is mandatory to avoid protrusion of the stent greater than 2 mm in the aorta. In these cases, it could be difficult to catheterize the renal artery if needed.
Renal artery thrombosis Renal artery thrombosis is rare13,19,40 and may be associated with a lack of appropriate antiplatelet preparation or by insufficient anticoagulation during the procedure. Dissection is the most common cause of arterial occlusion. Local thrombolysis, thromboaspiration, and thrombectomy devices may help to reopen the artery. In our series of 857 procedures, we had just one stent thrombosis during the procedure, rapidly and successfully treated by fibrinolysis (Figure 55.18). Segmental infarction of the kidney Segmental infarction of the kidney may be due to distal artery thrombosis following guide manipulation or to
Spasm of the renal artery Spasm may be seen and responds well to vasodilators. Access site complications Such complications have been reported as after all PTA: pseudoaneurysms, hematomas, hemorrhages, retroperitoneal hemorrhage, arteriovenous fistula, infection, and so on. Procedure-related death This is fortunately rarely reported in published series. In our series we had only one death after renal rupture.
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Figure 55.17
Post-angioplasty dissection and treatment with kissing balloon and stent.
Figure 55.18
Renal artery thrombosis and result after local fibrinolysis.
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Renal Artery Stenting: Procedural and Late Results
Authors
Year
Pts.(n)
Dorros (27) Iannone (34) White (38) Taylor (32) Blum (25) Harden (33) Tuttle (88) Roccha Singh (41) Bakker (68) Henry (23) Isles (Multic. St.) (50) Van de ven (26) Zeller (85) Henry Overall
1995 1996 1997 1997 1997 1997 1998 1999 1999 1999 1999 1999 2004 2006
76 63 100 29 68 32 129 150 106 235 379 42 268 744 2421
Lesions (n)
Primary Success (%)
92 83 133 32 74 32 148 180 120 274 416 42 320 857 2803
Renal angioplasty: results Technical results The primary success rate of the procedure in RAS is high in all published series (Table 55.1). Overall success rate was 98.5%. For Zeller et al.,85 the success rate was 100% in stenosed ostial lesions and 58% in total occlusions. Up to June 2006, we have treated 857 RAS (654 ostial lesions), of which 94.5% were atheromatous. The primary success rate was 99.9%. The restenosis rate at 6 months was = 15% (Table 55.1) and a restenosis is unusual after 1 year. The difference between the various stents used is not statistically significant,85 but there is a significant correlation between the vessel diameter and the restenosis rate. For Zeller et al.,85 the restenosis rate is 14% for vessels of 4 and 5 mm in diameter, 9% for 6 mm and 0% for 7 mm. This vessel diameter seems to be the only independent predictor of restenosis. Restenosis following angioplasty of FMD lesions is usually less than 10%. In our published series23 the restenosis rate was 11.5% for all lesions with no difference between ostial and non-ostial lesions (12 vs. 10.5%), and 17.3% with a vessel diameter = 5 mm, 10% with a vessel diameter = 6 mm. With Palmaz stent, the restenosis rate was 14.3%, and with Medtronic AVE stent, 8.9% (NS). The arterial long-term patency after renal artery stenting is excellent (Table 55.2) with a primary patency between 74 and 86.5% and a secondary patency between 85 and 98.5%.23,25,28,44 Effects on blood pressure (BP) Renal artery stenting of atherosclerotic lesions has been associated with a statistically significant decrease in blood pressure (Table 55.3) and the need for medication during long-term follow-up. About 15–20% of the patients are cured, and 50–60% are improved. In our series,23 19% were cured, 60% improved, and 21% unchanged. The number of drugs decreased from 2.7 before procedure to 1.1 after procedure (p < 0.02).
100 99 99 100 100 100 98 97 98 100 96-100 88 99 99,9 98,5
F.U. (Months)
Restenosis Rate (%)
6 10 8,7 6,7 27 6 8 13 8,5 25 6-12 6 22 36 11,1
25 14 19 16 11 12 14 12 16,9 11 16 14 9,6 11,5 14,7
White et al.38 reported a series of 100 patients. At 6-month follow-up, systolic blood pressure dropped from 173 ± 25 to 147 ± 23 (p < 0.001) and the diastolic blood pressure from 88 ± 17 to 76 ± 12 (p < 0.001). The average number of antihypertensive medications was reduced from 2.6 ± 1 to 2.0 ± 0.9 (p < 0.001). Zeller et al.40 recently reported a series of 340 patients. Systolic, diastolic, and mean blood pressure measurements significantly improved immediately after the intervention (132/72/93 vs. 144/79/102 mmHg at baseline p < 0.0001) and remained improved during follow-up (p < 0.0001). Blood pressure control was improved in 46%, unchanged in 43%, and deteriorated in 11% of the cases. The number of antihypertensive drugs taken before the intervention predicted improved BP control. Impaired BP control was seen in patients with bilateral RAS or patients with a short history of deteriorated renal function. Patients with unilateral intervention, severe nephrosclerosis (resistance index > 0.8) and diabetes mellitus also improved blood pressure control. Recent data from the Renaissance trial demonstrated a significant improvement in systolic hypertension 9 months after PTRA and stenting.52 For Rocha Singh et al.,41 clinical predictors of improved long-term BP control are mean arterial pressure > 110 mmHg and bilateral renal stenosis.
Table 55.2
Renal Artery Stenting: Long-Term Patency
Author
Year
Pts Lesions Max F.U. (n) (n) (Months)
Blum (25) Rodriguez Lopez (44) Henry (23) Zeller (28)
1997 1999
68 108
74 125
60 36
84,5 92,4 74 85
1999 2000
235 143
274 211
108 24
82,8 98,5 86,5 98
F.U = Follow Up PI = Primary Patency PII = Secondary Patency
PI %
PII %
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Table 55.3
Renal Artery Stenting: Effects on Blood Pressure (B.P.) B.P.
Authors
Year
Pts (n)
Dorros (27) Von Knorring (89) Taylor (32) Blum (25) Klow (90) Zuccala (91) Rodriguez (44) Henry (23) Zeller (40) Overall
1995 1996 1997 1997 1998 1999 1999 1999 2004
76 38 29 68 252 99 108 235 340 1245
F.U. (Months) 6 48 6 27 – – – 12 34 18,6
We have to point out that there is actually no randomized study available comparing stenting of severe RAS with medication to prove the superiority of endovascular procedure.92 However, arguing for sole medical therapy for treatment of hypertension in patients with RAS has to take into account the fact that a lot of patients do not take the drugs, which results in inadequate BP control. Furthermore, ACE inhibitors, diuretics, and other antihypertensive drugs may lead to an acute ischemic nephropathy in patients with severe RAS.93 In addition, under medical treatment alone, progressive development of chronic ischemic nephropathy has been described94 and progression of a RAS and loss of renal function are independent of the ability to medically control BP.18 For hypertensive patients with fibromuscular dysplasia or inflammatory diseases, renal angioplasty is the therapy of choice with cured or improved hypertension in 60–92% of the cases.74–95 Effects on renal function According to recent American Heart Association guidelines,96 a slowed decline in renal function is sufficient to support the
Table 55.4
Improved (%)
7 11 – 16 8 8 13 19 43 15,5
52 74 – 62 58 44 55 60 46 56
Year
Pts (n)
Dorros (27) Iannone (34) Taylor (32) Blum (25) Harden (33) Boisclair (51) Paulsen (43) Isles (50) Rodriguez Lopez (44) Henry (23) Rundback (97) Guerrero (47) Allaquaband (98) Haller (99) Zeller (40) Overall
1995 1996 1997 1997 1997 1997 1999 1999 1999 1999 1999 2002 2003 2004 2004
69 63 39 68 32 33 135 379 108 235 45 61 22 261 340 1890
Patients with baseline serum creatinine ≥ 1,5 mg/dl
Total (%) 59 85 50 78 66 52 68 79 89 71,5
claim that renal artery angioplasty is beneficial. Recent studies regarding the effects of peripheral renal angioplasty or stenting on renal function showed that a large percentage of patients seem to benefit from the procedure with a stabilization or improvement in renal function (Table 55.4). Renal stenting in selected patients could slow the progression of renovascular renal failure.33–45 In patients with a normal baseline creatinine level, renal function was mostly preserved.26,33,38,40,85 In a non-randomized study, PTRA improved renal function in 41–43% of patients.52 Blum et al. found no significant change in creatinine independent of baseline renal function.25 White et al.38 in his series of 100 patients found no significant change in the creatinine level. However in 9 of 44 patients with renal insufficiency, creatinine normalized. The effect of PTRA on renal function was demonstrated by La Batatide Alanore et al.54 After following 32 patients who underwent PTRA for a mean of 6 months, split renal function was detected using Captopril renal scintigraphy. The renal function of the treated kidney was found to improve significantly after PTRA. This suggests that PTRA improves the renal function in patients with unilateral RAS.
Renal Artery Stenting: Effect on Renal Function
Authors
*
Controlled (%)
Improved (%) 30 36 33 34 41 23 26 29 25 19 50 34 25,3
Stable(%) 48 46 29 100 34 35 56 48 95,5 67 43 50 23 36 39 53,3
Worse (%) 22∗ 18 38∗ 28∗ 24∗ 21∗ 26∗ 4,5 4 32 31∗ 27∗ 14 27 21,4
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Endovascular treatment of a renal artery stenosis: techniques, indications, and results There are few data on patients with severe renal dysfunction. In Zeller’s series,28,93 renal function improved in 71% of patients with severe renal insufficiency, 21% were unchanged, and 8% deteriorated. In 32%, planned chronic hemodialysis was deferred. In contrast, Pattynama et al.100 showed no improvement 1 year after the procedure in 40 azotemic patients with 61 RAS. In 60% of these patients, renal function was improved or preserved, and in 40% deteriorated. There was no difference found between bilateral and unilateral disease. Despite these generally favorable results, in many published series a decline in renal function was noted in a subset of patients even after successful initial technical results and a good long-term patency of the renal artery. Deterioration in the renal function may be seen in 20–30% of the patients (Table 55.4) or even more. In most of the series this depends on the renal function and the creatinine level at baseline.27,33,43–51 Dorros et al.27 reported a deterioration of the renal function in 47% of the patients with a creatinine level of over 2 mg/dl. Subramanian et al.46 demonstrated a worsening in renal function in 24% of non-diabetic patients and 27% of diabetic patients with renal insufficiency, and Guerrero et al.47 reported similar results in 31% of patients with renal insufficiency. Zeller et al.40,93 recently reported the long-term impact of stent-supported angioplasty on renal function in a series of 340 hypertensive patients. During a mean follow-up of 34 ± 20 months, serum creatinine significantly decreased from 1.45 ± 0.87 to 1.39 ± 0.73 mg/dl (p = 0.048). The renal function was improved in 34% of the patients, remained unchanged in 39%, and deteriorated in 27%. Baseline serum creatinine, bilateral intervention, percentage diameter stenosis, and three-vessel coronary diseases were independent predictors of improved renal function during follow-up. The serum creatinine decrease was not significant in patients with diabetes mellitus. Other reports33,34,39 suggest that only treatment of bilateral severe RAS is beneficial to renal function. In contrast to other series, the highest proportion (36%) of Zeller’s patients with deteriorated renal function was found in the subgroup with normal baseline serum creatinine. However in 90% of these patients, the increase in serum creatinine concentration was within the normal range. The more severe the renal dysfunction was at baseline, the more the patients benefited from the intervention: improved or unchanged mean serum creatinine concentrations were seen in 64% of patients with normal renal function, 82% of patients with moderate renal impairment, and 92% of those with severely impaired renal function. Improvement in renal function was also seen in 37% of the patients with nephrosclerosis and a resistance index of more than 0.8. Watson et al.45 assessed the effect of renal artery stenting on renal function in patients with chronic renal insufficiency (creatinine > 1.5 mg/dl) by comparing the slopes of the regression lines derived from the reciprocal of serum creatinine versus time plotted before and after stent deployment. Before stent deployment, all patients exhibited a negative slope indicating progressive renal insufficiency. After stent deployment the slopes were positive in 18 patients (72%), indicating improvement in renal function; and less negative in 7 patients (28%), indicating a persistence of decline in renal function deterioration (albeit at a lower rate than before the procedure in these 7 patients). Many factors may account
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for this functional deterioration: contrast media-induced nephrotoxicity, progression of concomitant nephrosclerosis, lesion recurrence, hyperperfusion syndrome, glomerular injury, and so on. However atheroembolism during the procedure seems to play an important role. Contrary to the earlier belief that atheroembolization is a “non-issue” during percutaneous angioplasty, there is now growing evidence to indicate that atherosclerotic debris commonly embolizes from lesions in many vascular territories during percutaneous intervention.101 Distal embolization seems to be the root cause of many procedural complications whenever atherosclerotic lesions are treated. Cholseterol atheromatous embolism is an increasingly recognized cause of renal function deterioration, due to instrument manipulation in the aorta and renal arteries, which result in detachment and embolism of atheromatous debris. Hiramoto et al.102 demonstrated that angioplasty and stenting of ex vivo aortorenal atheroma specimens using a 0.018-inch guidewire system was associated with thousands of atheroemboli. Each manipulation of the specimens, including simply advancing the guidewire through the lesion, released thousand of fragments. The number of fragments in each size category increased with decreasing particle size. Positioning and deploying the stent released an additional bolus of fragments similar to that released after balloon angioplasty. All of these fragments are of sufficient size to create vascular occlusions and initiate significant renal parenchyma damage. These authors conclude that the results of angioplasty procedures could be improved by placing distal protection devices to prevent atheroembolization. Even modern techniques and the use of low-profile systems cannot prevent atheroembolism and renal function deterioration, as recently reported by Nolan et al.103 who reported a series of 82 procedures with renal function deterioration in 24% of the patients at 1 year. The true incidence of atheroembolism is uncertain. In the Aspire 2 study, major embolic events occurred in 6.3% of the procedures.104 Many patients can have a silent course because of the large functional kidney reserve, which allows normal serum creatinine values despite a significant decline in total glomerular filtration capacity. Therefore only the most severe cases may be detected, especially in patients with preprocedural renal dysfunction and limited functional reserve. Abnormal serum creatinine may only be observed if 50% of the nephron population is destroyed. Most patients reach a peak serum creatinine level over 3–8 weeks but onset can also be sooner. Atheroembolism can give rise to different degrees of renal impairment but its diagnosis is difficult and the prognosis severe. No specific treatment can be proposed. The main problem is avoiding atheroembolism events during renal intervention. Selection of patients and technical considerations may limit atheroembolism, but protection devices similar to those used for carotid angioplasty are the main technique to avoid renal atheroembolism during renal angioplasty and stenting. Several studies have shown that protection devices with occlusion balloon or filters are efficient to reduce the risk of embolization to the brain, and that these techniques are mandatory in this field and the standard of care.105–107 We postulated that the same technique could be suitable in the management of renal angioplasty and stenting
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to reduce the risk of atheroembolism and reduce the risk of renal function deterioration. We have performed 124 RAS under protection in 105 hypertensive patients with atherosclerotic renal artery stenosis. Nine patients had solitary kidneys and 39 were in renal insufficiency. Different protection devices were used: occlusion balloon (n = 46) and filters (n = 78). In four cases we used the new FiberNet filter with success. With occlusion balloon we removed visible debris in any cases, with filters in 80% of the patients but with the new filter, visible particles were removed in all cases, five times more than with other filters. We had only one acute renal function deterioration probably due to contrast nephrotoxicity in a multivascular patient with severe renal insufficiency. This patient died with multiorgan failure. At 6-month follow-up (91 patients), 69 were stabilized, 21 had baseline renal insufficiency improved, and we had only one RF deterioration (1.1%) in a patient with moderate renal insufficiency. At 2 years (75 patients), 54 patients stabilized, 19 improved, and we had only 2 RF deteriorations (3%). This technique seems promising and the results better than those reported in most of the published data. It is possibly the technique of the future to improve the long-term results of RAS. Almost the same results were recently published by Holden et al.108 They performed 106 RAS in 90 patients with ischemic nephropathy and at a mean follow-up of 18.2 months; RF was improved in 36% of the cases and stabilized in 55%. He reported only 8% progressive decline of RF. Edwards et al.109 more recently used balloon occlusion and an aspiration catheter (Percusurge device) to treat 32 RAS. Ninety-two percent of the patients had renal insufficiency. RF response at 4–6 week follow-up was improved in 50% of the patients and unchanged in 50%. In no patient or after any procedure was RF observed to decline. Fifty-four percent of the patients with RF deterioration were improved. For the authors, the results with this technique of RAS under protection represent a marked improvement in short-term RF response rates compared with previously published experiences. They approximated the short-term results reported after open surgical revascularization and concluded that these data suggest that this technique may prevent RF harm during RAS as a result of atheroembolism and warrants further investigation.
Effects on patient survival Ischemic nephropathy is an important cause of end-stage disease and among hemodialysis patients, those with renovascular disease have the lowest survival and a > 80% 5-year mortality.110–112 We could therefore expect improved survival of patients with renal dysfunction after a successful interventional procedure. Two large series failed to prove a beneficial effect of revascularization on survival of patients with preprocedure severe renal dysfunction. Dorros et al.35 found baseline creatinine concentration > 1.5 mg/dl and bilateral diseases to be predictors for this increased mortality. Eight-five percent of patients with creatinine < 1.5 mg/dl are alive after 4 years and only 36% of those with creatinine = 2 mg/dl are alive after 4 years. Zeller93(9 in a subgroup analysis of 241 consecutive patients (mean follow-up of 27 ± 15 months) found that the cause of death was congestive heart failure or myocardial infarction (73%), stroke (13.5%), and malignant disease (13.5%). The highest mortality rate was found in patients with a serum creatinine concentration > 3 mg/dl (32%) and was significantly lower (p < 0.01) in patients with creatinine of 1.2–3 mg/dl (8%) as well as for patients with creatinine of < 1.2/dl (6%). The predictors for mortality are left ventricular dysfunction, age, diabetes mellitus, and creatinine > 3 mg/dl.
Conclusion Renal artery angioplasty and stenting is the first treatment to be proposed for patients suffering from renal artery stenosis. This procedure is largely performed with very good technical results, good anatomical results, low complication rate, and a good long-term patency. This technique has proven to be beneficial for the preservation of renal function and stabilization or improvement of blood pressure in a large number of patients. Nevertheless the deterioration of renal function after the procedure in 20–30% of the cases may limit the immediate benefits of this technique. Atheroembolism seems to play an important role. Renal angioplasty with protection devices seems a promising technique and might become the standard of care in the future. Larger and randomized studies are awaited to confirm the usefulness of the technique.
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Tuttle KR, Chovinard RF, Webber JT et al. Treatment of atherosclerotic ostial renal artery stenosis with the intravascular stent. Am J Kidney Dis 1998; 32: 611–22 Von Knorring J, Edgren J, Lepantalo M. Long term results of percutaneous transluminal angioplasty in renovascular hypertension. Acta Radiol 1996; 37: 36–40 Klow NE, Paulsen D, Vatne K et al. Percutaneous transluminal renal artery angioplasty using the coaxial technique. Acta Radiol 1998; 39: 594–603 Zuccala A, Zucchelli P. Ischemic nephropathy: diagnosis and treatment. J Nephrol 1998; 11: 318–24 Nordmann AJ, Woo K, Parkes R, Logan AG. Balloon angioplasty or medical therapy for hypertensive patients with atherosclerotic renal artery stenosis? A metaanalysis of randomised controlled trials. Am J Med 2003; 114: 44–50 Zeller T. Percutaneous endovascular therapy of renal artery stenosis. J Endovasc Ther 2004; 11 (suppl. II): II96–106 Caps MT, Zierler RE, Polissar NL et al. Risk of atrophy in kidneys with atherosclerotic renal artery stenosis. Kidney Int 1998; 53: 735–42 Van Bockel JH, Weibull H. Fibrodysplastic disease of the renal arteries. Eur J Vasc Surg 1994; 8: 655–7 Rundback JH, Sacks D, Kent KC et al. Guidelines for the reporting of renal artery revascularisation in clinical trials. American Heart Association. Circulation 2002; 106: 1572–85 Rundback JH, Manoni T, Rozenblit GN et al. Balloon angioplasty or stent placement in patients with azotemic renovascular disease: a retrospective comparison of clinical outcomes. Heart Dis 1999; 1: 121–5 Allaqaband S, Shaikh F, Zaidi S et al. Long term effects of renal artery stengin or renal function in patients with atherosclerotic renal artery stenosis and baseline creatinine of > 2.0 mg/dl (abstract). Am J Cardiol 2003; 92 (suppl.): 54L Haller ST, Kennedy D, Khuder S et al. Acute renal injury with renal artery stenting (abstract). Circulation 2004; 110 (suppl.): III614 Pattynama P, Becker GJ, Brown J et al. Percutaneous angioplasty for atherosclerotic renal artery disease: effect on renal function in azotemic patients. Cardiovasc Intervent Radiol 1994; 17: 143–6 Topol EJ, Yadav JS. Recognition of the importance of embolization in atherosclerotic vascular diases. Circulation 2000; 101: 570–80 Hiramoto J, Hansen KJ, Pan XM et al. Atheroemboli during renal artery angioplasty: an ex-vivo study. J Vasc Surg 2005; 41: 1026–30 Nolan BW, Schermerhom ML, Rowell E et al. Outcomes of renal artery angioplasty and stenting using low-profile systems. J Vasc Surg 2005; 41: 46–52 Rocha Singh K, Jaff MR, Rosenfield K. Evaluation of the safety and effectiveness of renal artery stenting after unsuccessful balloon angioplasty: the Aspire 2 study. J Am Coll Cardiol 2005; 46: 776–83 Henry M, Henry I, Klonaris C et al. Benefits of cerebral protection during carotid stenting with the Percusurge guardwire system: midterm results. J Endovasc Ther 2002; 9: 1–13 Reimers B, Corvaja N, Moshirirs A et al. Cerebral protection with filter devices during carotid artery stenting. Circulation 2001; 104: 12–5 Roubin GS. Carotid angioplasty and stenting under cerebral protection: the standard of care. Presented at the International Congress XV, Scottsdale, February 11–14, 2002 Holden A. Renal angioplasty and stenting with distal protection. Presented at the All That Jazz Meeting, New Orleans, 2005 Edwards MS, Craven BL, Stafford D et al. Distal embolic protection during renal artery angioplasty and stenting. J Vasc Surg 2006; 44: 128–35 Safian RD, Textor SC. Renal-artery stenosis. N Engl J Med 2001; 344: 431–42 Mailloux LO, Napolitano B, Bellucci AG et al. Renal vascular disease causing end-stage renal disease, incidence, clinical correlates, and out-comes: a 20-year clinical experience. Am J Kidney Dis 1994; 24: 622–9 Shannon HM, Gillespie IN, Moss JG. Salvage of the solitary kidney by insertion of a renal artery stent. AJR Am J Roentgenol 1998; 171: 217–22
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Renal angioplasty and stenting under protection devices M Henry, I Henry, A Polydorou, Ad Polydorou, and M Hugel
Introduction Atherosclerotic renovascular disease is increasingly recognized thanks to technical improvements in duplex ultrasound, magnetic resonance angiography, CT scanning, and routine renal angiography during cardiac catheterization, coronary procedures and particularly in hypertensive or multivascular diseased patients. It represents an important public health problem. A renal artery stenosis (RAS) is usually caused by atherosclerosis (80% of cases in patients over 40 years), and in rare cases is due to fibromuscular dysplasia (10% of cases and more often in young patients), arteritis (Takayasu’s disease), neurofibromatosis, or radiation. It can also be diagnosed in a renal transplant or in a renal bypass graft. The prevalence of RAS is high. Rihal et al. found RAS greater than 50% in 19.2% of patients during cardiac catheterization of 297 hypertensive patients.1 The prevalence of RAS is 35–45% in patients with peripheral vascular disease, 14–24% in patients with cerebrovascular disease, and 7–30% in patients with coronary heart disease.2–4 In patients with renal insufficiency, the incidence of unsuspected RAS is as high as 24%.5 RAS greater than 60% has been reported to be 6.8% in patients older than 65 years of age.6 The natural history of RAS depends on its etiology. Atherosclerotic RAS as well as renal artery stenosis due to Takayasu’s arteritis have a high tendency to progress with time, resulting in renal artery occlusion, loss of renal mass, and a subsequent decrease in kidney function. In the vessels with the most severe atherosclerotic stenoses, the result is total occlusion in 16% of the patients.7–11 On the other hand, renal artery stenoses due to fibromuscular dysplasia rarely tend to progress to occlusion.12,13 Atherosclerotic RAS can result in renovascular hypertension (secondary hypertension) and accounts for 1–5% of all cases of hypertension.14,15 Autopsies of subjects known to be hypertensive have revealed a substantially higher incidence (38–86%) of anatomic lesions in the renal arteries. Even normotensive subjects have a higher incidence of lesions (7–10%) in autopsy series. These data show that the presence of anatomic lesions, even severe stenoses, does not lead to hypertension in all cases and does not imply that hypertension, when present, is caused by the stenosis.13 Indeed hypertension is clearly recognized to cause progression of atherosclerosis in many vascular beds, so hypertension may cause renal vascular lesions rather than vice versa. Atherosclerotic RAS normally causes worsening of an already existing primary hypertension. A history of acceleration of previously mild hypertension
suggests renovascular hypertension.13 RAS can also lead to renal insufficiency. A rise in serum creatinine following initiation of antihypertensive therapy with ACE inhibitors may lead to the diagnosis of RAS. RAS may be severe enough to cause ischemia and tissue damage, as is often shown by asymmetry in renal size.13 Flash pulmonary edema is often the first clinical symptom of bilateral RAS.16 Renovascular hypertension is usually caused by non-atherosclerotic RAS such as fibromuscular dysplasia, which occurs in younger patients (< 40 years of age). It is probably the most common cause of hypertension in young children17,18 and has a higher prevalence in females. Atherosclerotic renovascular disease represents an important public health problem. It has been demonstrated that it increases cardiovascular and all-cause mortality. Aggressive treatment of a severe RAS (defined as a diameter stenosis of at least 70%) is recommended for patients with uncontrolled hypertension, renal insufficiency, congestive heart failure, unstable angina, and for patients with a solitary or a single functioning kidney. The treatment of RAS without hypertension or renal insufficiency is debatable but could be considered with a view to preserving renal function and renal artery patency. The treatment options for RAS include medical therapy, balloon angioplasty (with and without stenting) and surgery. Surgery carries a significant risk with a 2–7% peri-operative mortality rate and a 17–31% morbidity rate. In addition, deterioration in renal function occurs in 11–31% of patients, and reocclusion and restenosis in 5–18%.24–26 Indications for surgery are limited: failed percutaneous approach, hostile aorta, and infrarenal total occlusion (in association with aortic surgery). Percutaneous transluminal renal angioplasty (PTRA) has become the cornerstone of therapy for addressing RAS and is now the first treatment to be proposed. Balloon angioplasty alone was first proposed and is still the first line therapy for fibrodysplasic RAS. However, several authors have reported the successful use of endovascular stents for treating suboptimal angioplasty results and as a primary intervention for atherosclerotic lesions (particularly ostial lesions) with better immediate and long-term results than with PTA alone.27–32 Renal angioplasty stenting can be performed using the femoral approach in most cases. The brachial or radial approach can also be used. The technique benefits from the improvements of coronary technique: monorail systems for balloon and stents, low-profile devices, 0.014- or 0.018-inch guidewires allowing direct stenting in 80–90% of the procedures. Procedural success is excellent (98–100%) with a low 525
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complication rate, a low restenosis rate, and a good long-term patency rate of 85–98%.21–26 One of the benefits of PTRA includes a potential complete cure (7–19%) or at least easier management of hypertension (52–74%) in addition to preservation or improvement of renal function.27,28,31 However, post-procedural deterioration of the renal function occurs in a subset of patients after PTRA.32–34 We hypothesize that atheroembolism during the procedure is a precipitating factor for this complication and a major preventable factor limiting the benefits derived from PTRA. This hypothesis is supported by recent studies.35 In order to eliminate or reduce the risk of atheroembolic material being carried into the renal parenchyma, we applied the technique of distal embolic protection, using balloon or filters positioned distal to the lesion, a technique currently developed and approved for use in the coronary and cerebral circulations.36–38 Use of such devices during PTRA may increase the rate of beneficial clinical responses after revascularization.
Effects on renal function: rationale for protection devices The effects of renal angioplasty and stenting on renal function are controversial. There are no randomized studies comparing either balloon angioplasty or stenting with medical therapy. The meta-analysis reported by Nordmann et al.39 demonstrated no consistent difference in changes in the renal function. According to recent American Heart Association guidelines40 a slowed decline in renal function is sufficient to support the claim that renal artery angioplasty is beneficial. Recent studies regarding the effects of peripheral renal angioplasty or stenting on renal function showed that a large percentage of patients seem to benefit from the procedure with a stabilization or improvement in renal function (Table 56.1). Renal stenting in selected patients could slow the progression of renovascular renal failure.41–45,50–58 In patients with a normal baseline creatinine level, renal function was
Table 56.1
mostly preserved.31,43,50,54 In a non-randomized study, PTRA improved renal function in 41–43% of patients.59 Blum et al. found no significant change in creatinine independent of baseline renal function.30 White et al. in their series of 100 patients found no significant change in the creatinine level.54 However, in 9 of 44 patients with renal insufficiency, creatinine normalized. The effect of PTRA on renal function was demonstrated by La Batatide Alanore.60 After following 32 patients who underwent PTRA for a mean of 6 months, split renal function was detected using Captopril renal scintigraphy. The renal function of the treated kidney was found to improve significantly after PTRA. This suggests that PTRA improves the renal function in patients with unilateral RAS. There are few data on patients with severe renal dysfunction. In Zeller et al.’s series50 renal function improved in 71% of patients with severe renal insufficiency, 21% were unchanged, and 8% deteriorated. In 32%, planned chronic hemodialysis was deferred. In contrast, Pattynama et al.61 showed no improvement 1 year after the procedure in 40 azotemic patients with 61 RAS. In 60% of these patients, renal function was improved or preserved, and in 40% deteriorated. There was no difference found between bilateral and unilateral disease. Despite these generally favorable results, in many published series a decline in renal function was noted in a subset of patients even after successful initial technical results and a good long-term patency of the renal artery. Deterioration in renal function may be seen in 20–30% of the patients (Table 56.1) or even more. In most of the series this depends on the renal function and the creatinine level at baseline.32,34,42,44 Dorros et al. reported a deterioration of the renal function in 47% of the patients with a creatinine level of over 2 mg/dl.32 Subramanian et al.62 demonstrated a worsening in renal function in 24% of non-diabetic patients and 27% of diabetic patients with renal insufficiency while Guerrero et al.47 reported similar results in 31% of patients with renal insufficiency.
Renal artery stenting effect on renal function
Authors
Year
PTS (n)
Dorros32 Iannone41 Taylor42 Blum30 Harden43 Boisclair34 Paulsen44 Isles33 Rodriguez Lopez45 Henry28 Rundback46 Guerrero47 Allaquaband48 Haller49 Zeller50 Overall
1995 1996 1997 1997 1997 1997 1999 1999 1999 1999 1999 2002 2003 2004 2004
69 63 39 68 32 33 135 379 108 235 45 61 22 261 340 1890
* Patients with baseline serum creatinine ≥ 0.5 mg/dl
Improved (%)
Stable (%)
Worse (%)
30 36 33 – 34 41 23 26 – 29 25 19 50 – 34 25.3
48 46 29 100 34 35 56 48 95.5 67 43 50 23 86 39 53.3
22* 18 38* – 28* 24* 21* 26* 4.5 4 32 31* 27* 14 27 21.4
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Renal angioplasty and stenting under protection devices Zeller et al.50 recently reported the long-term impact of stent-supported angioplasty on renal function in a series of 340 hypertensive patients. During a mean follow-up period of 34 ± 20 months, serum creatinine significantly decreased from 1.45 ± 0.87 to 1.39 ± 0.73 mg/dl (p = 0.048). The renal function was improved in 34% of the patients, remained unchanged in 39%, and deteriorated in 27%. Baseline serum creatinine, bilateral intervention, percentage diameter stenosis, and triple vessel coronary diseases were independent predictors of improved renal function during follow-up. The serum creatinine decrease was not significant in patients with diabetes mellitus. Other reports41,43,55 suggest that only treatment of bilateral severe RAS is beneficial to renal function. In contrast to other series, the highest proportion (36%) of Zeller’s patients with deteriorated renal function was found in the subgroup with normal baseline serum creatinine. However in 90% of these patients, the increase in serum creatinine concentration was within the normal range. The more severe the renal dysfunction was at baseline, the more the patients benefited from the intervention: improved or unchanged mean serum creatinine concentrations were seen in 64% of patients with normal renal function, 82% of patients with moderate renal impairment, and 92% of those with severely impaired renal function. Improvement in renal function was also seen in 37% of the patients with nephrosclerosis and a resistance index of more than 0.8. Watson et al.58 assessed the effect of renal artery stenting on renal function in patients with chronic renal insufficiency (creatinine > 1.5 mg/dl) by comparing the slopes of the regression lines derived from the reciprocal of serum creatinine versus time plotted before and after stent deployment. Before stent deployment, all patients exhibited a negative slope indicating progressive renal insufficiency. After stent deployment the slopes were positive in 18 patients (72%), indicating improvement in renal function; and less negative in 7 patients (28%), indicating a persistence of decline in renal function deterioration, albeit at a lower rate than before the procedure in these 7 patients. Many factors may account for this functional deterioration: contrast media-induced nephrotoxicity, progression of concomitant nephrosclerosis, lesion recurrence, hyperperfusion syndrome, glomerular injury, and so on. However atheroembolism during the procedure seems to play an important role. Contrary to the earlier belief that atheroembolization is a non-issue during percutaneous angioplasty, there is now growing evidence to indicate that atherosclerotic debris commonly embolize from lesions in many vascular territories during percutaneous intervention.63 Distal embolization seems to be the root cause of many procedural complications whenever atherosclerotic lesions are treated. Evidence of distal embolization as a frequent complication was first seen in saphenous vein graft interventions.64 Distal protection devices have been able to recover embolic debris and significantly reduce the incidence of these complications. Clinical data are emerging suggesting that similar embolization and distalorgan complications also occur during catheter treatment of certain native coronary lesions,65 and during carotid stenting and renal stenting.36,38,66,67 Cholesterol atheromatous embolism is an increasingly recognized cause of renal function deterioration. Atheroembolism during the procedure could play an important role.
527
Cholesterol atheromatous embolism is caused by the release of microscopic plaque fragments and cholesterol crystals from the renal artery lesion or the atherosclerotic aorta into parenchymal renal vasculature during the procedure. Instrument manipulation in the aorta and renal arteries can result in detachment and embolism of atheromatous debris from ulcerated plaques. The large size of the devices used, an increased length or specific difficulties of the procedure may be contributory. Walker et al.67 recently demonstrated the great potential for embolic debris during the placement of the guiding catheter, sheath, or diagnostic catheter. He performed an aggressive aspiration of the guiding catheter or sheath before any contrast injection. Large particles of atherosclerotic debris (1–3 mm) were discovered in 41.7% of the patients. He proposed that careful aspiration of catheters before injections or interventions should routinely be performed. Patients with severe atheromatous disease of the aorta and its branches, ulcerated plaques, associated lesions such as aneurysm and dissection are candidates for these complications. Hiramoto et al.35 demonstrated that angioplasty and stenting of ex vivo aorto renal atheroma specimens using 0.018-inch guidewire system was associated with thousands of atheroemboli. Each manipulation of the specimens including simply advancing the guidewire through the lesion released thousand of fragments. The number of fragments in each size category increased with decreasing particle size. Positioning and deploying the stent released an additional bolus of fragments similar to that released after balloon angioplasty. All these fragments are of sufficient size to create vascular occlusions and initiate significant renal parenchyma damage. This author concludes that the results of angioplasty procedures could be improved by placing distal protection devices to prevent atheroembolization. Even modern techniques and the use of low-profile systems cannot prevent from atheroembolism and renal function deterioration as recently reported by Nolan et al.68 who reported a series of 82 procedures with a renal function deterioration in 24% of the patients at 1 year. The true incidence of atheroembolism is uncertain. Many patients can have a silent course because of the large functional kidney reserve, which allows normal serum creatinine values despite a significant decline in total glomerular filtration capacity. Therefore only the most severe cases may be detected, especially in patients with preprocedural renal dysfunction and limited functional reserve. Abnormal serum creatinine may only be observed if 50% of the nephron population is destroyed. Most patients reach a peak serum creatinine level over 3–8 weeks but onset can also be sooner. Few studies have addressed the problem of atheroembolism following RAS. Boisclaire et al. reported 4 cases in 33 procedures.34 Van de Ven et al. reported 2 cases in 24 procedures inducing renal insufficiency.27 More recently Commeau et al. reported acute deterioration of renal function due to cholesterol embolism necessitating hemodialysis.69 Morice et al. also published 2 cases of partial renal infarctions in a series of 80 patients despite the use of a new low-profile device and direct stenting.70 In the Aspire 2 study71 major embolic events occurred in 6.3% of the procedures. The clinical manifestations of atheroembolism are also non-specific. Thadhani et al.72 retrospectively evaluated 52 patients with both renal failure and histologically proven atheroembolism following angiography or cardiovascular
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surgery over a 10-year period. Within 30 days of their procedure, 50% of the patients had cutaneous signs of atheroembolism and 14% had documented blood eosinophilia. Most patients reached a peak serum creatinine level over 3–8 weeks73 but onset is usually sooner.31 Although proteinuria and nephritic syndrome are uncommon, Haqqie et al.73 reported 4 patients with histopathologically documented atheroembolism who developed nephrotic-range proteinuria. They suggested that atheroembolism should be considered in the differential diagnosis of nephrotic syndrome in elderly patients with serious vascular disease. Atheroembolism can give rise to different degrees of renal impairment: ● ● ● ●
●
only a moderate loss of renal function; severe renal failure requiring dialysis; abrupt and sudden onset of renal failure; more frequently a progressive loss of renal function over weeks (3–8 weeks); chronic stable and asymptomatic renal insufficiency.
Even in cases with high clinical suspicion, the diagnosis of an atheroembolism is difficult to establish using routine laboratory tests. Renal biopsy is the only definitive diagnostic tool; although it is valuable to exclude other potentially treatable disease processes, its routine application for confirmation of a disease amenable only to supportive treatment is problematic. For these reasons, it is not surprising that atheroembolism after renal artery interventions is often misdiagnosed as dyeinduced nephrotoxicity or the progression of nephrosclerosis. Dye-induced nephrotoxicity generally appears at 1 or 2 days after the procedure and often resolves within a few days or weeks. Its prevention is essential in patients with renal insufficiency and elderly patients with diabetes. Renal atheroembolism definitely poses a risk of renal function deterioration and decreased survival in patients undergoing endovascular procedures for RAS. Following to the increasing number of such patients, the cost of renal function deterioration and subsequent end-stage renal disease requiring dialysis represents a significant long-term problem. Its importance is clearly demonstrated in a recent work by Krishnamurthi et al.,74 who evaluated its impact on survival in 44 patients who had surgery for atherosclerotic RAS and concomitant intraoperative renal biopsy for detection of atheroemboli. Atheroembolic disease was identified in the biopsy specimens in 16 (36%) patients and correlated significantly with decreased survival (54% 5-year survival in this group vs. 85% in patients without atheroembolism, p = 0.011). Boero et al.75 recently emphasized the bad prognosis of renal atheroembolism. In a series of 22 patients with an onset of symptoms from a few hours to 60 days, 11 patients (50%) were put on dialysis with a partial functional recovery in 4, while 11 patients (50%) died. Thus it can be concluded that cholesterol embolism is a frequent cause of renal failure and is associated with a high mortality rate. No specific treatment can be suggested for renal atheroembolism. Therefore the main aim should be to avoid atheroembolic events during renal interventions. The selection of patients may limit the risk but more and more elderly high-risk patients with advanced atheromatous diseases need treatment and it is difficult to refuse these patients the benefits of the procedure.
Certain technical points are very important and need to be mentioned. The procedures should be as atraumatic as possible with use of small devices and adaptation of coronary angioplasty techniques. Direct stenting is not sufficient to avoid embolism. As mentioned, Walker et al. proposed the careful aspiration of the catheters.67 The “no touch” technique was also proposed to minimize atheroembolization.76 Beyond these technical considerations to circumvent atheroembolisms, we applied the concept of protected renal angioplasty and stenting.36–38 The rationale for distal embolic protection is similar to that of brain protection during angioplasty and stenting of the carotid arteries. Several studies have shown that protection devices with occlusion balloons or filters are effective in reducing the risk of embolization to the brain77,78 and that these techniques are now mandatory in this field and represent the standard of care.79 We postulated that the same technique could be suitable during renal angioplasty and stenting to reduce the risk of atheroembolism and to reduce the risk of deterioration of RF.
Impact of protection devices during angioplasty of RAS Techniques The technique has been previously described.36–38 All procedures are performed under local anesthesia and intravenous sedation. A 6–8-French guiding catheter is placed at the ostium of the renal artery, most of the time via a percutaneous femoral approach. Two types of protection devices can be used: ●
●
Occlusion balloon. The GuardWire system (Medtronic, Minneapolis, MN) is the same as that used for carotid protection (Figure 56.1–56.3). Filters: current filters available on the market can be placed in the renal artery (same filters as for carotid angioplasty) (Figures 56.4 and 56.5).
With the guiding catheter appropriately positioned, the protection device is carefully advanced across the lesion and positioned 2 or 3 cm beyond the target site. In the majority of
Figure 56.1
Percusurge occlusion balloon.
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(a)
(b)
(d) Figure 56.2
(c)
(e)
Percusurge technique.
(a)
(b) Figure 56.3
RAS under protection with Percusurge device. (See Color plates.)
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Figure 56.4
Filters.
the cases crossing the lesion with a protection device is easy and is the same technique as with any guidewire. In a few cases (angulated artery; tight, calcified stenosis) it could be helpful to first place a more supportive “buddy wire” in the renal artery before attempting to cross the lesion with the protection device. In cases of very tight stenosis a predilatation of the lesion with a coronary balloon may also be indispensable before crossing the lesion. With a Percusurge device, the Microseal adapter is attached and the occlusion balloon inflated to occlude the renal artery. On detaching the adapter, the occlusion balloon remains inflated.
Figure 56.5
With a filter it is deployed by carefully removing the delivery sheath. Contrast injection confirms the accurate positioning of the protection device. Angioplasty and stenting of the renal artery can be performed under protection using low-profile devices and the monorail technique. We perform a predilatation of the stenosis only in case of tight or calcified lesions. A direct stenting is done in the majority of the cases. After stent placement the protection device is retrieved. If a Percusurge device is used, after stent deployment the aspiration catheter is advanced over the wire to the level of the
(a)
(b)
(c)
(d)
RAS under protection with EPI filter.
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This technique of distal protection has some limitations: ●
●
●
●
●
Figure 56.6
RAS under protection: early bifurcation. ●
lesion and positioned adjacent to the protection balloon. Any debris are removed using a 20-ml syringe connected to the proximal end of the catheter. At least two aspirations are performed. After removing the aspiration catheter the Microseal adapter is reattached to the GuardWire and the occlusion balloon deflated allowing normal vessel flow. If the angiographic result is satisfactory, the device is removed. With filters, angiographic control is performed after stent deployment. If the result is satisfactory, the filter is withdrawn with the removal sheath. To facilitate protection device withdrawal and prevent it from getting caught on the stent, the guiding catheter is routinely advanced into the stent up its distal end. The aspirated blood or the filters are sent to the laboratory for analysis. In some cases with filters we can observe a slow or zero flow after stent deployment due to a clogged filter. In these cases, there is a stagnant column of blood proximal to the filter. Simply recapturing the filter will result in embolization to the kidney. It is indispensable to do an aspiration proximal to the filter prior to recapture of the device, either with an aspiration catheter or simply with the guiding catheter we can advance close to the filter. Aspiration catheters that can be used include: the Export Catheter (Medtronic), Pronto (Vascular Solutions Inc., Minneapolis, MN), or the Diver (Invatec, Roncadello, Italy).
Figure 56.7
FiberNet device.
The distal protection device does not prevent emboli from reaching the kidney during initial catheter manipulation or angiography and during crossing the lesion. The use of distal embolic protection devices may be limited by the renal anatomy and the lack of devices currently available on the market and dedicated for this application. In cases involving large vessels, we have to select carefully the device and to choose one device with a diameter at least equal to the diameter of the renal artery. In cases of early renal artery bifurcation, it is not possible to protect all arteries. The protection device should be placed in the main branch. To place the protection device we need a landing zone after the stenosis of at least 1.5–2.0 mm. One of the major limitations of the filters is the pore size, which in general is greater than 100 µm and allows small particles to go to the kidney.
To overcome some problems encountered with current filters a new filter was recently proposed and is in experiment. This filter, the FiberNet (Lumen Biomedical Inc., Plymouth, MN), consists primarily of polyester fibers located coaxially around the distal tip of a guidewire assembly (Figure 56.7). This filter is soft and conformable. When actuated, it expands radially to fill the vessel providing excellent apposition to the vessel wall. Contained and captured emboli are recovered/removed both by aspiration through the retrieval catheter and also by retention within the filter fibers when the filter is closed and retracted into the retrieval catheter. Aspiration is achieved through the retrieval catheter using the vacuum syringes to provide suctions. This filter enables the capture of emboli as small as 30/40 µm without compromising the flow through the filter and in our study the number of particles removed appears to be much higher than with other filters. The possibility of suction through the retrieval catheter during device removal is probably one of the major improvements with this device allowing cleaning of the dilated area and of the inner part of the stent. This technique allows aspiration of the debris, which can protrude through the struts of the stents after stent placement and dilatation and which
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could embolize after the procedure. The maximum diameter of this device is 7 mm, which is enough in most of the cases. The landing zone required to place this filter is shorter than with other devices (about 1 cm). We began the first human study with this new protection device, which seems very promising.
femoral approach in all patients except one patient presenting with total occlusion of both iliac arteries necessitating a brachial approach. Different protection devices were used: ● ● ●
Medication and patient surveillance As for all our stenting procedures, patients were given ticlopidine (500 mg/day) or clopidogrel (75 mg/day) and aspirin (100 mg/day) before the procedure. During the procedure, an intravenous bolus of 5000–10,000 units of unfractioned heparin is routinely administrated at the beginning of the procedure to have an activated clotting time around 250–300 seconds. The post-procedural drug regimen included aspirin (100 mg/day) indefinitely and ticlopidine (250 mg/day) or clopidogrel (75 mg/day) for one month. Patients remained in the hospital for 48 hours to monitor serum creatinine levels and adjust blood pressure medication. Renal duplex scanning is scheduled the day after the procedure, at 6 and 12 months, and then annually. Angiography is performed when a restenosis is suspected on the basis of positive clinical and duplex scan findings. Serum creatinine values are measured before and after the procedure (day 1) and at 1 and 6 months, with biannual measurements thereafter. For our final patients we evaluated the GFR (glomerular filtration reserve) which seems a more reliable parameter to appreciate the RF. Results Only single-center series on renal angioplasty and stenting under protection have been reported. Personal series From January 1999 to July 2006, 124 RAS were treated in 105 patients with poorly controlled hypertension (72 males and 33 females), mean age: 64.5 ± 11.7 years (range: 22–87) with percutaneous angioplasty and stenting under distal protection. All of these patients were diagnosed to have atherosclerotic RAS by renal duplex scanning and angiography. The indication for endovascular treatment was a stenosis greater than 70%. Written informed consent was obtained from all patients. One bilateral procedure was performed in 18 patients and we treated 2 renal arteries on the same side in one patient. Nine patients had a solitary or single functioning kidney (one transplant renal artery). Twenty-four patients had moderate renal insufficiency (serum creatinine 1.5–1.9 mg/dl) and 15 had severe renal dysfunction (serum creatinine ≥ 2 mg/dl). The RAS was located at the ostium in 108 cases. Mean percentage stenosis was 85.9 ± 8.3% (range: 70–99). Mean lesion length was 11.3 ± 3.0 mm (range: 8–29). The diameter of the artery was estimated at 6 mm in 87 arteries and 5 mm in 37 arteries. A total of 59 patients had diffuse severe atherosclerosis of the abdominal aorta. 32 patients had diabetes mellitus, 73 were current smokers, 66 had hyperlipidemia, and 73 had associated coronary disease. Cerebrovascular disease was found in 20 and lower extremity peripheral artery disease in 37. A 6–8-French guiding catheter was placed at the ostium of the renal artery via a percutaneous
● ● ● ●
Occlusion balloon (Percusurge): 46 procedures Filters: 76 procedures EPI (Boston Scientific, Natik, MA): 59 (Figures 56.1 and 56.2) Angioguard (Cordis, Warren, NJ): 7 Emboshield (Abbott Vascular, Redwood City, CA): 6 FiberNet (Lumen Biomedical, Plymouth, MN): 4 Accunet (Guidant, Indianapolis, IN): 2
Stenoses were easily crossed with the protection device in 123 cases due to their low profile and flexibility. One predilatation was required to cross a subocclusive calcified stenosis. We had no difficulty in deflating the occlusion balloons or in removing the protection devices. A direct stenting was performed in 96 cases. One hundred and twenty-seven different stent models were used: Boston Express (n = 27), Cordis Genesis (n = 29), Medtronic (n = 15), Guidant Herculink (n = 14), Cordis Corinthian (n = 11), Carbostent Sorin (n = 7), Cordis P154 (n = 6), Abbott (n = 6), Nir (n = 5), Stentec (n = 4), Cordis M3 (n = 2), Biotronik (n = 1). Three patients required two stents in the same artery to treat a long lesion. Technical success was obtained for all arteries (100%) with good stent deployment, no significant residual stenoses and complete covering of the lesion. Mean renal artery occlusion time with the Percusurge technique was 6.46 ± 2.42 mm. The mean time in situ for filters was 4.22 ± 1.18 mm, which is shorter than with the occlusion balloon. Two patients developed an arterial spasm (one with Percusurge, one with EPI filter) at the site of protection device, which immediately responded to local vasodilatator therapy. No dissection of the renal artery due to a protection device was seen. Particulate analysis With the Percusurge technique and the aspiration catheter, we aspirated visible debris in all patients (as with the carotid procedures). The aspirated blood samples were analyzed and studied by microscopy and scanning electron microscopy. Different particles were isolated and identified. Their number varied from 13 to 208 per procedure (mean ± SD: 98.1 ± 60.0), and diameter ranged from 38 to 6206 µm (mean ± SD: 201.2 ± 76.2 µm). The particles were atheromatous plaques, cholesterol crystals, necrotic cores, fibrin, fresh thrombi, organized thrombi, platelets, macrophage foam cells, and thrombogenic lipoid masses. Only fresh thrombi should be drug sensitive but these emboli were detected in only 10% of cases. The other particles are likely to be manageable only using mechanical means. With filters we removed visible debris in 80% of the cases. Two filters were totally blocked by large particles, with flow being totally interrupted. Two other filters were almost totally blocked with low flow. The flow was restored after removal of the filter. One patient was 26 years old. With the new filter FiberNet, visible debris were removed in all cases, five times more than with other filters. Minimum length was 28 µm, average length was 105 µm, and maximum length was 6.8 µm. Seventy percent of the particles were less than 100 µm. The average area for FiberNet
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Figure 56.8 Debris removed after RAS under protection with the FiberNet device.
debris captured was: 117.1 mm2 (range: 25.1–208 mm2). Atheromatous material was found in both aspirate and filter samples (65% in aspirate samples) (Figure 56.8). Follow-up Mean follow-up period was 18.3 ± 9 months (2–89 months). Four patients died from myocardial infarction, one at day 3 (patient who underwent coronary angioplasty shortly before renal stenting), one at 6 months, and one at 1 year of followup. One multivascular patient with severe renal insufficiency developed an acute renal failure after the procedure probably due to contrast nephropathy necessitating dialysis, and died 1 week later from multiorgan failure. Two patients were lost to follow-up after 1 year. Seven patients presented an in-stent restenosis, successfully treated by a new balloon angioplasty. We have not seen device-related late vascular lesions in the 38 angiographic controls performed during the follow-up. Hypertension During the follow-up we observed no difference with other published series of patients treated without protection. Systolic and diastolic blood pressure decreased significantly. The number of medications also declined significantly (2.8 vs. 1.2). Nineteen patients were cured (18%), 61 improved (59%), and 25 remained unchanged (22%).
Renal function As mentioned, we observed one acute function deterioration. Table 56.2 shows the mean value for urea and creatinine preprocedurally (D–1) and after the procedure (D+1), at 1 month, 6 months, 1 year, and 3 years. There is no statically significant difference during the follow-up. Table 56.3 shows the effects on the renal function (RF) at 6 months, 2, and 3 years in patients with normal renal function and in patients with moderate and severe renal insufficiency. At 6 months, (91 patients), we observed only one deterioration of the RF in a patient with moderate renal insufficiency at baseline, 21 improvements in patients with renal insufficiency, and 69 stabilizations. At 2 years (75 patients), we observed only two deteriorations of the RF (3%). One was in a patient with normal RF before the procedure, normal RF at 6-month follow-up and who developed a renal insufficiency at 2 years. This patient was treated for bilateral stenosis, one side without protection. The other was in a patient with moderate renal insufficiency. Ninety-six percent of the patients remained stabilized (n = 54) or improved (n = 19). At 3 years (37 patients), 93% of the patients remained stabilized (n = 26) or improved (n = 9). Twenty patients have RF deterioration. Other published series Several reports have been published in the literature. Holden et al. reported a first series of 46 procedures in 37 patients with preprocedural renal impairment performed with the Angioguard filter.66 They found the same results: renal function stabilized or improved in 95% of cases. Only 5% of the patients demonstrated an unchanged decline. No patients experienced acute post-procedural deterioration. These results are better than in most reports in the literature and also better than in a historic group of similar patients with ischemic nephropathy who underwent stent revascularization without distal protection at the same institution.55 The improved results are thought to be due to the prevention of cholesterol embolization during the procedure by distal filter baskets. A total of 65% of the filters contained embolic material, including fresh thrombus, chronic thrombus, atheromatous fragments, and cholesterol clefts. More recently, Holden80 published a larger series of 106 RAS treated under protection with filters in 90 patients
Table 56.2 The mean value for urea and creatinine preprocedurally and after the procedure, at 1 month, 6 months, 1 year, and 3 years Distal Protection during Renal Artery Stenting Follow up Renal Function Mean Follow-up 18,3 ± 9 Months (2 – 89) Number of patients D–1 D+1 D + 30 D + 180 2 Years 3 Years
105 105 103 91 75 37
Urea mean value G/L 0,46 ± 0,19 0,43 ± 0,18 0,41 ± 0,18 0,41 ± 0,14 0,42 ± 0,18 0,47 ± 0,19
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Cretinine mean value MG/L
P value
13,85 ± 5,04 12,15 ± 4,70 12,11 ± 3,85 11,92 ± 3,47 11,87 ± 2,71 12,71 ± 3,82
N.S. N.S. N.S. N.S. N.S. N.S.
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Textbook of peripheral vascular interventions Table 56.3 Effects on the renal function (RF) at 6 months, 2, and 3 years in patients with normal renal function and in patients with moderate and severe renal insufficiency Distal Protection during Renal Artery Stenting Follow-up Renal Function (R.F.) Nbr – 56 22 13 91
= 56 8 5 69
–→ 13 8 21
Nbr – 47 20 8 75
→
Normal R.F Moderate Renal Insufficiency Severe Renal Insufficiency Total
6 Months – 1 – 1
2 Years = 46 6 2 54
–→ 13 6 19
Nbr → 1* 1 – 2
– 25 9 3 37
3 Years = 24 2 – 26
–→ 6 3 9
→ 1* 1 – 2
→
= Stabilization R.F.: Creatine value within ± 0,2 mg/dl Improvement R.F.: Decreased Creatine value ≥ 0,2 mg/dl →Deterioration R.F.: Increased Creatine value ≥ 0,2 mg/dl * Patient with Bilateral Angioplasty (one without protection)
with ischemic nephropathy. He reported one acute deterioration of RF. At a mean follow-up of 18.2 months, RF was improved in 36% of cases, and stabilized in 55%. They reported only 8% of cases had a progressive decline of RF. Eggebrecht et al. published a case of renal angioplasty performed under distal protection with the Percusurge device for an in-stent restenosis.81 Histologic examination of blood retrieved from the distally occluded vessel showed foam cells and an amorphous lipoid substance as markers of atherosclerotic plaque debris. The authors concluded that the GuardWire could be included in routine angioplasty maneuvers. Li and colleagues also published a case of successful renal angioplasty and stenting under distal protection with the Percusurge GuardWire.82 Guerkens et al. used the Angioguard filters in six patients and retrieved macroscopic debris in every case.83 Edwards et al. more recently used balloon occlusion and aspiration catheter (the Percusurge device) to treat 32 RAS.84 Ninety-two percent of the patients had renal insufficiency. RF response at 4–6 weeks follow-up was improved in 50% of the patients and unchanged in 50%. In no patient or after any procedure was RF observed to be worsened. Fifty-four percent of the patients with RF deterioration were improved. For the authors the results with this technique of RAS under protection represent a marked improvement in short-term RF response rates compared with previously published experiences. They approximated the short-term results reported after open surgical revascularization and concluded that these data suggest that this technique may prevent RF harm during RAS as a result of atheroembolism and warrant further investigation. Discussion RAS is increasingly diagnosed in patients suffering from hypertension and renal insufficiency and in multivascular diseased patients. PTRA is now the first treatment to be proposed with a high technical success rate, a low complication rate, a low restenosis rate, and good long-term anatomical results. A large percentage of patients seem to benefit from the procedure concerning hypertension and renal insufficiency with stabilization or improvement in RF, and in selected patients, RAS could slow the progression of renovascular renal failure and may delay the need for renal replacement therapy.27–31,41–60
However, as we have noticed in many published series, a deterioration in RF may be detected in at least 20–30% of patients, not only in patients with renal insufficiency but also in those with normal RF at baseline, and even after successful initial technical results and good long-term patency.32,34,41–45,50 Atheroembolism during the procedure could play an important role. The risk of atheroembolism can be reduced with a good selection of patients and some technical points, but the use of protection devices seems the best technique to overcome this problem. This is the reason why we have applied the concept of protected renal angioplasty and stenting to circumvent atheroembolism. The rationale for distal embolic protection is similar to that of brain protection during carotid angioplasty and stenting of the carotid arteries. These techniques are now mandatory in this field and represent the standard of care.79 We have postulated that the same technique could be of value in the management of RAS in mitigating the risk of atheroembolism. Our results show only one acute deterioration of RF probably due to contrast nephropathy in a multivascular patient in poor condition and renal insufficiency at baseline. At 6-month follow-up, 98% of the patients were stabilized or improved and only two instances of deterioration (7%) appeared. Ninety-three percent of the patients remained improved or stabilized. These results seem to be favorable when compared with available published data and may well be attributed to the use of a protection device during the procedure. It is noteworthy that visible atherosclerotic debris were extracted in all cases with balloon occlusion techniques and in 80% of cases with current filters. But with the new filter FiberNet visible debris were removed in all cases, at least five time more than with other filters. Four filters were totally or almost totally blocked by debris, thereby highlighting the role of protection devices. Similar results were also recently published by Holden80 and Edwards et al.84 Both authors insist on the role of protection devices to reduce atheroembolism and the risk of RF deterioration. However this technique has some limitations as we have already mentioned: ●
The interventionist should remember that this technique does not protect the kidney from atheroembolism during
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●
●
●
●
●
attempts to initially catheterize the renal artery and cross the lesion. In the case of large vessels, the protection device has to be selected carefully, choosing a protection device with a diameter at least equal to the diameter of the renal artery. In case of an early renal artery bifurcation, it is not possible to protect all arteries. The protection device could be placed in the main branch (Figure 56.3a). We could use two protection devices, one protection device placed in each branch, but this technique could be limited by technical, anatomical problems, and by the cost. In fact, in daily practice 90% of the renal arteries can be protected with current protection devices. To place the protection device we need a landing zone of at least 1.5–2 mm, which may be a problem with long stenosis or non-ostial stenosis. Current protection devices are not dedicated to renal arteries and have to be modified and improved. Occlusion balloons have their own limitations and disadvantages. 䊊 It may deflate or may be non-occlusive during the procedure. 䊊 Some particles may be too large for suction (very rare). 䊊 Below the balloon there is a shadow zone where some particles may remain blocked and are difficult or impossible to aspirate with the aspiration catheter. These particles may migrate to the kidney when the balloon is deflated. 䊊 Occlusion balloon could lead to transient nephron ischemia. In our series the mean occlusion time was short (6.46 mm). We do not think that this transient ischemia could cause any damage to the kidney. This occlusion time is less than that of the campling required during a surgical procedure. Edwards et al.84 also used this technique without any complication. Filters have also limitations and disadvantages. 䊊 Bad wall apposition with the possibility of migration of some particles around the filters. 䊊 A filter may plug up with suspended particles that will embolize if we retrieve the filter. In this case before retrieving the filter we have to aspirate very carefully the blood below the filter. 䊊 A filter may thrombose: we need an effective anticoagulation with an ACT > 250–300 seconds. 䊊 Closure and retrieval of filters can dislodge their content collected during the procedure. 䊊 Some difficulties in retrieving a filter may be encountered. The filter could get caught on the struts of the stent during retrieval. 䊊 The major limitation of the filters is the pore size, which in general is greater than 100 µm. This is larger than the size of microcholesterol crystals85 and allows small particles going to the kidney. Atheroemboli typically occlude the medium-sized arterioles (150–200 µm in diameter) and glomerular capillaries. The pathogenesis of renal failure may be due entirely to occlusion of these vessels. But reactive inflammation surrounding the cholesterol crystals may play a significant role in causing the luminal occlusion and subsequent renal failure.86
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As we have mentioned, the new generation of filters like the FiberNet should reduce the risk of atheroembolism and of RF deterioration. Particles of 30–40 µm can be removed with this device and the possibility of suction with the retrieval catheter is an important improvement. Although no device-related complications occurred in this small series of patients, adding another instrument to the procedure while trying to prevent complications could create new problems. The potential for renal artery thrombosis during protection is extremely small, even with occlusion balloons, because the patients are on heparin and antiplatelet therapy. Moreover, the duration of occlusion is usually short, less than the time required to perform the distal anastomosis of a conventional aortorenal bypass. The risk of dissection with a protection device is negligible, but one has to consider the possibility of spasm (two cases in our series), which is, however, usually treatable medically. The indications for this technique of renal protection are debatable. Is the technique indicated for all patients? The indications for protection in patients with normal renal function need to be considered. The incidence of procedure-related decline in the renal function is considered to be low in this patient group. Many interventionists think that the extra cost of a renal protection system for these patients is not justified. However, we would like to point out the series recently published by Zeller et al.50 where the highest proportion (36%) of patients with worsened renal function was found in the subgroup with normal baseline creatinine. In our series, 66 hypertensive patients were treated with protection despite a normal serum creatinine. Only one patient experienced a renal function deterioration detected at 2-year follow-up. This technique of including renal protection may therefore become the standard of care in the future. At the present time, selective indications should at least be pointed out: ●
● ● ● ● ● ●
patients with renal insufficiency and a creatinine level of more than 1.4 mg/dl or possibly better still a GFR of less than 50 ml/min; elderly patients; patients with ischemic nephropathy; bilateral RAS; solitary or single functioning kidney; patients with diseased aorta and renal ostia; possibly diabetes.
As has been mentioned by Sos,85 physicians performing renal artery interventions must understand the non-linear relationship of renal function reserve (RFR) and serum creatinine (SCr) and its implication for the margin of safety (Figure 56.9). Severe iatrogenic renal parenchymal damage due to interventional or diagnostic procedures can be masked in patients with normal preintervention global SCr values. Thus 50% of total renal mass can be destroyed without any change in renal function. Patients with elevated SCr whose renal function is at the “knee” of this curve have very diminished renal reserve and are at much greater risk. An additional 10% loss of renal parenchyma can put such a patient on dialysis. There can be extensive damage to the kidneys that, in many patients with normal preintervention renal function, may not
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Textbook of peripheral vascular interventions protection system.80 New protection devices have to be developed, dedicated to the renal system.
Figure 56.9 Relationship of renal function reserve (GFR) and serum creatinine value (SCr).
be apparent during or after renal intervention. It is difficult to know exactly which patient needs protection. For example, a patient with 60% renal function reserve (normal SCr) before the procedure could be in renal insufficiency after the procedure if cholesterol embolism destroyed 20% of the nephrons. A good evaluation of the GFR is necessary before the procedure and particularly in patients with limited renal function, elderly patients and patients with extensive atheromatous disease. The choice of the protection device to use merits discussion. We have seen no difference between balloon occlusion and filter as in carotid angioplasty. Sos et al.85 reported that balloon occlusion protection devices seem more applicable, because the filters have a pore size of 100 µm or more allowing small particles and cholesterol crystals to go to the kidney. Holden feels that filters are the ideal renal
Conclusion Renal artery angioplasty and stenting is largely performed with very good technical success, good anatomical results, a low complication rate, and a good long-term patency rate. The effects on blood pressure are encouraging. However the deterioration of renal function after the procedure which may occur in 20–40% of cases may limit the immediate benefits of this technique. Atheroembolism seems to play an important role. Physicians dedicated to this field should be aware of the risks of atheroembolism and deterioration of renal function after renal interventional procedures. Renal protection is a new approach to improve the results of PTRA and stenting. Safety, feasibility, and efficacy of protected renal angioplasty has been demonstrated. Distal protection is not merely particulate retrieval. It may be the standard of care in the near future. Selective indications should be pointed out, particularly patients with renal insufficiency. Larger or randomized studies are awaited and will be needed to definitively address the utility of this approach and better document its beneficial effects on renal function and perhaps on hypertension, as well as on long-term prognosis. Some problems remain: ● ● ●
●
the cost of this technique; the best protection device needs to be determined; improvements in protection devices are needed and those specifically designed for renal protection; indications have to be specified.
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Rihal CS, Textor SC, Breen JF et al. Incidental renal artery stenosis among a prospective cohort of hypertensive patients undergoing coronary angiography. Mayo Clin Proc 2002; 77: 309–16 Missouris CG, Buckenham T, Cappucio FP et al. Renal artery stenosis: A common and important problem in patients with peripheral vascular disease. Am J Med 1994; 96: 10–14 Gross CM, Krämer J, Waigland J et al. Ostial renal artery stent placement for atherosclerotic renal artery stenosis in patients with coronary artery disease. Cath Cardiovasc Diagn 1998; 45: 1–8 Jean WJ, al-Bitar I, Zwicke DL et al. High incidence of renal artery stenosis in patients with coronary artery disease. Cath Cardiovasc Diagn 1994; 32: 8–10 O’Neil EA, Hansen KJ, Canzanello VJ et al. Prevalence of ischemic nephropathy in patients with renal insufficiency. Am Surg 1992; 58: 485–90 Hansen KJ, Edwards MS, Craven et al. Prevalence of renovascular disease in the elderly: a population based study. J Vasc Surg 2002; 36: 443–51 Schreiber MJ, Pohl MA, Novick AC. The natural history of atherosclerotic and fibrous renal artery disease. Uro Clin North Am 1984; 11: 383–92 Strandness DE Jr. Natural history of renal artery stenosis. Am J Kidney Dis 1994; 24: 630–5 Zierler RE. Screening for renal artery stenosis: is it justified. Mayo Clin Proc 2002; 77: 307–8 Subramanyan R, Joy J, Balakrishnan KG. Natural history of aortoarteritis (Takayasu’s disease). Circulation 1989; 80: 429–37 Sharma S, Jain AK. Natural history of non-specific aortoarteritis. In: Panja M, ed. Non Specific Aorto Arteritis. Marksman Media Services, Kolkata, 2001: 165
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Goncharenko V, Gerlock AJ, Schaff MI et al. Progression of renal artery fibromuscular dysplasia in 42 patients as seen on angiography. Radiology; 1981; 139: 45–50 Knutson DW, Abt AB. Pathophysiology, pathology, and clinical features of renovascular hypertension. In: Strandness E, Arena Van Breda JR, ed. Vascular Diseases. New York: Churchill Livingstone, 1994: 673 Berglund G, Anderson O, Wilhelmsent. Prevalence of primary and secondary hypertension studies in a random population sample. BMJ 1976; 2: 554–6 Pickering TG. Renovascular hypertension: medical evaluation and non surgical treatment. In: Laragh JM, Brenner BM, eds. Hypertension: Physiopathology, Diagnosis, and Management. New York: Raven Press, 1990: 1539 Messena LM, Zelenock GB, Yaok A et al. Renal vascularization for recurrent pulmonary oedema in patients with poorly controlled hypertension and renal insufficiency: a distinct subgroup of patients with atherosclerotic renal artery occlusive disease. J Vasc Surg 1994; 20: 76–87 Stane Y, Gyepes MT, Olson DL et al. Renovascular hypertension in children and adolescents. Radiology 1978; 129: 123–8 Sos TA, Pickering TG, Sniderman K et al. Percutaneous transluminal angioplasty in renovascular hypertension due to atheroma or fibromuscular hyperplasia. N Engl J Med 1983; 309: 274–8 Edwards MS, Craven TE, Borke GL et al. Renovascular disease and the risk of adverse coronary events in the elderly – a prospective, population based study. Arch Intern Med 2005; 165: 207–13 Fried LF, Shlipak MG, Crump C et al. Renal insufficiency as a predictor of cardiovascular outcomes and mortality in elderly individuals. J Am Coll Cardiol 2003; 41: 1364–72
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Johansson M, Herlitz H, Jensen G et al. Increased cardiovascular mortality in hypertensive patients with renal artery stenosis. Relation to sympathic activation, renal function, and treatment regimens. J Hypertens 1999; 17: 1743–50 Shlipak MG, Fried LF, Crump C et al. Cardiovascular disease risk status in elderly persons with renal insufficiency. Kidney Int 2002; 62: 997–1004 Shlipak MG, Fried LF, Crump C et al. Elevations of inflammatory and procoagulant biomarkers in elderly persons with renal insufficiency. Circulation 2003; 107: 87–92 Novick AC. Ziegelbaum M, Vidt DG et al. Trends in surgical revascularization for renal artery disease: Ten year’s experience. JAMA 1987; 257: 498–501 Weibull H, Bergqvist D, Bergentz SE et al. P.T.R.A. versus surgical reconstruction of atherosclerotic renal stenosis: a prospective randomized study. J Vasc Surg 1993; 18: 841–52 Cambria RP. Surgery: Indications and variables that affect procedural outcome, as well as morbidity and mortality. J Invas Cardiol 1998; 10: 55–8 Van de Ven PJ, Kaatee R, Beutler JJ et al. Arterial stenting and balloon angioplasty in ostial atherosclerotic renovascular disease: a randomized trial. Lancet 1999; 353: 282–6 Henry M, Amor M, Henry I et al. Stents in the treatment of renal artery stenosis: long-term follow-up. J Endovasc Surg 1999; 6: 42–51 Henry M, Amor M, Henry I et al. Stent placement in the renal artery: three-year experience with the Palmaz stent. J Vasc Interv Radiol. 1996; 7: 343–50 Blum U, Krumme B, Flugel P et al. Treatment of ostial renal artery stenosis with vascular endoprotheses after unsuccessful balloon angioplasty. N Engl J Med 1997; 336: 459–65 Van de Ven PJ, Beutler JJ, Kaatee R et al. Transluminal vascular stent for ostial atherosclerotic renal artery stenosis. Lancet 1995; 346: 672–4 Dorros G, Jaff M, Jain A et al. Follow-up of primary Palmaz–Schatz stent placement for atherosclerotic renal artery stenosis. Am J Cardiol 1995; 75: 1051–5 Isles CG, Robertson S, Hill D. Management of renovascular disease: a review of renal artery stenting in ten studies. Q J Med 1999; 92: 159–67 Boisclair C, Therasse E, Olivia VL et al. Treatment of renal angioplasty failure by perculaneous renal artery stenting with Palmaz stents: midterm technical and clinical results. AJR Am J Roentgenol 1997; 168: 245–51 Hiramoto J, Hansen KJ, Pan WM et al. Atheroemboli during renal artery angioplasty: an ex vivo study. J Vasc Surg 2005; 41: 1026–30 Henry M, Klonaris C, Henry I. Renal stenting with the Percusurge Guardwire device: a pilot study. J Endovasc Ther 2001; 8: 227–37 Henry M, Henry I, Klonaris C et al. Renal angioplasty and stenting under protection. The way for the future? Catheter Cardiovasc Interv 2003; 60: 299–312 Henry M, Henry I, Polydorou A et al. Renal angioplasty and stenting: long-term results and the potential role of protection devices. Expert Review Cardiovasc Ther 2005; 3: 321–34 Nordmann AJ, Woo K, Parkes R, Logan AG. Balloon angioplasty or medical therapy for hypertensive patients with atherosclerotic renal artery stenosis? A metaanalysis of randomized controlled trials. Am J Med 2003; 114: 44–50 Rundback JH, Sacks D, Kent KC et al. Guidelines for the reporting of renal artery revascularisation in clinical trials. American Heart Association. Circulation 2002; 106: 1572–85 Iannone LA, Underwood P, Nath A et al. Effect of primary balloon expandable renal artery stents on long-term patency, renal function, and balloon pressure in hypertension and renal insufficient patients with renal artery stenosis. Cathet Cardiovasc Diagn 1996; 37: 243–50 Taylor A, Sheppard D, MacLeod MJ et al. Renal artery stent placement in renal artery stenosis: technical and early clinical results. Clin Radiol 1997; 52: 451–7 Harden PN, MacLeod MJ, Rodger RS et al. Effect of renal artery stenting on progression of renovascular renal failure. Lancet 1997; 349: 1133–6 Paulsen D, Klow NE, Rogstad B et al. Preservation of renal function by percutaneous transluminal angioplasty in ischemic renal disease. Nephrol Dial Transplant 1999; 14: 1454–61 Rodriguez-Lopez JA, Werber A, Ray L et al. Renal artery stenosis treated with stent deployment: indications, technique and outcome in 108 patients. J Vasc Surg 1999; 29: 617–24 Rundback JH, Manoni T, Rozenblit GN et al. Balloon angioplasty or stent placement in patients with azotemic renovascular disease:
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a retrospective comparison of clinical outcomes. Heart Dis 1999; 1: 121–5 Guerrero, Kunjmmen B, Khaleel R et al. Stabilization of renal function after renal artery stenting. Am J Cardiol 2002; 90: 63H Allaqaband S, Shaikh F, Zaidi S et al. Long term effects of renal artery stenting or renal function in patients with atherosclerotic renal artery stenosis and baseline creatinine of > 2.0 mg/dl (abstract). Am J Cardiol 2003; 92 (suppl.): 54 L Haller ST, Kennedy D, Khuder S et al. Acute renal injury with renal artery stenting (abstract). Circulation 2004; 110 (suppl.): III–614 Zeller T, Frank U, Muller C et al. Stent supported angioplasty of severe atherosclerotic renal artery stenosis preserves renal function and improves blood pressure control. J Endovasc Ther 2004; 11: 95–106 Dorros G, Jaff M, Mathias L et al. Multicenter Palmaz stent renal artery stenosis revascularization registry report: four-year followup of 1058 successful patients. Catheter Cardiovasc Interv. 2002; 55: 182–8 Fiala LA, Jackson MR, Gillespie DL et al. Primary stenting of atherosclerotic renal artery ostial stenosis. Ann Vasc Surg 1998; 12: 128–33 Plouin PF, Chatellier G, Darne B et al. Blood pressure outcome of angioplasty in atherosclerotic renal artery stenosis: a randomized trial. Essai Multicentrique Medicaments vs. Angioplastie (EMMA) Study group. Hypertension 1998; 31: 823–9 White CJ, Ramee SR, Collins TJ et al. Renal artery stent placement: utility in lesions difficult to treat with balloon angioplasty. J Am Coll Cardiol 1997; 30: 1445–50 Dorros G, Jaff M, Mathiak L et al. Four-year follow-up of Palmaz–Schatz stent revascularization as treatment for atherosclerotic renal artery stenosis. Circulation 1998; 98: 642–7 Rocha Sing KJ, Miskkel GJ, Kathodi RE et al. Clinical predictors of improved long-term blood pressure control after successful stenting of hypertensive patients with obstructive renal artery atherosclerosis. Cathet Cardiovasc Intervent 1999; 47: 167–72 Von Knorring J, Edgren J, Lepantalo M. Long-term results of percutaneous transluminal angioplasty in renovascular hypertension. Acta Radiol 1996; 37: 36–40 Watson P, Madjipetrou P, Cow S et al. Effects of renal artery stenting on renal function and size in patients with atherosclerotic renovascular disease. Circulation 2000; 102: 1671–7 Rocha Singh K. Renaissance trial: a prospective multicenter trial to confirm the safety and efficacy of the express SD stent. Presented at ISET, Miami Beach, 2006 La Batide Alanore A, Azizi M, Froissart M et al. Split renal function outcome after renal angioplasty in patients with unilateral renal artery stenosis. J Am Soc Nephrol 2001; 12: 1235–41 Pattynama P, Becker GJ, Brown J et al. Percutaneous angioplasty for atherosclerotic renal artery disease: effect on renal function in azotemic patients. Cardiovasc Intervent Radio 1994; 17: 143–6 Subramanian R, Silva JA, Ramee SR et al. Beneficial effects of chronic renal insufficiency. Eur Heart J 2002; P577: 97 Topol EJ, Yadav JS. Recognition of the importance of embolization in atherosclerotic vascular diases. Circulation 2000; 101: 570–80 Baim DS, Wahr D, George B et al. Randomized trial of a distal embolic protection device during percutaneous intervention of saphenous vein aorto-coronary bypass grafts. Circulation 2002; 105: 1285–90 Limbruno U, Micheli A, De Carlo M et al. Mechanical protection of distal embolization during primary angioplasty: safety, feasibility, and impact on myocardial reperfusion. Circulation 2003; 108: 171–6 Holden A, Hill A. Renal angioplasty and stenting with distal protection of the main renal artery in ischemic nephropathy: early experiments. J Vasc Surg 2003; 38: 962–8 Walker C, Kowalski J, Knan M et al. Proximal protection before distal protection: preventing large atheroemboly during renal intervention. Am J Cardiol 2002; 90: 28H Nolan BW, Schermerhom ML, Rowell E et al. Outcomes of renal artery angioplasty and stenting using low-profile systems. J Vasc Surg 2005; 41: 46–52 Commeau P, Barragan P, Huret B et al. Direct stenting in the treatment of renal artery stenosis: immediate and in-hospital results. Am J Cardiol. 2001; TCT 74 Morice MC, Marco J, Laborde JC et al. The French registry on renal stenting. Am J Cardiol 2002; 90: 67H Rocha Singh K, Jaff MR, Rosenfield K. Evaluation of the safety and effectiveness of renal artery stenting after unsuccessful balloon angioplasty: the Aspire 2 study. J Am Coll Cardiol 2005; 46: 776–83
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Roubin GS. Carotid angioplasty and stenting under cerebral protection: the standard of care. Presented at the International Congress XV, Scottsdale, February 11–14, 2002 Holden A. Renal angioplasty and stenting with distal protection. Presented at the All That Jazz Meeting, New Orleans, 2005 Eggebrecht H, Haude M, Baumgart D et al. A new temporary occlusion and aspiration system prevention of distal embolization during percutaneous transluminal renal angioplasty. J Intervent Cardiol 2000; 13: 339–42 Li SS, Wang CH, Lam CW. Renal angioplasty under protection of the Percusurge Guardwire plus system. J Invasive Cardiol 2003; 15: 148–50 Guerkens U, Mueller R, Soblik S et al. A new protection device to prevent distal embolization in peripheral interventions. First results in renal and carotid arteries. Presented at the ACC Meeting, Anaheim, March 12–15, 2000 Edwards MS, Craven BL, Stafford J et al. Distal embolic protection during renal artery angioplasty and stenting. J Vasc Surg 2006; 44: 128–35 Sos T, Trost D. The importance of renal stenting in ischemic nephropathy. Endovasc Today 2003; 2: 44–6 Kulwant SH, Venkateswara KR. Atheroemboli renal disease. J Am Soc Nephrol 2001; 12: 1781–7
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Renal artery stenosis: when to refer to surgery? C Klonaris, A Katsargyris, and A Giannopoulos
Introduction Renal artery stenosis (RAS) may lead to several pathophysiologic disease processes such as secondary hypertension, renal insufficiency, and flush pulmonary edema, or may simply remain silent throughout life. It is caused by either atherosclerosis, or less frequently by a variety of entities including fibromuscular dysplasia, neurofibromatosis, and Takayasu’s arteritis. Atherosclerotic renal artery stenosis (ARAS) is a common entity, prevalent in patients suffering from coronary, carotid, and peripheral vascular disease. ARAS is a frequent cause of end-stage renal disease and is estimated to account for approximately 15% of the patients who require dialysis.1 Fibromuscular dysplasia most commonly affects young females and children, and usually is complicated with hypertension, while renal function is rarely impaired. The lesions involve predominantly the mid- and distal main renal artery, but can also extend to side branches. Progressive disease has been reported in up to 50% of those suffering from atherosclerotic occlusive disease of the renal artery and in up to 35% of patients with fibromuscular dysplasia.2,3 Treatment of renal arterial disease should serve to aid in the normalization of blood pressure, to preserve renal function, and possibly to reduce risk of cardiovascular events and mortality.4 Medical therapy is increasingly successful for RAS management. However, intervention remains a rational approach for progressive renal failure, failed antihypertensive medical treatment, and flash pulmonary edema especially in cases of progressive high-grade stenotic lesions. Although the outcome of any intervention has still to be compared with long-term results of the gold-standard surgical repair, the introduction of new, more potent percutaneous endoluminal techniques over the last decade has influenced surgical intervention for renovascular disease.5 One must be conscious of the fact that technological advances are rapidly overcoming the clinical limitations and long-term durability issues of endovascular procedures, thus increasing further the number of patients treated with minimally invasive techniques and restraining the space for conventional surgical repair. This chapter focuses on surgical intervention for RAS.
Indications for renal revascularization To date, there is no level A evidence (data derived from multiple randomized clinical trials or meta-analyses) supporting
either surgical or endovascular renal revascularization versus best medical treatment. Consequently, indications for intervention in renovascular disease are based on data derived from non-randomized studies, consensus opinion of experts, case studies, or standard of care (level of evidence B and C). Atherosclerotic renal artery disease Conditions for which there is evidence or general agreement that renal revascularization is beneficial, useful, and effective include: ●
●
●
●
hemodynamically significant stenoses with recurrent, unexplained congestive heart failure (CHF) or sudden, unexplained pulmonary edema; stenoses associated with accelerated, resistant to medication, or malignant hypertension; bilateral or unilateral to a solitary functioning kidney stenoses coexisting with chronic renal insufficiency; stenoses associated with unstable angina.
Conditions for which usefulness and efficacy of revascularization are less well established include: ●
●
●
asymptomatic patients with either bilateral or unilateral to solitary functioning kidney hemodynamically significant stenoses; asymptomatic patients with unilateral hemodynamically significant stenosis; patients with chronic renal insufficiency and unilateral stenosis.
In asymptomatic patients revascularization is appropriate only in cases of a viable kidney (linear length > 7cm). Fibromuscular dysplasia Revascularization in adults with fibromuscular dysplasia is recommended in cases of severe hypertension and hemodynamically and/or functionally significant renal artery stenosis. Clues to hypertension due to renal fibromuscular dysplasia include hypertension in childhood or adolescence, diastolic blood pressure > 115 mmHg in adult females < 45 years, hypertension resistant to medical management, abdominal bruit, hypertensive retinal arteriopathy, and differences in renal size or excretory function revealed with intravenous urographic or radionuclide studies. The hemodynamic significance 539
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Table 57.1 Operative techniques for renal revascularization Operative techniques Aortorenal bypass Renal endarterectomy Renal artery reimplantation Extra-anatomical splanchnorenal bypasses Ex vivo repair Primary nephrectomy Secondary nephrectomy
of dysplastic RAS can be determined with intra-arterial angiography. A pressure gradient of ~10 mmHg across the lesion, as well as demonstration of collateral vessels indicate significant RAS.6 The functional importance of RAS can be assessed via renin profiling.7
Important factors that should be considered in order to decide on the surgical technique include the condition of the native aorta, the existence of unilateral or bilateral renal artery disease, whether the stenotic lesion involves the ostium or the segmental branches of the renal artery, and the underline cardiopulmonary status of the patient. In cases of a hostile aorta due to intrinsic disease that is non-treatable without excessive patient risk, or in situations of very poor cardiac function, where aortic crossclamping would be hazardous, an extra-anatomical bypass may be appropriate. In patients who require open surgical treatment of AAAs or severe aortoiliac occlusive disease, an aortorenal bypass or endarterectomy simultaneously with an aortic reconstruction may be performed. In the case of single renal artery disease and a normal aorta an aortorenal bypass is preferred, while for the treatment of bilateral disease or multiple renal arteries of the same kidney, endarterectomy is favored.10,12,21,22
Surgery for RAS Surgical revascularization techniques A variety of open surgical procedures have evolved for the management of different clinical scenarios of RAS requiring intervention (Table 57.1). Although each method has its advantages, no single management provides optimal repair for all types of RAS. Aortorenal bypass is probably the most versatile approach; it is the most common open surgical procedure for the treatment of ARAS.8 Reversed autologous saphenous vein is used preferentially. However, use of a PTFE or polyester filament graft is also acceptable, especially when the graft originates from a concurrently placed synthetic aortic prosthesis.9 Renal endarterectomy is generally considered more technically demanding than conventional or extra-anatomical bypass.10 It is useful for ostial lesions involving both kidneys or multiple renal arteries11 and is also preferred by many surgeons when performed in concert with an aortic reconstructive operation.12 Renal artery reimplantation is probably the simplest and best option when the stenosis is orificial and there is sufficient vessel length. This technique has particular application in children with ostial lesions in whom the need for graft material can be avoided.13 It is also useful for combined repairs of aortic and renal disease in adults. Extra-anatomical splanchnorenal bypasses have received greater attention as an alternative method for surgical renal revascularization, especially in selected subgroups of patients at high risk for direct repair.14,15 However, it is widely believed that such procedures are not comparable with direct reconstructions, since they demonstrate reduced durability. Finally, ex vivo repair is used when extensive exposure is necessary for prolonged periods as in cases of fibromuscular dysplasia with renal artery branches stenoses, dissection or occlusion, and cases of degeneration of previously placed grafts to the distal renal artery.16 Primary nephrectomy is performed in patients with renal artery occlusion where surgical or endoluminal revascularization procedures are not possible, and only when a benefit, particularly regarding hypertension control, is expected after kidney removal.17,18 Secondary nephrectomy should only be performed in cases that reconstruction procedures have failed and can not be salvaged with reoperation.19,20
The technological advances in percutaneous endoluminal procedures along with the increasing clinical experience have influenced surgical intervention for renovascular disease. Recent data suggest that 85–95% of the patients that undergo surgery for RAS have ostial renal artery atherosclerosis, combined with diffuse extrarenal atherosclerotic disease and renal insufficiency.5,11,20 Although ostial atherosclerotic lesions represented an important limitation of percutaneous transluminal renal angioplasty (PTRA) during the past, primary stenting has been proven to be effective in the treatment of such lesions with good short and long-term results.23 Thus, currently renal artery stenosis involving the ostium is not considered as an absolute indication for surgical intervention. Similarly, renal artery stenosis coexistent with aortic aneurysm or aortoiliac occlusive disease is not anymore an absolute indication for open surgery, since both renal and aortic pathologies can be simultaneously repaired with percutaneous techniques. PTRA has also been documented to be effective in the treatment of fibrodysplastic lesions24–30 and it has become the dominant treatment in most centers. Surgery is preserved only for cases of renal artery stenosis with macroaneurysms, extensive branch vessel disease, or complex dissections, where the frequency of angioplasty complications is high. Consequently many clinicians limit nowadays surgical renal revascularization to cases of severe hypertension despite maximal medical therapy, failure of endovascular techniques, disease patterns not amenable to PTRA, or disease associated with excretory renal insufficiency.5 The American College of Cardiology/American Heart Association4 currently recommends surgical reconstruction for RAS in patients with: ●
●
●
fibromuscular dysplastic RAS with clinical indications for intervention, especially those exhibiting complex disease that extends into the segmental arteries and those having macroaneurysms (level of evidence: B); atherosclerotic RAS and clinical indications for intervention, especially those with multiple small renal arteries or early primary branching of the main renal artery (level of evidence: B); atherosclerotic RAS in combination with pararenal aortic reconstructions (in treatment of aortic aneurysms or severe aortoiliac occlusive disease) (level of evidence: C).
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Renal artery stenosis: when to refer to surgery? Surgical revascularization is associated with a 0.9–9% 30-day mortality. Improved or stable renal function during long-term follow-up is found in about 70% of patients, while improved or cured hypertension is documented in 65–95%. Graft restonosis or thrombosis rates range between 4 and 5%.11,31,32 On the other hand, primary stenting is initially successful in 97–100% of the cases, with minimal peri-operative mortality. Restenosis rates range between 11 and 21%.23,33–38 while two studies have documented 5-year primary patency rates of 79% and 84.5%, and secondary patency rates of 92.4 and 98%.23,35 Improvement or stabilization of renal function occurs in 43–96% of the patients with atherosclerotic RAS39–42 and improvement or cure of hypertension in 56–78% of the cases23,34–38,43 Obviously the optimal treatment for patients with RAS remains controversial. Surgical revascularization is associated with higher peri-operative mortality rates than renal artery stenting, providing however better long-term results in terms of restenosis, blood pressure control, and renal function preservation. Contrarily, minimal invasive percutaneous approaches are associated with lower morbidity and mortality allowing for quicker return to normal activity, but their longterm efficacy is frequently inferior to surgery. The attractive benefits of minimal invasive approaches should be attentively weighed against their limitations. Longer term assisted patency rates for PTRA and stenting are not currently available for direct comparison with surgical revascularization and in the entire field of renal revascularization there is only one prospective randomized study comparing endarterectomy with angioplasty.44 Although the latter concluded that PTRA combined with intensive follow-up and aggressive reintervention should be the first choice of therapy for atherosclerotic RAS causing renovascular hypertension, additional prospective randomized studies are needed in order to reach to safe conclusions and recommendations regarding surgical versus endovascular renal revascularization. Despite the absence of clear evidence, it is without doubt that currently percutaneous revascularization has become the dominant treatment of RAS in most centers. In our department almost all cases of RAS are treated percutaneously and surgical renal revascularization is performed most commonly
Figure 57.1 Retroperitoneal approach during surgical repair of a ruptured thoracoabdominal aortic aneurysm. Note the hematoma caused by the aneurysm rupture (arrow).
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Figure 57.2 Vessel loops for control of the left renal artery (arrow) and superior mesenteric artery (arrow head).
in concert with abdominal or thoracoabdominal aortic aneurysm repair (Figures 57.1–57.3). In our opinion, surgical reconstruction of renal artery in patients with clinical indications for intervention is absolutely indicated in cases of: 1. acute complications of PTRA/stenting (e.g. thrombosis, arterial rupture with severe hemorrhage) when percutaneous techniques such as thrombolysis or stent graft placement are not feasible; 2. rare configurations such as RAS with coexistent metastenotic aneurysm or complex segmental disease with macroaneurysms (fibromuscular dysplasia); 3. disease not amenable to percutaneous revascularization (e.g. severely calcified or ulcerated aorta, presence of thrombus in proximity with the renal orifice, and in rare cases where the arterial access site is not available).
Figure 57.3 Left renal artery reimplantation at dacron aortic graft after endarterectomy.
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Textbook of peripheral vascular interventions Table 57.2 Absolute and relative indications for RA surgery when revascularization is indicated Surgery for RAS Absolute indications
Relative indications
Acute complications of PTRA/stenting (thrombosis, arterial rupture with severe hemorrhage) RAS with metastenotic aneurysm Complex segmental disease with macroaneurysms (fibromuscular dysplasia) Disease not amenable to percutaneous revascularizaion
Short length or early branching of the main renal artery Multiple small renal arteries Stenosis in combination with pararenal aortic reconstructions Technical failures of PTRA/stenting Young, low-surgical-risk patients with progressive disease
Surgery should be also kept active in the therapeutic armamentarium, particularly for cases of short length or early branching of the main renal artery, multiple small renal arteries, stenosis in combination with pararenal aortic reconstructions, technical failures of PTRA/stenting, and younger, low-surgical-risk patients with progressive disease (Table 57.2).
Obviously, as endovascular device technology progresses along with improved operator skills, more patients will become candidates for endovascular treatment and will avoid surgery. Perhaps in the future, device failure may be the sole absolute indication for surgical intervention. At present, surgery is losing cases, but still has its day.
REFERENCES 1.
2. 3. 4.
5. 6. 7.
8. 9. 10.
Mailloux LU, Napolitano B, Bellucci AG et al. Renal vascular disease causing end-stage renal disease, incidence, clinical correlates, and outcomes: a 20-year clinical experience. Am J Kidney Dis 1994; 24: 622–9 Erdoes LS, Berman SS, Hunter GC, Mills JL. Comparative analysis of percutaneous transluminal angioplasty and operation for renal revascularization. Am J Kidney Dis 1996; 27: 496–503 Caps MT, Perissinotto C, Zierler RE et al. Prospective study of atherosclerotic disease progression in the renal artery. Circulation 1998; 98: 2866–72 Hirsch AT, Haskal ZJ, Hertzer NR et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease) endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. J Am Coll Cardiol 2006; 47: 1239–312 Hansen KJ, Starr SM, Sands RE et al. Contemporary surgical management of renovascular disease. J Vasc Surg 1992; 16: 319–30 Ernst CB, Bookstein JJ, Montie J et al. Renal vein renin ratios and collateral vessels in renovascular hypertension. Arch Surg 1972; 104: 496–502 Luscher TF, Greminger P, Kuhlmann U et al. Renal venous renin determinations in renovascular hypertension. Diagnostic and prognostic value in unilateral renal artery stenosis treated by surgery or percutaneous transluminal angioplasty. Nephron 1986; 44 (suppl. 1): 17–24 Khauli RB, Novick AC, Ziegelbaum M. Splenorenal bypass in the treatment of renal artery stenosis: experience with sixty-nine cases. J Vasc Surg 1985; 2: 547–51 Dean RH, Benjamin ME, Hansen KJ. Surgical management of renovascular hypertension. Curr Probl Surg 1997; 34: 209–308 Dougherty MJ, Hallett JW Jr, Naessens J et al. Renal endarterectomy vs. bypass for combined aortic and renal reconstruction:
11. 12.
13. 14. 15. 16. 17. 18. 19.
20. 21. 22. 23. 24.
is there a difference in clinical outcome? Ann Vasc Surg 1995; 9: 87–94 Cherr GS, Hansen KJ, Craven TE et al. Surgical management of atherosclerotic renovascular disease. J Vasc Surg 2002; 35: 236–45 Stoney RJ, Messina LM, Goldstone J, Reilly LM. Renal endarterectomy through the transected aorta: a new technique for combined aortorenal atherosclerosis – a preliminary report. J Vasc Surg 1989; 9: 224–33 Fry WJ, Ernst CB, Stanley JC, Brink B. Renovascular hypertension in the pediatric patient. Arch Surg 1973; 107: 692–8 Fergany A, Kolettis P, Novick AC. The contemporary role of extraanatomical surgical renal revascularization in patients with atherosclerotic renal artery disease. J Urol 1995; 153: 1798–801 Moncure AC, Brewster DC, Darling RC, Atnip RG, Newton WD, Abbott WM. Use of the splenic and hepatic arteries for renal revascularization. J Vasc Surg 1986; 3: 196–203 Dean RH, Meacham PW, Weaver FA. Ex vivo renal artery reconstructions: indications and techniques. J Vasc Surg 1986; 4: 546–52 Whitehouse WM, Jr., Kazmers A, Zelenock GB et al. Chronic total renal artery occlusion: effects of treatment on secondary hypertension and renal function. Surgery 1981; 89: 753–63 Oskin TC, Hansen KJ, Deitch JS, Craven TE, Dean RH. Chronic renal artery occlusion: nephrectomy versus revascularization. J Vasc Surg 1999; 29: 140–9 Stanley JC, Whitehouse WM Jr, Zelenock GB et al. Reoperation for complications of renal artery reconstructive surgery undertaken for treatment of renovascular hypertension. J Vasc Surg 1985; 2: 133–44 Hansen KJ, Deitch JS, Oskin TC et al. Renal artery repair: consequence of operative failures. Ann Surg 1998; 227: 678–89 Hansen KJ, Thomason RB, Craven TE et al. Surgical management of dialysis-dependent ischemic nephropathy. J Vasc Surg 1995; 21: 197–209 Cambria RP, Brewster DC, L’Italien G et al. Simultaneous aortic and renal artery reconstruction: evolution of an eighteen-year experience. J Vasc Surg 1995; 21: 916–24 Blum U, Krumme B, Flugel P et al. Treatment of ostial renal-artery stenoses with vascular endoprostheses after unsuccessful balloon angioplasty. N Engl J Med 1997; 336: 459–65 Baumgartner I, Triller J, Mahler F. Patency of percutaneous transluminal renal angioplasty: a prospective sonographic study. Kidney Int 1997; 51: 798–803
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Renal artery stenosis: when to refer to surgery? 25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35.
Grim CE. Percutaneous transluminal dilatation: the treatment of choice for renal artery stenosis causing hypertension. Am J Kidney Dis 1981; 1: 186–7 Grim CE, Yune HY, Donahue JP et al. Unilateral renal vascular hypertension: surgery vs. dilation. Vasa 1982; 11: 367–8 Martin EC, Diamond NG, Casarella WJ. Percutaneous transluminal angioplasty in non-atherosclerotic disease. Radiology 1980; 135: 27–33 Saffitz JE, Totty WG, McClennan BL, Gilula LA. Percutaneous transluminal angioplasty. Radiological–pathological correlation. Radiology 1981; 141: 651–4 Schwarten DE, Yune HY, Klatte EC, Grim CE, Weinberger MH. Clinical experience with percutaneous transluminal angioplasty (PTA) of stenotic renal arteries. Radiology 1980; 135: 601–4 Tegtmeyer CJ, Elson J, Glass TA et al. Percutaneous transluminal angioplasty: the treatment of choice for renovascular hypertension due to fibromuscular dysplasia. Radiology 1982; 143: 631–7 Rimmer JM, Gennari FJ. Atherosclerotic renovascular disease and progressive renal failure. Ann Intern Med 1993; 118: 712–9 Marone LK, Clouse WD, Dorer DJ et al. Preservation of renal function with surgical revascularization in patients with atherosclerotic renovascular disease. J Vasc Surg 2004; 39: 322–9 van de Ven PJ, Kaatee R, Beutler JJ et al. Arterial stenting and balloon angioplasty in ostial atherosclerotic renovascular disease: a randomised trial. Lancet 1999; 353: 282–6 Tuttle KR, Chouinard RF, Webber JT et al. Treatment of atherosclerotic ostial renal artery stenosis with the intravascular stent. Am J Kidney Dis 1998; 32: 611–2 Henry M, Amor M, Henry I et al. Stents in the treatment of renal artery stenosis: long-term follow-up. J Endovasc Surg 1999; 6: 42–51
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Rocha-Singh KJ, Mishkel GJ, Katholi RE et al. Clinical predictors of improved long-term blood pressure control after successful stenting of hypertensive patients with obstructive renal artery atherosclerosis. Catheter Cardiovasc Interv 1999; 47: 167–72 White CJ, Ramee SR, Collins TJ et al. Renal artery stent placement: utility in lesions difficult to treat with balloon angioplasty. J Am Coll Cardiol 1997; 30: 1445–50 Lederman RJ, Mendelsohn FO, Santos R et al. Primary renal artery stenting: characteristics and outcomes after 363 procedures. Am Heart J 2001; 142: 314–23 Hirshberg B, Sasson T, Grinblat I, Shustin L, Rubinger D. Prolonged renal dysfunction secondary to renal-artery stenosis in the elderly – it is never too late. Nephrol Dial Transplant 1998; 13: 982–4 Harden PN, MacLeod MJ, Rodger RS et al. Effect of renal-artery stenting on progression of renovascular renal failure. Lancet 1997; 349: 1133–6 Watson PS, Hadjipetrou P, Cox SV, Piemonte TC, Eisenhauer AC. Effect of renal artery stenting on renal function and size in patients with atherosclerotic renovascular disease. Circulation 2000; 102: 1671–7 Rocha-Singh KJ, Ahuja RK, Sung CH, Rutherford J. Long-term renal function preservation after renal artery stenting in patients with progressive ischemic nephropathy. Catheter Cardiovasc Interv 2002; 57: 135–41 Dorros G, Jaff M, Jain A, Dufek C, Mathiak L. Follow-up of primary Palmaz–Schatz stent placement for atherosclerotic renal artery stenosis. Am J Cardiol 1995; 75: 1051–5 Weibull H, Bergqvist D, Bergentz SE et al. Percutaneous transluminal renal angioplasty versus surgical reconstruction of atherosclerotic renal artery stenosis: a prospective randomized study. J Vasc Surg 1993; 18: 841–50
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Non-atherosclerotic renovascular disease JM Garasic and K Rosenfield
Introduction While atherosclerotic vascular disease is the most common cause of renal artery stenosis, a host of less common causes of non-atherosclerotic renovascular disease may be encountered. Thus, a good knowledge base on the topic is key to guiding appropriate disease-based evaluation and treatment.
Fibromuscular dysplasia Fibromuscular dysplasia (FMD) is an uncommon vasculopathy that primarily affects the small and medium-sized arteries. While involvement of the vascular system may occur in most any anatomic locale, the renal arteries are the most common site of involvement.1 Histologically, three main variants of FMD exist, and include intimal fibroplasia, medial dysplasia, and adventitial fibroplasia.2 Medial dysplasia can be subdivided into medial fibroplasia, perimedial fibroplasia, and medial hyperplasia in decreasing order of occurrence.3 The
(a)
most common histologic variety of medial dysplasia is medial fibroplasia which accounts for 75–80% of cases of FMD. Histologically, there are alternating segments of medial thinning and collagen-containing areas of medial thickening. These changes lend a typical “string of beads” appearance in which the bead diameter exceeds that of the unaffected adjacent artery (Figure 58.1a). Renal involvement of medial fibroplasia may be paired with carotid or other vascular involvement. Also, where atheromatous renovascular disease most commonly affects ostial or proximal segments of the renal artery, medial fibroplasia typically affects the distal twothirds of the main renal artery and its sub-branches. Perimedial fibroplasia is less common than medial fibroplasias, and accounts for roughly 10–15% of FMD cases. In this variant, there is diffuse collagen deposition in the outer half of the arterial media, and the associated angiographic characteristic is a “string of beads” appearance in which the beads are smaller than the unaffected adjacent artery. Medial hyperplasia is the least common form of medial dysplasia, and is due to smooth muscle hyperplasia. The resultant angiographic
(b)
Figure 58.1 A 43-year-old woman presented with new hypertension, refractory to medical therapy. Magnetic resonance angiography (MRA) of the renal arteries showed evidence of fibromuscular disease affecting the left renal artery. (a) The left main renal artery (white arrow) is seen to demonstrate a typical “string of beads” appearance with the beads being exceeds that of the unaffected adjacent artery. (b) Subselective right renal angiography in a young man with flank pain and wedge-shaped renal infraction after vigorous exercise. Proximal fibromuscular changes are seen (white arrow) as well as branch-vessel dissection, a potential complication of FMD (black arrows).
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Non-atherosclerotic renovascular disease appearance is a smooth concentric stenosis. Adventitial fibroplasia is a highly uncommon cause of renal FMD and will not be discussed further. Finally, intimal fibroplasia is the result of intimal deposition of collagen, with resultant smooth tubular or focal stenoses of the renal artery. Fibromuscular disease displays a clear female predilection, though cases may be sporadic, or follow an autosomal dominant inheritance with variable penetrance.4 Classically, fibromuscular disease of the renal arteries is considered a source of hypertension in young women, and is said not to cause renal insufficiency, though there is data to support an improvement in glomerular filtration rate (GFR) following revascularization for FMD.5 The primary motivation for revascularization of renal artery FMD is to assist in antihypertensive management, or in some cases as a true cure for hypertension. This circumstance is quite different from atherosclerotic renovascular disease where revascularization may aid in the management of hypertension, but rarely is it singularly curative. The management of renal FMD is most commonly medical on initial diagnosis. As in patients with atherosclerotic renovascular disease, hypertension is often quite responsive to angiotensin converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs). However, since hypertension that results from renal FMD is quite responsive to revascularization, and there is a desire to avoid life-long antihypertensive therapy if possible in this typically young patient cohort, revascularization is usually pursued. Revascularization for fibromuscular disease of the renal arteries may be surgical or percutaneous. In a surgical series, patients with fibromuscular disease revascularized with open bypass experienced significant improvements in glomerular filtration rate (GFR) and blood pressure control. In fact, more patients with FMD as a contributor to their elevated blood pressure experienced cure of hypertension than patients with atherosclerotic RAS treated surgically.5 Surgical revascularization in this particular series included renal autoimplantation, stenosis resection, splenorenal bypass, and orthotopic renal reimplantation. In the current era, percutaneous interventions are the modality of first choice in patients with FMD. Several series have supported the benefit of balloon angioplasty alone (PTA) in the management of renal FMD.6–9 In one series, hypertension was cured or improved in 98% of FMD patients treated with PTA.10 Angiographic success was achieved in 100% of treated stenoses, and balloon size was chosen based upon the reference vessel proximal and distal to the affected segment. There is little data comparing the relative merits of standalone PTA vs. stenting for renal FMD. Likewise, because of evidence supporting success with PTA alone, stenting has often been considered contraindicated in such a circumstance, though there is no negative data to support this notion. One final consideration in patients with renal FMD is the occurrence of spontaneous renal artery dissection. Dissection of carotid and renal arteries affected by FMD have been described to occur, and may be recurrent.11,12 Clinically, this may be asymptomatic or present with the sudden onset of flank pain. In cases where the dissected vessel is an arterial sub-branch, the management is typically conservative (Figure 58.1b). However, main or major branch vessel dissection may be amenable to percutaneous stenting.
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Takayasu’s arteritis Takayasu’s arteritis (TA) most commonly presents in the second and third decades of life, and is a potential source of non-atheromatous renovascular disease. Hypertension is common in these patients, and is frequently caused by renovascular disease. Notable is a tendency to underestimate central aortic blood pressure in patients with TA given frequent bilateral involvement of the brachiocephalic vessels. Once the presumptive diagnosis of Takayasu’s arteritis is made, however, abdominal aortic imaging will reveal underlying renovascular disease. MRA and duplex ultrasound are both excellent modalities for evaluating renal artery involvement in patients with TA. Both modalities can define the severity of stenosis, and document vessel wall thickness. Renovascular disease has been estimated to be present in 28–75% of patients with Takayasu’s.13–15 Arteriopathy in TA is characterized by both acute inflammatory and chronic fibrotic changes. For patients believed to be in the inflammatory phase of TA, steroids or other immunosuppressive therapies should precede revascularization.16,17 It is notable, however, that since steroids can worsen hypertension, TA patients with renovascular involvement can be particularly difficult to manage. For patients in the fibrotic phase with persistent renovascular disease, percutaneous intervention and surgical revacularization may be considered (Figure 58.3). Renal artery angioplasty is a safe and effective treatment for renal TA.18 While stenting is clearly safe and effective in cases of aorto-ostial lesions, marked elastic recoil, and dissection after PTA, its superiority over balloon angioplasty alone is unproven.19 If open aortic grafting is required, simultaneous renal bypass would be a preferable strategy.
Aneurysmal disease of the renal arteries Aneurysmal disease of the renal arteries is uncommon, though has potentially serious implications. Most renal aneurysms are asymptomatic, and may be found during imaging of the renal arteries for possible renovascular disease, incidentally on non-renal imaging, and has even been described in patients under evaluation as living renal donors.20 Hypertension is a common feature in patients with renal aneurysm.20–23 Potential etiologies of hypertension in this patient population include concomitant atheromatous or fibromuscular renal artery stenosis, segmental ischemia due to microembolism, parenchymal compression, and kinks in the involved vessel with resultant distal hypoperfusion. While surgical correction of the aneurysm is associated with improved control of hypertension, complete resolution is not universal (Figure 58.2). Indications for treating aneurysm of the renal artery are a topic of some controversy. Ultimately, while the primary concern in treating such aneurysms is to prevent rupture, management of hypertension and limitation of renal microembolism are also considered. Thus, while such characteristics as size and rate of growth may be considered in deciding upon the need for surgery, these additional reasons for treatment may be independently considered.
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(a)
(b)
Figure 58.2 In the setting of new hypertension, an 18-year-old woman was found on magnetic resonance angiography (MRA) of the abdomen to have a 1.2-cm right renal artery aneurysm. (a) The aneurysm is seen to arise at a site of renal artery bifurcation (white arrow), and was thought a poor location for coil embolization. Instead, open surgical repair was undertaken, and repeat angiography (b) shows resolution of the aneurysm without evidence of further aneurysms elsewhere. Of note, blood pressure was seen to improve after the surgical resection, supporting the notion that renal artery aneurysms can lead to arterial compromise and subsegmental renal ischemia.
Renal artery stenosis following renal transplantation Post-transplant renovascular disease is a consideration of particular interest in centers where renal transplantation is common. Iliac atheromatous disease, progressive atheromatous disease of the renal artery, and anastomotic compromise are potential causes of post-transplant renal artery stenosis, and renovascular disease of the transplanted kidney. The presence of pre-existing iliac artery stenosis proximal to the site of renal implantation is a potential source of early and late posttransplant renal insufficiency and hypertension.24 For this reason, anatomic evaluation of the iliac vessels is a reasonable
(a)
(b)
pre-operative step in patients with known coronary or peripheral vascular disease, abnormal ankle–brachial index, significant cardiovascular risk factors, or diminished lower extremity pulses.25 The presence of a pelvic bruit overlying the area of renal transplant anastomosis is only reflective of underlying vascular disease and/or turbulent vascular flow. This exam finding is not specific for the diagnosis of transplant renovascular disease, nor does the absence of such a bruit rule out transplant RAS.26–28 MRA and, if necessary, contrast angiography can be used to secure the diagnosis and define the details of iliac anatomy (Figure 58.4). Similarly, a donor can be evaluated by MRA to rule out underlying renovascular disease in the transplant kidney, that could threaten the organs future viability.29
(c)
Figure 58.3 A 45-year-old man presented with lower extremity claudication, upper extremity claudication, uncontrolled hypertension, and newly diagnosed renal impairment. After imaging studies showed aorto-ostial disease of the brachiocephalic vessels and the common iliac arteries, a presumptive diagnosis of Takayasu’s arteritis was made. (a) Concomitant involvement of the renal ostia was found, and confirmed at angiography (black arrows). Once active inflammation was ruled out by magnetic resonance angiography (MRA) of the aorta and inflammatory markers, balloon angioplasty and stenting; (b) were undertaken with an excellent angiographic and physiologic response. The stented segment of the left renal artery (black arrow) is seen to be comparable in diameter to the distal reference vessel. (c) However, a segment of marked post-stenotic dilatation (white arrow) is seen in the right renal artery just beyond the stented segment (black arrow).
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(a)
(b)
(c) Figure 58.4 A 65-year-old man with a history of end-stage renal disease (ESRD) presented 2 years after successful pelvic implantation of an orthotopic kidney with uncontrolled hypertension, mild progressive renal insufficiency, and bilateral thigh and buttock claudication. (a) MRA of the transplant renal artery shows anastomotic stenosis (white arrow) and (b) angiographic evaluation confirm transplant renal artery stenosis at the site of iliorenal anastomosis (white arrow) subsequently treated with stenting (double white arrows). (c) Severe stenosis of the right common iliac artery proximal to the renal artery anastomosis (black arrow) is also present, and was stented (double black arrows) via a right femoral artery approach.
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Medical treatment of hypertension, percutaneous intervention, or even surgical revascularization are options for treatment as the anatomy and clinical circumstances dictate.30 The development of renal artery atheromatous disease following renal transplantation will not be addressed in detail in this section. It is notable, however, that the transplant renal artery continues to be susceptible to the development of cholesterolbased plaque. While multiple modalities may be used to evaluate the post-transplant renal artery, renal artery duplex is an excellent non-invasive option in light of the superficial nature of the post-transplant kidney. Finally, surgical anastomotic stenoses can be a cause of post-transplant renal artery stenosis. Renal insufficiency or uncontrolled hypertension early post-transplant should prompt an investigation for possible stenosis at the iliorenal anastomosis. In the initial post-operative phase, open surgical revascularization may be considered over percutaneous intervention where an errant suture or arterial clamp injury is suspected. However, reoperation surgery comes with significant attendant risks, thus percutaneous intervention is usually viewed as the first-line therapy for transplant RAS.31–33 Percutaneous intervention can be accomplished from an ipsilateral or contralateral femoral artery approach.34 While concerns about the somewhat tenuous nature of the post-transplant kidney and the uninephric state may prompt the interventionalist to consider use of a distal atheroembolic protection device, the relatively short length of the post-transplant renal artery can limit the use of such devices due to anatomic constraints. Intravascular stents, while indicated for significant elastic recoil of flow-limiting dissection after renal angioplasty, are likely to provide superior outcomes to balloon angioplasty alone,35 and are used widely in the setting of transplant renovascular disease as well.35–37
Kawasaki’s disease Kawasaki’s disease (KD) is an inflammatory vasculitis that affects primarily the medium-sized arteries, including the renal arteries. The clinical criteria for diagnosing Kawasaki’s disease have been described elsewhere.48 While aneurysm is a more commonly considered complication of KD, arterial stenoses have also been observed.49,50 KD is the most common childhood vasculitide, and given that hypertension in the young should be considered secondary until proven otherwise, it is a diagnosis worth considering in this patient population. In one study of children with renovascular hypertension, a non-specified vasculitis was found to have occurred in 9% of cases.51 Evidence of a necrotizing vasculitis elsewhere may assist in making the diagnosis were a renal artery tissue diagnosis is not available.52 Both surgical bypass and percutaneous intervention have been described.
Polyarteritis nodosa Polyarteritis nodosa (PAN) is a necrotizing vasculitis affecting small and medium-sized arteries, of which the renal arteries are most commonly involved. Anatomically, involvement of the main renal arteries or immediate sub-branches is far less common than smaller arteriolar involvement. Furthermore, PAN is a potential etiology of small-vessel, syndromic renal arteriolar microaneurysm, renal infarcts, intrarenal and perirenal hemorrhage, renal insufficiency, and proteinuria.53 In cases where PAN-associated renal aneurysms are multiple and intraparenchymal in location, vascular surgical excision and repair may be difficult. Successful treatment of ruptured aneurysms with conservative management and endovascular embolization has been described, as has the need for nephrectomy to control hemorrhage.53–55
Neurofibromatosis Neurofibromatosis is a rare cause of non-atherosclerotic renovascular disease, and is a particular consideration in children with renal artery stenosis.38 The disease has autosomal dominant inheritance with variable penetrance, with typical findings including “café-au-lait” spots, cutaneous and plexiform neurofibromas, and learning disabilities. However, cardiovascular manifestations of neurofibromatosis do exist.39,40 The renal arteries are the most common site of involvement of the systemic vasculopathy associated with this disease, and hypertension is the clinical presentation in patients so afflicted.41 Compromise of the arterial lumen can result from proliferation of spindle cells in the wall, degeneration, healing, and subsequent muscle loss accompanied by extensive fibrosis.42,43 Intrarenal arterial aneurysm can also occur, and potentially coexist with obstructive lesions.44 Essential hypertension is still thought to be the most common cause of hypertension in patients with neurofibromatosis, but given the known possibility of renal artery compromise, a search for renovascular disease is recommended. Both contrast angiography and magnetic resonance angiography have been recommended as diagnostic modalities in cases of suspected renovascular neurofibromatosis, in part to aid in characterizing renovascular stenoses and aneurysms which may coexist, as well as to identify affected accessory renal arteries.40,45 Treatment with balloon angioplasty as well as surgical bypass has been described.46,47
Scleroderma Scleroderma, or progressive systemic sclerosis (PSS), is a systemic autoimmune infiltrative disorder characterized clinically by loss of cutaneous elasticity with skin thickening, Raynaud’s phenomenon, interstitial pulmonary fibrosis and pulmonary hypertension, myocardial fibrosis, esophageal infiltration, and renal involvement. PSS can affect the arterioles and small arteries of the skin, gut, lungs, heart, and kidneys.56 Scleroderma typically affects the medium-sized renal arteries and causes intimal and medial thickening with resultant renal hypoperfusion. As with large-vessel renovascular disease, there is resultant activation of the renin–angiotensin system, and accelerated hypertension and rapid loss of renal function can follow.57,58 Prompt treatment with angiotensin converting enzyme (ACE) inhibitors is crucial in preserving renal function during such scleroderma renal crises. As the diagnosis is usually made on a clinical basis, invasive imaging is usually unnecessary.
Radiation arteritis Radiation has been documented to cause obstructive medium to large-sized arterial lesions in a variety of anatomic locales:
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Non-atherosclerotic renovascular disease coronary, mesenteric, carotid, renal, and iliofemoral.7,59–61 The pathobiology of radiation arteriopathy varies depending upon the size of the affected vessel. Large arteries, such as those mentioned above, are thought to be relatively radiationresistant due to their high content of smooth muscle and connective tissue.59,62 However, endothelial injury can cause neointimal proliferation, and potentially hasten the process of atherosclerosis in the setting of hypertension and hyperlipidemia. Injury to the vaso vasorum has also been implicated to play a role in radiation arteritis.59,63 In fact, large-vessel radiation-induced renovascular disease is rarely described. Instead, most radiation-induced renovascular disease arises in the small intrarenal vessels, and causes interstitial thickening, proliferation, and fibrosis of the interlobular and arcuate arteries. This results in hypertension and renal insufficiency that may present decades after radiation exposure, and is uncommon in the current era of reduced-dose and directed radiation therapy for renal and lymphatic malignancies.59,64 While both percutaneous and open surgical means of revascularization have been described for management of
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radiation-induced vascular disease, there is no good evidencebased management of radiation RAS available.
Summary In summary, non-atherosclerotic causes of renovascular disease are uncommon, but important for vascular practitioners to recognize and understand. Of these, fibromuscular disease is the etiology most likely to be encountered, and is of particular importance given its occurrence in young patients, and the potential for FMD involvement in other vascular beds. Takayasu’s arteritis, while rare, is seen and managed by vascular practitioners, and has wide ranging anatomic implications as described. Finally, renal transplant arterial disease is of increasing importance in an era of widespread renal transplantation. In all of the above-described circumstances, there is considerable descriptive data to elucidate the pathobiology of renovascular involvement, however therapeutic management is still in evolution and is a fertile opportunity for further investigation.
REFERENCES 1. 2. 3. 4. 5. 6.
7. 8.
9.
10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21.
Gray BH, Young JR, Olin JW. Miscellaneous arterial diseases. In: Peripheral Vascular Diseases, second edition. Young JR, Olin JW, Bartholomew JR, eds. St. Louis: Mosby Yearbook, 1996: 425–40 Harrison EG, McCormack LJ. Pathologic classification of renal arterial disease in renovascular hypertension. Mayo Clin Proc 1971; 46: 161–7 Curr Op Rheumatol 2000; 12: 41–7 Rushton AR. The genetics of fibromuscular dysplasia. Arch Intern Med 1980, 140: 233–6 J Urol 2004; 171: 1043–5 Sos TA, Pickering TG, Sniderman K et al. Percutaneous transluminal renal angioplasty in renovascular hypertension due to atheroma or fibromuscular dysplasia. N Eng J Med 1983; 309: 274–9 Saddekni S, Sniderman KW, Hilton S, Sos TA. Percutaneous transluminal angioplasty of non-atherosclerotic lesions. AJR 1980; 135: 975–82 Mahler F, Probst P, Haertel M, Weidman P, Krneta A. Lasting improvement of renovascular hypertension by transluminal dilatation of atherosclerotic and nonatherosclerotic renal artery stenoses. Circulation 1982; 65: 611–7 Tegtmeyer CJ, Elson J, Glass TA et al. Percutaneous transluminal angioplasty: The treatment of choice for renovascular hypertension due to fibromuscular dysplasia. Radiology 1982; 143: 631–7 Circulation 1991; 83 [suppl. I]: I155–61 Meyers DS, Grim CE, Keitzer WF: Fibromuscular dysplasia of the renal artery with medial dissection: a case simulating polyarteritis nodosa. Am J Med 1974; 56: 412–6 Stroke 1985; 16(6) Lupi-Herrera E, Sánchez-Torres G, Marcushamer J et al. Takayasu arteritis. Clinical study of 107 cases. Am Heart J 1977; 93: 94–103 Kerr GS, Hallahan CW, Giordano J et al. Takayasu arteritis. Ann Intern Med 1994; 120: 919–29 J Clin Pathol 2002; 55: 481–6 Hall S, Barr W, Lie JT et al. Takayasu arteritis. A study of 32 North American patients. Medicine 1985; 64: 89–99 Kerr GS, Hallahan CW, Giordano J et al. Takayasu arteritis. Ann Intern Med 1994; 120: 919–29 Giordano JM. Surgical treatment of Takayasu’s arteritis. Int J Cardiol 2000; 75: S123–8 Sharma BK, Jain S, Bali HK et al. A follow-up study of balloon angioplasty and de-novo stenting in Takayasu arteritis. Int J Cardiol 2000; 75: S147–52 J Urol 1997; 158(2): 357–62 Martin RS III, Meacham PW, Ditesheim JA, Mulherin JL Jr., Edwards WH. Renal artery aneurysm: selective treatment for hypertension and prevention of rupture. J Vasc Surg 1989; 9: 26
22. 23. 24.
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34. 35. 36. 37. 38. 39. 40. 41.
Hupp T, Allenberg JR, Post K et al. Renal artery aneurysm: surgical indications and results. Eur J Vasc Surg 1992; 6: 477 Bulbul MA, Farrow GA. Renal artery aneurysms. Urology 1992; 40: 124 Voiculescu A, Hollenback M, Plum J et al. Iliac artery stenosis proximal to a kidney transplant: clinical findings, duplexsonographic criteria, and outcome. Transplantation 2003; 76: 332–9 Becker BN, Becker YT, McDermott JC et al. Abstracts of the 17th Annual Meeting of the American Society of Transplant Physicians, Chicago, May 9–13, 1998 Gray D. Renal artery stenosis in the transplanted kidney. Transplantation 1994; 58: 15–21 Lacombe M. Arterial stenosis complicating renal allo-transplantation in man. Ann Surg 1975; 181: 283–9 Morris P, Yadav R, Kincaid-Smith P et al. Renal artery stenosis in renal transplantation. Med J Aust 1971; 1: 1255–7 Bakker J, Ligtenberg G, Beek F, van Reedt Dortland R, Hené R. Transplantation 1999; 67(8): 1167–72 Merkus JW, Huysmanns FT, Hoitsma AJ et al. Renal allograft artery stenosis: results of medical treatment and intervention. A prospective analysis. Transplant Int 1993; 6: 111–5 Sniderman K, Sprayregan S, Sos TA. Percutaneous transluminal dilatation and renal transplant arterial stenosis. Transplantation 1980; 30: 440–4 Fauchald P, Vatne K, Paulsen D et al. Long term clinical results of percutaneous transluminal angioplasty in transplant renal artery stenosis. Nephrol Dial Transplant 1992; 7: 256–9 Rengel M, Gomes-Da-Silva G, Inchaustegui L et al. Renal artery stenosis after kidney transplantation: diagnostic and therapeutic approach. Kidney Int 1988; 54 (suppl. 68): S99–106 Spinosaa DJ, Isaacs RB, Matsumotoa AH et al. Curr Opin Urol 2001; 11: 197–205 Holder for KR paper on stents versus PTA Sierre SD, Raynaud AC, Carreres T et al. Treatment of recurrent transplant renal artery stenosis with metallic stents. J Vasc Interv Radiol 1998; 9: 639–44 Taube D. The use of expandable metal stents in transplant renal artery stenosis. Clin Radiol 1995; 50: 245–50 Holder Salyer WR, Salyer DC. The vascular lesions of neurofibromatosis. Angiology 1974; 25: 510–9 Lin AE, Birch PH, Korf BR et al. Cardiovascular malformations and other cardiac abnormalities in neurofibromatosis 1 (NF1). Am J Med Genet 2000; 95: 108–17 Friedman JM., Arbiser J, Epstein JA et al. Cardiovascular disease in neurofibromatosis 1: Report of the NF1 Cardiovascular Task Force. Gen Med 2002; 4(3): 105–11
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Textbook of peripheral vascular interventions Finley JL, Dabbs DJ. Renal vascular smooth muscle proliferation in neurofibromatosis. Hum Pathol 1988; 19: 107–10 Zochodne D. Von Recklinghausen’s vasculopathy. Am J Med Sci 1984; 287: 64–5 Huffman JL, Gahtan V, Bowers VD, Mills JL. Neurofibromatosis and arterial aneurysms. Am Surg 1996; 62: 311–4 Wasser MN, Westenberg J, van der Hulst VP et al. Hemodynamic significance of renal artery stenosis: digital subtraction angiography versus systolically gated three-dimensional phase-contrast MR angiography. Radiology 1997; 202: 333–8 Fossali E, Minoja M, Intermite R et al. Pediatr Nephrol 1995; 9: 5 Chalmers RTA, Dhadwal A, Deal J, Snell M, Wolfe JHN. The surgical management of renal artery stenosis in children. Brit J Surg 1988; 85 (suppl. 1): 40 Cassidy JT, Petty RE. Textbook of Pediatric Rheumatology, third edition. Philadelphia: WB Saunders, 1995: 372 Sasaguri Y, Kato H. Regression of aneurysms in Kawasaki disease: a pathological study. J Pediatr 1982; 100: 225–31 Roberti I, Reisman L, Churg J. Vasculitis in childhood. Pediatr Nephrol 1993; 7: 479–89 Deal JE, Snell MF, Barratt TM, Dillon MJ. Renovascular disease in childhood. J Pediatr 1992; 121: 378–84 BJ Foster, C Bernard, KN Drummond. Arch Dis Child 2000; 83: 253–5 Zapzalka DM, Thompson HA, Borowsky SS et al. Polyarteritis nodosa presenting as spontaneous bilateral perinephric hemorrhage: management with selective arterial embolization. J Urol 2000; 164: 1294–5
54. 55. 56. 57.
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Smith D, Wernick R. Spontaneous rupture of a renal artery aneurysm in polyarteritis nodosa: critical review of the literature and report of a case. Am J Med 1989; 87: 464 Chandrakantan A, Kaufman, J. Renal hemorrhage in polyarteritis nodosa: diagnosis and management. Am J Kidney Dis 1999; 33: e8 Abuelo G. Diagnosing vascular causes of renal failure. Arch Int Med 1995; 123(8): 601–14 Traub YM, Shapiro AP, Rodnan GP et al. Hypertension and renal failure (scleroderma renal crisis) in progressive systemic sclerosis: review of a 25-year experience with 68 cases. Medicine 1983; 62: 335–52 Gavras H, Gavras I, Cannon PJ, Brunner HR, Laragh JH. Is elevated plasma renin activity of prognostic importance in progressive systemic sclerosis? Arch Intern Med 1977; 137: 1554–8 Katras T, Baltazar U, Colvett K et al. Radiation-related arterial disease. Am Surgeon 1999; 65: 1176–9 Bigot JM, Mathieu D, Reizine D. Radiation arteriopathies. Ann Med Intern 1983; 134(5): 411–5 Hull MC, Morris CG, Pepine CJ, Mendenhall NP. Valvular dysfunction, and carotid, subclavian, and coronary artery disease in survivors of Hodgkin lymphoma treated with radiation therapy. JAMA 2003; 290: 2831–7 Fajardo LF. Morphologic pattems of radiation injury. Front Radiat Ther Oncol 1989: 23: 75–84 Fajardo LF, Berthrong M. Vascular lesions following radiation. Pathol Ann 1988; 23(1): 297–330 Fer MF, McKinney TD, Richardson RL et al. Cancer and the kidney: Renal complications of neoplasm. Am J Med 1981; 71: 704–18
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SECTION IX Celiac and mesenteric arteries
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Etiology, natural history, and pathophysiology of mesenteric ischemia JA Silva
Introduction Athero-occlusive disease of the mesenteric arteries occurs relatively frequently in the elderly population. On the other hand mesenteric ischemia is an uncommon clinical condition which generally manifests in its chronic form as post-prandial abdominal pain and weight loss, emaciation, and in its acute form or as an abrupt development of abdominal pain, lower gastrointestinal bleeding, and intestinal necrosis. Both conditions are inexorably fatal if they are left untreated. Although vascular disease causing acute intestinal gangrene had been recognized for centuries, and successful surgical treatment of intestinal infarction had been reported in the nineteenth century by Elliot1; the condition that we know today as Chronic Mesentric Ischemia was initially described by Goodman in 1918, who named it “angina abdominis” or abdominal angina, implying a similar pathophysiology to the recently described symptoms of coronary insufficiency.2 However, the existence of CMI was not fully accepted until 1936 when a publication by Dunphy provided irrefutable evidence of its existence. In his classic paper, Dunphy described a 47-year-old man who presented with worsening of his chronic post-prandial abdominal pain and severe weight loss, and suddenly died of acute abdominal pain, the necropsy showing intestinal infarction and severe three-vessel mesenteric atherosclerotic disease with superimposed thrombotic occlusion of the celiac trunk.3 In spite of giant advances in diagnostic techniques and procedures since the initial descriptions by Goodman and Dunphy, the diagnosis of mesenteric ischemia, particularly in its chronic form, remains challenging and under-recognized.
elderly individuals (> 65 years), found a 17.5% prevalence of significant (> 70%) stenosis, affecting at least one mesenteric artery.8 Furthermore, patients with renal artery stenosis have a very high (> 50%) prevalence of significant mesenteric artery stenosis.9 On the other hand, the development of symptoms of chronic mesenteric ischemia is relatively unusual, probably due to the rich communication among the three mesenteric vessels as well as the development of collaterals from other arteries. Although it is difficult to estimate the true incidence of this condition, mesenteric ischemia in its acute form has been reported to occur in 1 in 1000 hospital admissions, and in its chronic form in 1 in 100,000 individuals.10,11 Etiology Atherosclerotic disease is responsible for mesenteric arterial stenoses in more than 95% of the cases (Figure 59.1). These
Prevalence, etiology, and natural history Prevalence Mesenteric arterial stenoses occur commonly, particularly in the elderly population with established atherosclerotic disease. An angiographic study found a prevalence of asymptomatic mesenteric stenosis affecting at least one mesenteric artery in 40, 29, and 25% of patients with abdominal aortic aneurysm, aortoiliac obstructive disease, and peripheral atheroocclusive disease of the lower extremities, respectively.7 A recent study using duplex ultrasound in a non-selected group of
Figure 59.1 Atherosclerotic disease of the celiac and common hepatic artery (arising from the aorta, between the celiac trunk and the superior mesenteric artery).
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Textbook of peripheral vascular interventions patients with CMI develop acute mesenteric ischemia; however, the true incidence remains unknown.10 The other 50–80% of the patients continue with symptomatic chronic, post-prandial abdominal pain, weight loss, emaciation, and finally die.21 It is possible that a proportion of these patients may have attenuation or spontaneous relief of symptoms; however, this has not yet been documented. In spite of the etiology, abrupt interruption of perfusion of the small intestine and colon progresses from potentially reversible alterations in tissue integrity to complete transmural infarction with hemorrhagic necrosis. Consequently, acute mesenteric ischemia has a very poor prognosis with a mortality rate of 60–100% despite early treatment institution.10
Physiology, pathophysiology of mesenteric ischemia
Figure 59.2 Extrinsic compression of the celiac trunk by the median arcuate ligament of the diaphragm.
lesions are usually bulky and concentric, located in the ostium or the very proximal portion of the mesenteric artery, and are frequently caused by progressive atherosclerotic disease of the anterior aortic wall.12 Other vascular conditions such as fibromuscular dysplasia, Takayasu’s disease, Buerger’s disease, radiation, and autoimmune arteritis are uncommon causes of mesenteric arterial stenoses.13,14 The origin of the celiac trunk can be extrinsically compressed by the arcuate ligament of the diaphragm causing significant, sometimes critical, stenosis of this vessel (Figure 59.2).15 Whether isolated, extrinsic compression of the celiac trunk may lead to the development of symptomatic chronic mesenteric ischemia or the so-called “celiac axis compression syndrome,” has been the subject of great debate.16 However, there has been careful documentation showing that surgical decompression of this vessel leads to lasting symptom relief.17 Natural history There are scarce data in the literature addressing the progression of mesenteric arterial disease. Consequently, the natural history of this condition is still incompletely understood. Some investigators18 have suggested that progression of atherosclerotic mesenteric arterial stenoses occur at the same pace as that of renal atherosclerotic disease; that is, ~20% per year.19 In asymptomatic patients with established mesenteric atherosclerotic disease, development of symptomatic acute or chronic mesenteric ischemia has recently been shown to occur only in patients with multivessel disease. In a prospective study20 using invasive abdominal angiography in 980 patients, significant (> 50%) stenosis of at least one mesenteric artery was found in 82 patients. At a mean follow-up of 2.6 years, mesenteric ischemia developed only in the patients with three-vessel mesenteric arterial stenoses (27% of 15 patients). The natural history of patients with symptomatic CMI is dire. Some investigators have suggested that 20–50% of
Physiology Chronic mesenteric ischemia occurs as a result of insufficient oxygen delivery – that is, insufficient arterial blood supply – to the gut tissue, which is necessary to maintain normal intestinal functions such as secretion, absorption, and the increase in motility that follows food ingestion. In normal individuals, the intestine receives 10–20% of the cardiac output and up to 35% after meals, with 70% of this output supplying the intestinal mucosa.22 The splanchnic circulation has been shown to be subjected to a significant decrease in its arterial flow or to the development of ischemia in conditions of hypovolemia, shock, or extreme physical exercise.22–24 Studies using duplex ultrasound have demonstrated that after a 1000-calorie meal, flow velocities at the superior mesenteric artery (SMA) increase from 22.2 cm/second to 57 cm/second, and interestingly the Doppler waveform changes from high-resistance (triphasic), to a low-resistance pattern with high increased end-diastolic velocity.25 These changes in arterial flow velocities are the result of highly sophisticated and complex mechanisms that control vascular resistance, including intrinsic and neurohormonal mechanisms as well as extrinsic mechanisms. Among the intrinsic mechanisms of splanchnic blood flow autoregulation, it has been shown that a reduction in perfusion pressure leads to the release of adenosine and other metabolites of ischemia that directly produce a relaxation effect in the arteriolar smooth muscle of the splanchnic arterioles.22 In addition, during periods of hypoperfusion, the intestinal mucosa is capable of extracting larger amounts of oxygen. A study has shown that the human intestine has a fairly constant oxygen extraction until blood flow reaches a critical limit of 30 ml/minute/100 grams.26 Extrinsic mechanisms of splanchnic flow regulation include neural (the sympathetic nervous system) and hormonal (the renin– angiotensin system and vasopressin). Sympathetic tone is mainly provided by the preganglionic cholinergic fibers of the greater splanchnic nerves, which synapse in the paired celiac ganglia adjacent to the celiac trunk. On the other hand, parasympathetic fibers of the vagi also innervate the intestine, but probably exert negligible effect on the mesenteric vasculature.27 The renin–angiotensin system is stimulated under conditions of low extracellular flow volume, which promotes vasoconstriction through the direct action of angiotensin II
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Etiology, natural history, and pathophysiology of mesenteric ischemia and indirect action of adrenergic stimulation. Likewise, vasopressin is released from the pituitary gland triggering mesenteric arterial vasoconstriction and venorelaxation in conditions of blood loss and hyperosmolarity.28 Pathophysiology of acute mesenteric ischemia Acute mesenteric ischemia occurs as a result of sudden decrease or interruption of blood flow and oxygenation of the intestinal tissue, resulting in hypoxemia and compromise of the intestinal viability, which may lead to intestinal infarction if blood flow is not restored promptly. Acute mesenteric ischemia may be caused by embolism, thrombosis, non-obstructive vascular disease, or may be iatrogenic. Arterial embolism is the most common cause of acute mesenteric ischemia accounting for approximately 45–50% of cases.10,29 The heart is by far the most common source (~80%) of peripheral embolization, with atrial fibrillation the most frequent cause (~75%) for this condition, followed by recent myocardial infarction (~25%).30 Other embolic sources include cholesterol emboli from the aorta, septic emboli from the cardiac valves, tumor emboli such as atrial myxoma, mural thrombus from aortic aneurysms, and paradoxical emboli from the venous system in patients with patent foramen ovale or atrial septal defects.30 Thromboembolism due to rheumatic heart disease is rare at present, due to the low incidence and prevalence of rheumatic heart disease. Arterial thrombosis accounts for approximately 12% and venous thrombosis for 8% of the cases of acute mesenteric ischemia.10,29,31,32 Any condition leading to arterial or venous stasis, endothelial injury, or hypercoagulable states may result in thrombosis of the mesenteric circulation. Arteriosclerotic (by far the most common) and non-atherosclerotic vascular disease when severe, induce vascular stasis. Likewise, hospitalized patients receiving vasodilators and patients with congestive heart failure are also predisposed to arterial and venous stasis and thrombosis. Other less common causes of vascular stasis may result from mechanical or inflammatory causes, or from tumors, producing extrinsic compression of these vessels. The use of endovascular catheters and guidewires may also predispose to arterial and venous stasis as well as endothelial injury. Thrombophilias such as protein C and S deficiencies, antithrombin III deficiency, antiphospholipid antibodies, heparin-induced thrombocytopenia, factor V Leiden mutation, malignancies, the use of contraceptives, and malignancy, may all induce hypercoagulable states potentially leading to arterial or venous thrombosis of the mesenteric circulation and acute mesenteric ischemia.29,31–34 Non-occlusive acute mesenteric ischemia refers to ischemia not associated with anatomic arterial or venous obstructions, and occurs in approximately 20% of patients who develop acute mesenteric ischemia.29 This condition usually results from low cardiac output states, leading to a decrease of mesenteric perfusion below a critical ischemic threshold. Nonocclusive acute mesenteric ischemia has been described in patients with congestive heart failure, sepsis, profound hypotension, and hypovolemia. These conditions induce profound splanchnic vasoconstriction, and the release of vasoconstrictors as mentioned previously,27,28 which may lead to intestinal infarction. In addition, there are drugs that have
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been implicated in the development of splanchnic vasoconstriction such as ergot alkaloids, cocaine, and digitalis.35–38 Non-occlusive mesenteric ischemia most commonly occurs in very ill, elderly individuals with multisystemic disease, which often makes the diagnosis very challenging. There is a small but important group of patients who may develop acute mesenteric ischemia following cardiopulmonary bypass. Although its incidence has been reported to be 0.36%, the mortality rate in this group of patients ranges from 60 to 100%.40 The cause for this condition appears to be microembolism and/or hypoperfusion due to inadequate pump function from the heart or the bypass machine, in combination with a potential detrimental effect of vasopressors and intra-aortic balloon counterpulsation. Another iatrogenic cause of bowel ischemia includes inadequate or incomplete mesenteric revascularization following aortic aneurysm repair and compromise of mesocolic collaterals due to colonic resection.41 Pathophysiology of chronic mesenteric ischemia The development of symptoms of CMI usually results when at least two mesenteric vessels are affected by hemodynamically significant stenoses.18,20 Atherosclerosis, the most common cause of mesenteric arterial stenosis, progresses slowly in the majority of the cases, and thereby enables the recruitment of normally existing connections among the three mesenteric arteries, or the development of de novo collaterals (see the section on anatomy). Consequently, single-vessel stenosis rarely causes CMI, unless: (1) these mesenteric arterial interconnections are congenitally poorly developed; (2) there are acute or subacute stenoses where little time is available for the development of collaterals; or (3) the patient has previously been interrupted as a result of previous abdominal surgery or intestinal resection. Based on the previous discussion, the existence of CMI with single-vessel mesenteric arterial stenosis, particularly with isolated celiac trunk stenosis due to extrinsic compression (Figure 59.2) by the median arcuate ligament of the diaphragm, has been the subject of intense debate. This condition was initially described in 1963 by Harjola.41 Later, Bron and Redman showed that almost half of patients with isolated significant celiac artery stenosis or occlusion had abdominal symptoms.42 However, in a review of the literature, Szilagyi et al.,43 argued that in no single case could the existence of the celiac compression syndrome be conclusively proven, and that post-decompression symptom relief was placebo mediated. In the past three decades since that review, other investigators have provided careful documentation of the existence of this condition with lasting symptom relief after surgical decompression.44 It is important to understand that although the rich interconnection among the three mesenteric arteries has a protective effect against the development of intestinal ischemia, it may also promote a vascular steal phenomenon, a mechanism that appears to play a very important role in the pathophysiology of CMI. In an experimental dog model, using a 50% fixed stenosis of the celiac trunk in the SMA, the intramural pH in the small intestine (measured using tonometry) significantly decreased after the dogs were fed and the food reached the stomach. The interpretation for the drop in intestinal pH, was that blood was diverted from the intestine (which becomes ischemic) to the stomach, to satisfy the stomach metabolic demands
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stimulated by food.45 This experiment is important, because it explains the relatively early occurrence of abdominal pain (20–30 minutes after food intake) experienced by most patients with CMI, long before it has reached the intestinal wall. This blood shifting or intramesenteric steal has
also been proposed as the mechanism of abdominal pain or non-specific abdominal symptoms endured by patients with celiac trunk compression syndrome.46 Furthermore, intramesenteric steal has been reported to cause colon ischemia.47
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Elliot J. The operative relief of gangrene of intestine due to occlusion of the mesenteric vessels. Ann Surg 1895; 1: 9–23 Goodman EH. Angina abdominis. Am J Med Sci 1918; 155: 524–8 Dunphy JE. Abdominal pain of vascular origin. Am J Med Sci 1936; 192: 109–12 Kornblith PL, Boley SJ, Whitehouse BS. Anatomy of the splacnic circulation. Surg Clin North Am 1992; 72: 1–30 Chiene J. Complete obliteration of the coeliac and mesenteric arteries: viscera and their blood supply through the extra-peritoneal system of vessels. J Anat Physiol 1869; 3: 65–72 Fisher DF Jr, Fry WJ. Collateral mesenteric circulation. Surg Gyn Obs 1987; 164: 487–92 Valentine RJ, Martin JD, Myers SI, Rossi MB, Clagett GP. Asymptomatic celiac and superior mesenteric artery stenoses are more prevalent among patients with unsuspected renal artery stenoses. J Vasc Surg 1991; 14: 195–9 Hansen KJ, Wilson DB, Craven TE et al. Mesenteric artery disease in the elderly. J Vasc Surg 2004; 40: 45–52 Valentine RJ, Martin JD, Myers SI, Rossi MB, Clagett GP. Asymptomatic celiac and superior mesenteric artery stenoses are more prevalent among patients with unsuspected renal artery stenoses. J Vasc Surg 1991; 14: 195–9 Stoney RJ, Cunningham CG. Acute mesenteric ischemia. Surgery 1993; 114: 372–80 Marston A. Diagnosis and management of intestinal ischemia. Ann R Coll Surg Engl 1972; 50: 29–41 Reiner L, Jimenez FA, Rodriguez FL. Atherosclerosis in the mesenteric circulation: observations and correlations with aortic and coronary atherosclerosis. Am Heart J 1963; 66: 200–4 Palubinskas AJ, Ripley HR. Fibromuscular hyperplasia in extrarenal arteries. Radiology 1964; 82: 451–4 Harris MT, Lewis BS. Systemic diseases affecting the mesenteric circulation. Surg Clin North Am 1992; 72: 245–59 Stanley JC, Fry WJ. Median arcuate ligament syndrome. Arch Surg 1971; 103: 252–8 Bech FR. Celiac artery compression syndromes. Surg Clin North Am 1997; 77: 409–24 Reilly LM, Ammar AD, Stoney RJ et al. Late results following operative repair for celiac artery compression syndrome. J Vasc Surg 1985: 2: 79–91 van Bockel JH, Geelkerken RH, Wasser MN. Chronic splanchnic ischemia. Best Pract Res Clin Gastroenterol 2001; 15: 99–119 Zierler RE, Bergelin RO, Isaacson JS et al. Natural history of atherotic renal artery stenosis: a prospective study with duplex ultrasonography. J Vasc Surg 1994; 19: 250–7 Thomas JH, Blake K, Pierce GE, Hermreck AS, Seigel E. The clinical course of asymptomatic mesenteric arterial stenosis. J Vasc Surg 1998; 27: 840–4 Kwaan JH, Connolly JE. Prevention of intestinal infarction resulting from mesenteric arterial occlusive disease. Surg Gyn Obst 1983; 157: 321–4 Rosemblum JD, Boyle CM, Schwartz LB. The mesenteric circulation. Anatomy and physiology. Surg Clin North Am 1997; 77: 289–306 Heer M, Repond F, Hany A et al. Acute ischemic colitis in long distance runner. Gut 1987; 28: 896–9 Otte JA, Oostveen E, Geelkerken RH et al. Heavy exercise of short duration may provoke gastric ischemia in healthy subjects. Gastroenterology 1998; 114: A404
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Jager K, Bollinger A, Valli C et al. Measurement of mesenteric blood flow by duplex scanning. J Vasc Surg 1986; 3: 462–9 Desai TR, Sisley AC, Brown S et al. Defining the critical limit of oxygen extraction in the human small intestine. J Vasc Surg 1996; 23: 832–8 Granger DN, Richardson PD, Kvietys PR et al. Intestinal blood flow. Gastroenterology 1980; 78: 837– Reilly PM, Bulkley GB. Vasoactive mediators and splanchnic perfusion. Crit Care Med 1993; 21(2 suppl.): S55– Rivers S. Acute nonocclusive mesenteric ischemia. Sem Vasc Surg 1990; 3: 172– Elliot JP Jr, Hageman JH, Szilagyi E et al. Arterial embolization: problems of source, multiplicity, recurrence and delayed treatment. Surgery 1980; 88: 833–45 Schwartz LB, Gewertz BL. Mesenteric ischemia. Surg Clin North Am 1997; 77: 275–507 Rhee RY, Gloviczki P, Mendonca CT et al. Mesenteric venous thrombosis: still a lethal disease in the 1990s. J Vasc Surg 1994; 20: 688–97 Svensson PJ, Dahlback B, Resistance to activated protein C as a basis for venous thrombosis. N Engl J Med 1994; 330: 517–22 Greengard JS, Eichinger S, Griffin JH et al. Brief report: variability of thrombosis among siblings with resistance to activated protein C due to an Arg to Gln mutation in the gene for factor 5. N Engl J Med 1994; 331: 1559–62 Greene FL, Ariyan S, Stausel HC Jr. Mesenteric and peripheral vascular ischemia secondary to ergotism. Surgery 1977; 81: 176–9 Nalbandian H, Sheth N, Dietrich R et al. Intestinal ischemia caused by cocaine ingestion: report of two cases. Surgery 1985; 97: 374–6 Kim EH, Gewertz BL. Chronic digitalis administration alters mesenteric vascular reactivity. J Vasc Surg 1987; 5(2): 382–9 Levinsky RA, Lewis RM, Bynum TE et al. Digoxin induced intestinal vasoconstriction. The effects of proximal arterial stenosis and glucagon administration. Circulation 1975; 52(1): 130–6 Gennaro M, Ascer E, Matano R et al. Acute mesenteric ischemia after cardiopulmonary bypass. Am J Surg 1993; 166: 231–6 Geraghty PJ, Sanchez LA, Rubin BG et al. Overt ischemic colitis after endovascular repair of aortoiliac aneurysm. J Vasc Surg 2004; 40: 413–8 Harjola PT. A rare obstruction of the coeliac artery; report of a case. Annales Gynecologia Fenniae 1963; 52: 547–50 Bron KM, Redman HC. Splanchnic artery stenosis and occlusion. Incidence, arteriographic and clinical manifestations. Radiology 1969; 92: 323–8 Szilagyi DE, Rian RL, Elliot JP, et al. The coeliac compression syndrome: does it exist? Surgery 1972; 72: 849–63 Reilly LM, Ammar AD, Stoney RJ. Late results following operative repair for celiac artery compression syndrome. J Vasc Surg 1985; 2: 79–91 Poole JW, Sammartano RJ, Boley SJ. Hemodynamic basis for the pain of chronic mesenteric ischemia. Am J Surg 1987; 153: 171–6 Stanley JC, Fry WJ. Median arcuate ligament syndrome. Arch Surg 1971; 103: 252–8 Geelkerken RH, Schulze Kool LJ, Breslau PJ et al. Transient colonic ischemia: consequence of a rare anatomical variation of the mesenteric arteries. Eur J Surg 1996; 162: 827–9
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Assessment of mesenteric ischemia JA Silva
Introduction The diagnosis of mesenteric ischemia in its acute (AMI) and chronic (CMI) forms is frequently difficult, and the assessment of patients with these conditions may represent a challenge for clinicians. It is important to keep in mind that the majority of patients with AMI and CMI are generally elderly and often carry significant co-morbidities such as coronary, neurovascular, and peripheral athero-occlusive disease, and they may develop a myriad of symptoms before full manifestations of bowel ischemia are apparent. Furthermore, although CMI may follow a more indolent, repetitive, and to a certain degree predictable clinical course, AMI may at times develop in a more subtle and progressive way, or may be triggered by a different condition such as congestive heart failure, an acute coronary syndrome, dehydration, sepsis, and others. Consequently, when assessing patients with acute and/or chronic abdominal pain, clinicians must bear in mind a high degree of suspicion for mesenteric ischemia, particularly when evaluating elderly subjects with multiple risk factors or with a significant atherosclerotic disease burden.
Clinical presentation Acute mesenteric ischemia AMI affects, for the most part, elderly individuals who often have other co-morbid conditions as mentioned previously. It is not unusual for these patients to have a history of previous myocardial infarction and/or angina pectoris, congestive heart failure, stroke, claudication, chronic obstructive pulmonary disease (COPD), diabetes mellitus, among others.1,2 These patients may present with an acute (and usually serious) problem somewhere else, and during the course of their disease they may develop mesenteric ischemia. Consequently, their signs and symptoms may not lead the clinician to immediately suspect the presence of this condition. Due to their age as well as multiple ailments, these patients have a decreased physiologic reserve which renders them very vulnerable. Consequently, early diagnosis of this condition is of the utmost importance for decreasing morbidity and mortality and clinicians must keep in mind a high index of suspicion when assessing patients with abdominal pain and risk factors for mesenteric atherosclerotic disease and bowel ischemia. The presentation of AMI may be subtle, non-specific, and progressive before florid symptoms of AMI are established. However, the symptoms will depend on the site, cause and extent of arterial obstruction as well as the degree of collateral development.3 Abdominal pain is the dominant symptom, occurring in nearly 85% of the patients.4 However, only ~70%
of the patients with non-obstructive AMI develop this symptom.2,5 Change in mental status is also present in almost 30% of elderly patients.6 The abdominal pain is usually severe and typically out of proportion to the physical findings.7 The pain may initially be colicky but it subsequently becomes constant, and may be localized or diffuse. Localized pain is often peri-umbilical, and is usually related to small intestinal ischemia. In patients with CMI a history (often of long duration) of post-prandial abdominal pain and weight loss may be elicited, prior to the development of acute symptoms; however, the majority of patients with AMI have a history of abdominal pain of short duration. In those patients with along-standing history of CMI prior to the development of acute abdominal pain, acute arterial thrombosis superimposed on severe mesenteric atherosclerotic disease is the underlying pathologic event.8–10 In addition, mesenteric atherosclerotic disease and bowel ischemia should be considered when abdominal pain is absent, mild, or subclinical, particularly when patients with strong risk factors for developing atherosclerotic disease develop unexplained abdominal distention, lower gastrointestinal bleeding, metabolic acidosis, or sepsis.1,3 Frequently, these patients have the symptoms of mesenteric ischemia masked by other co-morbidities.3 Non-occlusive arterial disease must be suspected in patients without abdominal pain who develop diarrhea and bacteremia after cardiopulmonary resuscitation.11,12 Other common symptoms of acute mesenteric ischemia (Table 60.1) include diarrhea, nausea, and vomiting, which occur in ~50% of the patients.13 The diarrhea is frequently bloody, particularly when intestinal infarction is imminent.14 Gastrointestinal emptying with vomiting and diarrhea occurs as a result of intense muscular spasm and hyperperistalsis during early intestinal ischemia.15 Mesenteric venous thrombosis has a variable and usually more subtle/less severe clinical presentation. The progression toward more severe symptoms is also slower than when the arterial circulation is compromised. Abdominal pain (~85%), anorexia in (~50%), nausea and vomiting (~45%), upper Table 60.1 ischemia
Typical symptoms of acute mesenteric
Abdominal pain Distention Nausea and vomiting Diarrhea Lower gastrointestinal bleeding Fever Anorexia
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Table 60.2 ischemia
Common signs of acute mesenteric
Fever Tachycardia Abdominal distention Abdominal tympany High-pitched or hypoactive bowel sounds Abdominal tenderness on direct palpation Rebound abdominal tenderness Abdominal rigidity Fecal occult blood Hypotension Hyperventilation Lethargy, mental confusion
(~35%), and lower (~20%) gastrointestinal bleeding, as well as constipation (~10%) are the typical symptoms. The abdominal pain is usually diffuse but when localized it often affects the lower abdomen. Most typically, patients endure pain for several days (mean duration: 5 days) prior to seeking medical help.16,17 The physical examination (Table 60.2) in these patients is usually relatively benign, particularly at the beginning of the process. The abdomen is usually soft without or with minimal tenderness on direct deep palpation, and the bowel sounds are usually normal. With increasing and persisting bowel ischemia, the patient may develop abdominal distention and decreased bowel sounds as a result of hypoperistalsis from intestinal muscle ischemia. Abdominal distention also occurs from fluid accumulation of intramural leak. Nearly 75% of the patients will have fecal occult blood,14 and if ischemia progresses toward bowel infarction, they develop peritoneal signs such as abdominal rigidity and exquisite abdominal pain on palpation and rebound, fever, and tachycardia.3 If surgical intervention is not carried out at this point, patients develop overt sepsis, hypotension, renal failure, and finally die. Chronic mesenteric ischemia The typical symptoms of CMI include abdominal pain (usually triggered by food ingestion), weight loss, and an abdominal bruit localized in the epigastrium.8,18 The abdominal pain is usually described as dull aching or sometimes as “crampy,” in the peri-umbilical area. It begins within 1 hour (most frequently within 20–30 minutes) after food ingestion and subsides 1–2 hours later. Due to the post-prandial abdominal pain, patients develop the so-called “fear for food” and gradually decrease the amount of food and caloric intake that results in weight loss, which in some of cases may be profound. It is not unusual for patients with typical CMI to have a 20- to 40-pound weight loss by the time the diagnosis is made.19 More recently, some reports have shown that ischemic gastropathy and ischemic colitis are also manifestations of CMI. Ischemic gastropathy usually manifests as nausea, vomiting, fullness, right upper quadrant discomfort, abdominal pain, and weight loss.20–22 Ischemic colitis usually manifests as abdominal pain, gastrointestinal bleeding, and/or hematochezia.23,24 A mechanism of vascular stealing appears to play an important role in this type of presentation.25 Other less specific symptoms of CMI include nausea and change in bowel habits, with development of diarrhea and/or
constipation which in some instances may be related to intestinal malabsorption.19
Diagnosis of mesenteric ischemia Acute mesenteric ischemia As a general rule, simple laboratory and/or radiographic imaging studies cannot confirm or rule out the diagnosis of AMI. As mentioned earlier, the clinical presentation of abdominal pain in an elderly individual with multiple risk factors or with established atherosclerotic disease, and/or the development of abdominal distention and gastrointestinal bleeding in a critically ill individual must make the clinician suspicious for this condition. Acute intestinal ischemia causes a number of laboratory abnormalities, which are usually nonspecific. Leukocytosis with left shift is common.3,9,12,15 In a study of 43 patients with acute intestinal ischemia, 41 patients had leukocytosis, with most (n = 30), having a white count of > 15,000 cells/mm3.25 The serum amylase concentration may be elevated because of increased peritoneal absorption, as amylase leaks from the ischemic bowel.15,26 Acute ischemia also causes dysfunction of the bowel cell membrane enzymes, allowing sodium and water to enter the cells. Clinically, this is manifested as hemoconcentration and hypovolemia. Metabolic acidosis as a result of lactic acid accumulation develops in most of the patients as is usually the result of severe intestinal ischemia or infarction.9,12,27 In addition, intestinal necrosis is associated with elevation of serum lactate, phosphate, alkaline phosphatase, as well as prerenal azotemia, hypoxemia, bacteremia, and sepsis.25–31 Plain abdominal radiographs usually demonstrate no abnormalities until late in the clinical course. They are, however, useful in identifying other serious intra-abdominal conditions such as small bowel obstruction, adynamic ileus, colonic pseudo-obstruction and mechanical obstruction, which usually show non-specific radiographic patterns of intestinal dilation, focal gas-filled bowel loops, thickened bowel loops, and air–fluid levels. Specific radiographic findings develop with advanced intestinal ischemia in ~25% of the patients. These include “thumb printing” from intestinal edema, hemorrhage and muscle necrosis resulting in rigid aperistaltic bowel loops. Thumb printings are usually multiple, round, smooth, softtissue densities projecting into the air-filled intestinal lumen.32 Ominous roentgenographic findings include pneumoperitoneum as a result of intestinal perforation, pneumatosis intestinalis or portal vein pneumatosis (gas-forming bacteria in the bowel wall or extending into the portal vein).33 Duplex ultrasonography of the mesenteric arteries may be a useful diagnostic method to diagnose acute mesenteric occlusion. The major drawbacks of this diagnostic technique is that these patients usually require adequate preparation such as fasting as well as the use of semethicone to decrease the bowel for obtaining adequate ultrasound images, which is often not feasible in an emerging situation. In addition, a satisfactory study is very dependent on the technologist’s experience. Computed tomographic angiography (CTA) is a very sensitive and specific imaging modality to assess patency of the mesenteric arterial and venous system. It is at present available in most hospitals and has been proposed as a fast, effective,
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Chronic mesenteric ischemia The diagnosis of CMI is often challenging since the typical symptoms of post-prandial abdominal pain, weight loss, and epigastric bruit, in patients with significant mesenteric arterial stenoses may not always be present. Some investigators have reported that only 50% of patients with CMI develop these typical symptoms.37 We recently reported a series of 59 patients with CMI, and found typical presentation in 78% and ischemic gastropathy or ischemic colitis in 22% of the patients (Figure 60.1).38 Chronic mesenteric ischemia remains a clinical diagnosis and is based on the presence of symptoms of ischemic origin and the presence of hemodynamically significant stenoses in more than one mesenteric artery. As discussed in the chapter on pathophysiology, the presence of CMI in a patient with single-vessel mesenteric artery disease, although possible, is unusual and should be made only when other causes of abdominal pain have been excluded. In some patients with atypical or non-specific symptoms, the diagnosis is often made retrospectively based on the clinical success (or failure) of revascularization therapy. Due to these difficulties, some investigators advocate a multidisciplinary team
100 90 80
78%
70 Percent
and non-invasive way to determine the status of the mesenteric circulation. In addition, pneumatosis of the intestinal wall can be quickly diagnosed and three-dimensional reconstructions allow visualization of complex anatomy.33,34 Conventional angiography remains the gold-standard diagnostic test for confirming or excluding the diagnosis of mesenteric occlusive disease. Acute occlusion as a result of arterial thrombosis has a typical angiographic image of a lack of opacification of the mesenteric vessel from its origin (usually the superior mesenteric artery). On the other hand, emboli generally lodge at an arterial branch point with the proximal branches usually being spared. A typical meniscus and a typical angiographic “thrombus appearance” is usually noted at the point where the embolus has lodged. Angiography is also important for the definitive diagnosis of non-occlusive mesenteric ischemia. Non-selective and selective angiographic images in anteroposterior and lateral views are very useful not only to determine the cause of acute mesenteric ischemia, but also to plan the optimal revascularization strategy. Conventional angiography allows the identification of the appropriate sites for proximal anastomosis when considering surgical revascularization, and also enables the assessment of the feasibility of endovascular therapy such as thrombolysis followed by angioplasty and/or stent placement, or the use of vasodilators such as nitroglycerin and papaverine when the presence of arterial spasm is the cause of mesenteric ischemia. Some investigators advocate the use of conventional angiography, even when exploratory laparotomy is warranted, in the operating room, if feasible. On the other hand, there are patients in whom angiography cannot be obtained due their critical condition, such as severe hypotension, tachycardia, acidosis, or respiratory failure. With such conditions, the potential delay in performing the angiography may jeopardize the patient’s life. The decision to proceed with mesenteric angiography prior to exploratory laparotomy may be difficult in some circumstances and must be individualized according to the patient’s clinical condition.35,36
559
60 50 40 30 20
14%
10 0
Typical
Gartropathy
8% Ischemic colitis
Figure 60.1 Clinical presentation in 59 patients with chronic mesenteric ischemia.38
approach for the diagnosis and management of this challenging condition.39 The typical patients referred for non-invasive diagnostic imaging studies usually have significant peripheral, renal, coronary, and neurovascular atherosclerotic disease, and presumptive symptoms of chronic intestinal ischemia. It is not uncommon for some of these patients to have endured abdominal symptoms with or without weight loss for years before the clinician considers CMI as a possible diagnosis. Technical improvement in duplex ultrasonography, as well as the introduction of CTA and magnetic resonance angiography (MRA), is in the majority of the cases accurate enough to establish the diagnosis of mesenteric arterial stenosis.40–43 Conventional angiography remains the gold-standard diagnostic imaging modality for the diagnosis mesenteric arterial stenoses; however, due to the improvement in image quality and availability of non-invasive studies, clinicians resort to conventional angiography less frequently and it is at present recommended for patients with an inconclusive non-invasive imaging study, or in whom revascularization therapy is being entertained. At present, the main indications for performing invasive angiography are when patients have equivocal or contradictory non-invasive imaging results, or when revascularization is being considered. In addition, patients are often taken for confirmatory invasive angiographic diagnosis, after a non-invasive image modality has found significant mesenteric arterial stenoses in symptomatic individuals, with the purpose of proceeding with endovascular therapy during the same session, or as a preferred diagnostic modality by some vascular surgeons prior to surgical revascularization. Functional assessment Duplex ultrasound, CTA, MRA, as well as conventional angiography provide only anatomical information regarding the presence of significant stenosis in a particular mesenteric artery. However, these tests do not provide any physiological information and cannot be used to assess whether specific abdominal symptoms are manifestations of mesenteric ischemia. Tonometry and MRI are capable of providing functional information of intestinal ischemia, although their use has been limited to the research arena. Their development and clinical applicability are going to be of the utmost importance since they are going help clinicians to better select patients who require revascularization procedures, particularly those with atypical presentation of CMI or with single vessel disease.
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Tonometry measures intestinal mucosa pCO2 with a tonometer – a balloon-tip catheter – which is inserted and placed in contact with the stomach mucosa or the intestinal mucosa. The balloon is silicone gas-permeable, and enables carbon dioxide to freely equilibrate between the gastric or intestinal mucosa and the balloon lumen. The rational for the use of this functional test is that a decrease in intestinal blood flow promotes anaerobic metabolism, leading to an increase in pCO2, which is detected and measured by the tonometer balloon after pCO2 equilibrates.45,46 The diagnostic value of postprandial pCO2 is being debated, whereas post-exercise gastric tonometry appears as a promising provocative test for the diagnosis of gastrointestinal ischemia.47 Magnetic resonance imaging (MRI) is also capable of providing functional information of the mesenteric blood flow. Flow velocities and total flow volumes, using two-dimensional
cine-phase contrast velocity mapping, can be measured in the mesenteric vessels with MRI. Some studies have shown that compared to healthy volunteers, patients with CMI have decreased post-prandial flow volume augmentation.48,49 MRI has also been used to measure the oxygen saturation of hemoglobin in the superior mesenteric vein using MR oximetry. The principle behind this technology is that deoxyhemoglobin in erythrocytes is paramagnetic whereas oxyhemoglobin is not. Consequently, MR oximetry can calculate the percentage of circulating oxyhemoglobin in the superior mesenteric vein. As blood flow decreases, oxygen extraction augments to compensate and keep constant the total amount of oxygen delivery to the intestinal tissue. It has been shown that compared to normal volunteers, in whom percentage oxyhemoglobin increases after ingestion of meals, in patients with CMI, postprandial percentage oxyhemoglobin decreases.50
REFERENCES 1. 2. 3. 4.
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Reiner PM, Jimenez FA, Rodriguez FL. Atherosclerosis in the mesenteric circulation: observations and correlations with aortic and coronary atherosclerosis. Am Heart J 1963; 66: 200–9 Reinus JF, Brandt LJ, Boley SJ. Ischemic diseases of the bowel. Gastroenterol Clin North Am 1990; 19: 319–43 Capell M. Intestinal (mesenteric) vasculopathy I. Gastroenterol Clin North Am 1998; 27: 783–825 Kaleya RN, Boley SJ. Acute mesenteric vascular disease. In: Veith FJ, Hobson RW II, Williams RA et al., eds. Vascular Surgery: Principles and Practice, second edition. New York: McGraw-Hill, 1994: 762–80 Howard TJ, Plaskon LA, Wiebke EA et al. Nonocclusive mesenteric ischemia remains a diagnostic dilemma. Am J Surg 1996; 171: 405–8 Finucane PM, Arunachalam T, O’Dowd J et al. Acute mesenteric infarction in elderly patients. J Am Geriatr Soc 1989; 37: 355–8 Eldrup-Jorgensen J, Hawkins RE, Bredenberg CE. Abdominal vascular catatstrophes. Surg Clin North Am 1997; 77: 1305–20 Dunphy JE. Abdominal pain of vascular origin. Am J Med Sci 1936; 192: 109–12 Kaleya RN, Boley SJ. Acute mesenteric ischemia. An aggressive diagnostic and therapeutic approach. Can J Surg 1992; 35: 613–23 Endean ED, Barnes S, Kwolek CJ et al. Surgical management of thrombotic acute intestinal ischemia. Ann Surg 2001; 6: 801–8 Gaussorges P, Guergniant PY, Vedrinne JM et al. Bacteremia following cardiac arrest and cardiopulmonary resuscitation. Intensive Care Med 1988; 14: 575–7 Kaleya RN, Boley SJ. Acute mesenteric ischemia. Crit Care Clin 1995; 11: 479–512 Ottinger LW, Austen WG. A study of 136 patients with mesenteric infarction. Surg Gynecol Obstet 1967; 124: 251–61 Ottinger LW. The surgical management of acute occlusion of the superior mesenteric artery. Ann Surg 1978; 188: 721–31 Marston A, Taylor M. Acute mesenteric ischemia. In: Taylor MB, Gollan JL, Steer ML et al., eds. Gastrointestinal Emergencies, second edition. Baltimore: Williams & Wilkins, 1997: 555–70 Boley SJ, Kaleya RN, Brandt LJ. Mesenteric venous thrombosis. Surg Clin North Am 1992; 72: 183–201 Rhee RY, Gloviczki P, Medoza CT et al. Mesenteric venous thrombosis: still a lethal disease in the 1990s. J Vasc Surg 1994; 20: 688–97 Goodman EH. Angina abdominis. Am J Med Sci 1918; 155: 524–8 Van Bockel JH, Geelkerken RH, Wasser MN. Chronic splanchnic ischemia. Best Pract Res Clin Gastroenterol 2001; 15: 99–119 Liberski SM, Koch KL, Atnip RG, Stern RM. Ischemic gastroparesis: resolution after revascularization. Gastroenterology 1990; 99: 252–7 Babu SC, Shah PM. Celiac territory ischemic syndrome in visceral artery occlusion. Am J Surg 1993; 166: 227–30 Kathleen MC, Quigley TM, Kozarek RA, Raker EJ. Lethal nature of ischemic gastropathy. Am J Surg 1993; 165: 646–9
23. 24. 25. 26. 27. 28. 29. 30. 31.
32. 33. 34. 35. 36. 37. 38. 39. 40. 41. 42.
Geelkerken RH, Schulze Kool LJ, Breslau PJ et al. Transient colonic ischemia: consequence of a rare anatomical variation of the mesenteric arteries. Eur J Surg 1996; 162: 827–9 Cappell MS. Intestinal (mesenteric) vasculopathy II. Ischemic colitis and chronic mesenteric ischemia. Gastroenterol Clin North Am 1998; 27: 827– Boley SJ, Brandt LJ, Veith FJ. Ischemic disorders of the intestines. Curr Probl Surg 1978; 15: 1–85 Tsai CJ, Kuo YC, Chen PC et al. The spectrum of acute intestinal vascular failure: a collective review of 43 cases in Taiwan. Br J Clin Pract 1990; 44: 603–8 Boley SJ, Feinstein FR, Sammartano R et al. New concepts in the management of emboli of the superior mesenteric artery. Surg Gynecol Obstet 1981; 153: 561–9 Lange H, Jackel R. Usefulness of plasma lactate concentration in the diagnosis of acute abdominal disease. Eur J Surg 1994; 160: 381–4 Koborozos B, Vyssoulis G, Manouras A et al. Serum phosphate levels in acute bowel ischemia. Ann Surg 1985; 10: 242–4 Barnett S, Davison E, Bradley E. Intestinal alkaline phosphatase and base deficit in mesenteric occlusion. J Surg Res 1976; 20: 243–6 Brandt LJ, Smithline AE. Ischemic lesions of the bowel. In: Feldman M, Sleisenger MH, Scharschmidt BF, eds. Sleisenger and Fordtran’s Gastrointestinal and Liver Disease: Pathophysiology, Diagnosis, Management, sixth edition. Philadelphia: WB Saunders, 1998: 2009–24 Klein HM, Lensing R, Klosterhalfen B et al. Diagnostic imaging of mesenteric infarction. Radiology 1995; 197: 79–82 Wolf EL, Sprayregen S, Bakal CW. Radiology in intestinal ischemia: Plain film, contrast, and other imaging studies. Surg Clin North Am 1992; 72: 107–24 Perez C, Llauger J, Puig J et al. Computed a findings in bowel ischemia. Gastrointest Radiol 1989; 14: 241–5 Federle MP, Chung G, Jeffrey RB et al. Computed a findings in bowel infarction. AJR Am J Roentgenol 1984; 142: 91–5 Katzen BT. Current status of digital angiography in vascular imaging. Radiol Clin North Am 1995; 33: 1–14 Geelkerken RH, Van Bockel JH, De Roos WK et al. Chronic mesenteric vascular syndrome. Results of reconstructive surgery. Arch Surg 1991; 126: 1101–6 Silva JA, White CJ, Collins TJ et al. Endovascular therapy for chronic mesenteric ischemia. J Am Coll Cardiol 2006; 47: 944–50 Bradbury AW, Brittenden J, McBride K, Ruckley CV. Mesenteric ischaemia: a multidisciplinary approach. Br J Surg 1995; 82: 1446–59 Geelkerken RH, Van Bockel JH. Duplex ultrasound examination of splachnic vessels in the assessment of splachnic ischemic symptoms. Eur J Vasc Endovasc Surg 1999; 18: 371–4 Moneta GL, Lee RW, Yeager RA, Taylor LM, Porter JM. Mesenteric duplex scanning: a blinded prospective study. J Vasc Surg 1993; 17: 79–86 Behar JV, Nelson RC, Zidar JP, DeLong DM, Smith TP. Thin-section multidetector CT angiography of renal artery stents. AJR 2002; 178: 1155–9
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Maintz D, Tombach B, Juergens KU et al. Revealing in-stent restenoses of the iliac arteries: comparison of multidetector CT with MR angiography and digital radiographic angiography in a phantom model. Am J Roentgenol 2002; 179: 1319–22 Meaney JF, Prince MR, Nostrant TT et al. Gadoliniumenhanced MR angiography of visceral arteries in patients with suspected chronic mesenteric ischemia. J Magn Res Imag 1997; 7: 171–6 Dawson AM, Trenchard D, Guz A. Small bowel tonometry: assessment of gut mucosal oxygen tension in dog and man. Nature 1965; 206: 943–4 Kolkman JJ, Otte JA, Groeneveld AB. Gastrointestinal luminal pCO2 tonometry: an update on physiology, methodology, and clinical applications. Br J Anaesth 2000; 84: 74–86
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Kolkman JJ, Groeneveld AB, van der Berg FG et al. Increased gastric pCO2 during exercise is indicative of gastric ischemia: a tonometric study. Gut 1999; 44: 163–7 Li KC, Whitney WS, McDonnell CH et al. Chronic mesenteric ischemia: evaluation with phase contrast cine MR imaging. Radiology 1994; 190: 175–9 Burkart DJ, Johnson CD, Reading CC et al. MR measurements of mesenteric venous flow. Prospective evaluation in healthy volunteers and patients with suspected chronic mesenteric ischemia. Radiology 1995; 194: 801–6 Li KC, Dalman RL, Ch’en IY et al. Chronic mesenteric ischemia: use of in vivo MR imaging measurements of blood oxygen saturation in the superior mesenteric vein for diagnosis. Radiology 1997; 204: 71–7
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Conventional angiography, CTA, and MRA of the mesenteric arteries Y-W Chi and JA Silva
Introduction The diagnosis of chronic mesenteric ischemia (CMI) is challenging and for the most part relies on patient history and physical examination, in combination with an imaging diagnostic test showing significant stenosis of more than one mesenteric artery. Until recently, conventional and digital subtraction angiography (DSA) were considered the imaging techniques of choice for the diagnosis of mesenteric arterial stenosis. However, the development of non-invasive angiographic modalities such as computer tomographic angiography (CTA) and magnetic resonance angiography (MRA) have been shown to provide accurate anatomical detail and have challenged conventional angiography as the gold-standard test for the diagnosis of mesenteric arterial stenosis. In the present chapter we will discuss these three diagnostic imaging techniques for the diagnosis of mesenteric arterial stenosis.
Mesenteric anatomy The mesenteric or splanchnic arterial circulation consists of three main arteries: the celiac trunk, the superior mesenteric artery (SMA), and the inferior mesenteric artery (IMA). Embryologically, these three arteries develop as paired vessels, but they eventually merge, providing the potential for abundant and persistent collateral connections. The celiac trunk arises on the ventral portion of the abdominal aorta at the level of T12 to L1, between the diaphragmatic crura. The SMA arises just distal to the celiac trunk at the level of L1 to L2 also on the ventral portion of the abdominal aorta. The IMA arises on the anterior to left lateral aspect of the abdominal aorta at the level of L3 to L4, about 8–10 cm distal to the SMA. The stomach and upper half of the duodenum comprise the foregut and are supplied by the celiac trunk. The lower half of the duodenum, jejunum, ileum, cecum appendix, ascending colon, and proximal two-thirds of the transverse colon comprise the midgut and are supplied by the SMA. The lower third of the transverse colon, sigmoid colon, descending colon, sigmoid colon, rectum, and the upper part of the anal canal comprise the hindgut and are supplied by the IMA.1 The origin of the celiac trunk is usually encased in the median arcuate ligament of the diaphragm, a fibrous portion of the central and posterior portion of this muscle. The celiac trunk divides soon after its origin into the common hepatic, left gastric, and splenic arteries. The first branch of the SMA 562
is the inferior pancreatoduodenal artery, which courses superiorly to join the superior pancreatoduodenal artery (a branch of the gastroduodenal artery), to form one of the most important connections between the celiac trunk and the SMA. The next important branches are the middle colic (supplying flow to the proximal two-thirds of the transverse colon), right colic (for the mid and distal ascending colon), and the iliocolic (for the distal ileum, cecum, appendix, and proximal and ascending colon). The IMA branches into the left colic artery which connects with the middle colic artery of the SMA (marginal artery of Drummond), the sigmoid, and superior rectal arteries. The most important branches and anatomical distribution of the three mesenteric arteries are described in Figure 61.1. In about 1% of the population, the SMA arises directly from the celiac trunk constituting the celiomesenteric trunk. The hepatic artery may also arise from the SMA in about 12% of cases, and the common hepatic artery may originate directly from the abdominal aorta (usually below the celiac trunk) in about 2% of cases.2 There is a rich communication among the three mesenteric vessels in normal conditions which becomes more important and prominent during chronic ischemia, particularly when one or more mesenteric arteries develop significant stenoses or occlusions. Well-known communications between the celiac trunk and the SMA (superior and inferior gastroduodenal arteries), as well as the SMA and IMA (marginal artery of Drummond) have already been mentioned. Another important connection between the SMA and IMA is the meandering mesenteric artery which connects the ascending branch of the left colic artery with a branch of the SMA that arises proximal to the origin of the middle colic artery and often becomes prominent during chronic occlusion of one of this arteries. Other connecting systems among these three vessels as well as significant collateral flow to the mesenteric circulation from other aortic branches such as the lumbar intercostal, middle sacral, mammary, and internal iliac arteries are also present (Figure 61.1).1
Conventional angiography Invasive non-selective and selective mesenteric angiogram, with and without digital subtraction imaging, has remained the gold-standard against all other image modalities, and are compared for the diagnosis of mesenteric arterial stenosis. More recently, however, with the advances in image quality of CTA, MRA, and duplex ultrasonography, this concept has been
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Figure 61.1 Anatomic representation of the mesenteric arterial circulation. (Reproduced with permission from Scharwtz et al. The vascular system. In: Lyerly HK, Gaynor JW Jr, eds. The Handbook of Surgical Intensive Care, 3rd ed. St Louis, Mosby Year Book, 1992, p 287).
challenged, and clinicians rely less frequently on conventional angiography for the diagnosis of mesenteric arterial stenoses. At present, the main indications for performing invasive angiography are when patients have equivocal or contradictory non-invasive imaging results, or when revascularization is being considered. It is common practice to take patients to the catheterization suite, with the diagnosis of mesenteric arterial stenosis by a non-invasive image study, for confirmatory angiographic diagnosis with the purpose of proceeding with endovascular therapy during the same session. Alternatively, some vascular surgeons may prefer confirmatory invasive angiography prior to surgical revascularization.
For the acquisition of adequate images, it is necessary to use a radiographic gantry with angulation capability in both the axial and sagittal planes as well as a large-field (14- to 16-inch or 36- to 41-cm) image intensifier capable of capturing the larger regions of interest such as the entire aortic arch, entire pelvic vasculature, and both legs.3 Image recording of peripheral studies has conventionally been obtained using film-screen radiographic techniques and mechanical rapid cut-film changers. This has now been replaced by digital angiography, which allows immediate monitor display of the acquired image, as well as electronic processing to enhance contrast, reduce noise, and subtract
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overlying bony and soft-tissue density. Although not available in all angiographic suites as yet, digital subtraction angiography (DSA) enhances significantly the angiographic anatomical detail, and allows the use of less contrast as well as shortening the procedural time. A preliminary image is recorded immediately prior to contrast injection, so that any background density (bone, calcifications, soft tissue, and air densities) can be subtracted from subsequent images, which then show only the contrast-filled vessels of interest (Figure 61.2a). Quantitative online angiographic analysis, available in many angiographic suites, is also very helpful for the interventionist since it
provides an objective method to measure the diameter stenosis, length, and reference vessel diameter, helping the operator to choose the appropriate equipment.3 Regarding contrast agents, the majority of catheterization suites, at present, utilize low-osmolar contrast agents because compared to high-osmolar agents, the former cause less sideeffects such as nausea, vomiting, lightheadedness, or target organ pain leading to better patient tolerability.4 In addition, low-osmolar agents carry a lower osmotic load and promote less fluid retention which is always desirable in patients with impaired left ventricular and renal function. In recent years,
(b)
(a)
(c)
Figure 61.2 (a) Digital subtraction angiogram showing mild stenosis in the celiac trunk and severe stenosis in the superior mesenteric artery. This is seen on the volume rendering view; (b) Multiplanar reformation; (c) Severely stenotic superior mesenteric artery.
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Conventional angiography, CTA, and MRA of the mesenteric arteries two new contrast agents have been developed as alternatives to patients with severely impaired renal function and a history of life-threatening contrast allergy: carbon dioxide (CO2), and gadolinium (gadopentetate dimeglumine). The former has been tested in many vascular beds but, as a general rule, its use should be avoided for angiograms above the diaphragm to minimize the risk of distal embolization and stroke.5–7 The latter has traditionally been used with magnetic resonance imaging, and although is relatively non-toxic, it is recommended that the dose should not exceed 0.4 mmol/kg.8 Procedure The performance of angiography of mesenteric arteries requires that the operator be familiar with the retrograde common femoral and brachial arterial accesses. As is the case for the renal arteries, before selective angiography is performed, an abdominal aortogram should be obtained in the anteroposterior and lateral projections. After the origin of the mesenteric vessels has been identified, selective angiography is carried out in the lateral view using a 5- or 6-French internal mammary, right Judkins-4, renal double curve, or a hockeystick diagnostic catheter. The IMA often arises in a very acute caudal angle on the ventral portion of the abdominal aorta, and a Simmons-1 catheter is often very useful to engage this vessel. Selective engagement of the mesenteric arteries also allows measurement of the pressure gradient, since, as is the case for the renal arteries, the majority of stenoses in these vessels are located in their ostium or the very proximal portion.9 Using hand injections, selective angiogram is performed in the lateral and anteroposterior views, which allows good visualization of the ostium, as well as the rest of the mesenteric vessels and their main branches.2
Computed tomographic angiography Computer tomographic angiography (CTA) is becoming one of the preferred non-invasive imaging modalities for the diagnosis of peripheral arterio-occlusive disease and visceral arterial stenoses. The use of computed tomography began in the 1970s, and is based on the generation of a three-dimensional image from the internal structure of an object. Multiple series of two-dimensional x-ray images which are taken around a single axis of rotation marked the beginning of cross-sectional and multiplanar imaging.10 The basic principle of CT is the same as in conventional x-ray techniques: x-rays are generated by an x-ray tube and as they penetrate the anatomical area to be imaged, they get attenuated (weakened). These differences in x-ray attenuation are then measured by an image intensifier and the resulting image is caught by a camera. In modern angiography systems, each frame of the analog signal is then converted to a digital frame and stored by a computer in its memory and/or on hard magnetic disk. These x-ray “movies” can be viewed in real time as the angiography is being performed, or they can be stored in digital memory for later review. CTA imaging of the mesenteric arteries was initially attempted using a single-detector-row scanner, with suboptimal results.11 It was not until the introduction of the multiple-detector-row CT in the 1990s, that images of the
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entire mesenteric vascularture became much improved. Multidetector CTA is achieved by synchronizing the intravenous contrast medium injection, timed to the arterial phase, with the thin-section spiral computed tomographic acquisition. The dataset is then processed to generate the two- (2D), and the three- (3D) dimensional images. The spiral four-detector-row CT, combines multiple rows of detectors and fast gantry rotation with a narrow collimation.12 At present, 16-, 64-, and 128-channel detector CT are commercially available with submillimeter acquisition of the entire mesenteric vascular tree.10 Since the introduction of the 16-row multidetector CTA, the sensitivity and specificity of CTA for detecting normal and abnormal mesenteric vasculatures have been found to be well over 95% when compared to DSA (Figure 61.2).13 In addition to assessing the degree of arterial stenosis, multidetector CTA is of great use in patients with suspected mesenteric ischemia because it can also detect changes in the affected bowel wall such as wall thickening, edema, submucosal hemorrhage, pneumatosis, as well as potential causes of ischemia such as atherosclerotic plaque and debris, thrombus, occlusion, tumor compression, or traumatic etiologies. CTA imaging of the mesenteric arterial system usually starts with an anterior–posterior view. Non-enhanced images are typically obtained first to identify high-density materials such as vascular calcifications, residual intravenous contrast, endovascular stents/stent grafts, surgical clips, grafts, and foreign bodies, which may be confused or obscured with the injected contrast medium.13 The next phase involves contrast enhancement of the mesenteric arteries. Optimization of contrast medium is crucial for attaining good quality images. After the radiocontrast is administered, the degree of mesenteric vasculature enhancement defined by the changes in Hounsefield units (HU), is dependent on the sufficient delivery of radioiodine dose at the appropriate rate. Arterial enhancement should reach a minimum of 250–300 HU. The recommended minimum radioiodine dose is 1.1–1.7 ml/kg delivered at a rate of 3.4–4.3 ml/second for a 350 mg/ml concentration.13 The multidetector CTA is activated once the contrast reaches the supraceliac aorta using either a test bolus or automatic bolus triggering techniques. The former is performed by injecting 15–20 ml of contrast medium at a rate equivalent to that planned for the CTA, usually 4 ml/second. Tranverse sections are obtained every 2 seconds. A region of interest (ROI) is placed in the supraceliac aorta generating a time-attenuation curve. The peak of this time-attenuation curve is defined as the contrast medium transit time and is used by the CT technologist to activate the multidetector CTA and to start acquiring the images. The second technique, the automaticbolus tracking, is more popular due to its ability to provide a more homogenous enhancement and higher HU. In this protocol the multidetector CTA is automatically turned on after the ROI reaches a predetermined threshold, usually 150 HU above the baseline attenuation value. For either technique, approximately 80–120 ml of iodinated contrast medium is usually used. Table 61.1 illustrates scanning parameters for 4 and 16 multidetector CTA. Historically, three types of contrast mediums are available for imaging. The high-osmolar mediums of which diatrizoate is one of the most representative, has an osmolality of
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Scanning and reconstruction parameters
Parameter
4 detector row CT
16 detector row CT
Colimation (mm) Table speed (mm/rotation) Pitch Kilovolts Gantry time (ms) Range Acquisition time (s)
1 4–6 1–1.5 120 500 300–350 25–37.5
0.75 12–18 1–1.5 140 750 300–350 8.3–12.5
Contrast material Access Cannula (gauge) Type (mg of iodine/ml) Volume (ml) Rate (ml/s) Saline flush (ml)
Antecubital 18–20 300–400 120–150 3–4 50
Antecubital 18–20 300–400 80–100 4 50
2016 mOsm/kg of H2O, much higher than the plasma osmolality, and is not used in clinical practice due to their significant nephrotoxicity. The more commonly used contrast mediums are the low-osmolar contrast media such as iohexol and the isosmolar contrast media represented by iodixanol. Biochemically, iodixanol most closely resembles the osmolality of blood and has been established as the safer contrast medium to use among the currently commercially available agents.14 The final step of multidetector CTA is imaging rendering or post-processing. There are five principles in visualization techniques (Table 61.2): multiplanar reformation (MPR); curved planar reformation (CPR); maximum intensity projection (MIP); shaded surface display (SSD); and volume rendering (VR). SSD has become obsolete and replaced by VR as a more important technique. By rotating the images in multiple axes, a great deal of anatomical detail can be obtained. In addition, this technology allows assessment of stent patency, with negligible artifact effect, which is of particular importance since these devices are so frequently used in percutaneous revascularization therapies (Figure 61.3).
Table 61.2
The major advantages with the use of CTA as a diagnostic imaging modality include less physician depedency during image acquisition, faster scanning speed with minimal breath holds, decreased image acquisition time, higher spatial resolution able to define pertinent internal structures contiguous to the blood vessels, and availability. The disadvantages are the requirement for iodine-based contrast which can cause contrast nephrotoxicity and/or allergic reactions, radiation exposure, and lengthy post-processing time. From the interpreter’s viewpoint, the pitfalls of CTA are artifacts caused by calcified plaques which may cause a “blooming” phenomenon, and asymmetric contrast distribution due to upstream stenosis or occlusion which impairs arterial enhancement.15,16
Magnetic resonance angiography Magnetic resonance imaging (MRI) is a non-invasive diagnostic method for assessing anatomical morphology without the use of radiation or radio-contrast material. The MRI scanner
CTA visualization techniques
Mode
Display
Principle use
Advantages
Disadvantages
MPR
2D
Structure Vessel lumen Vessel wall
Limited spatial display
CPR
2D
Vessel lumen Vessel wall
MIP
2D
Angiographic overview
SSD
3D
VR
3D
Angiographic overview Angiographic overview
“Slice” through dataset in coronal, sagittal, and oblique projections Simplify image interpretation Accurate display of stenoses, occlusions, calcifications and stents Longitudinal vessel display Display of stenoses, occlusions, calcifications and stents Depict small caliber vessels Depict poorly enhancing vessels Communicate findings Depicts structural relationships Communicate findings “Slice” through dataset in axial, coronal, sagittal, and oblique projections Depict structural relationships Accurate spatial perception Communicate findings
Operator dependent Vessel/bone/visceral overlap Limited grading of stent lumen Limited by calcium burden Vessel/bone/visceral overlap Threshold dependent Opacity-transfer function dependent
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combined with a gadolinium–chelate injection, the arterial phase and then the portal phase can be shown in a highspatial resolution. The contrast between blood and tissue is significantly improved but the resolution among the extravascular structures is reduced. As a result, spin-echo or gradientecho sequences are often used to offset this limitation. Using 3D gadolinium-enhanced MR angiography, the saturation effects and respiratory motion artifacts are minimized or eliminated allowing for a detailed visualization of the mesenteric vasculature. These improvements in contrast resolution are achieved regardless of the plane of acquisition, therefore the number of image sections required to display a large vascular territory as well as the overall image acquisition time may be reduced. Overall, gadolinium-enhanced MRA has a high correlation (as assessed by k values) with conventional angiography in the common hepatic artery, the splenic artery, superior and inferior mesenteric arteries as well as the celiac trunk (Figures 61.4 and 61.5).16,18 Nevertheless, this correlation significantly decreases when assessing branch vessels. In clinical practice, when assessing the mesenteric circulation, the test bolus and the automatic bolus triggering techniques
(b) Figure 61.3 (a) 3D volume-rendering view of celiac and superior mesenteric artery (SMA) stents as well as collateral circulation between the inferior mesenteric artery and SMA; (b) patent celiac stent and occluded SMA stent view via curve and multiplanar reformation.
applies magnetism and radio waves to obtain pictures of the human anatomy. MRI technology is based on a phenomenon discovered in the 1930s called nuclear magnetic resonance (NMR), in which magnetic fields and radio waves energize atoms and cause the release of radio signals as electromagnetic energy that is measured and analyzed by a computer, which then forms 2D or 3D images that may be viewed on a monitor. Its clinical use for the assessment of mesenteric vasculatures started in the 1990s. Traditional magnetic resonance angiography (MRA) techniques are based on non-enhanced velocity-dependent inflow time-of-flight or phase-contrast methods to evaluate mesenteric circulation. However, these methods were initially hampered by longer data acquisition times, motion, flow, artifacts from metallic devices or surgical clips, signal loss secondary to areas of complex flow and in-plane flow saturation effects.17 With the advent of gadolinium, it was possible for MRI technology to create a 3D gadolinium-enhanced MR angiography, and many of the problems associated with time-of-flight and phase-contrast were resolved. The newer conventional MR devices allow acquisition within 6–20 seconds and when
Figure 61.4 Short occlusion of the superior mesenteric artery by MRA. Published courtesy of Hagspiel KD, Leung DA, Angle JF et al. MR angiography of the mesenteric vasculature. Radiol Clin North Am 2002; 40(4): 867–86.
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Figure 61.5 Ostial celiac and inferior mesenteric artery stenosis by MRA. Published courtesy of Laissy JP, Trillaud H, Douek P. MR angiography: noninvasive vascular imaging of the abdomen. Abdom Imaging 2002; 27(5): 488–506.
are frequently used. However, unlike CTA in which the automatic bolus triggering is very commonly used, in MRA the technique applied varies according to the physician preference and experience. For the test bolus technique, 30–40 cm3 of gadolinium contrast is injected at a rate of 2 cm3/second.
Weight-adjusted volumes are preferred in patients with low body weights, never exceeding 0.3 mmol/kg of body weight. For the bolus-triggering technique, a trigger threshold of 20% signal increase will detect the leading edge of the contrast agent bolus. The images are usually obtained 5–6 seconds following contrast injection. Atherosclerotic disease in the celiac trunk, SMA, and IMA are usually well visualized with this technology and, as is the case for CTA, three-dimensional reconstruction and attainment of images in any desired plane is possible using maximum-intensity projections or surface rendering techniques. All of this technical sophistication enables clinicians to visualize the ostium and the rest of the target mesenteric artery with a great deal of detail. In a study of 14 patients using simultaneous conventional angiography as control, stenosis was found in seven celiac trunks, six SMAs, and four IMAs. In two cases the IMA stenosis was overestimated. The sensitivity and specificity of MRA in this small study was 100 and 95% respectively.19 Advantages of MRA over CTA include: (a) a more favorable safety profile of paramagnetic agents compared with that of iodinated contrast agents; (b) the ability to tailor the imaging plane of acquisition to correspond with the vascular territory under consideration; (c) simpler 3D MRA dataset; (d) lack of ionizing radiation; and (e) high tissue contrast.17 A potential limitation of MRA relates to the fact that it indirectly relies on the detection of vascular signals. In some cases, degradation of these signals can occur, usually as a result of turbulence, which may lead to overestimation of the degree of stenosis. It has also been shown that the sensitivity of MRA to detect calcification and spatial resolution is lower compared to CTA. Furthermore, the inability to visualize vessels with stents due to signal void caused by metallic material is an additional limitation.20 Other disadvantages of MRA include limited availability and cost. As discussed previously, typical MR protocols use 3D contrast-enhanced MR angiography supplemented with phase-contrast MRA for additional functional information. Such protocol takes 30–60 minutes to complete, considerably longer than with CTA.
REFERENCES 1. 2. 3.
4. 5. 6. 7.
Uflacker R. Abdominal aorta and its branches. In: Uflacker R, ed. Atlas of Vascular Anatomy. An Angiographic Approach. Philadelphia: Lippincott Williams & Wilkins, 1997: 405–604 Kornblith PL, Boley SJ, Whitehouse BS. Anatomy of the splanchnic circulation. Surg Clin North Am 1992; 72: 1–30 Cardella JF, Casarella WJ, DeWeese JA et al. Optimal resources for the examination and endovascular treatment of the peripheral and visceral vascular systems. AHA Intercouncil Report on Peripheral and Visceral Angiographic and Interventional Laboratories. Circulation 1994; 89: 1481–93 Krouwels MM, Overbach EH, Guit GL. Iohexol versus ioxaglate in lower extremity angiography: a comparative randomized doubleblind study in 80 patients. Eur J Radiol 1996; 22: 133–8 Hawkins IF. Carbon dioxide digital subtraction arteriography. Am J Roentgenol 1982; 139: 19–27 Kerns SR, Hawkins IF. Carbon dioxide digital subtraction angiography: expanding applications and technical evolution. Am J Radiol 1995; 164: 735–43 Caridi JG, Hawkins IF. CO2 digital subtraction angiography: potential complications and their prevention. J Vasc Interv Radiol 1997; 8: 383–91
8.
9. 10. 11. 12. 13. 14.
Kaufman JA, Geller SC, Waltman AC. Renal insufficiency: gadopentetate dimeglumine as a radiographic contrast agent during peripheral vascular interventional procedures. Radiology 1996; 198: 579–86 Derrick JR, Pollard HS, Moore RM. The pattern of atherosclerotic narrowing of the celiac and superior mesenteric arteries. Ann Surg 1959; 149: 684–9 Fleischmann D, Hallett RL, Rubin GD. CT angiography of peripheral arterial disease. J Vasc Interv Radiol 2006; 17(1): 3–26 Cademartiri F, Raaijmakers RH, Kuiper JW et al. Multi-detector row CT angiography in patients with abdominal angina. Radiographics 2004; 24(4): 969–84 Rydberg J BK, Cademyer KS et al. Multisection CT: scanning techniques and clinical application. Radiographics 2000; 20: 1787–806 Hellinger JC. Evaluating mesenteric ischemia with multidetectorrow CT angiography. Tech Vasc Interv Radiol 2004; 7(3): 160–6 Aspelin P AP, Fransson SG, Strasser R, Willenbrock R, Berg KJ. Nephrotoxic effects in high-risk patients undergoing angiography. N Engl J Med 2003; 348: 491–9
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Schertler T, Wildermuth S, Alkadhi H et al. Sixteen-detector row CT angiography for lower-leg arterial occlusive disease: analysis of section width. Radiology 2005; 237(2): 649–56 Laissy JP, Trillaud H, Douek P. MR angiography: noninvasive vascular imaging of the abdomen. Abdom Imaging 2002; 27(5): 488–506 Bradbury MS, Kavanagh PV, Bechtold RE et al. Mesenteric venous thrombosis: diagnosis and noninvasive imaging. Radiographics 2002; 22(3): 527–41
18. 19. 20.
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Hagspiel KD, Leung DA, Angle JF et al. MR angiography of the mesenteric vasculature. Radiol Clin North Am 2002; 40(4): 867–86 Meaney JF, Prince MR, Nostrant TT et al. Gadolinium-enhanced MR angiography of visceral arteries in patients with suspected chronic mesenteric ischemia. J Magn Res Imag 1997; 7: 171–6 Batels LW SH, Bakker CJ, Viergever MA. MR imaging of vascular stents: effects of susceptibility, flow, and radiofrequency eddy currents. J Vasc Interv Radiol 2001; 12: 365–71
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Duplex ultrasound of the mesenteric arteries Y-W Chi and JA Silva
Principles of duplex ultrasound Duplex ultrasound (DU) is one of the most commonly used non-invasive diagnostic modalities for the screening of stenoses in many vascular territories including the mesenteric arteries. The application of this technique is based on the physical principle of using sound waves to create images as well as deriving information from blood flow and flow velocities. The term ultrasound denotes sound-wave frequencies above 20 kHz which are out of the audible range. Ultrasound produces images of anatomic structures by using pulse-echo techniques. An ultrasonic transducer is placed in contact with the skin, often coupled with liquid gel to maximize sound transmission. The transducer then emits brief pulses of sound at a fixed repetition rate (pulse-wave technique). After the sound is generated, its transmission into the tissue may be absorbed, scattered, or reflected. Only the reflected sound waves can be caught by the transducer in between the brief intermittent periods of pulse-wave emission. These reflected sound waves are ultimately amplified and processed into a format suitable for display. Therefore, the images in B mode or brightness mode, are created with varying degrees of intensity which are proportional to the reflected echo signal amplitude and the depth (distance between the transducer the studied anatomical structure) (Figure 62.1). The use of B mode in combination with Doppler spectral analysis is termed duplex ultrasound. Briefly, Doppler spectral analysis relies on the differences in ultrasound-wave frequencies between those transmitted and those received by the transducer. The transmitted frequencies come from the transducer and the received frequencies are reflected from the moving blood including cells and macroparticles. This difference is termed Doppler shift and is calculated based on the Doppler equation, 2fVcosθ/C. The Doppler spectral analysis consists of all the Doppler shifts displayed in a wave format so that the peak systolic velocity and end diastolic velocity can be measured. Furthermore, the Doppler shifts can also be transformed into different color codes which are used to display flow (Figure 62.2).
After ingestion of a meal, the flow in the intestine markedly increases and the fasting high-resistive (low or near-zero Diastolic flow velocities) pattern turns into a post-prandial low-resistive flow pattern, characterized by augmented flow velocities during diastole.3 In contrast to SMA and IMA, the celiac trunk shows a low-resistive flow pattern continually because most of the blood flow in this vessel is directed to the
(a)
Application of duplex ultrasound in the mesenteric circulation In the superior mesenteric (SMA) and in the inferior mesenteric (IMA) arteries, the flow pattern during the fasting state are characterized by diminished flow velocities during diastole.1,2 570
(b) Figure 62.1 (a) Incidental wave and reflected wave forming the basis of ultrasound imaging; (b) b-mode imaging.
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(a)
(b) Figure 62.2 Physical properties of ultrasonography and analysis of velocity spectrum: (a) Doppler shift and equation; (b) spectral analysis. (See Color plates.)
liver and spleen which have low-resistance capillary beds.4 Normal fasting values for SMA peak systolic velocity (PSV) do not exceed 156 cm/second and end diastolic velocity (EDV) ranges from 11 to 16 cm/second. After food ingestion, SMA PSV increases by about 40% but mean flow velocity increases much more (by about 160%) because of a massive increase in diastolic flow.4 Celiac artery PSV in normal fasting subjects does not exceed 120 cm/second and EDV ranges from 32 to 35 cm/second. Normal flow values for IMA have not been established.1 There are two important aspects of duplex ultrasound for the diagnosis of chronic mesenteric ischemia. The first is the assessment of the flow resistance pattern in the SMA. The presence of a low-resistance flow pattern in the SMA or IMA in a fasting state is suggestive of mesenteric ischemia.1 A highresistance flow pattern is normal in the SMA or IMA during the fasting state. Consequently, a low-resistance pattern during the fasting state would be an indication of decreased capillary resistance as a compensatory measure to overcome a significant anatomical stenosis and strongly suggests the presence of mesenteric ischemia.5 The second aspect of mesenteric ischemia concerns the duplex detection of anatomical stenosis or occlusion of the celiac artery, SMA or IMA. Only stenosis
causing ≥ 70% diameter reduction or occlusion is thought to be of clinical significance.
Ultrasound examination procedure Protocols for the assessment of the mesenteric arteries vary according to the vascular laboratory, but there is agreement in certain principles: 1. The patient should always be examined in a fasting state and scanned in the supine position. The post-prandial state interferes with diagnostic accuracy by producing excessive bowel gas which limits sound-wave transmission. In addition, the aforementioned increase in flow in both systole and diastole during digestion of food can be misread as the presence of a hemodynamically significant stenosis. More importantly, there is no established velocity criteria to evaluate mesenteric ischemia in the post-prandial state. 2. Longitudinal aortic view and mesenteric vessel ostia should always be investigated for any evidence of atherosclerosis, aneurysms and obstruction.
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3. For the celiac artery, high velocity or disturbance should be noted, and common hepatic artery flow direction should be documented. 4. For SMA and IMA, peak systolic velocity and spectral analysis should be obtained.
Clinical studies of mesenteric arterial stenosis Although employed for more than 20 years for assessing the mesenteric vasculature, the role of duplex ultrasound is not fully defined. The diagnosis of mesenteric artery stenosis using color-flow Doppler is based on the visualization of an increased flow velocity in combination with post-stenotic flow disturbance (turbulence).5 There is agreement that in the SMA, a stenosis of ≥ 70% generates a PSV of ≥ 275 cm/second, and an EDV of ≥ 45 cm/second, during the fasting state (Figure 62.3). In the celiac trunk, a ≥ 70% stenosis usually generates a PSV of at least 200 cm/second and an EDV of at least 55 cm/second (Figure 62.4). Some authorities have used PSV
exclusively to diagnose mesenteric ischemic while others validated the use of EDV prospectively as the most sensitive tool.1,5 Ultrasound examination of celiac trunk and the SMA are adequate in more than 90% of patients making it a highly effective diagnostic tool.1,5 IMA can be visualized with color Doppler examination in 92% of normal middle-aged subjects, but little information exists in the literature regarding ultrasound diagnosis of IMA stenosis.7 For the SMA and celiac arteries, color-flow Doppler examination offers a high level of accuracy. Doppler sensitivity ranges from 89 to 100%, and specificity from 91 to 96% for stenosis ranging from 50% to greater than 70%.4–6 Although post-prandial scanning has been suggested as a means of increasing the sensitivity of the test, it only marginally improves it and at present is not routinely performed in most laboratories.8 Occlusion of a mesenteric artery is diagnosed with ultrasound when blood flow is absent in a portion of the vessel on color flow or spectral Doppler examination. The finding of flow reversal in the gastroduodenal or common hepatic arteries is highly suggestive of celiac trunk occlusion.6
(a)
(b) Figure 62.3 SMA stenosis by color image and velocity spectral analysis: (a) SMA stenosis color image; (b) SMA stenosis spectral analysis. Adapted from Zwiebel WJ. Ultrasound Assessment of the Splanchnic Arteries. In: Zwiebel WJ, ed. Introduction to Vascular Ultrasonography, 4th ed. Philadelphia: W.B. Saunders Company; 2000: p. 425. (See Color plates.)
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(a)
(b) Figure 62.4 Celiac stenosis by color image and velocity spectral analysis: (a) celiac stenosis color image; (b) celiac stenosis spectral analysis. (See Color plates.)
Conclusion Duplex ultrasonography is a useful diagnostic method for detecting mesenteric arterial stenoses and in the hands of experienced sonographers, the sensitivity for detecting
significant celiac or SMA stenosis is over 90%. Compared with other non-invasive diagnostic image modalities such as computed tomographic angiography or magnetic resonance angiography, or with conventional angiography, ultrasonography confers the highest safety profile.
REFERENCES 1. 2. 3. 4.
Moneta GL, Yeager RA, Dalman R et al. Duplex ultrasound criteria for diagnosis of splanchnic artery stenosis or occlusion. J Vasc Surg 1991; 14(4): 511–8; discussion 8–20 Geelkerken RH, van Bockel JH. Mesenteric vascular disease: a review of diagnostic methods and therapies. Cardiovasc Surg 1995; 3(3): 247–60 Geelkerken RH, van Bockel JH. Duplex ultrasound examination of splanchnic vessels in the assessment of splanchnic ischaemic symptoms. Eur J Vasc Endovasc Surg 1999; 18(5): 371–4 Zwiebel WJ. Ultrasound assessment of the splanchnic arteries. In: Zwiebel WJ, ed. Introduction to Vascular Ultrasonography, fourth edition. Philadelphia: WB Saunders, 2000: 421–9
5. 6. 7. 8.
Zwolak RM, Fillinger MF, Walsh DB et al. Mesenteric and celiac duplex scanning: a validation study. J Vasc Surg 1998; 27(6): 1078–87; discussion 88 Korotinski S, Katz A, Malnick SD. Chronic ischaemic bowel diseases in the aged – go with the flow. Age Ageing 2005; 34(1): 10–6 Denys AL, Lafortune M, Aubin B et al. Doppler sonography of the inferior mesenteric artery: a preliminary study. J Ultrasound Med 1995; 14: 435–9 Gentile AT, Moneta GL, Lee RW et al. Usefulness of fasting and postprandial duplex ultrasound examinations for predicting highgrade superior mesenteric artery stenosis. Am J Surg 1995; 169: 476–9
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Endovascular therapy for mesenteric ischemia JA Silva
Introduction The treatment of mesenteric ischemia has historically been surgical. In the last few years, however, percutaneous, catheterbased treatment has profoundly changed the approach of patients with significant athero-occlusive disease in many vascular territories and has challenged surgical revascularization as the treatment of choice in many vascular territories. Endovascular therapy has also been shown to play a crucial role in patients with mesenteric atherosclerotic disease and mesenteric ischemia, particularly those with CMI. In the present chapter we discuss the role of percutaneous revascularization strategies in the treatment of acute and chronic mesenteric ischemia.
Acute mesenteric ischemia General measures As was discussed in previous chapters, patients with acute mesenteric ischemia (AMI) are frequently hypotensive, dehydrated, acidotic, and septic. Therefore, these individuals require aggressive fluid resuscitation and hydration with crystalloid and/or colloid solutions. In addition, they must have correction of their metabolic acidosis and electrolyte imbalance as well as adequate antibiotic coverage for gram negative and anaerobic bacteria. Intestinal decompression with a nasogastric tube is also important, and discontinuation of medications that promote splanchnic vasoconstriction such as vasopressin and digoxin is also recommended.1–3 Endovascular therapy The traditional treatment for AMI has been surgical revascularization with exploratory laparotomy for assessment of intestinal viability and resection of the infarcted bowel.4 Van Deinse et al. were the first to report the successful treatment of AMI with balloon angioplasty.5 In the last few years, other investigators have also reported successful use of percutaneous endovascular techniques for the treatment of AMI in selected patients, in conjunction with exploratory laparotomy when clinically indicated for removal of necrotic intestine; however the experience is still scarce.6–9 Endovascular revascularization procedures are carried out immediately after invasive angiography has been obtained. The angiographic findings usually define the etiology of 574
AMI; that is, embolic, thrombotic, or non-occlusive AMI. The reported experiences with endovascular therapy for the treatment of AMI are very limited and anecdotal. In two case reports, the authors described the successful treatment of patients with acute exacerbation of CMI treated with endovascular stent placement of an occluded superior mesenteric artery in one report,6 or in two critical stenoses of the celiac trunk and inferior mesenteric artery in a second report.7 In a series of 58 patients with AMI, 50 patients were treated with open surgical revascularization and 8 patients were treated with endovascular procedures: transcatheter vasodilator therapy (n = 6), balloon angioplasty (n = 1), and catheter directed thrombolysis (n = 1). Five patients (63%) required bowel resection, and six patients (75%) died within 30 days. In this series of 58 patients, the overall mortality rate was 80% for nonocclusive mesenteric ischemia, 31% for embolism, and 32% for thrombosis.8 In a more recent publication, three patients with AMI were successfully treated with endovascular therapy using thrombectomy followed by stent placement. Because these three patients were treated promptly, none of them developed intestinal infarction or required bowel resection. The patients remained alive and symptom-free at 16 months of follow-up.9 Several small series have also shown the successful use of local infusions of fibrinolytic therapy for thrombotic occlusions of mesenteric arteries causing AMI.10–14 In a report of ten cases, infusion of urokinase was successful in treating seven patients with AMI due to embolism into the superior mesenteric artery.11 Some experts believe that this form of therapy should be considered in patients with no peritoneal signs, short duration of symptoms, and when angiography can be carried out without delay.15 The major drawback of catheter-directed fibrinolysis is that reperfusion may take several hours, potentially jeopardizing intestinal viability or worsening intestinal ischemia/infarction. For this reason these patients need close surveillance and the persistence of abdominal pain and/or the development of peritoneal signs should prompt the endovascular therapist for their immediate referral for surgical therapy and exploratory laparotomy. Patients with non-occlusive mesenteric ischemia may benefit with selective infusion of vasodilator therapy.16–18 Although several vasodilators may be useful for relieving vasospasm in the splanchnic circulation (such as papaverine, tolazoline, nitroglycerin, glucagon, prostaglandin, etc.) the largest experience is with papaverine.17 Kaleya et al. recommend the use of selective infusions of papaverine in the superior mesenteric artery at doses of 30–60 mg/hour.18
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Endovascular therapy for mesenteric ischemia This medication is, however, contraindicated in patients with hypotension, because peripheral vasodilation may worsen the condition and further decrease splanchnic perfusion. Papaverine infusion is continued for approximately 24 hours, after which angiography is repeated usually using the same infusion catheter. Clinical evidence of therapeutic responses includes decrease or relief of abdominal pain, amelioration or normalization of abdominal signs, stabilization of vital signs, and improvement of laboratory abnormalities such as metabolic acidosis and leukocytosis. Angiographic evidence of therapeutic responses includes mesenteric vasodilation, and faster passage of radio-contrast material. If patients develop or do not rapidly have remission of peritoneal signs during papaverine infusion, they should be referred for exploratory laparotomy without delay for assessment of intestine viability and possible resection of infarcted bowel.17 The success of endovascular strategies for the treatment of AMI will ultimately depend on the promptness of its detection and the swiftness of therapy institution. The endovascular therapist must always assess these patients very closely after endovascular treatment even if the procedure has been successful. Whether every patient with AMI should undergo laparoscopic assessment or exploratory laparotomy to rule out bowel infarction is debatable. Most surgical authorities advocate the use of routine surgical exploration for assessment of intestinal viability and removal of necrotic bowel.8 On the other hand, it has recently been suggested that patients with an angiographically successful endovascular procedures in whom the clinical and laboratory abnormalities immediately improve or subside can be managed with minimal invasive laparoscopic assessment for intestinal viability or no exploration at all.7,9 If this last strategy is chosen, the operator must have a very low threshold for referring these patients for exploratory laparotomy if they have any persistent clinical signs or laboratory abnormalities suggestive of splanchnic ischemia or if they develop recurrence of symptoms after an initial clinical improvement.
Chronic mesenteric ischemia Medical therapy Patients with CMI, like other patients with atherosclerotic vascular disease, should be treated with aggressive lipid-lowering therapy, smoking cessation, optimization of blood pressure, diabetes control, and the use of antiplatelet drugs such as aspirin. Because of the experimental data of angiotensin II leading to splanchnic vasoconstriction, there may be a theoretical role in the use of angiotensin converting enzyme (ACE) inhibitors and/or angiotensin receptor blocker (ARB) in these patients.19 In addition, due to the detrimental actions of digoxin in the splanchnic circulation causing vasoconstriction and ischemia, this drug must be avoided in these individuals.20,21 Although it is possible that a small proportion of patients with CMI may have improvement or relief of symptoms with medical therapy, this has not yet been documented, and as a general rule these patients have a progression of disease (see natural history) toward development of acute mesenteric ischemia or inanition and death, unless revascularization is carried out. For this reason the current recommendations of
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the ACC/AHA guidelines are that all patients with CMI should be referred for revascularization therapy, either endovascular or surgical.22 Endovascular therapy Endovascular revascularization techniques have dramatically changed the treatment of peripheral athero-occlusive disease and are at present accepted as alternatives to surgery in many vascular territories. Compared to surgical revascularization, percutaneous catheter-based therapy offers several distinct advantages such as the use of local instead of general anesthesia, allowing the treatment of patients who are at high-risk for general anesthesia. The morbidity and mortality from endovascular therapy is very low when compared to surgical revascularization. Problems secondary to angioplasty are generally related to vascular access. Following endovascular therapy, patients are usually ambulatory on the day of treatment and unlike vascular surgery, they can often return to normal activity within 24–48 hours of an uncomplicated procedure. Finally, endovascular therapies may be repeated if necessary, generally without increased difficulty or increased patient risk compared to the first procedure, and prior angioplasty does not preclude surgery if required at a later date. Chronic mesenteric ischemia frequently leads to malnourishment. In addition, patients with CMI often have significant atherosclerotic disease in other vascular territories such as the coronary and neurovascular circulation. Furthermore, stenoses of the mesenteric arteries are usually focal, preferentially located in the ostium or the very proximal portion of these vessels. These clinical and vascular characteristics of patients with CMI, make percutaneous transluminal intervention a very attractive treatment modality for this condition. Percutaneous transluminal angioplasty Furrer and Gruentzing were the first to report the successful treatment of chronic mesenteric ischemia using percutaneous transluminal angioplasty in a superior mesenteric artery in 1980.23 Since that publication, the use of percutaneous transluminal angioplasty in the mesenteric circulation has been reported in small series but has shown that this revascularization technique yields a high procedural success rate and low morbidity and mortality rates. The procedural success rate for balloon angioplasty in patients with CMI has been reported to be between 79 and 100%, with clinical success rates between 63 and 91%. Symptom recurrence occurred in 5–7%; however, the number of patients treated in these series was smaller and the follow-up shorter than the surgical studies (Table 63.1).24–32 Endovascular stent placement Aorto-ostial stenoses are difficult to treat with balloon angioplasty alone due to elastic recoil. Stent placement minimizes this recoil resulting in larger final lumen diameter and higher procedural success rate than for balloon dilation alone. In renal artery atherosclerotic aorto-ostial stenoses, the use of stents has been shown to be superior to balloon angioplasty alone.33,34 There are still limited data in the literature addressing the role of endoluminal stents for the treatment of CMI (Table 63.2). In one of the initial studies of 33 patients
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Textbook of peripheral vascular interventions Table 63.1 Summary of patients with chronic mesenteric ischemia treated with percutaneous transluminal angioplasty
Allen24 Hallisay25 Matsumoto26 Sniderman27 Simonetti28 Nyman29 Matsumoto30 Kasirajan31 Landis32
N
Tech success
19 15 19 14 22 23 33 28 29
95% 87% 79% 86% 95% 90% 87% 100% 97%
Stent
Clinical success
Complications
Symptom recurrence
83% 93% 63% 86% 91% 74% 88% — 90
11% 0% 16% 0% 0% 0% 12% 11% 3.4
3% 4% 2% 5% 2% 3% 5% 5% —
0% 0% 0% 0% 0% 0% 36% 82% —
(47 arteries) with CMI undergoing percutaneous transluminal intervention (12 patients and 15 vessels received stents), the technical success rate was 81% for balloon angioplasty alone and 100% for stenting. Complete or partial resolution of symptoms occurred in 82 and 6% of the patients respectively.30 In another study of 12 patients treated with stent placement, the reported technical success rate was 92%.35 One patient developed bowel infarction and died in the hospital despite a technically successful procedure. The primary and the primary-assisted patency rates were 74% and 83% respectively and the secondary patency rate was 83%. In a more recent study of 25 patients and 26 arteries treated with primary stenting, technical success was obtained in 96% and symptom relief in 88%.36 There was no procedural mortality and the only complications were the development of a pseudoaneurysm (n = 2), and renal failure (n = 1). At a mean follow-up of 15 months, the primary clinical benefit (no recurrence of symptoms) was 83%, and the restenosis rate was 18%. We have reported results of primary stent placement for CMI in 59 patients (79 vessels) also with quite favorable outcomes.37 The angiographic and the procedural success rates were 97 and 96% respectively, with symptom relief in 88%. We were unable to cross two chronic total occlusions in one patient. One patient died in the hospital due to sepsis and renal failure, despite an angiographically successful procedure. At a mean follow-up of 38 ± 15 months, 17% had recurrence of symptoms but none developed acute mesenteric ischemia and all of them underwent successful revascularization without any complication (Figure 64.1). Follow-up was obtained in 90% of the patients and 90% of the vessels, with computed
Table 63.2
Assisted primary patency 72% 62% 58% 71% 80% 96% 85% — 88
tomographic angiography, conventional angiography or duplex ultrasound showing a restenosis rate of 29%. Other investigators have obtained comparable results.38–41 Although there are no prospective controlled data comparing outcomes of balloon angioplasty versus stent placement for the treatment of mesenteric arterial stenoses, recent studies suggest that endovascular stent placement confers superior immediate and long-term results than balloon angioplasty alone, for which stent revascularization should be the percutaneous treatment of choice. Likewise, there are no controlled randomized data comparing surgical versus percutaneous revascularization strategies. Because patients with CMI are usually malnourished and frequently carry significant cardiac and neurovascular morbidity, it is not surprising that surgical revascularization (discussed in the next chapter) carries a high procedural morbidity (~45%) and high mortality rates (~15%).42 Whether patients who survive surgery have higher patency rates and symptom-free survival than patients treated with stent revascularization remains controversial (see next chapter).31,37,40 The results of percutaneous revascularization have prompted several investigators to advocate the use of this strategy as the treatment of choice for patients with CMI,43 or as bridging for further surgical revascularization in patients who develop recurrence of symptoms after percutaneous treatment once the surgical risk has been decreased.44 Technical aspects Aspirin is started at least one day prior to the procedure. Heparin is given after vascular access had been obtained to achieve an activated clotting time (ACT) of > 250 seconds.
Studies of patients with CMI treated with stent placement
Study (reference)
N
Sheeran35 Sharafuddin36 Silva37 Aburahma38 Resch39 Brown40 Schaefer41
12 25 59 22 17 14 19
Procedural Success 92% 96% 96% 96% 94% 100% 96%
Symptomrelief 83% 88% 88 95% 82% 100% 78%
In-hospital Mortality 8% 0% 1.7% 0% 5.8% 0% 10%
Procedural Complications 0% 12% 2.5% 0% 5.8% 0% 0%
Symptom Recurrence
Primary Patency Rate
18% 17% 17% 34% 17% 50% 22%
83% 92% 71% 30% 69% 43% 82%
Follow-up (months) 15.7 15 38 26 14 13 17
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Figure 63.1 Kaplan–Meir survival curves showing the 5-year cumulative probability of survival (72%), symptom-free (80%), and symptom-free survival (57%) of 59 patients with chronic mesenteric ischemia. (From Silva et al. J Am Coll Cardiol 2006; 47: 944–50; reprinted with permission).
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We often use retrograde common femoral arterial (CFA) access; however, in cases in which the origin of the mesenteric vessel is significantly caudally oriented, the brachial arterial access is preferred. A non-selective aortogram in the anteroposterior and lateral views are initially obtained using a pigtail diagnostic catheter to determine the origin of the mesenteric arteries as well as to visualize their patency and the presence of ostial stenosis. Selective mesenteric arterial imaging is then performed with 4–6-Fr diagnostic (internal mammary, Cobra, Simmons, Sos, or Judkins’ right configuration) catheters using hand injections of contrast. After angiography is completed and the decision to proceed with intervention is confirmed, a soft-tip exchange-length 0.035-inch (Wholey wire, Malinckrodt, St. Louis, MO) or a 0.014-inch steerable guidewire is advanced over the diagnostic across the stenosis. The diagnostic catheter is then exchanged over the Wholey wire for a 6–8-French hockeystick or internal mammary angioplasty guiding catheter (or any of the guiding catheters now available for renal angioplasty) and positioned in contact
Figure 63.2 A 72-year-old with typical symptoms of chronic mesenteric ischemia and critical stenoses of the superior and the inferior mesenteric arteries, successfully treated with a biliary (SMA) and a coronary (IMA) stent. (From Silva et al. J Am Coll Cardiol 2006; 47: 944–50; reprinted with permission).
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Figure 63.3 A 61-year-old female with symptoms of ischemic gastropathy for over 1 year, consisting of persistent nausea, poor appetite, easy fullness, vomiting, and abdominal pain only occasionally related to food intake. She had lost over 40 pounds when she underwent an abdominal aortogram showing total occlusion of all three mesenteric arteries. The superior mesenteric artery was successfully recanalized and stented with immediate resolution of her chronic symptoms and she experienced weight gain. (From Silva et al. J Am Coll Cardiol 2006; 47: 944–50; reprinted with permission).
with the ostium of the vessel. When using 6-French angioplasty guiding catheters, a 0.014-inch steerable guidewire is usually necessary to cross the lesion. When the brachial arterial access is used, a 6- or 7-French, 90-cm-long vascular sheath (Daig, Minnetonka, Minnesota) is advanced over the guidewire and positioned in the abdominal aorta immediately above the target mesenteric artery. A 6-French multipurpose diagnostic catheter is then introduced through the long arterial sheath and used to engage the mesenteric artery. A soft-tip exchange-length 0.035-inch steerable guidewire (Wholey wire, Malinckrodt, St. Louis, MO) is used to cross the mesenteric artery. Alternatively, 0.014-inch guidewires can be used if the operator plans to use a 6-Frenchcompatible balloon and stent systems. Keeping the 6-French multipurpose diagnostic catheter engaging the ostium of the mesenteric artery, and the Wholey wire distally engaging the branch of the mesenteric artery, the arterial sheath is advanced over the multipurpose catheter and positioned in contact with the ostium of the target mesenteric artery. The 6-French multipurpose diagnostic catheter is then removed, leaving the guidewire in the mesenteric artery branch, and the arterial sheath in contact with the ostium of the vessel. After the reference vessel diameter (RVD) is measured with online quantitative angiography, a peripheral angioplasty balloon (4–8 mm in diameter, 2 cm long) is advanced over the Wholey wire (or a 0.014-inch guidewire) and positioned at the lesion site. The lesion is then dilated with a balloon (sized 1:1 ratio with the RVD), using the lowest pressure that will fully expand the balloon. A balloon-expandable stent, long enough to cover the lesion, is used to scaffold the lesion and maximize the angiographic result. The balloon-expandable stent is advanced over the guidewire, still within the sheath or guiding
catheter, to the lesion site. The sheath or the guiding catheter is withdrawn, uncovering the stent, and with contrast injections through the sheath or the guiding catheter the stent is positioned at the lesion site. The stent is deployed at 6–8 atmospheres, and then the balloon is withdrawn into the sheath or the guiding catheter. Angiography is then performed and if inadequate expansion of the stent is observed, the operator repeats dilation of the stent at a higher inflation pressure or with a larger balloon (Figures 63.2–63.4).
Complications of endovascular therapy The complication rate of endovascular therapy is relatively low with a reported incidence of 0–12% after stent placement (Table 63.1). These complications are usually related to vascular access and include hematomas, pseudoaneurysms, abrupt occlusion and retroperitoneal bleeding. In the larger three studies published in the literature, three complications (12%) occurred (one transient contrast-induced nephropathy, and two pseudoaneurysms) in one study,36 three complications (5%) in the second study (two vascular brachial arterial access occlusion, and one death from multiorgan failure),37 and three complications (14%) in the third study (two groin hematomas and one mesenteric artery dissection requiring surgery).32 Distal embolization leading to bowel infarction is a potentially serious complication, for which some investigators have advocated the use of distal protection devices for the treatment of these patients.40 Nevertheless, its clinical occurrence appears to be low.35 Other complications include vessel dissection and thrombosis which have also been reported in some series.24,32,43
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Figure 63.4 A 67-year-old man with ischemic cardiomyopathy who developed symptoms of ischemic colitis (abdominal pain and lower gastrointestinal bleeding). Selective mesenteric angiography reveals high-grade stenosis in the celiac trunk and the inferior mesenteric artery, which successfully underwent stent placement. A 2-year follow-up angiogram revealed patent stents (last upper and lower panels on the right) (From Silva et al. J Am Coll Cardiol 2006; 47: 944–50; reprinted with permission).
REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Kaleya RN, Boley SJ. Acute mesenteric ischemia. An aggressive diagnostic and therapeutic approach. Can J Surg 1992; 35: 613–23 Kaleya RN, Boley SJ. Acute mesenteric ischemia. Crit Care Clin 1995; 11: 479–512 Ottinger LW, Austen WG. A study of 136 patients with mesenteric infarction. Surg Gynecol Obstet 1967; 124: 251–61 Cleveland TJ, Nawaz S, Gaines PA. Mesenteric arterial ischemia: diagnosis and therapeutic options. Vasc Med 2002; 7: 311–21 Van Deinse WH, Zawacki JK, Phillips D. Treatment of acute mesenteric ischemia by percutaneous transluminal angioplasty. Gastroenterology 1986; 91: 475–8 Loomer DC, Johnson SP, Diffin DC, DeMaioribus CA. Superior mesenteric artery stent placement in a patient with acute mesenteric ischaemia. J Vasc Interv Radiol 1999; 10: 29–32 Leduc FJ, Pestieau SR, Detry et al. Acute mesenteric ischemia: minimal invasive management by combined laparoscopy and percutaneous transluminal angioplasty. Eur J Surg 2000; 166: 345–7 Park WM, Gloviczki P, Cherry KJ Jr et al. Contemporary management of acute mesenteric ischemia: factors associated with survival. J Vasc Surg 2002; 35: 445–52 Demirpolat G, Oran I, Tamsel S et al. Acute mesenteric ischemia: endovascular therapy. Abdom Imaging (in press) Calin GA, Calin S, Ionescu R et al. Successful local fibrinolytic treatment and balloon angioplasty in superior mesenteric arterial embolism: a case report and literature review. Hepatogastroenterology 2003; 50: 732–4
11. 12.
13. 14. 15. 16. 17. 18. 19. 20.
Simo G, Echenagusia AJ, Camunez F et al. Superior mesenteric arterial embolism: local fibrinolytic treatment with urokinase. Radiology 1997; 204: 775–9 Turegano Fuentes F, Simo Muerza G, Echenagusia Belda A et al. Successful intraarterial fragmentation and urokinase therapy in superior mesenteric artery embolism. Surgery 1995; 117: 712–4 McBride KD, Gaines PA. Thrombolysis of a potentially occluding superior mesenteric artery thromboembolus by infusion of streptokinase. Cardiovasc Interv Radiol 1994; 17: 164–6 Boyer L, Delorme JM, Alexandre M et al. Local fibrinolysis for superior mesenteric artery thromboembolism. Cardiovasc Intervent Radiol 1994; 17: 214–6 Gallego AM, Ramirez P, Rodriguez JM et al. Role of urokinase in the superior mesenteric artery embolism. 1996; 120: 11–113 Bakal CW, Sprayregen S, Wolf EL. Radiology in intestinal ischemia: angiographic diagnosis and manangement. Surg Clin North Am 1992; 72: 125–141 Capell M. Intestinal (mesenteric) vasculopathy I. Gastroenterol Clin North Am 1998; 27: 783–825 Kaleya RN, Sammartano RJ, Boley SJ. Aggressive approach to acute mesenteric ischemia. Surg Clin North Am 1992; 72: 157–182 Reilly PM, Bulkley GB. Vasoactive mediators and splanchnic perfusion. Crit Care Med 1993; 21(2 suppl.): S55 Kim EH, Gewertz BL. Chronic digitalis administration alters mesenteric vascular reactivity. J Vasc Surg 1987; 5(2): 382–9
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23. 24. 25. 26. 27.
28. 29. 30.
31. 32.
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Textbook of peripheral vascular interventions Levinsky RA, Lewis RM, Bynum TE et al. Digoxin induced intestinal vasoconstriction. The effects of proximal arterial stenosis and glucagon administration. Circulation 1975; 52(1): 130–6 Hirsh AT, Haskal ZJ, Hertzer NR et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): Executive summary. J Am Coll Cardiol 2006; 47: 1239–312 Furrer J, Gruentzig J, Kugelmeir J, Goebel N. Treatment of abdominal angina with percutaneous dilatation of an arterial mesenteric superior stenosis. Cardiovasc Interv Radiol 1980; 3: 43–4 Allen RC, Martin GH, Rees CR et al. Mesenteric angioplasty in the treatment of chronic mesenteric ischemia. J Vasc Surg 1996; 24: 415–23 Hallisay MJ, Deschaine J, Illescas FF et al. Angioplasty for the treatment of visceral ischemia. J Vasc Interv Radiol 1995; 6: 785–91 Matsumoto AH, Tegtmeyer CJ, Fitzcharles EK et al. Percutaneous transluminal angioplasty of visceral arterial stenoses: results and long-term clinical follow-up. J Vasc Interv Radiol 1995; 6: 165–74 Sniderman KW. Transluminal angioplasty in the management of chronic intestinal ischemia In: Strandness DE, van Breda A, eds. Vascular Diseases: Surgical and Interventional Therapy. New York: Churchill Livingston, 1994: 803–9 Simonetti G, Lupetelli L, Urigo F et al. Interventional radiology in the treatment of acute and chronic mesenteric ischemia. Radiol Med 1992; 84: 98–105 Nyman U, Ivancev K, Lindh M, Uher P. Endovascular treatment of chronic mesenteric ischemia: report of five cases. Cardiovasc Intervent Radiol 1998; 21: 305–13 Matsumoto AH, Angle JF, Spinosa DJ et al. Percutaneous transluminal angioplasty and stenting in the treatment of chronic mesenteric ischemia: results and longterm clinical follow up. J Am Coll Surg 2002; 194: S22–31 Kasirajan K, O’Hara PJ, Gray BH et al. Chronic mesenteric ischemia. Open surgery versus percutaneous angioplasty and stenting. J Vasc Surg 2001; 33: 63–71 Landis MS, Rajan DK, Simons ME et al. Percutaneous management of chronic mesenteric ischemia: outcomes after intervention. J Vasc Interv Radiol 2005; 16: 1319–25
33. 34. 35. 36. 37. 38. 39. 40. 41. 42.
43. 44.
Van de Ven PJ, Kaatee R, Beutler JJ et al. Arterial stenting and balloon angioplasty in ostial atherosclerotic renovascular disease: a randomized trial, Lancet 1999; 353: 282–6 Leertouwer TC, Gussenhoven EJ, Bosch JL et al. Stent placement for renal artery stenosis: where do we stand? A meta-analysis. Radiology 2000; 216: 78–85 Sheeran SR, Murphy TP, Khwaja A, Sussman SK, Hallisay MJ. Stent placement for the treatment of mesenteric artery stenosis or occlusions. J Vasc Interv Radiol 1999; 10: 861–7 Sharafuddin MJ, Olson CH, Sun S, Kresowik TF, Corson JD. Endovascular treatment of celiac and mesenteric arteries stenoses: applications and results. J Vasc Surg 2003; 38: 692–8 Silva JA, White CJ, Collins TJ et al. Endovascular therapy for chronic mesenteric ischemia. J Am Coll Cardiol 2006; 47: 944–50 AbuRahma AF, Stone PA, Bates MC et al. Angioplasty/stenting of the superior mesenteric artery and celiac trunk: early and late outcomes. J Endovasc Ther 2003; 10: 1046–53 Resch T, Lindh M, Dias N et al. Endovascular recanalisation in occlusive mesenteric ischemia – feasibility and early results. Eur J Endovasc Surg 2005; 29: 199–203 Brown DJ, Schermerhorn ML, Powell RJ et al. Mesenteric stenting for chronic mesenteric ischemia. J Vasc Surg 2005; 42: 268–74 Schaefer PJ, Schaefer FK, Hinrichsen H et al. Stent placement with the monorail technique for treatment of mesenteric artery stenosis. J Vasc Interv Radiol 2006; 17: 637–43 Derrow AE, Seeger JM, Dame DA et al. The outcome in the United States after thoracoabdominal aortic aneurysm repair, renal artery bypass, and mesenteric revascularization. J Vasc Surg 2001; 34: 54–61 Steinmetz E, Tatou E, Favier-Blavoux C et al. Endovascular treatment as first choice in chronic intestinal ischemia. Ann Vasc Surg 2002; 16: 693–9 Biebl M, Oldenburg WA, Paz-Fumagalli R et al. Endovascular treatment as a bridge to successful surgical revascularization for chronic mesenteric ischemia. Am Surg 2004; 70: 994–8
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Mesenteric ischemia: surgical revascularization and indications for surgery JA Silva and DE Allie
Introduction Acute and chronic mesenteric ischemia are rare clinical conditions which carry significant morbidity and are often fatal if left untreated. The successful surgical treatment for acute mesenteric ischemia (AMI) and intestinal infarction was first reported in the nineteenth century by Elliot1 but it was not until 1957 that Mikkelsen described the first successful surgical revascularization in a patient with chronic mesenteric ischemia (CMI).2 Since those two publications the traditional treatment for these conditions has been surgery. Despite significant progress in diagnostic procedures and surgical techniques, AMI continues to carry a very high mortality rate. Whether new percutaneous approaches may decrease the fatality rate in patients with AMI remains to be seen, but at present there are only anecdotal reports in selected patients on the percutaneous treatment of AMI as was discussed in the previous chapter. If successfully discharged from the hospital, surgery usually confers lasting symptom relief in the majority of the patients with CMI. However, the procedural morbidity and mortality rates are high which makes catheter-based therapy more attractive for this sick group of patients. In the present chapter the surgical treatment and the surgical indications for both acute and chronic mesenteric ischemia are discussed.
Acute mesenteric ischemia Early aggressive resuscitation with volume replacement and correction of electrolyte and metabolic acidosis is crucial in the treatment of these patients. In addition, immediate institution of broad spectrum antibiotics, particularly when patients have peritoneal signs and bowel infarction is suspected is also critical.3,4 For the treatment of acute thrombosis and embolism, the initial steps after laparotomy is to determine and/or confirm the cause and extent of the mesenteric occlusive disease (particularly in patients who have not undergone preoperative mesenteric angiography), as well as to assess bowel viability.5,6 Although most experienced surgeons can differentiate between viable and necrotic intestine by simple visual inspection, in some instances this assessment may be difficult.7,8 The extent of bowel damage is usually determined by the cause.
In situ thrombosis triggered by atherosclerotic plaque rupture or ulceration usually causes ischemia and necrosis of the whole small bowel, since atherosclerotic plaques affecting the ostium of the small mesenteric artery are usually involved. In contrast, systemic embolization usually spares the proximal small bowel and local arterial embolization often leads to patches of ischemic bowel with spared segments of small intestine.6 The surgical treatment of AMI includes mesenteric arterial embolectomy and mesenteric artery bypass, in addition to removal of necrotic bowel during the surgical procedure. Embolectomy is performed by exposing the superior mesenteric artery (SMA) at its origin. An arteriotomy is performed and a 3- to 4-French Fogarty catheter is passed proximally to extract the clot and re-establish arterial flow. If this technique does not re-establish flow, bypass surgery is performed. In a report of 82 patients with embolic AMI, 34 patients required embolectomy alone and 20 patients required embolectomy and bowel resection. The patients who required embolectomy alone had a 35% mortality rate whereas those who needed embolectomy and intestinal resection had a 68% mortality (p < 0.05).9 These investigators and others have concluded that early diagnosis and treatment is critical to decrease the incidence of intestinal infarction and the need for bowel resection and has a dramatic impact on the procedural mortality.9–11 Bypass grafting is a much more complex operation than surgical embolectomy which requires not only the exposure of the SMA but also of the aorta and the iliac vessels. It is usually performed in patients with thrombosis of the SMA in whom thrombotic occlusion is superimposed to significant atherosclerotic disease, usually causing severe stenosis at the ostium or very proximal portion of this vessel. The type of technique depends on the surgeon’s experience, but most operators generally use the infrarenal abdominal aorta as the proximal anastomosis since the supraceliac aorta is usually less familiar and more time consuming. In addition, despite many surgeons preference for employing prosthetic grafts, it is recommended that autogenous vein (saphenous vein) bypass be used when patients have already developed intestinal infarction or when infarction is suspected or impending, in order to minimize the risk of later graft infection.5,6 Park et al.12 pooled data from 24 publications and 1234 patients with AMI treated surgically, between the years 1967 and 581
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2000 and found a mortality rate of 69% (range: 24–92%). In the same publication, the authors described their results in 58 patients with AMI (thrombosis: 37 patients; embolism: 16 patients; and non-occlusive: 5 patients) treated with surgery (n = 43) or endovascularly (n = 8). Open mesenteric revascularization was performed in 43 patients with bypass grafting (n = 22), thromboembolectomy (n = 19), patch angioplasty (n = 11), endarterectomy (n = 5), or reimplantation (n = 2). All patients underwent surgical exploration and 53% required bowel resection. The 30-day and 1-year mortality rates were 32 and 57% respectively. On multivariate analysis, an age less than 60 years, no recent surgery and bowel resection were predictors of increased survival at 529 days of follow-up. In comparison, of the 8 patients who underwent endovascular therapy (6 patients had non-occlusive AMI), 75% died at 30 days of follow-up.12 Determination of bowel viability and removal of necrotic bowel is critical since infarcted intestine causes bowel perforation, peritonitis, and sepsis. Several different methods to confirm questionable viable tissue have been recommended such as the use of Doppler ultrasound pulsatile signals, the use of intravenous fluorescein in combination with the Wood’s lamp, surface oximetry, among others.8,13–15 In some instances, when questionable viable intestine is not removed at the time of initial laparotomy, patients are returned to the operating room for a “second look” laparotomy 12–36 hours after the initial surgical procedure. At this time, the viability of the intestinal segment in question by visual inspection is usually obvious. The decision to proceed with a second-look laparotomy is usually made at the time of the initial operation and should be individualized.7 In short, surgical treatment for AMI has the advantage of allowing the operator to proceed not only with revascularization of the ischemic bowel, but also to assess intestinal viability and to proceed with bowel resection. As discussed in the chapter on the assessment of mesenteric ischemia, conventional angiography should ideally be obtained immediately prior to surgery to determine the etiology and the extent of intestinal ischemia so long it can be performed expediciously. Despite significant advances in diagnostic and surgical procedures, AMI carries a very high mortality rate, and its early detection and surgical intervention directly correlate with the survival rate.
Table 64.1
Chronic mesenteric ischemia Surgical treatment for CMI is challenging for the vascular surgeon and usually entails a careful selection of patients regarding the etiology of the symptoms and the assessment of the operative risks, as well as the choice of surgical technique. A variety of surgical techniques have been suggested including reimplantation, transarterial and transthoracic endarterectomy, antegrade and retrograde aortovisceral bypass using vein or arterial autograft bypasses and prosthetic bypass, with a reported early success rates of 91–96% and late success rates between 80 and 90%.16 Although there is lack of controlled data regarding the best surgical technique for this condition, it has been suggested by most centers with large experience that antegrade revascularization or transaortic endarterectomy of both the celiac trunk and the SMA confer the best long-term results.16,17 Irrespective of the technique used, surgical revascularization carries significant procedural morbidity and mortality rates. In Table 64.1 we have summarized the outcome of 12 surgical studies, showing a mortality rate ranging from 0% to 29%, and a morbidity rate ranging from 9 to 62%.18–29 These results have been confirmed by a recent surgical study of 336 patients from the Nationwide Inpatients sample as part of the Healthcare Cost and Utilization Project, showing that surgical revascularization for CMI had an in-hospital mortality of 14.7%, a complication rate of 44.6%, and a median hospital stay of 14 days.30 Patients with CMI usually have significant coronary, neurovascular, renal, and peripheral atherosclerotic disease. These co-morbidities put these individuals at a high risk for developing post-operative vascular events such as myocardial infarction, stroke, renal failure or non-cardiogenic pulmonary edema, causing death or a difficult post-operative course and a very prolonged hospital stay. However, of the patients who were discharged from the hospital, the majority had lasting symptom relief, with a recurrence rate of 10–30% at a follow-up of 3–5.5 years (Table 64.1). Due to these significant complication rates, percutaneous catheter-based revascularization techniques have challenged surgical revascularization as a more suitable revascularization modality for this sick group of individuals, as was discussed in the previous chapter.
Results of surgical revascularization
N Hollier18 Cunningham19 Cormier20 McAfee21 Christensen22 Gentile23 Johnston24 Taylor25 Mateo26 Foley27 Cho28 English29
56 85 103 58 53 23 21 58 85 49 25 58
Procedural mortality 8.9% 12% 4% 10% 0% 0% 0% 0% 8% 12% 4% 29%
Procedural morbidity — 47% — 49% — — 19% 9% 33% 35% 60% 62%
Symptoms relief 96% 97% — 96% — 100% — — 81% — — 94%
Symptoms recurrence 26.5% 14% 4% 10% 30% 10% 14% 4% 24% 21% 21% 43%*
Follow-up (years) 3 5 5.5 3.3 — 3.3 — 4.5 4.8 3.5 5.3 3
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Mesenteric ischemia: surgical revascularization and indications for surgery Surgical versus endovascular therapy The growing application of endovascular therapy for the treatment of peripheral arterio-occlusive disease as well as the recent publication of studies demonstrating that percutaneous intervention is an important treatment for CMI, has given way to intense debate regarding the best revascularization strategy for this condition. Unfortunately, there are no controlled prospective randomized studies, comparing these two treatment modalities and therefore firm conclusions cannot be drawn with the existing data. From the previous discussion it is clear that because patients with CMI are a very sick group of individuals – that is, malnourished, and frequently with severe coronary and neurovascular disease – and because of the characteristics of their disease, such as proximity and focal nature of the atherosclerotic lesions, this group of patients is ideally suited for endovascular therapy. Results from surgical reports and endovascular stent series as well as comparative studies show that in the majority of patients, the immediate clinical success and procedural morbidity and mortality are superior in the endovascular group. Another aspect where percutaneous intervention may be superior over surgery is that graft failure after surgery often presents abruptly, as sudden occlusion, either in the early post-operative period or at follow-up, leading to bowel infarction and death in the majority of the patients.18,19,26 This occurrence is rare after endovascular therapy. We recently reported the results of 59 patients treated with endovascular stent revascularization, and in no single case did the development of in-stent restenosis lead to mortality. None of our patients had acute mesenteric ischemia, either early after the procedure or at follow-up. There were no acute or subacute post-procedural stent thrombosis events, and the cases of in-stent restenosis led to gradual development of symptoms.31 The major controversy stems from whether a particular treatment option confers superior lasting clinical benefits. Four non-randomized retrospective studies have attempted to compare surgical revascularization versus endovascular treatment for CMI.32–35 One small study32 compared the outcomes of nine patients treated with bypass graft and eight patients treated with balloon angioplasty alone. Although the immediate and long-term outcomes were comparable in the two groups, it is difficult to draw meaningful conclusions from this small study. A second study,33 compared the results of 28 patients treated percutaneously (23 patients received stents), and 85 patients treated with surgery. The patients in the endovascular treatment group were older and had a significant higher prevalence of coronary artery disease. The procedural related mortality was 10.7 for the endovascular treatment group and 8.2% for the surgical group (p = 0.71); however, serious complications were significantly less common (19 vs. 40%; p = 0.03), and hospital stay shorter (5 vs. 13 days; p = 0.08) in the percutaneously treated group. The long-term mortality and patency rates were similar in the two groups. Recurrence of symptoms was more frequent in the endovascularly treated group than in the surgically treated group (34 vs. 13%; p = 0.001); however, the large majority (86%) of the patients with recurrent symptoms in the endovascular treatment group had patent vessels, whereas 90% of the patients with recurrence of symptom in the surgical group had graft or vessel occlusion.
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A more recent study34 comparing outcomes of 60 patients treated with surgery (n = 41) or endovascular therapy (n = 19; 89% received stents), found a much lower morbidity rate and a shorter in-hospital stay in the percutaneously treated group. The 30-day mortality and 3-year cumulative survival were similar in both groups. The 6-month symptom-recurrence was significantly higher in the percutaneously treated group despite similar cumulative patencies rates (83 vs. 68%, p = NS). Comparable results were obtained in a different a study of 14 patients treated with stent revascularization. At a mean follow-up of 13 months, 50% developed recurrence of symptoms, and 57% developed in-stent restenosis requiring repeat endovascular treatment.35 When the authors compared their results with historical surgical controls at the same institution, vessel patency was significantly higher in the surgically treated group. These results, however, contrast with our study of 59 patients and 79 arteries, where we found an in-stent restenosis rate of 29% of the arteries (37% of the patients), at a mean follow-up of 38 ± 15 months (Figure 64.1), comparable with most surgical series (Figure 64.1).31 Recent reports have also suggested a strategy of endovascular therapy as bridging to surgical revascularization, thereby allowing patients to improve their surgical risk profile (nutritional status, treatment of co-morbidities such as coronary artery disease, etc.) and proceeding with more definitive surgical treatment at a later stage if necessary.36,37 More studies – ideally prospective randomized – will be needed to draw a definitive conclusion; however, in light of the current evidence, a large and increasing proportion of practitioners including the authors, refers patients with CMI for endovascular stent therapy as the treatment of choice, reserving surgical revascularization for those patients in whom percutaneous intervention fails (like patients with chronic total occlusions) or those who develop symptom recurrence due to in-stent restenosis, where surgery may be considered instead of repeat percutaneous intervention.
Figure 64.1 Kaplan–Meir survival curves showing the 5-year cumulative probability of survival (72%), symptom-free (80%), and symptom-free survival (57%) of 59 patients with chronic mesenteric ischemia. (From Silva et al. J Am Coll Cardiol 2006; 47: 944–50; reprinted with permission).
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ACC/AHA indications for surgical revascularization in mesenteric ischemia Acute mesenteric ischemia Surgery remains the gold-standard treatment for AMI because it has the advantage of allowing intestinal reperfusion, and at the same time enables the assessment of intestinal viability and resection of necrotic bowel if necessary, as discussed previously. There are still little data on endovascular therapy for this condition, but perhaps it may be considered in selected patients with angiographic documentation of obstructive AMI during the early stages of this condition. In the current ACC/AHA guidelines,38 surgical treatment for obstructive AMI has a class I level of evidence B recommendation meaning that there is general agreement among experts regarding the benefit of the procedure based upon a single randomized trial or on non-randomized studies. Surgical treatment includes revascularization, resection of necrotic bowel, and (when appropriate) a “second look” operation after revascularization. In the case of non-obstructive AMI, laparotomy and resection of non-viable bowel is indicated in patients with persistent symptoms despite appropriate medical treatment, also as a class I level of evidence B recommendation. In the same guidelines,38 percutaneous interventions for AMI have a class IIb level of evidence C recommendation, meaning that the usefulness and efficacy of this form of therapy is less well established based upon evidence and/or expert opinion. The guidelines state that this treatment may be considered in selected patients with acute arterial obstructions; however, these patients may still require laparotomy for assessment of bowel viability or resection. The use of catheter-directed vasodilators for non-obstructive AMI with evidence of vasospasm is recommended as class IIa level of evidence B, meaning that although there are conflicting opinions, the weight of evidence favors the use of this form of therapy.
Chronic mesenteric ischemia Until recently, surgical treatment was considered the treatment of choice for patients with CMI. Due to the high procedural complication and mortality rate with surgical revascularization and the encouraging results in recently published studies using endovascular therapy, more patients with CMI are referred for the latter. It remains to be determined which treatment modality confers the higher symptom-free survival and patency rates in patients successfully discharged from the hospital. However, it appears clear that patients with catheterbased treatment for CMI have lower procedural complications and mortality rates than surgically treated patients. In the current ACC/AHA guidelines,38 surgical treatment for CMI has a class I level of evidence B recommendation, meaning that there is general agreement among experts regarding the benefit of the procedure based upon a single randomized trial or non-randomized studies. Surgical revascularization of asymptomatic patients with intestinal arterial obstructions may be considered in patients undergoing aortic and/or renal artery surgery for other indications as a class IIb level of evidence B recommendation. The usefulness and efficacy of this form of therapy is less well established based on evidence and/or expert opinion. Recent reports have also suggested a strategy of endovascular therapy as a bridge to surgical revascularization, thereby allowing patients to improve their surgical risk profile (nutritional status, treatment of co-morbidities such as coronary artery disease, etc.) and proceeding with more definitive surgical treatment at a later stage if necessary.36,37 More data are needed to draw a definitive conclusion; however, in light of the current evidence, it is the author’s opinion that patients with CMI should be referred for endovascular stent therapy as the treatment of choice. Surgical revascularization should be reserved for patients in whom percutaneous intervention fails, such as those with chronic total occlusions, or who develop symptom recurrence due to in-stent restenosis. In such cases, surgery may be preferable to repeat percutaneous intervention.
REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.
Elliot J. The operative relief of gangrene of intestine due to occlusion of the mesenteric vessels. Ann Surg 1895; 1: 9–23 Mikkelsen WP. Intestinal angina: Its surgical significance. Am J Surg 1957; 94: 262–7 Kaleya RN, Boley SJ. Acute mesenteric ischemia. An aggressive diagnostic and therapeutic approach. Can J Surg 1992; 35: 613–23 Kaleya RN, Boley SJ. Acute mesenteric ischemia. Crit Care Clin 1995; 11: 479–512 Mansour MA. Management of acute mesenteric ischemia [surgical technique]. Arch Surg 1999; 134: 328–30 Endean ED, Barnes SL, Kwolek CJ et al. Surgical management of thrombotic acute intestinal ischemia (scientific papers of the southern surgical association). Ann Surg 2001; 233: 801–8 Moore EM, Endean ED. Treatment of acute intestinal ischemia caused by arterial occlusions. In: Rutherford RB, ed. Vascular Surgery, sixth edition. Philadelphia: Elsevier Saunders, 2005: 1718–28 Ballard JL, Stone WM, Hallet JW et al. A critical analysis of adjuvant techniques used to assess bowel viability in acute mesenteric ischemia. Am Surg 1993; 59: 309–11 Batellier J, Kieny R. Superior mesenteric artery embolism: eightytwo cases. Ann Vasc Surg 1990; 4: 112–6 Levy PJ, Krausz MM, Manny J. Acute mesenteric ischemia: improved results – a retrospective analysis of 92 patients. Surgery 1990; 107: 372–80
11. 12. 13. 14. 15. 16. 17. 18. 19.
Lazaro T, Sierra L, Gesto R et al. Embolization of the mesenteric arteries: surgical treatment in twenty-three consecutive cases. Ann Vasc Surg 1986; 1: 311–5 Park WM, Gloviczki P, Cherry KJ Jr et al. Contemporary management of acute mesenteric ischemia: factors associated with survival. J Vasc Surg 2002; 35: 445–52 Wright CB, Hobson RW. Prediction of intestinal viability using Doppler ultrasound technique. Am J Surg 1975; 129: 642–5 Carter MS, Fantini GA, Sammartano RJ et al. Qualitative and quantitative fluorescein fluorescence in determining intestinal viability. Am J Surg 1984; 147: 117–21 Locke R, Hauser CJ, Shoemaker WC. The use of surface oximetry to assess bowel viability. Arch Surg 1984; 119: 1252–6 van Bockel JH, Geelkerken RH, Wasser MN. Chronic splanchnic ischemia. Best Pract Res Clin Gastroenterol 2001; 15: 99–119 Cleveland TJ, Nawaz S, Gaines PA. Mesenteric arterial ischemia: diagnosis and therapeutic options. Vasc Med 2002; 7: 311–21 Hollier LH, Bernatz PE, Pairolero PC, Payne WS, Osmundon PJ. Surgical management of chronic intestinal ischemia: A reappraisal. Surgery 1981: 90: 944–6 Cunningham CG, Reilly LM, Rapp JH, Schneider PA, Stoney RJ. Chronic visceral ischemia. Three decades of progress. Ann Surg 1991; 214: 276–88
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25. 26. 27. 28. 29.
Cormier JM, Fichelle JM, Vennin J et al. Atherosclerotic occlusive disease of the superior mesenteric artery: late results of reconstructive surgery. Ann Vasc Surg 1991; 5: 510–8 McAfee MK, Cherry KJ, Naessens JM et al. Influence of complete revascularization on chronic mesenteric ischemia. Am J Surg 1992; 164: 220–4 Christensen MG, Lorentzen JE, Schroeder TV. Revascularization of atherosclerotic mesenteric arteries: experience in 90 consecutive patients. Eur J Vasc Surg 1994; 8: 297–302 Gentile AT, Moneta GL, Taylor LM et al. Isolated bypass to the superior mesenteric artery for intestinal ischemia. Arch Surg 1994; 129: 926–31 Johnston KW, Lindsay TF, Walker PM, Kalman PG. Mesenteric arterial bypass grafts: early and late results and suggested surgical approach for chronic and acute mesenteric ischemia. Surgery 1995; 118: 1–7 Taylor LM, Porter JM. Treatment of chronic visceral ischemia. In: Rutherford, RB, ed. Vascular Surgery. Philadelphia: WB Saunders, 1995; 1301–11 Mateo RB, O’Hara PJ, Hertzer NR et al. Elective surgical treatment of symptomatic chronic mesenteric occlusive disease: early results and late outcomes. J Vasc Surg 1999; 29: 821–32 Foley MI, Moneta GL, Abou-Zamzam AM et al. Revascularization of the superior mesenteric artery alone for the treatment of intestinal ischemia. J Vasc Surg 2000; 32: 37–47 Cho JS, Carr JA, Jacobsen G et al. Long-term outcome after mesenteric artery reconstruction: a 37-year experience. J Vasc Surg 2002; 35: 453–60 English WP, Pearce JD, Craven TE et al. Chronic visceral ischemia: symptom-free survival after open surgical repair. Vasc Endovasc Surg 2004; 38: 493–503
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Derrow AE, Seeger JM, Dame DA et al. The outcome in the United States after thoracoabdominal aortic aneurysm repair, renal artery bypass, and mesenteric revascularization. J Vasc Surg 2001; 34: 54–61 Silva JA, White CJ, Collins TJ et al. Endovascular therapy for chronic mesenteric ischemia. J Am Coll Cardiol 2006; 47: 944–50 Rose SC, Quigley TM, Raker EJ. Revascularization for chronic mesenteric ischemia: comparison of operative bypass grafting and percutaneous transluminal angioplasty. J Vasc Interv Radiol 1995; 6: 339–49 Kasirajan K, O’Hara PJ, Gray BH et al. Chronic mesenteric ischemia. Open surgery versus percutaneous angioplasty and stenting. J Vasc Surg 2001; 33: 63–71 Sivamurthy N, Rhodes JM, Lee D et al. Endovascular versus open mesenteric revascularization: immediate benefits do not equate with short term functional outcomes. J Am Coll Surg 2006; 202: 859–67 Brown DJ, Schermerhorn ML, Powell RJ et al. Mesenteric stenting for chronic mesenteric ischemia. J Vasc Surg 2005; 42: 268–74 Schaefer PJ, Schaefer FK, Hinrichsen H et al. Stent placement with the monoriel technique for treatment of mesenteric artery stenosis. J Vasc Interv Radiol 2006; 17: 637–43 Biebl M, Oldenburg WA, Paz-Fumagalli R et al. Endovascular treatment as a bridge to successful surgical revascularization for chronic mesenteric ischemia. Am Surg 2004; 70: 994–8 Hirsh AT, Haskal ZJ, Hertzer NR et al. ACC/AHA 2005 Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): Executive summary. J Am Coll Cardiol 2006; 47: 1239–312
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SECTION X Lower extremity
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Epidemiology and pathophysiology of peripheral arterial disease of the lower extremities C Klonaris, A Papapetrou, and A Giannopoulos
Introduction The adult population is most commonly the “target group” of vascular sciences worldwide, with atherosclerosis being the predominant etiologic factor for vascular diseases. Chronic lower limb ischemia represents a large portion of the so-called “vascular patients” and is associated with increased morbidity and mortality. Walking disability, referred to as intermittent claudication (IC), is the most common clinical presentation and is associated not only with increased risk for amputation, but is also a marker of concomitant cardiovascular and cerebrovascular diseases and of limited life expectancy.1
Terms and definitions Intermittent claudication is defined as pain in the leg musculature during exercise, which is relieved by rest. Pain can be located in the muscles of calf, thigh, or buttock depending on the site of arterial compromise (Figures 65.1 and 65.2). As the arterial disease progresses in severity, symptoms become more intense and persistent, the pain-free walking distance lessens and the pain may become constant. The latter is defined as “rest pain” and typically affects the foot, is aggravated when the leg is elevated in bed during the night, and is relieved by dependency. Further deterioration of the disease leads to leg hypoperfusion, tissue loss, gangrene, and ultimately amputation in one-third of patients with critical limb ischemia (CLI). These patients have an annual mortality of 20%.1
Diabetes mellitus is strongly related to the development of PAD. Many studies have shown that IC is two times more common in diabetics than in non-diabetics. Diabetes mellitus affects more the infrainguinal and infrageniculate vessels as well as the microcirculation of the extremities. PAD is more aggressive in patients with diabetes and several studies have showed the increased rates of acute ischemia and amputation in these patients when compared with non-diabetics.7 When diabetes is coupled with chronic renal insufficiency then morbidity and mortality rates are also increased.8,9 Smoking is another risk factor that seems to have a strong impact in development and progress of PAD. Intermittent claudication is three times more common among smokers than non-smokers. Almost 80% of patients with PAD are current or former smokers and there is a strong association between the number of cigarettes smoked daily and the severity of the symptoms.10,11 Consequently, smoking cessation is strongly recommended and represents an integral part of the conservative treatment of PAD. Elevated serum lipids are also a significant risk factor. Elevated total cholesterol, low-density lipoprotein (LDL), and decreased high-density lipoprotein (HDL) are found more frequently in patients with lower extremity PAD than in the age-matched control group.12,13 Hypertension is also involved in the creation of lower PAD, but there seems to be a stronger relationship between hypertension and cerebrovascular events than PAD.14,15 Elevated levels of serum homocysteine and C-reactive protein (CRP) are also strongly associated with PAD development.16,17
Etiology
PAD and concomitant vascular diseases
Atherosclerosis is the predominant cause for peripheral arterial disease. The risk factors that are responsible for developing atherosclerosis are implicated in the pathogenesis of peripheral arterial disease (PAD). Since atherosclerosis is a long-standing procedure, PAD is most commonly a disease of the elderly. In large population studies there is a sound agreement that in men around the age of 60 years, the prevalence of intermittent claudication is 3–6%. In all these studies the prevalence in men is greater than in women.2–6
Concomitant presentation of atherosclerosis in the human vasculature is not infrequent. Atherosclerosis tends to affect all arteries and as such it is quite common to find patients suffering from PAD, coronary artery disease (CAD), and cerebrovascular disease (CVD) at the same time. Several studies have attempted to estimate the prevalence of CAD in patients with intermittent claudication. CAD can be asymptomatic if exercise is limited because of claudication. Past medical history, clinical examination, and electrocardiography reveal that 40–60% of patients with PAD also have 589
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Figure 65.2 Obstruction of the left external iliac artery with an extensive collateral network.
Figure 65.1 Focal stenosis at the lower abdominal aorta producing severe bilateral thigh and limb claudication.
concomitant CAD.18,19 However in an interesting study published in 1984, Hertzer et al.20 found that 90% of all patients admitted for elective peripheral vascular surgery had atherosclerotic lesions in the coronary arteries diagnosed with coronary angiograms. Twenty-eight percent had severe three-vessel disease and only 10% had normal coronary arteries. Interestingly, it is also true that the prevalence of PAD among patients suffering primarily from CAD is higher.21 It seems that the correlation of PAD with CVD is not as strong as with CAD. Several investigators estimated the prevalence of CVD in patients with PAD using carotid artery duplex ultrasonography and found that 26–50% of these patients had carotid artery disease.22,23 Conversely, according to Aronow’s study, 33% of patients with CVD had also PAD.21
Pathophysiology from a hemodynamic perspective Over the past decade, there has been meticulous research in an attempt to elucidate the hemodynamic behavior of human blood flow and it would be quite helpful to underline some significant points. Critical stenosis A stenosis becomes critical when the cross-sectional area of a vessel is reduced by more than 75% (usually 80–95%), which
corresponds to 50% reduction in vessel diameter.24 Under these circumstances significant drops in pressure and flow are noted, contributing to the energy loss of the fluid. Besides the degree and length of the stenosis, the velocity of blood flow distally to the stenosis plays a significant role in the estimation of energy losses. Blood flow velocity after the stenosis depends on the resistance of the run-off vasculature. When the blood flow velocity distal to the stenosis is high (low-resistance run-off bed), the drop in pressure and flow reaches a critical level with less narrowing of the vessel. So, in low-resistance run-off beds like the cerebral, coronary, and limb in exercise circulation, a smaller narrowing is needed for compromising perfusion and creating symptoms (e.g. angina pectoris, intermittent claudication).25,26 In contrast, in high-resistance arterial beds (e.g. the leg at rest), the vasculature is closed, blood flow velocity distal to the stenosis is lower, the need for blood supply is minimal, and so a stenosis can be asymptomatic. When atherosclerosis progresses and a stenosis becomes narrower, the blood supply of the lower limb becomes inadequate even during rest, which results in rest ischemia or critical limb ischemia.25,26 Multilevel disease (sequential stenoses) The existence of several stenoses in series in a major arterial axis, called multilevel disease, is a rather frequent pattern of atherosclerosis (Figure 65.3). Evaluation of energy losses of blood flow through a narrow segment has contributed a lot to better understanding of PAD pathophysiology. Energy losses are principally due to the viscosity of blood and to its inertia (viscous and inertial energy losses). Poiseuille’s law describes energy losses (drop in energy) due to
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(a)
(b)
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Figure 65.3 Multilevel peripheral arterial disease at (a) left external iliac; (b) common femoral; and (c) superficial femoral arteries resulting in critical limb ischemia.
its viscosity within a narrow segment in an ideal model (viscous energy losses): P1 – P2 = Q • 8Lη/πr4 where P1–P2 is the drop in potential energy; Q is the flow; L is the length of the stenosis; r is the radius of the stenotic lumen; and η is the coefficient of viscosity. Inertial energy losses of the blood are encountered at the entrance and the exit of a stenosis, and in fact energy losses at the exit are larger compared to those at the entrance of the narrowing. All of the above can be described by the following equation: ∆P = k • ρ/2 • (vs – v)2 = k • ρ/2 • v 2 • {(r/rs)2 – 1}2 where P is the loss of energy; vs is the velocity within the stenosis; v is the velocity beyond the stenosis; rs is the radius of stenotic lumen; and r is the radius of the distal lumen. The biggest portion of energy losses is attributable to inertial losses (viscous losses calculated by Poiseuille’s law underestimates the total energy losses). The length of a stenotic segment mostly affects viscous losses. It enters Poiseuille’s law in the first power, in contrast to the radius which is elevated to the fourth power, making the radius the more significant factor of a stenosis. A stenosis of double length would double only the viscous component of energy losses so the total amount of energy lost would be slightly bigger. In contrast, two separate sequential stenoses of equal length create approximately double the energy loss because the entrance and exit effects (inertial losses) occur two times. This explains how two “non-critical” stenoses in the same arterial axis can compromise critically the perfusion of the distal arterial bed.27,28 Implementation of hemodynamic behavior of blood in clinical practice is remarkable and has a significant impact
in treatment strategies. The most common diagnostic manipulation is the measurement of blood pressure of the arteries at the level of ankle during rest and post-exercise. Ankle pressure is a non-invasive marker of blood flow. In normal arteries, ankle pressure is equal or slightly greater than the brachial artery pressure. Exercise produces little or no drop in ankle pressure, whereas a rapid recovery of pressure is observed during the first minutes of rest. An arterial stenosis proximally reduces markedly the ankle pressure depending on the location of the stenosis. Several clinical studies have correlated the drop in pressure and the location of the stenosis; infrageniculate popliteal artery, superficial femoral artery, aortoiliac and multilevel disease, in increasing order, produce a significant drop in pressure during exercise.29 This means that blood flow is unable to meet the requirements of the muscle in exercise, anaerobic metabolic products are accumulated in the ischemic muscle, which ultimately results in the expression of pain. Further reduction of blood flow is observed with progress of the disease and perfusion of the limb is compromised even during rest. Ischemic rest pain is located in the toes and can lead to gangrene. According to current clinical practice, it is quite rare for a single stenosis to produce severe symptoms or even to threaten the limb, whereas multilevel disease usually requires therapeutic intervention.
Conclusion It is quite remarkable that the number of interventions for lower limb atherosclerotic disease has increased over the last decade, but limb amputations are still an inevitable part of current practice. It is apparent that further research at a molecular level for elucidation of atherosclerotic disease etiology and advance of vascular technologies and biomechanics will contribute to the best treatment of peripheral arterial disease.
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Ouriel K: Peripheral arterial disease. Lancet 2001; 358(9289): 1257–64 Hughson WG, Mann JI, Garrod A: Intermittent claudication: prevalence and risk factors. Br Med J 1978; 1(6124):1379–81 De Backer G, Kornitzer M, Sobolski J, Denolin H: Intermittent claudication––epidemiology and natural history. Acta Cardiol 1979; 34(3):115–24 Reunanen A, Takkunen H, Aromaa A: Prevalence of intermittent claudication and its effect on mortality. Acta Med Scand 1982; 211(4): 249–56 Fowkes FG, Housley E, Cawood EH, Macintyre CC, Ruckley CV, Prescott RJ: Edinburgh Artery Study: prevalence of asymptomatic and symptomatic peripheral arterial disease in the general population. Int J Epidemiol 1991; 20(2): 384–92 Meijer WT, Hoes AW, Rutgers D, Bots ML, Hofman A, Grobbee DE: Peripheral arterial disease in the elderly: The Rotterdam Study. Arterioscler Thromb Vasc Biol 1998; 18(2):185–92 Criqui MH, Fronek A, Klauber MR, Barrett–Connor E, Gabriel S: The sensitivity, specificity, and predictive value of traditional clinical evaluation of peripheral arterial disease: results from noninvasive testing in a defined population. Circulation 1985; 71(3): 516–22 Dormandy JA, Murray GD: The fate of the claudicant––a prospective study of 1969 claudicants. Eur J Vasc Surg 1991; 5(2):131–3 Most RS, Sinnock P: The epidemiology of lower extremity amputations in diabetic individuals. Diabetes Care 1983; 6(1): 87–91 Price JF, Mowbray PI, Lee AJ, Rumley A, Lowe GD, Fowkes FG: Relationship between smoking and cardiovascular risk factors in the development of peripheral arterial disease and coronary artery disease: Edinburgh Artery Study. Eur Heart J 1999; 20(5): 344–53 Cole CW, Hill GB, Farzad E, Bouchard A, Moher D, Rody K, Shea B: Cigarette smoking and peripheral arterial occlusive disease. Surgery 1993; 114(4): 753–56; discussion 756–7 Kannel WB, Shurtleff D: The Framingham Study. Cigarettes and the development of intermittent claudication. Geriatrics 1973; 28(2): 61–8 Murabito JM, Evans JC, Nieto K, Larson MG, Levy D, Wilson PW: Prevalence and clinical correlates of peripheral arterial disease in the Framingham Offspring Study. Am Heart J 2002; 143(6): 961–5 Hooi JD, Stoffers HE, Kester AD, Rinkens PE, Kaiser V, van Ree JW, Knottnerus JA: Risk factors and cardiovascular diseases associated with asymptomatic peripheral arterial occlusive disease. The Limburg PAOD Study. Peripheral Arterial Occlusive Disease. Scand J Prim Health Care 1998; 16(3):177–82 Novo S, Avellone G, Di Garbo V, Abrignani MG, Liquori M, Panno AV, Strano A: Prevalence of risk factors in patients with peripheral arterial disease. A clinical and epidemiological evaluation. Int Angiol 1992; 11(3): 218–29
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Taylor LM, Jr., Moneta GL, Sexton GJ, Schuff RA, Porter JM: Prospective blinded study of the relationship between plasma homocysteine and progression of symptomatic peripheral arterial disease. J Vasc Surg 1999; 29(1): 8–19; discussion 19–21 Pradhan AD, Manson JE, Rossouw JE, Siscovick DS, Mouton CP, Rifai N, Wallace RB, Jackson RD, Pettinger MB, Ridker PM: Inflammatory biomarkers, hormone replacement therapy, and incident coronary heart disease: prospective analysis from the Women's Health Initiative observational study. Jama 2002; 288(8): 980–7 Szilagyi DE, Elliott JP, Jr., Smith RF, Reddy DJ, McPharlin M: A thirty–year survey of the reconstructive surgical treatment of aortoiliac occlusive disease. J Vasc Surg 1986; 3(3): 421–36 Brewster DC, Okada RD, Strauss HW, Abbott WM, Darling RC, Boucher CA: Selection of patients for preoperative coronary angiography: use of dipyridamole–stress––thallium myocardial imaging. J Vasc Surg 1985; 2(3): 504–10 Hertzer NR, Beven EG, Young JR, O'Hara PJ, Ruschhaupt WF, 3rd, Graor RA, Dewolfe VG, Maljovec LC: Coronary artery disease in peripheral vascular patients. A classification of 1000 coronary angiograms and results of surgical management. Ann Surg 1984; 199(2): 223–33 Aronow WS, Ahn C: Prevalence of coexistence of coronary artery disease, peripheral arterial disease, and atherothrombotic brain infarction in men and women > or = 62 years of age. Am J Cardiol 1994; 74(1): 64–5 Klop RB, Eikelboom BC, Taks AC: Screening of the internal carotid arteries in patients with peripheral vascular disease by colour–flow duplex scanning. Eur J Vasc Surg 1991; 5(1): 41–5 Alexandrova NA, Gibson WC, Norris JW, Maggisano R: Carotid artery stenosis in peripheral vascular disease. J Vasc Surg 1996, 23(4):645–9. May AG, Van De Berg L, Deweese JA, Rob CG: Critical arterial stenosis. Surgery 1963; 54: 250–9 Moore WS, Malone JM: Effect of flow rate and vessel calibre on critical arterial stenosis. J Surg Res 1979; 26(1):1–9. Sydorak GR, Moore WS, Newcomb L, Campagna G, Hall AD: Effect of increasing flow rates and arterial caliber on critical arterial stenoses. Surg Forum 1972; 23(0): 243–4 Flanigan DP, Tullis JP, Streeter VL, Whitehouse WM, Jr., Fry WJ, Stanley JC: Multiple subcritical arterial stenoses: effect on poststenotic pressure and flow. Ann Surg 1977; 186(5): 663–8 Karayannacos PE, Talukder N, Nerem RM, Roshon S, Vasko JS: The role of multiple noncritical arterial stenoses in the pathogenesis of ischemia. J Thorac Cardiovasc Surg 1977; 73(3): 458–69 Wolf EA, Jr., Sumner DS, Strandness DE, Jr.: Correlation between nutritive blood flow and pressure in limbs of patients with intermittent claudication. Surg Forum 1972; 23(0): 238–9
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Lower extremity arterial disease assessment KF Murphy, K Irshad, A Sinha, and DB Reid
Introduction
Clinical history
The assessment and treatment of lower extremity arterial disease is a relatively modern phenomenon, although the condition has been recognized for centuries. Leonardo da Vinci described arteriosclerosis in anatomical sketches in the fifteenth century, and amputation for gangrene has been performed since ancient times.1 The modern era really began with the introduction of aortography by dos Santos in 1929.2 The arterial system could then be visualized, the site of lesions identified, and treatment planned. Following this initial breakthrough, there have been many techniques developed to aid the assessment of the arterial supply of the lower limb, including non-invasive evaluation that can be used in the symptomatic and asymptomatic patient. Although technological advances have improved our understanding of vascular disease and its management, careful history taking and clinical examination remain the most useful tools in assessing the lower limb arterial supply. Such an assessment is important because symptomatic arterial disease of the lower limb affects up to 5% of men and 2.5% of women 60 years or older.3 With an aging population the incidence is likely to increase, and the sex difference disappears after 70 years of age. Arterial disease is slowly progressive, and while after 5–10 years 70% or more will report no change or an improvement in symptoms, 20–30% will have advancing disease, and approximately 10% go on to require amputation. (This figure is up to seven times higher in diabetics). Despite the rather benign course, intermittent claudication is a marker of systemic atherosclerosis, and patients with symptomatic peripheral vascular disease have a threefold increase in cardiovascular mortality.4,5 This chapter identifies frameworks for evaluating lower limb ischemia and discusses their relative merits. History taking and examination allow you to assess the severity and location of arterial disease, and guide investigations. Noninvasive diagnostic measures are then used to confirm or grade functional severity. The degree of functional limitation and the natural course of disease must then be weighed against the risk and success of any potential intervention. If further information is required to guide treatment, more invasive investigations can be carried out such as preprocedural diagnostic arteriography. All of these methods of preliminary assessment together with the techniques to evaluate treatment in the operating room are discussed in this chapter.
The assessment of the patient presenting with symptoms suggestive of lower extremity arterial disease should begin with a detailed clinical history. As well as the history of presenting complaint, a full past medical history looking particularly for evidence of atherosclerotic disease elsewhere, family history, drug history, personal, and social history should be included.6 Exercise-induced calf, thigh, or buttock muscle pain, relieved by rest after a predictable distance (intermittent claudication) is the typical symptom of restricted blood flow due to arterial stenosis or occlusion. The term claudication comes from the Latin for “to limp” – “claudicare” or “claudicatio.” It has come to mean pain/disability associated with exercise. The clinical severity of disease has been classified by Fontaine (Table 66.1).7 The clinical presentation depends on the site and extent of arterial disease and the efficiency of the collateral circulation. The impact this has on a patient’s lifestyle/occupation is an important consideration for future management. A typical presentation of calf pain coming on after 100–200 yards is usually due to an occlusion of the superficial femoral artery in the adductor canal.1 This is present in 75% of claudicants.1 Exercise-induced calf pain can also be caused by popliteal artery entrapment, cystic degeneration of the popliteal artery, and chronic compartment compression syndrome.1,6 Nerve root compression may also present in a similar way, but can usually be identified from a careful history.7 Foot claudication is less common, but typically comes on after only 40–50 yards. There is pain and numbness in the foot and the lesion is usually a popliteal occlusion. A common cause of distal peripheral arterial disease is the tibial vessel involvement of diabetes mellitus. Thigh and buttock claudication is classically due to aortoiliac disease, with a reduction in blood flow in the internal iliac arteries. This may not be felt as the same cramping pain of calf claudication, but as an aching associated with weakness of the muscles. Symptoms may be difficult to differentiate from osteoarthritis of the hip or from spinal stenosis. However, it is the predictable exercise distance and relief with rest that differentiates claudication. Venous occlusion may also cause thigh claudication-like symptoms.6 Progression of disease, with a further reduction in blood flow, leads to peripheral extremity pain which is present at rest 593
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Table 66.1
Fontaine classification of PVD7
Stage Stage Stage Stage Stage
Symptom I II III IV
Asymptomatic Intermittent claudication Ischemic rest pain Ulceration /gangrene
and relieved by dependency, known as ischemic rest pain. When the leg is elevated the effect of gravity aiding the blood down the leg is lost. Rest pain typically occurs at night while in bed and affects the foot distal to the tarsal bones. The patient will usually quickly learn to sleep with the foot hanging out of the bed, or even upright in a chair. This may progress to ulceration/skin loss, and eventually gangrene (Table 66.2). While the presence of risk factors such as smoking, family history of peripheral vascular disease, and diabetes may help clinch the diagnosis (Table 66.3), risk factor modification is the best way of halting the progression of peripheral vascular disease, and history taking should include a thorough evaluation of these.
Clinical examination Clinical examination should commence from the end of the bed, and include the radial pulses and a full cardiovascular examination. Patients with arterial disease generally look older than their years.1 Their posture may give an indication of the degree of pain and symptoms – the patient with rest pain will be sitting up with the legs dependent, and will have edema of the lower leg and foot because of this chronic dependency. Examination of the lower limbs includes the abdomen to the toes, and the patient should be appropriately undressed (removal of trousers, skirt, tights, socks, and shoes) to allow this. Inspection Beginning with inspection, skin changes associated with ischemia should be looked for, such as atrophic, polished skin;
Table 66.3
Table 66.2
Causes of ischemic rest pain
Arteriosclerosis Diabetic gangrene Thromboangiitis obliterans (Buerger’s disease) Raynaud’s syndrome Arterial embolism Venous and cardiac gangrene1 Trauma Blood dyscrasias Drug-induced gangrene Reflex sympathetic dystrophy
thick, tough nails; and loss of hair. Ulcers and areas of gangrene should be looked for in the typical sites (see Table 66.4). Palpation Capillary refill is affected by room temperature, cardiac output, and shock, and is not the most reliable indication of perfusion especially in an acutely ill patient. It should be assessed by pressure on the pulp of the great toe. Normal capillary refill takes < 2 seconds. The abdomen must be palpated for the presence of an occult aortic aneurysm. Palpation and documentation of all pulses in the arms and legs is necessary for a full assessment. Femoral pulses are best palpated with the hip slightly externally rotated. The vessel is then palpated over the pubic ramus of the ileum, about two finger breadths from the pubic tubercle. The popliteal pulse may be difficult to palpate, yet if too easily felt it raises the possibility of a popliteal aneurysm. With the patient supine, the knee is held very slightly flexed by the examiner. Six fingers are placed in the posterior dent behind the knee. Pressure from the thumbs placed either side of the patellar tendon then pushes the artery down onto the six fingers.1 The posterior tibial pulse is felt in the hollow behind the medial malleolus, and the dorsalis pedis on the dorsum of the foot between the first and second metatarsal bones. In 10% of normal subjects, one or other of these will not be felt, and a lateral tibial pulse may be felt higher in the foot, just below the ankle, medial to the bony prominence of the fibula.6 Elevating the ischemic leg leads to pallor and venous guttering; dependency causes hyperemia. The speed at which
Common risk factors for peripheral vascular disease
Risk factor
Comments3
Smoking
The diagnosis of peripheral vascular disease is made a decade earlier in smokers than non-smokers. It is a strong risk factor with relative risk ratios of 1.7:7.5 Incidence increases with age. In men under 50 years the prevalence of intermittent claudication is 1–2%, in those above 50 years, 5%. At 50 years the prevalence in men is 5%, 2.5% in women. This difference disappears after 70 years of age. Patients with diabetes have a seven-fold increase in amputation rate. Epidemiological links peripheral vascular disease with hypertension. Almost 50% of patients with lower extremity arterial disease have hyperlipidemia. There is evidence that the treatment of this reduces both the progression of atherosclerosis and the incidence of intermittent claudication.
Age Male sex Diabetes Hypertension Hypercholesterolemia
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Common sites of ulceration1
Site Nail bed of the great toe Nail bed of fifth toe Medial side of great toe, over head of first metatarsal Lateral side of fifth toe and head of fifth metatarsal Adjacent sides of fourth and fifth toes Dorsum of foot Front of the lower leg Hack on heel
postural change occurs appears directly related to the severity of the ischemia. Loss of sensation to fine touch is an early sign of severe ischemia and occurs before loss of function. Auscultation A bruit is heard where there is narrowing of the artery and is closely related to (and most intense at the site of) a stenosis. Common sites are aortic, iliac, femoral vessels, and the adductor canal. Clinical investigation Other clinical tests should include blood pressure measurement, and a full blood count to check for anemia or polycythemia which can both make symptoms worse. Urea and electrolytes are taken to check renal function; and blood glucose for impaired glucose tolerance and cholesterol/ lipids/triglycerides. Hyperlipidemia is found in 37% of PVD patients.8 This figure is higher for the under 50s.
Acute lower limb ischemia The clinical signs of acute lower limb ischemia can point to the location of arterial occlusion.1 The typical signs of a femoral embolism or acute femoral occlusion are pain in the foot and calf, with mottling from just above the knee, numbness of the lower half of the leg, and loss of function of the ankle and toes. A popliteal artery occlusion usually presents with a white foot, pain in the foot and toes, numbness of the toes, loss of function of the toes, but retained function of the ankle. In aortic occlusion there is mottling from the groin down, pain throughout the whole of both legs, numbness from the knees down, and loss of function of the knees, ankles, and toes. Despite these often typical presentations which point to the site of disease, modern vascular assessment with imaging is usually performed to confirm the diagnosis and reveal treatment options.
Non-invasive investigations Non-invasive investigations are used to confirm the clinical impression, and can give an indication of the severity of the disease, and how severe the physiological impairment is. They will show whether significant occlusive disease is present and where the lesions are, and in multilevel disease, which segments
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are most severely affected. In limbs with tissue loss they may reveal the potential for primary healing and help in the planning of treatment. Ankle–brachial pressure index The ankle–brachial pressure index (ABPI) was described by Yao in 1969.9 The index is the ratio of the highest systolic pressure at the ankle relative to the brachial systolic pressure. This should normally be greater than or equal to 1. It is simple, quick, and cost-effective. Patients with intermittent claudication typically have an index of 0.9–0.4, those with rest pain < 0.4, and those with gangrene 0.9 In diabetic patients, the ABPI reading may be falsely high due to calcification of the vessels which makes them incompressible by the blood pressure cuff. The ABPI is usually stable from one examination to the next in a particular individual, and it is therefore an effective means of following a patient’s progress. After successful intervention, the ABPI will rise; a fall may indicate progressive arterial disease or a failed intervention. The ABPI is an independent predictor of all-cause and cardiovascular mortality.10 Exercise ABPI This is a particularly useful test when there is a good history of claudication but normal resting ABPI, and it differentiates claudication from pseudoclaudication.11 When arterial disease of the lower limb is present, a reduction in systolic pressure occurs distal to the stenosis/occlusion following exercise. If the systolic pressure at the ankle falls by 20% or more, or takes 3 minutes or more to recover, there is significant vascular disease.10 Conversely, if systolic BP does not fall after a brisk 5 minute walk, occlusive vascular disease in that limb can be excluded.10 A standardized protocol has been developed, which objectively documents the magnitude of symptom limitation. This requires a treadmill machine and experienced staff.11 The treadmill is set at 2 mph, with a gradient of 10–12°. Initial ankle and brachial pressures are measured with the patient supine at rest for 20 minutes. They then walk, with ankle cuffs in place, for 5 minutes, or until pain occurs, whichever is sooner. The patient immediately lies down, and the pressures are measured. Although conventionally brachial pressures are repeated, this is not strictly necessary as the most important variable is the degree by which the ankle pressure drops, and the time it takes to recover. Brachial pressure will rise with exercise. Measure-ments are repeated every 2 minutes until back to resting levels, or 10 minutes have elapsed.3,12 In the presence of obstructive arterial disease there will be a drop in ankle pressure, and the magnitude of this reflects the functional disability. The location of the arterial disease also affects the degree of drop, and in general the more proximal the lesion, the greater the effect on ankle pressure in response to exercise. More proximal vessels supply a greater muscle mass, therefore there is a greater and more prolonged diversion of blood away from the lower leg. Toe pressures The measuring of toe pressures is not commonly used in routine clinical practice, but allows accurate assessment of distal circulation. They are not influenced by the calcification
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of pedal vessels, and therefore are useful in diabetics. Very small cuffs are used, and normal toe pressures are in the range 90–100 mmHg (absolute pressures, not ratios). A pressure of 30 mmHg or less indicates critical ischemia.10 Toe pulse oximetry Toe pulse oximetry is a simple and easily reproducible study, particularly useful in assessing patients with leg ulcers and their suitability for compression bandaging when the ABPI cannot be measured.13,14 The measure is a ratio of toe to finger pulse oximetry, and correlates well with the ABPI. Color flow Doppler ultrasound The commonest indication for duplex ultrasound in lower extremity arterial disease is to identify potential percutaneous intervention in patients with intermittent claudication. It establishes the diagnosis, the anatomical site of disease, and can define the severity of a focal stenosis. It can help decide whether to proceed with angiography, and aid the planning of the optimum treatment approach to a lesion.15 It is a potential substitute for angiography in patients requiring reconstructive surgery, and may find suitable, patent distal vessels not seen on angiography. Another useful function is in graft surveillance, particularly vein grafts. It is less good for prosthetic grafts. The downside is reduced accuracy in aortoiliac disease due to overlying bowel gas or obesity, and the presence of dense calcification. Sensitivity is also reduced downstream from a proximal stenosis. The technique uses pulsed Doppler and real-time B mode ultrasound to image vessels and any stenotic lesion. Flow and pressure waveforms can also be assessed.16 The greyscale image identifies plaque and thrombus, while the color flow Doppler assessment provides a measure of blood velocity, demonstrates flow and indicates the degree of vessel narrowing. The flow velocity increases at the stenosis. A stenosis of 50% or more is present if the peak systolic velocity doubles when compared with the velocity in an adjacent segment.10 A normal Doppler wave form is triphasic, with rapid antegrade flow in systole, a transient reverse flow early in diastole, and slow antegrade flow in late diastole in general the presence of a triphasic velocity pattern excludes a flow-limiting lesion proximal to the recording site.10 In the presence of arterial stenosis, distal to the lesion there will be a decreased rate of rise of the antegrade flow, reduced amplitude of forward velocity, and loss of the reverse flow in early diastole, giving a biphasic waveform. In severe stenosis there will be monophasic flow.10 Color flow Doppler ultrasound is operator dependent. When compared with angiography, duplex ultrasound has a sensitivity of 80% and specificity 90% for detecting femoral and popliteal disease. It is not as effective in the tibial and peroneal arteries. In the surveillance of infrainguinal bypass grafts it is very good, identifying stenosis before complete graft occlusion, and before any symptoms occur or there is a reduction in ABPI.10 Pulse-generated run-off The rapid cycling of a proximal cuff generates an arterial pulse wave. Pulse-generated run-off (PGR) allows functional testing
of distal artery patency, for example when angiography fails to show them, but is rarely used in clinical practice. Magnetic resonance angiography Magnetic resonance angiography (MRA) produces (relatively) non-invasive, three-dimensional, cross-sectional images. It is very effective in the evaluation of stenoses,11 where it has a sensitivity of 99.5% and specificity of 98.8% when compared with DSA (digital subtraction angiography). It is costeffective, and superior to DSA in that it will demonstrate the vessel from any rotational angle and also in seeing distal vessels in some patients.17 MRA can also be used to evaluate results after treatment, to monitor grafts, and to look for post-operative complications such as pseudoaneurysms. It enables the selection of patients for endovascular intervention or surgery11 (see Figure 66.1). One limitation is that it tends to overestimate stenoses, and may be inaccurate in the presence of stents. A “cast” of the blood vessel is displayed, showing the lumen. This means aneurysms are not well imaged by MRA, and can be missed. There are also a number of contraindications to MRI, for example the presence of a pacemaker, or cerebral artery clip.11 MRI utilizes a large external magnetic field, with gradients applied across it and an oscillating magnetic field known as the radiofrequency field or RF field. This combination allows the operator to produce signals from inside the patient which are used to generate the MR images.17 MR images depend on the characteristics of the object being imaged. T2 weighted images display simple fluids like urine, bile, or CSF as bright and other tissues as darker. T1 weighted images display flow effects, MRI contrast agents, fat and methemoglobin as bright, and are therefore used in MRA and MRV. Contrast-enhanced MRI produces superior MRA images. The contrast (gadolinium) shortens the T1 value of the protons in the local vicinity, making them more conspicuous on T1 weighted sequences.17 Gadolinium still has some nephrotoxic effects, but is less nephrotoxic than iodinated contrasts, and much less is required in MR than either CT or conventional angiography.
Invasive investigations Conventional angiography This is the “definitive” method for anatomical evaluation of lower limb arterial disease when revascularization is planned. It is an invasive procedure, which requires an intra-arterial catheter, usually accessed from the femoral artery. The catheter is inserted using the Seldinger technique, passing a guidewire through the needle, and feeding a catheter over the wire,18 and contrast injected. Digital subtraction imaging is frequently used. It is generally a safe procedure, performed under local anesthetic. Conventional angiography shows the outline of the lumen, and therefore the outline of the artery wall, and where there is narrowing, and to some extent the severity of the arterial disease process at each location (see Figure 66.2). Occlusions and length of occlusions are seen, as well as collaterals and the quality of collateral blood flow. Importantly the quality of the
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Figure 66.1 Magnetic resonance angiography showing: (a) diffuse bilateral common iliac disease (note the blush of contrast in the cecum from a previous barium examination); and (b) left superficial femoral artery occlusion.
(a) Figure 66.2
(b) Conventional angiogram showing a left common iliac stenosis.
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profunda femoris is demonstrated, and the presence and quality of the popliteal artery. Angiography may point to either open or endovascular repair. Complications associated with angiography include those due to contrast (anaphylaxis, toxic reactions, worsening renal function) and those due to intra-arterial instrumentation (hematoma, arterial spasm, subintimal dissection, false aneurysm, AV fistula and emboli). Computerized tomography angiography CT angiography (CTA) can assess peripheral vascular anatomy and significant stenosis, and select candidates for further intervention. It is particularly useful in diagnosing and assessing aortic aneurysms and provides associated soft tissue diagnostic information in the lower limb vessels, for example popliteal entrapment and cystic adventitial disease.11 With the use of CTA or 3D reconstructions or both, CT effectively shows the location and extent of aneurysmal disease (see Figure 66.3). The use of CT to image infrainguinal vascular disease has been increasing with the development of improved computer software and hardware for CT scanners. Computerized 3D reconstruction enables a large number of fine slices from one CT scan to be reproduced as high-quality 3D images of the
Figure 66.3 Spiral CT reconstruction showing the “cast” of an aortic aneurysm. Note the ulcerated plaque inside the aneurysm. (See Color plates.)
contrast enhanced vessels. The fast scan time allows all the data to be collected during the first pass of an intravenous bolus of contrast through the arteries.10 This reduces the artifact caused by patient movement. This technology enables CT angiography, and the resolution of the images of contrastenhanced vessels is adequate for evaluating occlusive disease. Used to supplement history and physical examination, CT can rule out significant occlusive disease in the superficial femoral or popliteal arteries.19 The latest advance in CTA is fast multislice CT (64 and 128 slice) which provides outstanding detail of the peripheral vessels. Intraoperative assessment Lower extremity arterial disease assessment is also required during treatment in the operating room environment. During endovascular procedures, angiography is performed immediately prior to intervention to confirm the lesion to be treated, and subsequently to assess the completeness of treatment. Arterial pressure measurements are also useful, particularly in assessing the physiological severity of aortoiliac disease which is often underestimated by other techniques. Measurements can be resting or following an injection of intra-arterial papaverine to produce peripheral vasodilatation. A hemodynamically significant lesion is present when the systolic pressure drop is more than 20 mmHg12 or 14%20 after injection of papaverine into the intra-arterial catheter. A papaverine test may reveal the significance of a lesion, particularly in the iliac arteries, which did not look very significant on angiography, leading to stenting.21 A third modality used during endoluminal repair is intravascular ultrasound (IVUS) – a miniature ultrasound probe used within the vessel lumen that gives magnified details of atherosclerotic plaque. It has become a safe and valuable surgical tool in assessing the severity of disease and the completeness of treatment during endovascular procedures.22 The IVUS probe is passed into the vessel lumen to examine the artery being treated and because the ultrasound probe is in such close proximity to the artery wall, great detail is possible with significant magnification of the images compared with conventional extracorporeal ultrasound. IVUS provides histological detail of the vessel wall and also demonstrates blood flow within the lumen.22 The most recent advances, color flow and virtual histology IVUS, greatly improve the quality and interpretation of the images.22,23 In peripheral arteries IVUS has a complimentary role to arteriography. It allows a greater appreciation of the vessel wall constituents and can distinguish between soft plaque and calcification. Intimal flaps, thrombus formation, and ulceration are also visible and IVUS can detect lesions missed on conventional arteriography24 (see Figure 66.4). IVUS also checks the accuracy of stent and stent graft deployment. Illustrative case example using “triple assessment”: A 60-year-old male patient with bilateral iliac artery disease (Figure 66.1) underwent bilateral iliac stenting. After femoral
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(b)
(c) Figure 66.4 Intraoperative angiography and IVUS: (a) the stenoses are demonstrated pre-treatment; (b) post-stenting a narrowing is seen on the angiogram, which is shown with IVUS to be an intimal flap; (c) following the stenting of this lesion there is a good angiographic result, confirmed on IVUS.
artery access, angiography confirmed the lesions to be treated (Figure 66.4a). These stenoses were further examined using IVUS, which demonstrated a 70% stenosis, greater than that indicated by angiography. IVUS measurements were also used to choose balloon and stent size. Following the deployment of the stents, angiography showed a new stenotic lesion distal to
where the stents had been deployed on the right-hand side. There was a 50 mmHg pressure gradient across this lesion. IVUS demonstrated that it was caused by an intimal flap at the distal end of the stent just at the iliac bifurcation (Figure 66.4b). A further stent was deployed over the flap. This “triple” assessment24 was repeated with satisfactory
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completion angiography, IVUS, and resolution of the gradient (Figure 66.4c).
Conclusion The majority of patients presenting with arterial disease of the lower limb will be managed conservatively, and by best medical therapy to reduce their cardiovascular risk. Since most patients with lower extremity disease have co-morbidities it is particularly important to be able to assess them by non-invasive means. Assessment begins with clinical history and examination.
The impact of symptoms on quality of life is usually the driving factor for deciding whether further treatment is required. APBIs can offer a measure of disease severity. If further investigation is deemed appropriate, exercise testing can give an objective measure of functional limitation (or exclude a vascular problem), and duplex can help to locate the exact site of the occlusion or degree of stenosis. MRA then provides detailed images of the vessels prior to any invasive procedure. If a suitable lesion is identified the patient can then be put forward for endovascular or open repair. Assessment is continued during intervention to assess the requirement and completion of treatment.
REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11.
Reid W, Pollock J. The Surgeon’s Management of Gangrene. Baltimore: University Park Press, 1978 dos Santos R, Lamas A, Pereira CJ. L’arteriographie des membres de l’aorte et ses branches abdominales. Bull Soc Nat Chir 1929; 55: 587–601 Weitz JI, Byrne J, Clagett GP et al. Diagnosis and treatment of chronic arterial insufficiency of the lower extremities: a critical review. Circulation 1996; 94: 3026–49 Reunanen A, Takkunen H, Aromaa A. Prevalence of intermittent claudication and its effect on mortality. Acta Med Scand 1982; 211: 249–56 Jelnes R, Gaardsting O, Hougaard JK et al. Fate in intermittent claudication: outcome and risk factors. Br Med J (Clin Res Ed) 1986; 293: 1137–40 Rutherford RB. Essentials of Clinical Evaluation. In: Rutherford RB, ed. Vascular Surgery, sixth edition. Philadelphia: Elsevier Saunders, 2006: 1–13 Beard JD. ABC of arterial and venous disease: Chronic lower limb ischaemia. BMJ 2000; 320: 854–7 Ballantyne D, Lawrie TD. Hyperlipoproteinaemia and peripheral vascular disease. Clin Chim Acta 1973; 47: 269–76 Yao ST, Hobbs JT, Irvine WT. Ankle systolic pressure measurements in arterial disease affecting the lower extremities. Br J Surg 1969; 56: 676–9 Donnelly R, Hinwood D, London NJ. ABC of arterial and venous disease. Non-invasive methods of arterial and venous assessment. BMJ 2000; 320: 698–701 Hirsch AT, Haskal ZJ, Hertzer NR et al. ACC/AHA 2005 guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): executive summary. A collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease) endorsed by the American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and
12. 13. 14. 15. 16. 17. 18. 19.
20. 21. 22. 23. 24.
Vascular Disease Foundation. J Am Coll Cardiol 2006; 47: 1239–312 Zierler RE, Sumner DS. Physiologic assessment of peripheral arterial occlusive disease. In Rutherford RB, ed. Vascular Surgery, sixth edition. Philadelphia: Elsevier Saunders, 2006: 197–222 Bianchi J, Douglas WS, Dawe RS et al. Pulse oximetry: a new tool to assess patients with leg ulcers. J Wound Care 2000; 9: 109–12 Bianchi J, Douglas S. Pulse oximetry vascular assessment in patients with leg ulcers. Br J Community Nurs 2002; 22, 24, 26, passim Rzucidlo EM, Zwolak RM. Arterial duplex scanning. In: Rutherford RB, ed. Vascular Surgery, sixth edition. Philadelphia: Elsevier Saunders, 2006: 246–53 Lunt MJ. Review of duplex and colour Doppler imaging of lowerlimb arteries and veins. J Tissue Viability 1999; 9: 45–55 Insko EK, Carpenter JP. Magnetic resonance imaging and angiography. In: Rutherford RB, ed. Vascular Surgery, sixth edition. Philadelphia: Elsevier Saunders, 2006: 356–77 Seldinger SI. Catheter replacement of the needle in percutaneous arteriography; a new technique. Acta Radiol 1953; 39: 368–76 Fillinger MF, Whittaker DR. Computer tomography, CT angiography, and 3D reconstruction for the evaluation of vascular disease. In: Rutherford RB, ed. Vascular Surgery, sixth ed. Philadelphia: Elsevier Saunders, 2006: 316–53 Murie JA, Quin RO, Forrest H, Sheldon CD. Pressure contour analysis in the assessment of arterial stenosis. Angiology 1983; 34: 445–51 Quin RO, Evans DH, Bell PR. Proceedings: The haemodynamic effect of papaverinee in peripheral arterial disease. Br J Surg 1976; 63: 661 Diethrich EB, Irshad K, Reid DB. Virtual histology and color flow intravascular ultrasound in peripheral interventions. Semin Vasc Surg 2006; 19: 155–62 Irshad K, Reid DB, Miller PH et al. Early clinical experience with color three-dimensional intravascular ultrasound in peripheral interventions. J Endovasc Ther 2001; 8: 329–38 Reid DB, Irshad K, Diethrich EB. Intravascular ultrasound applications. In: AbuRahma AF, Bergans JJ, eds. Noninvasive Vascular Diagnosis: A Practical Guide to Therapy, second edition. London: Springer-Verlag, 2007: 506–16
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Lower extremity: other techniques ML Brennan and L Cho
Introduction It is critical to distinguish between arterial and non-arterial etiology in evaluating patients with suspected claudication. Peripheral arterial disease is the most common cause; however, the differential diagnosis is broad and includes vasculitis, deep venous thrombosis, musculoskeletal injury, neuropathy, and spinal stenosis. The first step in assessment of the lower extremity is obtaining a complete patient history and a physical exam that includes evaluation of cardiovascular risk factors. Based on clinical suspicion of claudication, a number of non-invasive physiologic monitoring and imaging techniques are available for diagnostic purposes (summarized in Table 67.1). 1. Physiologic testing that allows determination of vascular systolic pressures and impairment are: 䊊 ankle–brachial index (ABI) and toe–brachial index (TBI); 䊊 segmental blood pressure measurements; 䊊 pulse volume recordings (PVR); 䊊 segmental Doppler ultrasound; 䊊 exercise testing; 䊊 duplex ultrasound; 䊊 transcutaneous oximetry. 2. Imaging modalities that enable visualization of location and extent of stenosis, occlusion or anatomic changes are: 䊊 magnetic resonance angiography (MRA); 䊊 computed tomographic angiography (CTA); 䊊 angiography. With the exception of duplex ultrasound (which is covered in Chapter 62), the clinical indication for each technique and information gained from each will be discussed in turn below.
Physiologic testing Ankle–brachial index and toe–brachial index The ankle–brachial index (ABI) is the ratio of systolic blood pressure in the foot versus the arm. It is reproducible, informative, and can be done in the physician’s office. The patient lies down for 5 minutes and blood pressure cuffs are placed on the arm above the antecubital fossa and at the ankle. The target arteries are the brachial and dorsalis pedis or posterior tibial arteries. The blood pressure cuff is inflated to suprasystolic
pressure (20 mmHg greater than brachial systolic pressure) and deflated at 2–5 mmHg per second. Sphygmomanometer readings are taken when the pulse is heard via Doppler ultrasound. Systolic measurements are taken in both arms and both legs and the higher measurements at each site are noted. Sources of error in pressure measurements include inadequate rest period, inappropriately sized cuff, excessive deflation rate, multiple occlusions between cuff and probe, and subclavian obstruction. The normal range of ankle–brachial indices is 1.0–1.3. ABIs in healthy persons are greater than 1.0 due to peripheral systolic pressure in the lower extremities being 10–20 mmHg greater than systolic arm pressure. ABIs of 0.8–0.9 indicate mild peripheral arterial disease whereas values between 0.6 and 0.8 indicate moderate stenosis. ABIs less than 0.6 represent severe peripheral arterial disease. ABI values greater than 1.3 are due to calcification and loss of elasticity of the vasculature. These measurement values are correct but inappropriately high for the purposes of test interpretation. These readings are observed in diabetics, end-stage renal disease patients, and the elderly. ABIs greater than 1.4 are associated with increased cardiovascular risk.1 In situations of ABIs greater than 1.3, measurement of toe pressure is indicated since the digital vessels of the foot are slow to calcify and are a suitable alternative measurement point. Toe–brachial indices (TBIs) can also be used in situations where a clot is distal to pedal pulses. There is a normal pressure drop of 20–30 mmHg between the ankle and the toe and this affects the cutpoint for diagnosis. A TBI less than 0.6 is abnormal and indicative of peripheral arterial disease. ABIs less than 0.9 are diagnostic of peripheral arterial disease with 95% sensitivity and 100% specificity compared with angiography. ABIs have been shown to predict mortality, and cardiovascular events.2,3 Furthermore, it can be used to stratify patients with peripheral arterial disease. The 2005 ACC/AHA guidelines on peripheral artery disease document that in persons >50 years of age with peripheral arterial disease, 20–50% of persons are asymptomatic and only 10–35% of patients exhibit claudication symptoms.4 With such a high percentage of persons not presenting with “classic” symptoms, a simple test such as this is useful in basic cardiovascular evaluation and should be measured in all patients with suspected claudication. Segmental pressure examination To perform segmental pressure examination, blood pressure cuffs are placed on each arm above the antecubital fossa, thigh (upper and lower or just middle), calf (middle), ankle, 601
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Table 67.1
Non-invasive physiologic monitoring and imaging techniques
Test
Reason for test
Considerations
Ankle–brachial index Toe–brachial index Segmental blood pressure measurements Pulse volume recordings
Used to determine if stenosis is present in extremities Used to localize site of stenosis and vessel pressure changes Used to localize site of stenosis and vessel pressure changes Allows exacerbation of underlying pathology and quantification of functional capacity Used to determine oxygenation status
Toe pressure should be measured in cases of calcification Can be used to localize segment if calcification is not present Provides information about vessel pressures changes regardless of calcification status Can be done with or without ABIs
Exercise testing Transcutaneous oximetry Magnetic resonance angiography
Quantitative imaging of stenosis
Computed tomographic angiography Angiography
Quantitative imaging of stenosis Quantitative imaging of stenosis
transmetatarsal, and toe. A brachial systolic pressure is measured and then pressure increased to suprasystolic pressure in each cuff starting in the toe, and progressing bilaterally and sequentially up the legs. The Doppler ultrasound probe can be placed on the posterior tibial artery for all segments except the toe to detect pulse following inflation of each segment. Segmental pressure examination allows localization of stenosis to a segment of the vasculature. It is typically done in conjunction with pulse volume recordings. It has a reported 86% accuracy.5 Calcification affects segmental pressures in the same way ABIs are affected. Information is gained by examining pressure differences within and between extremities. If a pressure difference >30 mmHg is present between consecutive cuffs, then a stenosis or occlusion is present in the distal segment. The segments are informative for the following vessels: ● ● ● ● ●
upper thigh – aortoiliac; lower thigh – superficial femoral; upper calf – distal superficial femoral or popliteal; lower calf – infrapopliteal; toe – digital artery.
If a > 20 mmHg difference exists in measurement of each leg, then a stenosis or occlusion exists in the leg with the lower value. A high arm versus thigh pressure suggests stenosis in the aorta, ipsilateral iliac artery, common femoral artery, or proximal superficial femoral artery. Pulse volume recordings Pulse volume recordings are used in conjunction with segmental pressure measurements to assess the location of arterial disease. It is also called volume plethysmography. Pressure cuffs are inflated to 60–65 mmHg, which puts pressure on but does not occlude the vessel. The resultant change in blood volume affects the waveform tracing and this is recorded by plethysmography. The waveform shape, signal, and amplitude are assessed. A normal pulse volume recording
Useful in determining amputation site and healing potential Uses non-ionizing radiation and can be done without IV contrast, lower resolution than CT or angio. May overestimate severity of lesion Uses ionizing radiation, uses IV contrast, lower resolution than angio Gold standard for imaging of vascular changes
looks like an arterial pulse waveform. There is a rapid systolic upstroke and downstroke with dicrotic notch. With increasing stenosis, the waveform becomes attenuated, widened, and flattened. Changes in pulse volume contour indicate arterial obstruction. This test is accurate regardless of vascular calcification. Data from the test is most useful for comparison within vascular beds of an individual patient. It is not appropriate for comparison between patients as cardiac output and vasomotor tone affect readings. When done in combination with segmental pressure recordings, there is a 95% diagnostic accuracy for prediction of significant stenosis.5 Figure 67.1 shows a representative segmental pressure and pulse volume recordings. Doppler ultrasound Doppler ultrasound can be used in lieu of pulsed volume recordings and in conjunction with segmental pressures. However, this is rarely done due to higher cost. The arterial waveform is recorded using continuous Doppler. The normal waveform observed is triphasic with forward and reverse flow components. This represents the outflow pulse from the heart being reflected in periphery (reverse flow) and pushed back again at the closed aortic valve (forward flow). With stenosis, there is loss of reverse flow and the waveform becomes biphasic. With disease progression, only forward flow may be observed and a monophasic waveform results. The waveform amplitude is also blunted with severity of disease due to turbulent flow causing varying velocities that broaden the peak. The sensitivity and specificity of ultrasound for detection of femoropopliteal disease was 80 and 90%, respectively.6 Potential sources of error are insensitivity at low blood pressures and misreading of arterial versus venous pulses. Exercise treadmill testing Exercise testing provides an opportunity to assess the impact of claudication on functioning by documenting
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Figure 67.1 Segmental pressure and pulse volume recordings. A 20 mmHg drop in segmental pressures is noted between the aortoiliac and distal superficial femoral or popliteal arteries, suggesting a focal stenosis. A 30 mmHg drop in segmental pressures is observed between the popliteal and dorsalis pedal arteries in the right leg, suggesting a significant stenosis in the anterior tibial artery. Note the abnormal metatarsal waveform has a diminished amplitude and flattened peak.
exercise capacity. The type of exercise testing will depend on the patient. The Gardner protocol, which increases grade and speed in 2–3 minute stages, is frequently used. It is terminated when the patient exhibits symptoms. A less strenuous walk test is an alternative option and may be more appropriate for elderly patients. Other types of exercise stress include tiptoeing, knee bending, and hyperemia induced by tourniquet applied for 3 minutes above the knee. Fixed or graded treadmill tests can also be used to assess maximum walking distance in persons who need exercise training for rehabilitation for peripheral arterial disease. Exercise testing combined with ankle–brachial measurements is used to evaluate patients with suspected peripheral arterial disease that have pain, but borderline ABIs between 0.85 and 1.0. Typically, treadmill testing with constant speed, 12% gradient, and 2 miles per hour for 5 minutes is used to exacerbate underlying pathology. ABIs are taken every minute following completion. Increased oxygen demands associated with exercise cause vasodilation and decreased peripheral resistance. Ankle pressures in a normal individual show an increase or no change following exercise because there are parallel increases in systemic pressures in upper and lower extremities. Pressures quickly return to normal
within 1 minute. However, in regions of stenosis, a decrease of 15 mmHg or a >20% change is considered positive and indicative of peripheral arterial disease. The time to return to baseline pressures is also increased. Transcutaneous oximetry This technique uses oximetry to assess blood oxygenation. It is performed by placing a probe on the patient’s chest and the limb under observation The chest and limb probe readings should be similar. Deoxygenated blood absorbs more red light from the oximeter than oxygenated blood does and differences in values between chest and limb suggest areas lacking oxygenation. This is used in determining amputation site and in prediction of tissue healing. A 20 mmHg or greater difference predicts healing with 79% accuracy and has 82% sensitivity and 64% specificity.7
Imaging modalities Imaging modalities allow the determination of stenosis location, extent and severity. Visualization techniques are critical in
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(a)
(b)
Figure 67.2 Magnetic resonance imaging of right lower extremity: (a) anterior view showing total occlusion of right superficial femoral artery; (b) decreased distal run-off is shown in the right lower extremity.
Figure 67.3 CT angiography of bilateral lower extremities. Bilateral lower extremity shown with occlusion of bilateral superficial femoral artery occlusion with collateral blood supply.
Figure 67.4 Angiography of common iliac arteries. Occlusion of the right external iliac artery is noted on the angiogram.
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Lower extremity: other techniques appropriate determinations for staging, revascularization, and amputation. These techniques are not typically needed in patients with normal exercise ABI unless there are suspected anatomic changes accounting for the ischemia such as entrapment. Non-invasive imaging is newer and shows real promise for clinical applications, particularly early detection, but the applications of these technologies are still being defined and developed. Magnetic resonance angiography (MRA) (Figure 67.2) Magnetic resonance angiography is useful for evaluation of vessels for revascularization, bypass, sites of anastamoses, and evaluation of the extent of the disease. Routine use in surveillance is not an option due to cost. Magnetic resonance angiography is magnetic resonance imaging with threedimensional angiograms. There are several types of magnetic resonance angiography. All capture images of blood movement and suppress surrounding tissue in generation of images. Phase contrast allows examination of a specific area but is not widely used. Time-of-flight allows examination of flow patterns and permits visualization of the complete lower peripheral circulation. There is a sensitivity and specificity of 85 and 81%, respectively, for detection of significant stenosis.8 A problem with time-of-flight MRA is that due to decreased blood movement at the site of stenosis, there is a loss of information. The result is that the stenosis can be falsely diagnosed as occluded. MRA can be done with gadolinium. Gadolinium-enhanced MRA increases signal intensity, and is higher resolution and more diagnostically accurate than time-of-flight. It has a sensitivity of 92% and specificity of 97%.9
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Computed tomographic angiography (CTA) (Figure 67.3) Computed tomographic angiography uses x-rays taken from different angles to generate images. It allows the evaluation of the anatomic location of significant stenosis. It is a suitable substitute for patients unable to undergo MRA or when better resolution is needed than with MRA. CT angiography identified stenosis > 50% with a sensitivity of 93% and specificity of 96% compared to angiography. Additional studies are needed to continue to compare, validate, and standardize noninvasive imaging modalities. Intra-arterial angiography (Figure 67.4) Angiography is the oldest of the imaging techniques and is considered the gold standard. Angiography allows visualization of prelesional flow, site of stenosis, outflow, and collateral bed. It is useful when revascularization is being evaluated. Vascular access is usually at the common femoral artery at the level of the center of femoral head. A 4–6-French sheath and catheter is used. Contrast material is injected and visualization of vasculature is done using x-rays. Images can be generated for both legs simultaneously, above the aortic bifurcation. If the problem area is in the area of the catheter, brachial access is used as well. A pelvic/abdominal aortogram is used for imaging distal aorta and iliac arteries. A lower extremity angiogram will image iliac, femoral, and tibial bifurcations in profile without vessel overlap. Digital subtraction is recommended for contrast angiography to enhance imaging. Angiography has risks associated with it including contrast allergies, kidney problems, and atheroemboli.
REFERENCES 1.
2. 3.
4.
Resnick HE, Lindsay RS, McDermott MM et al. Relationship of high and low ankle brachial index to all-cause and cardiovascular disease mortality: the Strong Heart Study. Circulation 2004; 109: 733–9 Criqui MH, Langer RD, Fronek A et al. Mortality over a period of 10 years in patients with peripheral arterial disease. N Engl J Med 1992; 326: 381–6 O’Hare AM, Katz R, Shlipak MG, Cushman M, Newman AB. Mortality and cardiovascular risk across the ankle-arm index spectrum: results from the Cardiovascular Health Study. Circulation 2006; 113: 388–93 Hirsch AT, Haskal ZJ, Hertzer NR et al. ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to Develop Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed by the American Association of Cardiovascular
5. 6. 7. 8.
9.
and Pulmonary Rehabilitation; National Heart, Lung, and Blood Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease Foundation. Circulation 2006; 113: e463–654 Rutherford RB, Lowenstein DH, Klein MF. Combining segmental systolic pressures and plethysmography to diagnose arterial occlusive disease of the legs. Am J Surg 1979; 138: 211–8 Koelemay MJ, den Hartog D, Prins, MH et al. Diagnosis of arterial disease of the lower extremities with duplex ultrasonography. Br J Surg 1996; 83: 404–9 Wutschert R, Bounameaux H. Determination of amputation level in ischemic limbs. Reappraisal of the measurement of TcPo2. Diabetes Care 1997; 20: 1315–8 Baum RA, Rutter CM, Sunshine JH et al. Multicenter trial to evaluate vascular magnetic resonance angiography of the lower extremity. American College of Radiology Rapid Technology Assessment Group. JAMA 1995; 274: 875–80 Ruehm SG, Hany TF, Pfammatter T et al. Pelvic and lower extremity arterial imaging: diagnostic performance of three-dimensional contrast-enhanced MR angiography. AJR Am J Roentgenol 2000; 174: 1127–35
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Iliac occlusive diseases DT Cragen and RR Heuser
Introduction Approximately one-third of lower extremity occlusive disease occurs in the iliac arteries, with the remaining two-thirds of disease in the femoral, popliteal, and infrapopliteal systems. Surgical revascularization has been the mainstay of invasive treatment of aortoiliac disease for decades. More recently, percutaneous techniques have been developed and shown to have similar efficacy with less associated morbidity and mortality. As supporting technology improves and new percutaneous techniques are developed, a greater number of patients and their physicians are choosing percutaneous repair over surgical bypass. Furthermore, symptoms can be treated sooner with percutaneous repair due to its lower morbidity and mortality, thus helping patients maintain active lifestyles that will further slow the progression of atherosclerotic obstruction. Traditional surgical revascularization of iliac occlusive disease involved aortoiliac, aortofemoral, or femoral–femoral bypass grafting and has been highly effective, its success only being limited by its significant morbidity and mortality. The Veterans Administration Cooperative Study demonstrated in a randomized trial nearly two decades ago that percutaneous transluminal angioplasty (PTA) produced similar results to surgery with similar symptomatic relief, durability, and freedom from amputation.1 PTA was somewhat less successful acutely (15% failure rate) but had fewer complications and no deaths while three deaths (2.4%) occurred in the surgical arm. At 4-year follow-up, these results were sustained and there was a trend in survival favoring the PTA arm.2 Similar results were obtained in a randomized, single-center Swedish study with similar success and complication rates for both arms.3 Advances in technology during the last two decades have allowed more complicated lesions to be treated endovascularly with ever-increasing procedural success. While most patients with iliac disease are asymptomatic, patients may present for evaluation with a range of symptoms from mild exertional claudication to acute critical limb ischemia. Claudication from iliac occlusive disease usually involves both the thigh and the calf of the ipsilateral leg, but buttock claudication and vasculogenic impotence occur and suggest iliac stenosis. The severity of symptoms varies according to the degree of stenosis, the recruitment of collateral circulation, and the presence of other proximal and/or distal stenoses. Percutaneous intervention has become the mainstay of therapy for patients with iliac occlusive disease who have acute limb ischemia, critical limb ischemia, and stable claudication refractory to exercise and medical programs. 606
In addition, percutaneous revascularization of the iliac artery can be critical in order to maintain a patent conduit for coronary and carotid catheters in these patients with diffuse atherosclerosis.
Diagnosis While most significant occlusive iliac disease is discovered in response to patient symptoms, more patients are being seen with asymptomatic disease—in part because of the rapid proliferation of other angiography procedures, especially coronary, which require passage of guidewires and catheters through the femoral and iliac systems to access the aorta and its branches. Iliac disease may impede guidewire and catheter advancement, require additional manipulation of guidewires and catheters, or even prohibit passage altogether. Finally, routine angiography of the iliofemoral system on the access side is routinely done at the conclusion of these procedures to assess puncture location and adequacy for closure devices and this may frequently uncover occult disease. Known or suspected iliac occlusive disease should prompt a thorough history and physical exam. Special attention should be given to history of co-morbidities, functional status, and cardiopulmonary symptoms including angina and dyspnea. A detailed exploration of exertional limb discomfort should be undertaken as ipsilateral limb claudication is the most common presenting symptom in patients with significant plaque burden. Care should be taken to distinguish the symptoms from those of other disease processes that may overlap significantly such as pseudoclaudication from spinal stenosis, peripheral neuropathies, and venous insufficiency. Any history of non-healing ulcers should be elicited and prompt further evaluation. Correctable and treatable risk factors such as nicotine usage, physical inactivity, diabetes mellitus, hyperlipidemia, and hypertension should be identified and management options discussed with the patient. Physical examination should focus on the cardiac and pulmonary systems to assess for co-morbid conditions of significance such as obstructive pulmonary disease, valvular heart disease, cardiomyopathy, and arrhythmias. A detailed examination of the peripheral pulses in the upper and lower extremities should be undertaken and documented. Finally, non-invasive studies such as ankle–brachial indices with or without segmental pressures, Doppler imaging of the extremities, and pulse volume recordings can assist in
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Iliac occlusive diseases localizing obstructive disease as well as determining the severity. Advances in both computed tomography and magnetic resonance imaging allow these powerful modalities to more exactly define the nature and extent of disease burden.
Vascular access An important part of planning any interventional procedure is determining the access point that will permit the greatest likelihood of procedural success and least risk of complication. Generally, the ipsilateral retrograde femoral artery (FA) can be chosen for high iliac lesions if the FA is relatively free of disease and there is an adequate “landing zone” for the sheath. This ipsilateral approach is favored when intervention is planned near the aortic bifurcation as positioning a PTA balloon or a stent accurately using the crossover technique from the contralateral FA can be very difficult due to the angulation of the guidewire and/or sheath. Contralateral retrograde femoral artery access with a crossover sheath is very effective for most common iliac, internal iliac, and external iliac lesions. This technique provides excellent support and is especially useful if the patient’s ipsilateral disease hinders access or advancement of the vascular sheath. Certain lesions may require both ipsilateral and contralateral femoral access, particularly with aortoiliac bifurcation disease (Figure 68.1), chronic occlusions, and during interventions when a dissection may have occurred and it is critical to preserve the vessel via the true lumen. In uncommon scenarios, popliteal access may also be required (Figure 68.2). Finally, brachial or radial artery access may be indicated in patients with severe aortoiliac bifurcation disease or when bilateral iliofemoral disease limits access from the femoral arteries. This approach can provide optimal guidewire angulation for precise delivery of balloons and stents to the aortoiliac bifurcation. Of critical importance is that once vascular access is obtained via any route, care must be taken to avoid losing that access. It can often be quite difficult to obtain initial access when there is a heavy disease burden and loss of access can lead to multiple complications including hematomas, vascular dissections, excess radiation exposure to the patient and operators, and sometimes cancellation or postponement of the procedure.
Angiography Angiography of the abdominal aorta and bifurcation is generally performed with a pigtail or similar side-hole catheter placed in the mid-abdominal aorta. As needed, each iliac can be selectively entered with a catheter and/or sheath and selective views can be obtained to further demarcate lesion sites and severity. Both inflow and outflow of each lesion should be clearly demarcated by the films and run-off views of bilateral lower extremities should be obtained. Once all views are obtained, a working view should be selected. A radio-opaque ruler placed in the field adjacent to the diseased artery is useful to establish landmarks to guide precise sizing and deployment of balloons and stents.
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Selecting revascularization: endovascular vs. surgical Multiple studies have shown that the site of stenosis is highly predictive of both immediate procedural success and durability of results. The TransAtlantic Inter-Society Consensus statement proposed a widely adopted classification system for iliac stenoses that categorizes them in increasing risk for poor endovascular procedural outcomes (Table 68.1).4 The consensus statement proposed that type A iliac lesions should be treated by percutaneous revascularization and type D lesions were best managed surgically. Type B and C lesions are intermediate risk and there was less consensus over the preferred treatment. The consensus statement said that percutaneous management for type B and surgical management for type C lesions are the preferred approach, but there is no clear evidence to support this recommendation. Over the past several years, endovascular methods have been refined, interventionists are becoming more adept at advanced techniques, and stent technology in particular has improved and greatly expanded the scope of endovascular management. It has become common practice for interventionists to treat TASC type B, C, and even complex D lesions successfully with endovascular procedures. A recent study published by the Cleveland Clinic presented their findings in 89 patients who underwent 92 endovascular procedures for symptomatic iliac occlusions (TASC B, C, and D lesions).5 Their reported procedural success was 91% overall but 95 and 94% in TASC B and C lesions respectively. The most common intraoperative complication was flow-limiting dissection (5/92) but all of these were successfully treated with prolonged balloon inflation and stent placement. Primary and secondary (i.e. after repeat revascularization) patency of the treated artery was 76% and 90% respectively at 36 months. Limb salvage rate was an impressive 97%. Peri-procedural mortality was 3.3%: one patient died of complications from distal embolization and two patients died of cardiorespiratory events. This compares favorably to open aortobifemoral grafting which also carries a peri-operative mortality of approximately 3.3% in recent studies.5 Endovascular treatment has become the mainstay of revascularization of iliac artery occlusive disease for the aforementioned reasons. This has been paralleled by a significant and sustained decrease in aortobifemoral graft surgery as patients and providers opt for the efficacy, safety, and durability of endovascular repair.6,7 As further refinements occur, we can only expect that endovascular repair will be more and more widely adopted.
Peri-procedural medical considerations Patients with known or suspected peripheral vascular disease should be managed with aggressive medical therapy (aspirin, statins, cilostazol, etc.) before considering endovascular therapy for refractory symptoms. If the patient is not on aspirin at initial presentation, they should be started on a daily dose (preferably 325 mg daily) several days prior to planned intervention. After completing diagnostic angiography, if intervention is indicated then the appropriate interventional sheath is placed in the access site. Once the sheath exchange has been performed and before significant guidewire and
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(a)
(b)
(c)
(d)
Figure 68.1 ‘Kissing’ stents at aortoiliac bifurcation. A 61-year-old female with a 75-pack-year history of smoking, uncontrolled hypertension, and hyperlipidemia had 12 months of bilateral hip and buttock claudication and developed blue toe syndrome 6 weeks previously on the right. Her ABIs were 0.53 and 0.58 on the right and left, respectively. (a) Initial angiography with access obtained from the right common femoral artery revealed high-grade bilateral proximal common iliac artery stenoses. A second arterial access was obtained in the left common femoral artery to permit simultaneous balloon deployment on both sides; (b) After predilatation with 6 × 40 mm kissing balloons, two 8 × 37 mm stents were deployed in ‘kissing’ fashion with approximately 1 cm overlap in the distal aorta; (c) Angiography performed after the stents were deployed revealed resolution of the disease proximally, but residual complex disease at the distal edge of the right common iliac stent; (d) A third stent, 8 × 27 mm, was deployed in an overlapping fashion and the final angiogram shows an excellent result. On the day after this procedure, her ABIs were 1.0 and 0.91 on the right and left, respectively, and the patient was discharged home in good condition.
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(b)
(c)
(d)
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Figure 68.2 A complicated external iliac artery case. A 52-year-old man with a history of coronary disease, tobacco abuse, and hyperlipidemia presented for symptomatic claudication of the right leg reproducible at < 1 block of walking and refractory to medical therapy and exercise. (a) Initial angiography showed occlusion of the external iliac artery just distal to the take-off of the internal iliac artery; and (b) reconstitution of the distal external iliac artery via collaterals; (c) After angioplasty and stenting of the external iliac artery, initial angiography showed a perforation with a free-flowing jet of contrast. An angioplasty balloon was reinflated at the perforation site until a covered stent could be deployed; (d) Angiography after covered-stent deployment confirmed resolution of the perforation but poor distal run-off. Further evaluation confirmed that the stents had been deployed in a dissection plane and there was no significant antegrade flow to the common femoral artery. The patient returned 1 month later and access was obtained from both the contralateral femoral artery and the ipsilateral popliteal artery. Once the true lumen was crossed, angioplasty and stenting was performed and the previously placed stents were crushed to the side.
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(e) Figure 68.2, cont’d (e) Final angiography confirmed excellent antegrade flow and the patient experienced resolution of his symptoms.
catheter manipulation, intravenous heparin (3000–6000 units) is routinely given in our laboratory. During prolonged (>1 hour) procedures or if thrombus is observed in catheters or on guidewires, strong consideration should be given to administering further heparin either empirically or to target a modestly elevated activated clotting time (ACT) of at least 200 seconds. In the absence of serious perforation or bleeding complications, we do not routinely reverse heparin after the intervention. Postprocedurally, sheaths should be left in place until the ACT is 10 cm) 10. Unilateral occlusion involving both the CIA and EIA 11. Bilateral EIA occlusions 12. Diffuse disease involving the aorta and both iliac arteries 13. Iliac stenoses in a patient with an abdominal aortic aneurysm or other lesion requiring aortic or iliac surgery CIA, common iliac artery; EIA, external iliac artery; CFA, common femoral artery.
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Iliac occlusive diseases planned intervention would suffice as an estimate of vessel size. It may also be appropriate in some instances to use intravascular ultrasound guidance to facilitate vessel measurements and assess lesion morphology and composition. The balloon diameter should be chosen 0–1 mm larger than the reference vessel diameter such that when inflated it causes 15–20% overdilation of the lesion.16 The length of the balloon should allow it to extend just beyond the lesion margins proximally and distally to minimize barotrauma to the surrounding segments. Inflation of the balloon should be carried out at the minimal pressure that eliminates the waist, or pinching, of the balloon at the site of stenosis. Repeat angiography should be performed to determine success of the procedure; generally a residual stenosis of < 30% is considered acceptable and appropriate with balloon angioplasty. A translesional gradient should be measured with the sheath or guide catheter and should be < 5 mmHg to document resolution of the hemodynamically significant stenosis. If results are not optimal (> 30% residual stenosis or translesional gradient of >5 mmHg) or if a significant dissection occurs, consideration should be given to further angioplasty and/or stent placement. Stents As described above, PTA alone of the iliac artery is highly successful but limited by elastic recoil of the vessel which decreases acute gain, acute closure, and restenosis of the occluded segment; and by intimal dissections which can sometimes be flow limiting. In addition, PTA has been less successful with certain lesion characteristics: irregular, ulcerated stenoses, occlusions, eccentric, or long lesions. The deployment of stent endoprostheses primarily or immediately after PTA has significantly reduced the impact of each of these limitations and contributed to the success of endovascular revascularization. A 4-year multicenter trial done by Palmaz et al. documented the results of placing the Palmaz stent in the iliac artery of 486 patients and 567 limbs and showed angiographic patency was 92% at 8.7 months.17 A smaller study examined the results of deployment of Palmaz stents in the iliac arteries of 83 patients and 103 limbs.18 This study showed a primary patency rate of 87.5% at a mean follow-up of 10.4 months and sustained clinical benefit in 86.4% of patients at 4 years. A retrospective study of 288 patients showed high initial success rates, low complication rates, and similar patency data as had previously been reported with PTA use alone.19 More recent reports have sought to examine long-term results of stent deployment. Vorwerk et al. reported a 4-year primary patency of 78% and secondary patency of 82% in a small study of 100 patients.20,21 Schurmann and colleagues reported a similar patency rate of 83% at 5-year follow-up using nitinol self-expanding stents in 110 patients.22 Park et al. recently reported 10-year follow-up data on 249 limbs in 203 patients in which technical success was very high (98%) and the primary patency of the stents was 87%, 83%, 61%, and 49% at 3, 5, 7, and 10 year follow-up, respectively.23 Factors that predicted loss of stent patency included stent diameter and lesions in the external iliac artery alone and tandem lesions in the common and external iliac artery. These results are comparable to results obtained with surgery but
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with significantly less complications, morbidity, and mortality associated with the index procedure.24 Given the favorable data supporting the use of stents, they are utilized in the vast majority of percutaneous interventions in the iliac arteries. Deployment of the stents is similar to PTA as described above in terms of sizing of the stent. As stent technology improves, stents are increasingly lower profile, more flexible, and hence more deliverable. Balloon-expandable stents are preferred when precise placement is desired. Occasionally, the stent may be difficult to deliver to the region due to calcification or vessel irregularity. In these cases, it may be useful to advance the delivery sheath or catheter across the lesion, advance the stent to the treatment site, and then unsheathe the stent by withdrawing the sheath while fixing the stent in place. Balloon-expandable stents are generally sized 1:1 to the reference vessel diameter. As with PTA, during deployment of balloon-mounted stents, the operator should seek to achieve full expansion of the balloon and stent with no evidence of a “waist” within the stent length. Post-dilatation may be required for persistent narrowing within the stented region or if there is a concern of malapposition of the stent to the vessel wall. There is concern that post-dilatation may be a significant source of intraprocedural embolic material as material is extruded through the stent struts, so it should be employed judiciously. Self-expanding stents are generally sized approximately 1 mm larger than the reference vessel diameter such that they will continue to exert radial pressure along the length of the lesion. They are also sized approximately 1 cm longer than the lesion due to the difficulty in precise deployment of the stent and because the stent will shorten beyond its nominal length as it is post-dilated. Once positioned and deployed, postdilatation is routine with self-expanding stents to assure wall apposition circumferentially and to prevent migration of the stent. Perforation of the iliac artery, or its major branches, was previously often catastrophic due to the large vessel size and high flow rates through the artery. Initially, a balloon was reinflated at the site of perforation to tamponade the artery until definitive therapy could be performed or hemostasis was achieved. Recently, placement of a polytetrafluoroethylenecovered stent has become routine and has been safe and effective (Figure 68.3). These stents are either available in balloon-mounted versions for precise delivery or the more common self-expanding variety.
Conclusion The care of iliac occlusive disease has been revolutionized over the last two decades with the advent and development of percutaneous endovascular techniques. Angioplasty and stenting of the iliac artery is the procedure of choice for the vast majority of patients and clinicians when local expertise in these endovascular procedures is available. Studies have consistently shown that percutaneous intervention in the iliac artery is effective, safe, and produces durable results that rival those of surgical bypass techniques. As interventionists become more facile with advanced endovascular techniques and incorporate the latest technological advances, the scope and severity of disease that can be treated percutaneously will continue to grow.
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(c) Figure 68.3 Exclusion of an internal iliac aneurysm. A 64-year-old man with hypertension, hyperlipidemia, and recent onset impotence was found to have an infrarenal abdominal aortic aneurysm (AAA) on computed tomography of the abdomen performed for unrelated reasons. It was recommended that he proceed with angiography and then endoluminal grafting (ELG) of the AAA. (a) On angiography, he was found to also have aneurysmal dilatation of the left common iliac artery and a focal aneurysm of the proximal left internal iliac artery with occlusion of the right internal iliac artery. Given the difficulty of contralateral access after placement of ELG, we opted to proceed with exclusion of the left internal iliac artery aneurysm prior to placement of the ELG; (b) Once access was obtained with a 0.035-inch guidewire, a balloon-mounted 7 × 59 mm iCast PTFE-covered stent (Atrium Medical Corp, Hudson, NH) was deployed across the aneurysm with successful; (c) exclusion of the aneurysm. The patient underwent successful ELG placement a few weeks later.
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REFERENCES 1.
2.
3.
4. 5. 6. 7. 8. 9. 10. 11. 12.
Wilson S, Wolf G, Cross A. Percutaneous transluminal angioplasty versus operation for peripheral arteriosclerosis. Report of a prospective randomized trial in a selected group of patients. J Vasc Surg 1989; 9: 1–9 Wolfe G, Wilson S, Cross A et al. Surgery or balloon angioplasty for peripheral vascular disease: a randomized clinical trial. Principal investigators and their Associates of Veterans Administration Cooperative Study Number 199. J Vasc Interv Radiol 1993; 4: 639–48 Holm J, Arfvidsson B, Jivegard L et al. Chronic lower limb ischaemia. A prospective randomised controlled study comparing the 1-year results of vascular surgery and percutaneous transluminal angioplasty. Eur J Vasc Surg 1991; 5: 517–22 Management of peripheral arterial disease (PAD). TransAtlantic Inter Society Consensus (TASC). J Vasc Surg 2000; 31(suppl.): 1–296 de Vries S, Hunink M. Results of aortic bifurcation grafts for aortoiliac occlusive disease: a meta-analysis. J Vasc Surg 1997; 26: 558–69 Leville C, Kashyap V, Clair D et al. Endovascular management of iliac artery occlusions: extending treatment to TransAtlantic Inter-Society Consensus class C and D patients. J Vasc Surg 2006; 43: 32–9 Whitely M, Ray-Chaudhuri S, Galland R. Changing patterns in aortoiliac reconstruction: a 7-year audit. Br J Surg 1996; 83: 1367–9 Freiman D, Spence R, Gatenby R et al. Transluminal angioplasty of the iliac and femoral arteries: follow-up results without anticoagulation. Radiology 1981; 141: 347 Johnston K. Iliac arteries: reanalysis of results of balloon angioplasty. Radiology 1993; 186: 207–12 Van Andel G, Van Erp W, Krepel V et al. Percutaneous transluminal dilatation of the iliac artery: long-term results. Radiology 1985; 156: 321 Gallino A, Mahler F, Probst P et al. Percutaneous transluminal angioplasty of the arteries of the lower limbs: a 5 year follow up. Circulation 1984; 70: 619–23 Becker GJ, Katzen BT, Dake MD. Non coronary angioplasty. Radiology 1989; 170: 403–12
13. 14. 15. 16.
18. 19. 20. 21. 22. 23. 24.
Van Andel GJ, Van Erp W, Krepel M. Percutaneous transluminal dilatation of the iliac artery. Long term results. Radiology 1985; 156: 321–3 Tegtmeyer CJ, Hartwell GD, Selby JB et al. Results and complications of angioplasty in aortoiliac disease. Circulation 1991; 83(suppl I): 153–60 Wilson SE, Wolf GL. Cross AP. Percutaneous transluminal angioplasty versus operation for peripheral atherosclerosis. J Vasc Surg 1989; 9: 1–9 Kalman P, Johnston K, Sniderman K. Indications and results of balloon angioplasty for arterial occlusive lesions. World J Surg 1996; 20: 630–417. Palmaz JC, Laborde JC, Rivera FJ et al. Stenting of the iliac arteries with the Palmaz stent: experience from a multicenter trial. Cardiovasc Intervent Radiol 1992; 15: 291–7 Murphy KD, Encarnacion CE, Le VA, Palmaz JC. Iliac artery stent placement with the Palmaz stent: follow-up study. J Vasc Interv Radiol 1995; 6: 321–9 Richter GM, Roeren T, Noeldge G et al. Initial long-term results of a randomized 5-year study: iliac stent implantation versus PTA. Vasa – Supplementum. 1992; 35: 192–3 Vorwerk D, Gunther R, Schurmann K et al. Primary stent placement for chronic iliac artery occlusions: follow-up results in 103 patients. Radiology 1995; 194: 745–9 Vorwerk D, Gunther R, Schurmann K et al. Aortic and iliac stenoses: follow-up results of stent placement after insufficient balloon angioplasty in 118 cases. Schurmann K, Mahnken A, Meyer J et al. Long-term results 10 years after iliac arterial stent placement. Radiology 2002; 224: 731–8 Park K, Do Y, Kim J et al. Stent placement for chronic iliac arterial occlusive disease: the results of 10 years experience in a single institution. Kor J Radiol 2005; 6: 256–66 Devries SO, Hunink MG. Results of aortic bifurcation grafts for aortoiliac occlusive disease: a meta analysis. J Vasc Surg 1997; 26: 558–69
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Procedures for the hypogastric artery J Cynamon and P Prabhaker
Introduction For a long time the hypogastric artery was a neglected vessel, with few procedures being performed by interventional radiologists except for a limited number of angioplasties done for significant claudication or erectile dysfunction. Recently, this vessel has become of prime importance to various procedures. Fibroids are currently treated by embolizing the uterine artery as it stems from the anterior division of the hypogastric artery. Pudendal arteriography and iliac angioplasty are being performed for evaluation and management of impotency. Rarely, buttock claudication, which can be due to significant hypogastric artery stenosis, can be treated by angioplasty. The most frequent intervention of the hypogastric artery performed at our institution is preoperative hypogastric artery coil embolization for stent-graft or operative repair of abdominal aortic and iliac artery aneurysms to prevent collateral endoleaks. This chapter will review these indications and techniques that have now become commonplace in the angiography suite.
Claudication Since angioplasty for claudication has been around for many years, we will begin with this topic, Isolated hypogastric artery stenosis causing significant claudication occurs rarely (Figure 69.1).1 Occasionally, an external iliac artery occlusion occurs with a proximal hypogastric artery stenosis. In this situation, where the common femoral artery and the distal vessels are supplied by the hypogastric artery, a focal stenosis of the hypogastric artery may lead to severe thigh or calf claudication and thus may warrant treatment via angioplasty. An alternative to angioplasty would be recanalization of the external iliac artery, which is significantly more invasive than a focal hypogastric artery angioplasty. Unfortunately, there are no large series reporting the initial and long-term results of hypogastric artery angioplasties for the treatment of claudication.
Erectile dysfunction The evaluation and possible treatment of impotency is another procedure that involves the hypogastric artery. Although there are many methods of evaluation of the cause of impotency, such as duplex ultrasonography, magnetic resonance imaging, and radionuclide imaging, pudendal arteriography remains the gold standard for penile arterial assessment. Pudendal arteriography allows for an anatomic study of the causes of 614
impotence, which is necessary when considering penile arterial reconstructive surgery. The distal aorta, common iliac artery, proximal hypogastric artery, and pudendal arteries must be evaluated. Pudendal arteriography is best performed by bilaterally catheterizing the hypogastric arteries and using the image intensifier to visualize in the ipsilateral anterior oblique projection, with the penis positioned across the contralateral thigh so that the dorsal and cavernosal arteries become visible (Figure 69.2). The angiogram is performed after injecting 60 mg of papaverine directly into the cavernosum using a 25 or 27 gauge needle.2 This causes a partial or complete erection in most patients, which improves flow and helps visualize the dorsal penile artery. The classic penile anatomy is the dorsal penile, cavernosal, and bulbar arteries stemming from each pudendal artery.3,4 A great deal of variation exists, with only 18% of cases in one study having the classic pudendal anatomy.5 To avoid misinterpretation of normal variants, such as the dorsal penile artery branching from the iliac or common femoral artery, these variants should be searched for if a dorsal penile artery is not seen with hypogastric artery injection (Figure 69.3). If a stenosis is identified in one of the inflow vessels such as the common iliac or proximal hypogastric arteries, the patient may benefit from transluminal angioplasty. In addition, a focal lesion in the pudendal artery can be dilated with a small vessel balloon.6 However, many patients with arterial erectile dysfunction do not have a focal lesion amenable to angioplasty. These patients can benefit from a surgical bypass to the dorsal penile artery.
Uterine artery embolization Transcatheter uterine artery embolization was once an uncommon procedure performed for emergency control of hemorrhage related to pelvic trauma, post-partum and postcesarean bleeding, placental abnormalities, ectopic pregnancy, hemorrhage from gestational trophoblastic disease, intraoperative bleeding, and pelvic arteriovenous malformations.7 Recent use of uterine artery embolization for the treatment and management of symptomatic uterine leiomyomas has further stretched the application of this procedure. Uterine leiomyomas produce significant morbidity by causing uterine enlargement, abnormal bleeding, anemia, pelvic pain, and infertility. Prior therapeutic techniques, such as treatment with gonadotrophin-releasing hormone (GnRH) analogs, myomectomy, or hysterectomy, have proved to be either inadequate or associated with significant morbidity, mortality, and potential infertility. Thus, the utilization of uterine artery embolization to shrink
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Figure 69.1 (a) A 62-year-old man with three block buttock claudication with a focal stenosis of the proximal hypogastric artery. (b) Percutaneous transluminal angioplasty (PTA) with a 6 × 4 balloon performed via an ipsilateral common femoral artery puncture. (c) Post-PTA angiogram demonstrating a good result. The patient no longer suffered from buttock claudication.
leiomyomas by obstructing their blood supply appears to be a better and less-invasive approach to the treatment of symptomatic fibroids.8,9 Uterine artery embolization is performed via selective catheterization of the hypogastric and uterine arteries. Bilateral embolization is required for treatment of symptomatic leiomyomas since bilateral arterial anastomoses provide the blood supply to fibroids. The most common agents used include Gelfoam sponges and polyvinyl alcohol particles (Figure 69.4).10 Other agents such as Biospheres and Onyx are being evaluated. Complications have been infrequent, with the most common complication being groin hematomas and arterial perforations. Post-embolization pain resulting from
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leiomyoma ischemia is also fairly common and is controlled with appropriate narcotics. Other observed but very rare complications include endometritis and ischemia to pelvic organs seen with emergency embolization done for hemostasis. Studies have shown a high rate of success, with decreased symptomatology and reduction in leiomyoma volume of between 20 and 80%. Limited follow-up of patients undergoing uterine artery embolization has prevented knowledge of the exact frequency of embolization failure and of the consequences on post-embolization fertility. However, successful pregnancies have been reported after the procedure, which offers hope that uterine artery embolization may one day be the main modality of treatment for symptomatic uterine fibroids.
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Figure 69.2 Right anterior oblique view of a selective right hypogastric artery (a) before and; (b) after injection of 60 mg papaverine. The pudendal artery is visualized and is seen as it enters the dorsum of the penis and becomes she dorsal penile artery. The cavernosal and bulbar arteries are also seen. Note this elongated view of the dorsal penile artery can only be obtained in the anterior oblique projection with the penis draped across the contralateral thigh.
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Figure 69.3 (a) The left dorsal penile artery is not seen on the selective hypogastric artery injection; (b) An external iliac artery injection demonstrates the dorsal penile artery to be a branch off the superficial femoral artery, which is an unusual variant.
Randomized clinical trials should be performed to further elucidate the applications of and indications for uterine artery embolization.7,11–13
Hypogastric artery embolization Stent-grafts have become an alternative to standard surgical repair in the management of aortoiliac aneurysms. Two grafts are currently FDA (Food and Drug Administration) approved and others are in clinical trials. If an endoleak occurs, which is the leakage of blood into a treated aneurysm, the procedure is considered a failure, Endoleaks may occur as a result of an incomplete seal around the proximal or distal attachment of a stent-graft (type I) or due to retrograde flow from collateral arterial branches (type II). Midgraft tears or modular disconnections are called type III endoleaks, and type IV endoleaks are due to graft porosity. When a stent-graft crosses the origin of one of the hypogastric arteries, cross-pelvic collaterals may allow retrograde flow through the hypogastric artery and into the treated aneurysm, resulting in a type II endoleak. To prevent this occurrence, coils can be placed in the hypogastric artery prior to placing the endovascular graft across its origin. Stent-grafts will cross the origin of the hypogastric artery in the following circumstances: 1. abdominal aortic aneurysms (AAAs) with short common iliac arteries (CIAs), making stent anchorage in one of the common iliac arteries difficult;
2. CIA aneurysms extending near the CIA bifurcation; 3. an AAA with an aorto-unifemoral stent-graft, a cross-femoral bypass, and a contralateral CIA occlusion device, such as the type placed frequently at our institution (The Montefiore Endovascular Graft System (MEGS)) (Figure 69.5). Hypogastric artery coil embolization can decrease the incidence of these endoleaks. It will prevent retrograde flow via the hypogastric artery into the aneurysm. The hypogastric artery branches can still continue to be perfused via crosspelvic collaterals. Unfortunately, many patients treated in this manner will develop buttock claudication. This occurred in 41% of all patients in a study conducted at our institution.14 The location at which the hypogastric artery is coil embolized is important in reducing the incidence of buttock claudication. A more proximal embolization may have a lower incidence of buttock claudication. In our study, 10% of patients with proximal hypogastric artery coil embolizations developed buttock claudication versus 55% of those with distal embolizations. Coils, as opposed to other embolic agents, permit proximal placement while also preventing backflow, but still preserve distal vessel patency, thus minimizing possible resultant ischemia, Proximal occlusion of the hypogastric artery at its origin, before its anterior–posterior bifurcation, sufficiently impedes retrograde filling of the aneurysm and the development of endoleaks, In addition, proximal occlusion still allows collaterals to contribute to the anterior and posterior divisions of the hypogastric artery and permits continued communication between the anterior and posterior divisions.
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Figure 69.4 (a) A 44-year-old patient with a large fibroid and severe pelvic pain related to menstruation. Pelvic angiogram demonstrates hypertrophied uterine arteries. Bilateral uterine artery embolization performed with polyvinyl alcohol (250–400 µm particles); (b) The hypertrophied uterine arteries are no longer seen. The patient’s symptoms have dramatically improved.
The vessels distal to the embolization site continue to fill via collaterals and can thus help prevent ischemia-induced claudication (Figure 69.6).14,15 To ensure more accurate proximal placement of embolization coils and maintain communication between the branches of the hypogastric artery, non-fibered GDC coils can be used in conjunction with Gianturco coils. GDC coils may be used in cases where Gianturco coils are likely to embolize to the hypogastric bifurcation or beyond, which can occur in patients with difficult anatomy, such as a hypogastric artery that does not taper as one moves distally towards its bifurcation. A non-fibered GDC coil will prevent microcoils and Gianturco coils from embolizing into the branches of the hypogastric artery while still allowing communication between the anterior and posterior divisions of the hypogastric artery even if it is lodged at the hypogastric bifurcation. In addition, GDC coils can be useful in difficult ipsilateral hypogastric artery catherterizations where a reversed curve catheter may be necessary to adequately seal the proximal hypogastric artery. Gianturco coils cannot always easily advance through a reverse curve catheter. Instead, a non-fibered GDC coil can be first placed to prevent distal embolization and then followed by Tornado or Vortex coils placed through a Tracker catheter (Figures 69.7 and 69.8).16
When treating a hypogastric artery aneurysm, one must occlude the distal and proximal end of the hypogastric artery. If the anterior and posterior divisions arise from the body of the aneurysm, as they often do in a hypogastric aneurysm, proximal embolization would not be possible. Coil embolization of its branches and a common iliac artery to external iliac artery endoluminal graft would isolate or occlude the aneurysm. If there is enough space in the proximal hypogastric artery, an occluder can be placed in this vessel instead of the common iliac to external iliac stent-graft (Figures 69.9 and 69.10).17 Common iliac aneurysms or arteriovenous fistulas involving the common iliac arteries provide another challenge. The usual hypogastric artery embolization may not prevent endoleaks into the aneurysm or flow through the fistula even after the proximal common iliac artery to external iliac artery stent-graft is placed. This occurs because of a communication between the iliolumbar and lumbar arteries that allows flow into the common iliac artery and through the fistula, in these cases, coils should extend above the iliolumbar artery or be placed into the iliolumbar artery to prevent a persistent lumbar to iliolumbar collateral (Figure 69.11).14 Hypogastric artery embolization prior to the surgical repair of aortoiliac or iliac aneurysms may also prove advantageous.
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Figure 69.5 (a) Common iliac artery with enough normal distal common iliac artery so anchor the distal stent-graft above the hypogastric artery. Therefore, embolization of the hypogastric artery is not needed; (b–d) Iliac and aortoiliac aneurysms with insufficient normal common iliac artery requiring extension of the stent-graft into the external iliac artery. Coil embolization of the hypogastric artery is thus indicated.
Cases where hypogastric artery embolization would be most useful include those in which the proposed surgical procedure would require either a surgical anastomosis at the common iliac artery bifurcation or ligation of the hypogastric artery. This can be difficult with a common iliac artery aneurysm, especially on the left side because of the need to mobilize the sigmoid mesocolon. A study performed at our institution revealed that in all cases after hypogastric artery embolization, the actual surgical procedure was modified to an external iliac
artery or common femoral artery bypass with ligation of the proximal artery, thereby excluding the common iliac artery aneurysm. This technique avoids the need to operate in the region of the iliac aneurysm, thus signifi-cantly simplifying the operation. Our study demonstrated simplification of the open aneursysm repair with a low occurrance of complications, which suggests that hypogastric artery embolization should be considered for patients with iliac aneurysms prior to open aortoiliac or iliac aneurysm repair (Figure 69.12).
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Figure 69.6 (a, b) Aortic and right common iliac artery aneurysms. Coil embolization of the right hypogastric artery was performed via an ipsilateral common femoral artery approach; (c) Measurement of the hypogastric artery helps us choose the coil size required to limit the incidence of coil migration; (d) Selective catheterization with a Cobra catheter is performed in the posterior oblique projection; (e) The anterior and posterior divisions are best seen in the anterior oblique projection; (f, g) Adequate coil placement in the hypogastric artery proximal to the bifurcation and the iliolumbar artery.
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Figure 69.7 (a) A common iliac artery aneurysm; (b) Reverse taper of the hypogastric artery. Note that any coil placed in the proximal hypogastric artery is likely so embolize as the artery is enlarging as it nears the bifurcation; (c) A GDC coil is being placed in the hypogastric artery; (d) Post-GDC coil and proximal Gianturco coil embolization.
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Figure 69.8 (a) Aorto–right common iliac artery aneurysm; (b, c) The origin of the hypogastric artery is not easily identified on either oblique view; (d, e) Craniocaudal angulation demonstrates the origin of the hypogastric artery, allowing its catheterization with an SOS Omni catheter. (f) Measuring the diameter of the hypogastric artery. (g) GDC coil placed via a Tracker catheter; (h) Post-microcoil embolization. The microcoils were not able to travel beyond the GDC coil; (i) Post-embolization completion angiogram demonstrates well-positioned coils above the hypogastric artery bifurcation and cessation of prograde flow in the hypogastric artery.
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Figure 69.9 Hypogastric artery aneurysms are managed by coil embolizing its branches and occluding the proximal hypogastric artery by either (a) using a stent-graft from the common iliac artery to the external iliac artery or; (b). If an adequate proximal neck exists, an occluder can be placed in the proximal hypogastric artery.
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Figure 69.10 (a) A patient with a hypogastric artery aneurysm; (b) Branches of the hypogastric artery are coil embolized; (c) An occluder is placed in the proximal hypogastric artery; (d) The hypogastric aneurysm is isolated and thrombosed.
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Figure 69.11 (a) A 49-year-old man s/p back surgery developed a right common iliac artery-to-vein fistula; (b, c) The planned procedure was a common iliac artery to external iliac artery stent-graft to prevent retrograde flow in the hypogastric artery from leaking into the common iliac artery behind the stent-graft and having a persistent fistula, and thus the hypogastric artery was embolized; (d) Follow-up 3 months later shows a persistent small fistula; (e) There was no proximal or distal endoleak; (f) The leak turned out to be a lumbar to iliolumbar collateral. in retrospect, the most proximal coil was just beyond the iliolumbar artery. This allowed a persistent lumbar to iliolumbar collateral with retrograde flow in the proximal hypogastric artery and in the common iliac artery behind the stent-graft and through the fistula.
So far, our discussion has focused on unilateral hypogastric artery, Bilateral hypogastric artery embolization is usually avoided for fear of causing significant morbidity in the form of perineal necrosis, severe lower extremity neurological deficits, ischemic colitis, impotency, and buttock claudication.18 Bilateral occlusion is more likely required in aortic aneurysm cases that also affect the iliac arteries. This occurs in about 20% of aortic aneurysms, which often involve the distal common iliac artery.19 Interruption of one or both hypogastric arteries may be necessary in these cases along with aortoiliac or aortofemoral bypass in order to completely exclude the aneurysm. A study performed by vascular surgeons at our institution reveals that the incidence of severe morbidity might actually be quite low for bilateral hypogastric artery interruption.20 No patients in this study suffered perineal necrosis, ischemic colitis, or death. In addition, only a small percentage experienced impotency, neurological deficits,
or persistent buttock claudication after occlusion of the hypogastric artery unilaterally or bilaterally. These results suggest that unilateral or bilateral hypogastric artery occlusion is most probably not a dangerous procedure and thus can be performed to completely exclude aneurysms that involve the iliac bifurcation or hypogastric arteries. It is proposed that the complications seen in other series are more likely due to other intraoperative events such as hypotension and severing of important collaterals that stem from the distal external iliac, common femoral, and profunda femoral arteries. In conclusion, the hypogastric artery has become a very important vessel in interventional radiology. More knowledge and research is needed to prevent unanticipated complications that may occur when treating claudication, impotency, uterine leiomyomas, and most importantly, aortoiliac aneurysms.
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Figure 69.12 (a) A patient with an aortoiliac aneurysm. Surgical options include a bifurcated graft to the right common iliac artery and to the distal left common iliac artery. This can be a difficult operation. A less optimal alternative is; (b) a bifurcated graft to the right common iliac artery and ligation of the proximal left common iliac artery and its external iliac artery, with the left limb of the bifurcated graft inserting into the left external iliac artery below the ligation. This procedure does not address preventing retrograde left hypogastric artery flow and maintains a pressurized left common iliac artery. If the left hypogastric artery is coil embolized; (c) prior to open repair, the latter procedure can be performed (d) and there is no concern regarding retrograde flow so the common iliac artery aneurysm will also occlude.
REFERENCES 1. 2. 3. 4.
Smith G, Train J, Nitty H, Jacobson J. Hip pain caused by buttock claudication. Clin Orthop Ref Res 1992; 284: 176–80 Wahl S, Rubin M, Bakal C. Radiologic evaluation of penile arterial anatomy in arteriogenic impotence. Int J Impot Res 1997; 6: 93–7 Ferner H, Strubesand J, eds. Sobotta atlas of human anatomy, Vol. 2, 10th edn. Baltimore: Urban & Schwartzberg, 1983: 200–1 Kadir S. Atlas of normal and variant angiographic anatomy. Philadelphia: WB Saunders, 1991: 227–93
5. 6. 7.
Bookstein JJ, Lang EV. Penile magnification pharmacoarteriography: details of intrapenile arterial anatomy. Am J Radiol 1987; 146: 883–8 Valji K, Bookstein J. Transluminal angioplasty in the treatment of arteriogenic impotence. CVIR 1988; 11: 245–52 Abulafia O, Sherer D. Transcatheter uterine artery embolization for the management of symptomatic uterine leiomyomas. Obst Gynecol Sur 1999; 54(12): 746
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Textbook of peripheral vascular interventions Wallach E. Myomectomy. In: Thompson J, Rock J, eds. Je Lindess operative gynecology, 7th edn. Philadelphia: Lippincott, 1992: 647–62 Dubuisson J, Lecuru F, Foulot H. Laparoscopic myomectomy. In: Sutton C, Diamond M, eds. Endoscopic surgery for gynaecologists. London: WB Saunders, 1993: 71–6 Markoff G, Quagliarello J, Rosen R, Bechman E. Uterine arteriovenous embolization successfully embolized with a liquid polymer isobutyl 2-cyanoacrylate. Am J Obst Gynecol 1987; 156: 1179–80 McLucas B, Goodwin S, Vedantham S. Embolic therapy for myomata. Minimally Invas Ther Allied Technol 1996; 5: 336–8 Braf Z, Knootz W. Gangrene of bladder: complications of hypogastric artery embolization. Urology 1977: 9: 670–1 Stancato-Pasik A, Mitty H, Richard H, Eshkar N. Obstetric embolotherapy. effects on menses and pregnancy Radiology 1996; 201: 179 Cynamon J, Lerer D, Veith F et al. Hypogastric artery coil embolization prior to endoluminal repair of aneurysms and fistulas: buttock claudication, a recognized but possibly preventable complication. J Vase Intervent Radiology 2000; 11(5): 573–7
15. 16. 17. 18. 19. 20.
Lee C, Kaufman J, Fan C et al. Clinical outcome of internal iliac artery occlusions during endovascular treatment of aortoiliac aneurysmal diseases. J Vase Intervent Radiology 2000; 11(5): 567–71 Cloft H, Joseph G, Tong et al. Use of three-dimensional Guglielmi detachable coils in the treatment of wide-necked cerebral aneurysms. Am J Neuroradiol 2000; 21(7); 1312–4 Cynamon J, Marin M. Veith F et al. Endovascular repair of an internal iliac artery aneurysm with use of a stented graft and embolization coils. J Vase Intervent Radiology 1995; 6: 509–12 Andriole G, Sugarbaker P. Perineal and bladder necrosis following bilateral internal iliac artery ligation. Report of a case. Dis Colon Rectum 1985; 28(3): 183–4 Armon M, Wenham P, Witake S et al. Common iliac artery aneurysms in patients with abdominal aortic aneurysms. Eur J Vase Endovas Surg 1998; 15(3): 255–7 Mehta M, Veith F, Ohki T et al. Unilateral and bilateral hypogastric artery interruption during aortoiliac aneurysm repair in 154 patients: a relatively innocuous procedure. Presented at the 54th Annual Meeting of the Society of Vascular Surgery, June 10–14, 2000
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Femoropopliteal disease E Calabrese and F Camerano
Introduction
Treatment
In the proximity of the inguinal ligament, the common femoral artery gives origin to the profunda femuris, continuing its straight course in the thigh as the superficial femoral artery (SFA). The profunda originates several small branches and, besides supplying blood to the thigh, builds up a network of collaterals interlacing with the distal arteries of the limb. This profunda network may eventually partially replace a chronically occluded superficial femoral artery in supplying blood to the leg and foot. Occlusive diseases of the profunda, when it is not associated with stenosis or occlusion of the SFA, will often give no clinical symptoms. If the SFA is occluded, severe stenosis of the profunda will produce critical ischemia; the simultaneous complete occlusion of the profunda and the SFA will induce ischemic loss of the limb. The profunda is usually the last of the two branches affected by stenosis, often due to the extension of severe calcific disease at the femoral bifurcation. The SFA is the vessel that is most often affected by symptomatic disease in the lower extremities and its occlusive disease produces pain when walking (claudicatio). In diabetic patients, FSA disease, in presence of neuropathy or infection, may produce non-healing ulcerations and gangrene of the foot, thus requiring immediate therapeutic attention in all patients with tissue loss. The SFA runs initially in the anterior aspect of the thigh, then moves medially, crosses the adductor canal and travels posterior to the distal part of the femur. It then becomes the popliteal artery as it reaches the knee area. The popliteal artery, which runs behind the knee, is most affected by the repetitive movements of the knee and may kink sharply during squatting and extreme joint flexion.1 Due to its length and course, the femoropopliteal artery needs to adjust to the complex, repetitive movements of the knee and thigh that produce elongation, torsion, shortening, smooth or sharp curving, and even temporary kinking.2 Studying in depth the behavior of this vessel under physiologic conditions has helped us to better understand the correct way to approach occlusive femoral artery disease. Advancement in age and appearance of calcifications in various segments of the femoral artery further complicate the adaptation of the artery, due to its increased rigidity in the affected segments. Several advancements in knowl-edge, technique and materials have had a significant influence on the progress of interventional technique involving the SFA.3
Claudicatio Occlusive disease of the femoropopliteal artery, if symptoms are absent or limited to mild claudicatio, can be treated conservatively with smoking cessation, control of cholesterol, maintenance of arterial blood pressure below 140/90 in nondiabetics and 130/80 in diabetics, accurate control of blood sugar, and antiplatelet therapy. If symptoms of claudicatio impair the quality of life, a supervised exercise program should be considered. Several drugs have been evaluated in the medical treatment of claudicatio. Cilostazol (a phosphodiesterase III inhibitor) is the most effective available drug and has been shown to be superior to pentoxifylline in increasing peak treadmill performance and quality of life. However, it can have side-effects such as headache, diarrhea, and palpitations and is contraindicated in congestive heart failure.4,5 Naftidrofuryl (a 5-hydroxytryptamine type 2 antagonist with few, mild sideeffects) improves by 26% treadmill performance when compared with placebo.6 Pentoxifylline and buflomedil have few side-effects but their clinical impact on claudicatio seems very limited when compared with placebo. Vasodilators are ineffective, as are antiplatelet drugs, but this latter group is essential in preventing further complications and advancement of cardiovascular disease. Intravenous prostaglandins improve performance in the treadmill test while effectiveness of oral prostaglandins has not been proven and cannot be currently recommended in the treatment of claudicatio.4 Research is still under way to evaluate the efficacy of fibroblast growth factor and vascular endothelial growth factor. If supervised exercise programs, drug therapy, and smoke cessation fail to obtain improvement of symptoms and if the patient observes a worsening in the quality of life, then a more aggressive approach is justified. Critical limb ischemia Prostanoids have been used to reduce limb loss and help heal ulcers with mixed success.4 Because of their limited effectiveness and unpredictable response, their use is currently reserved exclusively to those patients who cannot be revascularized in a highly specialized center and after issuance of a reliable second opinion on the possibility of surgery or PTA. Conservative therapy has very limited success in critical limb ischemia (CLI) and its use is not justified whenever surgical or endovascular reconstructions are feasible. If a medical center does not have sophisticated endovascular or surgical experience in 625
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limb salvage, the patient should be rerouted to a highly competent service that can handle the most distal bypasses and complex endovascular procedures. Time is critical and patients should be referred as rapidly as possible to obtain appropriate treatment whenever SFA occlusion is associated with foot infection, skin lesions, tissue loss, or significant trauma. Maximal blood flow is needed to heal most lesions, even if they were not originally caused by ischemia. Antibiotic delivery to infected areas is maximized with optimal blood supply, increasing the chances of healing. Increasing the flow by opening a stenotic or occluded SFA may help save a limb even if infragenicular disease is not amenable to corrective treatment. Either surgery or interventional procedures, or both combined, can usually increase blood flow across the femoral artery and help save the limb. TASC The Trans-Atlantic Inter-Society Consensus for the Management of Peripheral Arterial Disease (TASC) was updated in 2007 (TASC II) with arterial lesions still stratified in four groups but with the recommendations for preferred treatment changed, due to advances in techniques.4 TASC II recommends that type A lesions be treated preferentially with the endovascular technique due to its excellent results in this group. The endovascular technique should also be the initial approach in type B lesions unless there are specific reasons that indicate a surgical approach. Type C lesions do better with surgery and the endovascular approach should be reserved for patients who are at a high risk for open repair. Type D lesions, in TASC II stratification, do not yield good enough results with endovascular methods to justify them as primary treatment. TASCII classification of femoropopliteal lesions for the year 2007 is reported as follows: ●
●
●
●
Type A lesions: 䊊 Single stenosis < 10 cm in length 䊊 Single occlusion < 5 cm in length Type B lesions: 䊊 Multiple lesions of < 5 cm in length 䊊 Single lesion not involving infragenicular popliteal artery and < 15 cm in length 䊊 Single or multiple lesions with non-tibial-vessel continuity 䊊 Heavily calcified occlusion < 5 cm in length 䊊 Single popliteal stenosis Type C lesions: 䊊 Multiple lesions > 15 cm in length 䊊 Recurrent lesions after two endovascular interventions Type D lesions: 䊊 Chronic total occlusion of CFA or SFA (> 20 cm involving the popliteal artery) 䊊 Chronic total occlusion of the popliteal artery and proximal trifurcation vessels
Endovascular treatment in type C lesions should be chosen only if there are significant co-morbidities that discourage a surgical approach as a primary choice, if the patient prefers endovascular over surgical treatment, and if the operator has extensive experience and good personal results with the endovascular approach.
The endovascular approach in type D lesions of the femoropopliteal tract should be chosen only for limb salvage and if no other viable options are available, with surgery not feasible or absolutely contraindicated, or if the patient adamantly refuses bypass surgery and the operator has extensive experience and acceptable results in complex distal endovascular procedures. Only centers with extensive experience in limb salvage should be involved in treating type D lesions with the endovascular technique, and only in carefully selected cases as a last resort for limb salvage.7
Endovascular treatment As techniques and instrumentations have improved over time, endovascular techniques for revascularization of the diseased superficial femoral artery have been gaining ground over surgery. In a meta-analysis of several reported series, Muradin et al. observed a technical and clinical success rate of PTA generally exceeding 95%.8 Bolia’s subintimal technique has been successful in restoring patency in long segment occlusion and appear effective in long term studies.9 A study published in the Lancet in 2005 showed no significant difference between bypass surgery and PTA in amputation-free survival at 6 months.10 Earlier studies still showed a clear superiority of surgery in treating long SFA occlusions, but such a difference seems to be disappearing with the advancement of stenting techniques and the advent of subintimal techniques. Patients with critical limb ischemia have poorer results than those with simple claudicatio: the length of lesion and presence and degree of infragenicular disease have a direct influence on long term success of PTA procedures. Schillinger et al. in 2002 observed the impact of elevated CRP (C-reactive protein) levels on the 6-month patency rate.11 The understanding of the limits of balloon expandable stents with their limited flexibility and their susceptibility to permanent deformation from extrinsic pressure have helped advance research on new materials and design. The advent of nitinol self-expanding stents, their improvement in design to achieve both flexibility and sufficient stability, and their metallurgic refinements to increase resistance to repeated stress have made better stents available to the operators.3 Permanent deformation of balloon-expandable stents interfering with flow and patency were originally reported by Rosenfield et al. who observed how such problems could not be easily detected on standard angiography. Intravenous ultrasound (IVUS) helped detect stenoses, which recurred in all cases after redilatation. Most operators have long since abandoned the use of balloon-expandable stents in the SFA12 (Figure 70.1). A German multicenter retrospective study comparing the stainless steel BS Wallstent with nitinol Cordis SMART stents showed a highly significant difference in 1-year primary patency rates (61 ± 5% in the SMART group and 30 ± 5% in the Wallstent group; p < 0.0001) Results were also better in the SMART group when assisted and secondary patency were evaluated.13 The authors concluded that nitinol gave overall superior results when compared to steel. In this study, superiority could have been affected by the completely different design and construction behavior of the two stents. The Wallstent is a closed cell system that increases rigidity of
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Figure 70.1 A crashed and thrombosed balloon expandable stent in the SFA.
the vessel and elongates or shortens significantly with changes in the vessel diameter; the SMART stent is a more flexible system with higher radial force, which adapts to changes in diameter with minimal changes in its length. We may nowadays consider nitinol to be our primary choice for SFA stenting material but we do not in fact have enough uncontroversial data to affirm the superiority of titanium over steel in stents of similar design and mechanical behavior. New steel leagues may show an improved performance in terms of flexibility, adaptability, radial force, and resistance to repeated stress if appropriate stent designs are utilized. Resistance to stress has been another important issue with controversial reports on the importance of stent fracture on patency. Biamino et al.14 reported an increase in stent thrombosis when fracture was observed, but their study, including both xxxK and SMART stents, on closer scrutiny suggested a poorer performance of the xxxK, which is less flexible and more sensitive to the effect of strut fractures. The well-designed SIROCCO study failed to show any association between stent fractures and restenosis in a series of SMART stents inserted in the SFA.15 Stents that are resistant to stress fracture are a desirable option provided that flexibility is not adversely affected. Guidant-Abbott embarked on attentive metallurgic studies and refinements to increase the resistance to stress of its Absolut stents and several other companies followed suit. Modern nitinol stents generally show a higher resistance to stress fracture than previous generations. Drug binding to stent structure has been widely used in coronary interventions, initially with enthusiastic comment but lately with a more critical attitude. The only major study on drug elution is being conducted by Cordis, utilizing self-expanding SMART nitinol stents laced with sirolimus in the SFA. The initial study, SIROCCO I, approached both short and long lesions, utilizing up to three sequential stents, with the sirolimus being eluted fairly fast from the stents. Several stent fractures (in about 30% of cases) were observed in this series, possibly due to the loss of natural flexibility in the arterial tree due to the insertion of several sequential stents, built with a six-interlink system that characteristically gives SMART stents good stability but higher rigidity during critical flexions. A second study, SIROCCO II, used a slower eluting stent and approached lesions of limited length, never exceeding two sequential stents in the initial treatment of any lesion. The fracture rate dropped significantly in the SIROCCO II study. Both studies were prospective randomized double-blind comparative studies between bare stents and drug-eluting stents.
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Preliminary 6-month data showed an advantage in the drug-eluting branch of the study, but over time the two groups fared similarly with no significant advantage reported in the drug-eluting group. The most important result of the SIROCCO study was the demonstration of an excellent long-term primary patency of the SMART stent in the SFA position.15 This study was instrumental in canceling the negative data on SFA stenting reported by Gray et al. several years earlier in the Journal of Vascular Surgery.16 The conclusions coming out of this study may have slowed down the diffusion of SFA stenting. It evaluated the performance of balloonexpandable stents and Wallstents, devices that are not appropriate for SFA insertion due either to susceptibility to external compression or to poor adaptability to flexion. The issue of primary versus rescue stenting in SFA has been resolved in a paper published in the New England Journal of Medicine in 2006. A prospective randomized comparison was made between a group treated with primary stenting of the SFA and another group treated with PTA and secondary stenting in case of suboptimal results with PTA alone (32% of patients had secondary stent implantation). Patients treated with primary stenting had a 12-month echographic restenosis rate of 37% while those treated with PTA and secondary stenting had a much higher restenosis rate of 63% (p = 0.01). Free walking distance at 6 and 12 months was better in the primary stent group. Thus primary stenting clearly appears to be a better choice over simple PTA when treating SFA disease.17 Endoprosthesis has been evaluated for use in the SFA and studies with the Viabahn-Haemobahn endograft have recently been published. In a retrospective study in 60 limbs of 57 patients, primary and secondary patency rates for ViabahnHemobahn were 90 and 95% at 30 days (n = 59), 57 and 80% at 3 years (n = 49), 45% and 69% at 5 years (n = 32). In this study the authors identified a subgroup of patients as optimal candidates for insertion of SFA endoprosthesis having no heavy calcifications, no popliteal obstruction, with a least one run-off vessel and with adequate antiplatelet therapy. This “optimal” subgroup had a 5-year primary and secondary patency rate of 62 and 90% (n = 21).18 A prospective randomized study comparing results of Viabahn implantation with those of a standard surgical Dacron and PTFE femoropopliteal bypass in 100 limbs showed no significant difference between the two groups both in primary and secondary patency rates at 12-month follow-up. In this study, 1-year primary patency was 73.5% in the Viabahn group and 74.2% in the surgical group, and secondary patency was 83.9 and 83.7%, respectively.19 Adverse effects and thrombogenicity of the PTFE endograft have also been reported in the SFA.20 Further investigation with longer follow-up is needed to understand better what happens in cases when the insertion of Viabahn sacrifices collaterals at the beginning and at the end of the obstructed segment. Does sacrificing these collaterals influence limb salvage when the prosthesis eventually occludes? Bare stents do not usually interfere with patency of collaterals, and when nitinol stents occlude, sometimes collaterals take over again, providing some distal flow that can be critical to limb salvage beyond the patency span of the stent itself. Hydrophilic guides and, among them, the remarkable Terumo guides, have greatly improved the capability of crossing lesions completely occluding the vessel. Several techniques to
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approach total occlusion and severely calcified lesions have been tried over the years with limited success. Retrograde canalization through the popliteal artery or by puncturing the dorsalis pedis and passing a guide into the SFA and across the occlusion is an effective technique and helps cross occlusions that could not be negotiated through an antegrade approach. Long-term patency data are not yet available with this technique and the destiny of the punctured artery (thrombosis?) needs to be better understood over time. Excimer lasers have been utilized to open completely obstructed FSA but its results were not brilliant and a prospective study with 3-year follow up on 312 patients with short occlusion of the SFA (average 7.5 cm; range 1–10 cm) showed an 8.3% failure rate in canalization and a poor 3-year primary patency rate of 40.2% while the assisted and secondary patency were respectively 76.5 and 86.3%.21 Atherectomy with a Rotablator performs poorly. The CRAG (Collaborative Rotablator Atherectomy Group) study on 72 patients (79 limbs and 107 arteries including iliac femoral and infragenicular vessels treated at UCLA, Montefiore Hospital, and Stanford) had a cumulative patency rate of 31% at 12 months and 18.6% at 24 months. In this study 84% of the femoral atherectomy procedures were initially successful but there were reports of hemoglobinuria, emboli, dissection, perforation, and hematomas.22 At present, lasers and Rotablators have little place in the treatment of femoral artery disease. Cryoplasty is an approach recently introduced by Boston Scientific with the purpose of reducing vessel injury, elastic recoil, neointimal hyperplasia, constrictive remodeling, and the need of stent implantation. In cryoplasty, a specially designed PTA balloon applies cold thermal energy while dilating the plaque and the vessel wall. Several studies have reported encouraging results. Samson et al. treated 32 patients (33 limbs and 47 arterial lesions) with a technical success rate of 96% and their 12-month freedom from lesion restenosis was 82.2%.23 Laird et al. did a multicenter study treating lesions no longer
than 10 cm in the femoral artery and achieved an 83.2% freedom from target lesion revascularization at 300 days.24 However, the use of cryoplasty and its effectiveness has been challenged both on a biological and clinical basis. Wildgruber et al. tried to confirm in humans the claims based on in vitro models that cryothermal energy induces apoptosis and reduces proliferation rate. To study the process in vivo, the authors studied the role of adhesion molecules (ICAM, VCAM, e-selectin, p-selectin, MCP-1), growth factors (TGFb, bFGF) and the cytokine TNFa and their changes 4 weeks after angiography, angioplasty, and cryoplasty on 29 patients. ICAM, VCAM, e-selectin and MCP-1 increased similarly in angioplasty and cryoplasty. P-selectin and TGFb decreased after cryoplasty, but this change was not significant.25 Karthik et al. applied cryoplasty to challenging cases of recurrent stenosis after a conventional PTA and/or stenting. There was a 100% initial success rate with non-flow limiting dissection in two cases, but 50% of cases developed restenosis within 6 months and the remaining ones had progressive restenosis appear between 6 and 12 months after the cryoplasty. The series was small (only ten cases) but the technique showed a 50% failure rate at 6 months and 100% at 12 months and appeared to be of no value in treating restenotic lesions of the ileofemoral tract.26 Restenosis is a difficult problem to solve and a method that has been evaluated, with initial promising results, is brachytherapy. The Vienna-2 trial, a prospective randomized study, compared the efficacy of a dose of 12 Gy of adjunctive endovascular brachytherapy against no further treatment after successful PTA in long-segment femoropopliteal lesions. At 6 months follow-up, the restenosis rate was significantly lower in the brachytherapy group (29.4 vs. 56.9%; p 0.99).27 New techniques appear frequently
(a)
(b)
(c)
(d)
Figure 70.2 (a) Long segment stenting of the SFA; (b) good flow on straight line angiography; (c) inappropriate results shown on flexion angiography; (d) defect under flexion corrected by adding a distal sequential stent.
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Femoropopliteal disease in the endovascular field and it takes some time before effective ones can be distinguished from the useless ones that are enthusiastically promoted in initial investigations. Currently, primary SFA stenting seem to have been successful, standing the test of time provided that it is correctly performed.
Technique for SFA stenting Distal SFA lesions and popliteal lesions can be approached with an antegrade puncture of the femoral artery while proximal SFA lesions should be treated through a contralateral approach with a reinforced introducer. The lesion is first crossed with a straight Terumo 0.035-inch guide, then with a 4-French straight catheter. The guide is removed and contrast is injected through the catheter to insure its proper positioning inside the distal lumen. A 0.014- or 0.018-inch guide is inserted and the catheter is removed. If severe stenosis or complete occlusion is present a predilatation is performed with a 3 or 4 mm balloon. A stent of appropriate length is inserted and more stents are inserted as required, superimposing partially for 1–2 cm the proximal and distal end of two contiguous stents. An appropriate balloon is chosen and final dilatation is completed from within the stent. Final angiographic control is performed first with the knee extended then with a 90 º flexion of the knee and with the thigh flexed and extra-rotated to simulate physiological
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movements of the artery and stent. Unsatisfactory flexion angiography should be given accurate attention and further stenting or adjustments may be needed to achieve a proper result (Figures 70.2a-d). Flexion angiography is absolutely required whenever retrogenicular vessels are treated; that is, whenever the stenting approaches or crosses the knee line. In these critical procedures early results of retrogenicular stenting improve ten-fold with the use of flexion angiography (54 vs. 5% early failure rate, p < 0.01).7
Conclusion Avoidance of balloon-expandable stents subject to deformation and development of elastic, resilient nitinol stents, and a better understanding of the physiology and pathology of the femoropopliteal tract during movement and rest have greatly improved the results of stenting. Today, PTA with stenting is clearly superior to PTA alone and it seems to be the preferred choice to achieve the highest possible patency rate. Subintimal angioplasty and PTFE covered endoprostheses also have some place in the treatment of selected cases. The introduction of longer stents (over 200 mm) to avoid superimposition of sequential stents and the investigation of newer materials and designs may further improve results and extend application of PTA. In time, we may expectendovascular techniques to supplant most surgical procedures in the femoropopliteal artery.
REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13.
14. 15.
Avisse C, Marcus C, Ouedraogo T et al. Anatomoradiologicalstudy of the popliteal artery during knee flexion. Surg Radiol Anat 1996; 17: 255–62 Wensing PJ, Scholten FG, Buijs PC et al. Arterial tortuosity in the femoropopliteal region during knee flexion: a magnetic resonance angiographic study. J Anat 1995; 187(1): 133–9 Smouse HB, Nikaronov A, LaFlash D. Biomechanical forces in the femoro-popliteal arterial segment. Endovasc Today 2005; 1–6 Norgren L, Hiatt WR, Dormandy JA et al. on behalf of the TASC II Working Group. Eur J Vasc Endovasc Surg 2007; 33: S1–75 Dawson D, Cutler B, Hiatt W et al. A comparison of cilostazol and pentoxifilline for treating intermittent claudication Am J Med 2000; 109(7): 523–30 Lehert P, Comte S, Gamano S, Brown TM. Naftidrofuryl in intermittent claudication: a retrospective analysis. J Cardiovasc Pharmacol 1994; 23 (suppl. 3): S48–52 Calabrese E. Stenting below the knee in limb salvage: long-term results Am J of Cardiology Suppl 2004; 94(6): 7E Muradin G, Bosch J, Stijnen T, Hunink M. Balloon dilatation and stent implantation for treatment of femoropopliteal arterial disease: meta-analysis. Radiology 2001; 221(1): 137–45 Desgranges P, Boufi M, Lapeyre M et al. Subintimal angioplasty feasible and durable. Eur J Vasc Endovasc Surg 2004; 28(2): 138–41 Adam DJ, Beard JD, Cleveland T et al. Bypass versus angioplasty in severe ischemia of the leg (BASIL): multicentre, randomized controlled trial. Lancet 2005; 366(9501): 1925–34 Schillinger M, Exner M, Mlekusch W et al. Vascular inflammation and PTA of the femoropopliteal artery: association with restenosis. Radiology 2002: 225(1): 21–6 Rosenfield K, Schainfeld R, Pieczek A, Haley L, Isner JM. Restenosis of endovascular stents from stent compression. J Am Coll Cardiol 1997; 29(2): 328–38 Hayerizadeh B, Zeller T, Krankenberg H et al. Long-term outcome of SFA stenting using nitinol stents compared with stainless steel stents: a multicenter study. Poster at Transcatheter Cardiovascular Therapeutics (TCT 2003) Washington, DC Scheinert D, Scheinert S, Sax J. Prevalence and clinical impact of stent fractures after femoropopliteal stenting. J Am Coll Cardiol 2005; 45(2): 312–5 Duda SH, Bosiers M, Lammer J et al. Drug-eluting and bare nitinol stents for the treatment of atherosclerotic lesions in the superficial
16.
17. 18.
19.
20. 21. 22. 23. 24. 25.
26. 27.
femoral artery: long-term results from the SIROCCO trial. J Endovasc Ther 2006; 13(6): 701–10 Gray BH, Sullivan TM, Childs MB, Young JR, Olin JW. High incidence of restenosis/occlusion of stents in the percutaneous treatment of long segment superficial femoral artery disease after subintimal angioplasty J Vasc Surg 1997; 25: 74–83 Schillinger M, Sabeti S, Loewe C et al. Balloon angioplasty versus implantation of nitinol stents in the superficial femoral artery. N Engl J Med 2006; 354(18): 1879–88 Fischer M, Schwabe C, Schulte KL. Value of the hemobahn / viabahn endoprosthesis in the treatment of long chronic lesions of the superficial femoral artery: 6 years of experience. J Endovasc Ther 2006; 13(3): 281–90 Kedora J, Hohmann S, Garrett W et al. Randomized comparison of percutaneous Viabahn stent grafts vs prosthetic femoral-popliteal bypass in the treatment of superficial femoral arterial occlusive disease J Vasc Surg 2007; 45: 10–16 Bray PJ, Bray AE. Thrombogenicity of the Hemobahn/Viabahn in the SFA.: J Endovasc Ther 2006; 13(6): 783–4 Laird JR, Zeller T, Gray BH et al. Limb salvage following laserassisted angioplasty for critical limb ischemia: results of the LACI multicenter trial. J Endovasc Ther 2006; 13(1): 1–11 Peripheral atherectomy with the rotablator: a multicenter report. The Collaborative Rotablator Atherectomy Group (CRAG). J Vasc Surg 1994; 19(3): 509–15 Samson RH, Showalter DP, Lepore MR, Ames S. Cryoplasty therapy of the superficial femoral and popliteal arteries: a single center experience. Vasc Endovascular Surg 2006; 40(6): 446–50 Laird JR, Biamino G, McNamara T et al. Cryoplasty for the treatment of femoropopliteal arterial disease: extended follow-up results. J Endovasc Ther 2006; 13 (suppl. 2): II52–9 Wildgruber M, Weiss W, Berger H et al. Early endothelial and haematological response to cryoplasty compared to balloon angioplasty of the superficial femoral artery – a pilot study. Br J Radiol 2007; 954(80): 430–6 Karthik S, Tuite DJ, Nicholson AA et al. Cryoplasty for arterial restenosis. Eur J Vasc Endovasc Surg 2007; 33(1): 40–3 Wolfram RM, Budinsky AC, Pokrajac B, Potter R, Minar E. Endovascular brachytherapy for prophylaxis of restenosis after femoropopliteal angioplasty: five-year follow-up – prospective randomized study. Radiology 2006; 240(3): 878–84
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When to refer to surgery for femoropopliteal disease N Morrissey
Introduction Important differences exist between the peripheral circulation and other vascular beds with respect to the need for treatment. Unlike in the coronary and carotid circulations, there is no evidence to suggest that intervention on asymptomatic disease is indicated. Treatment of significant lower extremity arterial disease in the absence of symptoms does not protect the patient against future events in the same way a coronary or carotid intervention can prevent myocardial infarction or stroke. As all interventionalists understand, once we treat a blood vessel, we start a response to injury which often leads to restenosis or occlusion. With this in mind, it is important to approach each case with an understanding of the symptoms that are being treated and avoid unnecessary intervention. Although techniques have become less invasive, the indications for intervention should remain firm. Disabling claudication, rest pain and tissue loss continue to be the indications for any intervention.
Superficial femoral artery (SFA) disease Decisions regarding the appropriate therapy for peripheral arterial occlusive disease require that the clinician consider anatomic as well as physiologic factors. Durability is a significant concern especially for patients who have longer life expectancies. With respect to the superficial femoral and proximal popliteal arteries, treatment of isolated disease in these segments is typically for claudication, although these patients may also suffer rest pain, ulcer and gangrene. Durability of bypass for SFA and popliteal disease is in the 50–70% range at 5 years depending on the conduit used.1–4 In contrast, percutaneous interventions in the same territory have 1 year patency around 50–75%.5,6 From the standpoint of durability alone, bypass has a slight advantage, however, the physiologic status of the patient, the anatomy of the disease, and the morbidity of the procedure are factors to consider.4 For example, a 50-year-old patient who suffers from claudication but is otherwise quite healthy will most likely have a long life expectancy and require a durable procedure. In such a case, a long SFA occlusion may be best treated by bypass initially or bypass after a single failed percutaneous procedure. Alternatively, if the patient has only a short focal lesion where the likelihood 630
of long-term success is greater, percutaneous methods are the preferred initial treatment. A patient with severe cardiac, pulmonary, and renal disease who has a non-healing ulcer or gangrene may require that a procedure be durable only until the patient’s wounds healed. Such a patient may only be able to undergo a minimally invasive procedure and may benefit from a less durable outcome. An important factor to consider during any catheter based procedure on peripheral arteries is the vessel beyond the lesion. It is critical that the interventionalist not harm the artery beyond the lesion in order to preserve that as a distal target for bypass. Propagation of a dissection beyond the distal aspect of a stenosis or occlusion can force the surgeon to perform a bypass to a more distal target vessel than originally planned. Given the importance of the target vessel size and quality in the success of bypass, harming a proximal target vessel can result in a worse clinical outcome for the patient. A good example of this is when the operator cannot re-enter the vessel lumen in the above-knee segment although the artery is normal there. Propagation of the dissection to the Below-knee artery may change the necessary bypass from an above-knee to below-knee popliteal bypass. This principle holds true for all vessels treated.
Long segment SFA /popliteal disease Numerous devices have been developed to treat stenoses and occlusions of the SFA and popliteal arteries. In spite of some exciting and promising new technology, no one percutaneous method of treatment seems far superior to the others.7–9 In general, lesion severity predicts long-term success of therapy. TASC A-B lesions tend to have more durable outcomes compared to TASC C or D lesions regardless of the device used to treat the disease. Open surgical bypass for femoropopliteal disease has a long history of success.3 The durability of bypass depends on the inflow, the run-off and the conduit. In cases where there is long segment disease, the patient’s health is good, and there is adequate saphenous vein for bypass, surgical revascularization should be considered as initial therapy. Having said that, an initial attempt at percutaneous revascularization may be undertaken as long as two conditions are met: 1. The patient and interventionalist understand that durability may be less than conventional surgery and there may be a need for repeat intervention or eventual surgical bypass.
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When to refer to surgery for femoropopliteal disease 2. The interventionalist adheres to the principle stated above and does not convert a good target vessel into an unusable artery thus mandating a more distal bypass. In cases where the patient’s physiology is suboptimal, percutaneous treatment is considered first-line therapy even in cases of long segment disease. This decision also depends on the symptoms of the disease. For example, a patient with a long total occlusion of the SFA who has severe heart failure may not be able to walk far enough to claudicate. In the absence of other symptoms, the patssient requires no treatment for this “asymptomatic” femoral disease until or when their cardiac status improves to the point where they can walk enough to claudicate significantly and can tolerate a procedure. In cases where femoropopliteal occlusive disease results in limb-threatening ischemia, treatment of some kind is mandatory to avoid amputation. The patient’s physiology and the need for durability again are important factors in determining which is the best approach for revascularization.10 Failed percutaneous interventions are common with currently available technology.7–9,11–3 Failure may be more common in the case of long lesions. Early failure (less than 6 months) may be a significant predictor of repeat failure. In these cases of early failure, anatomic factors such as outflow disease, inflow disease and residual stenosis or dissection may predispose to early reocclusion. In cases of early failure, referral for open surgical bypass should be strongly considered if the patient can tolerate such a procedure. In the absence of adequate conduit for bypass, patients may be best suited with repeat percutaneous interventions given the poor patency of prosthetic bypass grafts to distal vessels.
Tibial disease Patients with below-knee disease tend to present with limb threatening ischemia. Once again, the presence of disease itself is not an indication for treatment, symptoms are. Rest pain, non-healing ulcers, and gangrene are indications to treat tibial vessels. Bypass with vein to tibial vessels can be expected to have limb salvage rates in the 80–90% range REF and patency rates around 50–70% at 3–5 years REF. Percutaneous therapy may be favored in patients with severe tibial disease since they tend to have more severe co-morbidities than patients with SFA disease.13 The ability to get continuous flow to the foot via at least one vessel is usually enough to heal wounds and salvage limbs. After wounds heal, reocclusion of the vessel may not result in new symptoms and therefore durability beyond this point may not be needed. In the case where tibial intervention fails, or if there is ongoing gangrene or sepsis of the foot in spite of optimal endovascular treatment, surgical bypass is warranted. In the case of diabetics, we have found that severe foot infection or gangrene may require recanalization of at least two vessels via a percutaneous approach in order to maximize flow. In some cases, in spite of technically successful endovascular treatment of a tibial vessel, flow is not adequate and bypass to a pedal vessel with vein graft is needed. These cases need to be followed closely and referred early for surgery if necrosis and infection progress despite optimal percutaneous intervention.
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Special considerations Placement of stents in the immediate above-knee segment will eliminate an above-knee popliteal bypass as an option should the intervention fail. Below-knee bypasses have inferior patency to above-knee and such a maneuver will adversely affect the durability of subsequent procedures. In the case of limb salvage, patients tend to have more severe co-morbidities and perhaps shorter life expectancy. In such cases, especially in the face of severe co-morbidities, we have taken an aggressive percutaneous approach in order to create inline flow to heal wounds or alleviate rest pain. In some cases, we have noted poor wound healing with single vessel treatment and have attempted to open at least two tibial vessels in cases of severe ischemia. Should an aggressive percutaneous approach fail to provide adequate flow to heal wounds, bypass with autogenous conduit should be planned. With sufficient endovascular optimization of inflow vessels (popliteal or SFA) a shorter bypass such as a popliteal to posterior tibial or dorsalis pedis can be performed using shorter segments of vein, which may be a precious resource. Should percutaneous revascularization fail, an attempt at bypass should be made in order to salvage a limb except where co-morbidities are prohibitive. Failed percutaneous interventions frequently require open surgical salvage in order to avoid limb loss. When a patient is being treated for non-limb threatening ischemia and as a result of complications related to the procedure develops limb-threatening symptoms, early referral for definitive therapy may be needed. Since the manipulations we perform can cause significant arterial trauma, it is possible to cause dissections, perforations, and embolization which may result in more severe ischemia. When this occurs, consideration should be given to possible open surgical salvage. While percutaneous methods of salvage may be effective, there is often a need for prompt restoration of flow or cessation of hemorrhage, which may be best suited to open surgical intervention.
Summary As more clinicians enter the arena of lower extremity revascularization, it is important that each intervention has all options discussed with the patient in a forthcoming manner. In our practice, we offer the option of open or percutaneous treatment but typically find patients choosing less invasive treatments at least during their first intervention. There are a certain number of patients who will opt for the standard of care which is open surgical revascularization, and it is important that this option be well described to them by whoever their provider is. Failure to present all options, or to minimize the value of one treatment or another does a disservice to our patients. The era of doctors telling their patients what to do is past, and the benefits of thorough, informed discussions with our patients are many. As we view our patients as partners in the process, so too are the other members of the interventional team who may provide therapies beyond the scope of our own practice. The importance of relationships between surgeons and other interventionalists when treating peripheral vascular disease cannot be overstated. An interventionalist who does not perform open surgery needs to have confidence in the availability and ability of their surgical partners.
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REFERENCES 1.
2. 3.
4. 5.
6. 7.
Cox JL, Chiasson DA, Gotlieb AI. Stranger in a strange land the pathogenesis of saphenous vein graft stenosis with emphasis on structural and functional differences between veins and arteries. Prog Cardiovasc Dis 1991; 34: 45–68 Taylor LM Jr, Edwards JM Porter JM. Present status of reversed vein bypass grafting five-year results of a modern series. J Vasc Surg 1990; 11: 193–205 Klinkert P, Schepers A, Burger DH, van Bockel JH, Breslau PJ. Vein vs. polytetrafluoroethylene in above-knee femoropopliteal bypass grafting: five year results of a randomized controlled trial. J Vasc Surg 2003; 37: 149–55 Nolan B, Finlayson S, Tosteson A, Powell R, Cronenwett J. The treatment of disabling claudication in patients with superficial femoral artery occlusive disease–Decision analysis. J Vasc Surg 2007; 45: 1179–84 Myers SI, Myers DJ, Ahmend A, Ramakrishnan V. Preliminary results of subintimal angioplasty for limb salvage in lower extremities with severe chronic ischemia and limb-threatening ischemia. J Vasc Surg 2006; 44: 1230–46 Kalbaugh CA, Taylor SM, Blackhurst Dw et al. One year prospective quality of life outcomes in patients treated with angioplasty for symptomatic peripheral arterial disease. J Vasc Surg 2006; 44: 296–302 Duda SH, Bosiers M, Lammer J et al. Drug eluting and bare stents for the treatment of atherosclerotic lesions in the superficial
8. 9. 10. 11. 12.
13.
femoral artery: long-term results from the SIROCCO trial. J Endovasc Ther 2006; 13: 701–10 Laird J, Jaff MR, Biamino G et al. Cryoplasty for the treatment of femoropopliteal arterial disease: results of a prospective, multicenter registry. J Vasc Interv Radiol 2005; 16: 1067–73 Keeling WB, Shames ML, Stone PA et al. Plaque excision with the Silverhawk catheter: early results in patients with claudication or critical limb ischemia. J Vasc Surg 2007; 45(l): 25–31 Lazaris AM, Salas C, Tsiamis AC et al. Factors affecting patency of subintimal infrainguinal angioplasty in patients with critical lower limb ischemia. Eur J Vasc Endovasc Surg 2006; 32: 668–74 Cheng SW, Ting AC, Ho P. Angioplasty and primary stenting of high-grade long segment superficial femoral artery disease: is it worthwhile? Ann Vasc Surg, 2003; 17: 430–7 Feiring AJ, Wesolowski AA, Lade S. Primary stent-supported angioplasty for treatment of below-knee critical limb ischemia and severe claudication: early and one year outcomes. J Am Coll Cardiol 2004; 44: 2307–14 Faglia E, Antero M, Caminiti M, Caravaggi C, et al. Extensive use of peripheral angioplasty, particularly infrapopliteal, in the treatment of ischemic diabetic foot ulcers: clinical results of a multicentric study of 221 consecutive diabetic subjects. J Intern Med 2002; 252: 225–32
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Infrapopliteal arterial diseases: angioplasty and stenting E Calabrese
Introduction The efficacy of dorsalis pedis, tibialis posterior, and even plantar artery bypass in limb salvage have been repeatedly demonstrated, showing a high long-term patency rate and a significant improvement in the clinical status of the limb.1 While they are possibly the standard of care for long infragenicular arterial obstructions, distal bypasses are long and technically demanding procedures which require the availability of a suitable long vein and a reasonable minimal distance between the surgical field of the distal anastomosis and the gangrenous or infected area. Patients with severe cardiac disease and deteriorated general conditions may sometimes be poor candidates for lengthy surgery, even if performed with sophisticated anesthesia and attentive monitoring. Several diabetic patients have extensively infected feet, which do not respond to local and antibiotic treatment unless proper blood supply is provided. This subset of patients with no suitable veins available, with extensive infection in the proximity of a planned distal anastomosis, and with expected poor tolerance for long surgery, is an ideal candidate for alternative minimally invasive procedures (Table 72.1) but recent advances in techniques may extend the indications of endovascular procedures to a wider range of patients. During the early nineties, a few centers around the world started performing infragenicular percutaneous transluminal angioplasty (PTA) with some encouraging results. The crudeness of the earlier available tools had limited the reach and efficacy of the technique, and during the eighties, infrapopliteal PTA was performed with boogies and tapered catheters.2 It is assumable that unreported failures must have been widespread: the procedure did not gain favor for several years until the application of delicate coronary angioplasty instrumentation to the lower limbs rendered distal PTA a less traumatic procedure. Sivantnantham et al. from Leeds in England, reported a 96% technical success rate performing tibial artery angioplasty and a 58% clinical improvement rate. They observed the improvement of ankle–brachial index in 52% of the treated limbs and improvement in the isotope flow studies in 43% of the limbs. Angiograms were not used to assess patency, except in those few cases where PTA failed. The authors correctly pointed out the need of relieving the arterial spasm that occurs during below-the-knee angioplasty.3 Treiman et al., from Los Angeles, in a joint study performed by surgeons and radiologists, observed early recurrence of previously dilated stenosis as the main cause for early failure,
and deemed the clinical results from the procedures unsatisfactory.4 Their angiographic observation of locally recurrent stenosis formed the basis for later studies at the National Center for Limb Salvage, based on the insertion of tiny stents in the treatment of short occlusions and difficult stenosis. Appropriate medical treatment was also an issue and while Treiman et al. could not observe any benefit from the use of Persantine plus aspirin, Bull et al.5 emphasized the use of Coumadin: the drug was not recommended either in more recent studies or in our experience. Bull et al. also noticed a very poor success rate in angioplasty of completely occluded tibial segments.5 Lofberg et al.,6 reported a Swedish study from Uppsala on 94 infragenicular procedures performed on 82 patients, 90% of whom were in Fontaine stage IV, between 1989 and 1993. In this series, 196 PTAs were performed, involving either the infragenicular vessels only or both the infragenicular and femoral vessels. Seventy-one of the procedures were performed for complete occlusion (none longer than 5 cm below the knee and none longer than 10 cm above the knee). Patients were followed up at 6, 12, 24, and 36 months post-PTA: the primary clinical success rate was respectively 55, 51, 36, and 36%. The cumulative secondary clinical success rate was 44%, while limb salvage was 72% at 36 months. Clinical success was defined as a subjective improvement of symptoms and possibly an associated increase of ankle–brachial index of 0.10, based on the old reporting standards of the SVS-ISCVS (Society of Vascular Surgery-International Society for Cardiovascular Surgery), published in 1986. The presence of diabetes, preop ABPI (Ankle Brachial Pressure Index) < 0.2, and the type of lesion (occlusion vs. stenosis) did not affect long-term results. Performance of a surgical bypass, major amputation or death were considered endpoints in this study. Of the 82 patients, one patient had immediate bypass for acute ischemia post-PTA; 13 patients had elective bypass because of PTA occlusion at a mean 7.2 months post-PTA; and 20 patients underwent amputation at a mean 4.7 months after reocclusion of PTA. Of the remaining patients, 15 died during follow-up (10.8 months mean; range: 1–40 months). The remaining 34 patients were followed for mean 16.2 months (range: 1–60 months). Eventually, 34 out of the 82 patients (41%) were alive and had retained their limbs at a mean 16.2 months follow-up. The data from the Lofberg study pointed out both the efficacy of infragenicular procedures for limb salvage and the high mortality associated with severe peripheral vascular disease.6 633
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Table 72.1 ●
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Indications for infragenicular PTA
No suitable vein available for bypass Severe infection near the sites of planned anastomosis Poor general conditions and high surgical risk Short lesions Patient’s refusal of surgery Previously failed bypass Unavailability of highly skilled surgeon
ABPI, Doppler analysis, and clinical observation may be inaccurate in determining patency rates for the procedure, and the only certain determining factor of complete success is having been able to save a limb in a patient that is still alive, with digital subtraction angiography or NMR-angiography (Nuclear Magnetic Resonance Angio) showing patency of the vessels subjected to PTA or stenting. Brown et al., while reporting enthusiastic results on infragenicular PTA, observed dismal failure rates when PTA was associated with surgical bypass.7 In our series, when distal angioplasty was performed after bypass, results became excellent whenever stenting was used to support PTA of distal anastomoses or to warrant long-term patency of stenosed run-off arteries. Veith et al. supported the use of distal PTA in combination with bypass and confirmed the higher mortality of bypass (3.3% in their series) when compared with PTA.8 Fraser et al.9 in 1996, and Bakal et al.10 reviewed the literature on infragenicular PTA, observing how accurate selection of patients for PTA improved results. They also noticed that clinical results and limb salvage after PTA were higher than the patency rate, while in surgical bypasses, patency always exceeded limb salvage rate. Bakal et al.’s specifically emphasized the need for the achievement of a so-called “straight-line flow” to the foot to achieve a good outcome. We were unable to reproduce Bakal et al.’s findings in our studies and, in fact, we observed that straight-line flow to the foot is not a requirement to achieve long term patency and limb salvage, especially when stenting is utilized. We did notice that the status of distal run-off vessels is much less critical after infragenicular PTA than after surgical bypass in maintaining long-term patency. Fraser et al. observed that diabetic patients fared slightly worse than non-diabetic ones. Establishing limb salvage as a main goal instead of hemodinamic patency gave a significant push to the popularity of infra-genicular PTA, because it was repeatedly noticed that healed ischemic lesions do not often recur even if the dilated vessel restenoses in time.10 In 2001, in a paper published in Circulation, Dorros et al. reported data on 284 ischemic limbs treated with tibioperoneal angioplasty. Their initial success rate was 95% and clinical 5-year follow-up showed a 91% limb salvage rate. Major amputations were performed in 9% of patients but 8% of patients in this series required bypass surgery during follow-up. Their Fontaine stage IV patients had a 5-year survival rate of 33%, compared to the 58% of Fontaine stage III and 56% of the whole series (most cases were in Fontaine stage III). Their results point out the efficacy of infragenicular PTA, but also the need of attentive follow-up and general medical work-up to improve a dismal survival rate. Careful aggressive studies
and treatment of associated coronary, renal artery, and cerebrovascular diseases may significantly improve survival.11 Boyer et al., working in France, did a retrospective study on 49 patients who underwent 71 infrapopliteal PTAs. Immediate technical success was achieved in 91%, but two of the four failures required major amputation. Operative mortality was 2% and morbidity 16%. They reported an exceptional three-year limb salvage of 87% and a primary patency rate of 81% determined by duplex ultrasound.12 Söder et al., working in Finland, had a realistic 48% primary patency, 56% secondary patency, and 80% cumulative limb salvage at 18 months. Angiographic follow-up at 10 months showed a 32% rate of restenosis for arteries successfully treated for subocclusive disease and a higher 5% restenosis rate when completed occlusions had been successfully treated. Presence of renal insufficiency and failure to obtain angiographic improvement at the site of ischemia were independent predictors of poor long-term clinical results.13 Graziani and his collaborators in Italy, have performed a large number of infragenicular PTAs with success, and having cooperated with internists, diabetes specialists and surgeons, achieved encouraging rates of limb salvage at 14-month follow-up.14 Nasr et al. observed how, in their series, PTA had progressively replaced surgery, obtaining a limb salvage rate of 85% at 5 years, but still observing a high patient mortality of 55% in the same period of time.15 Bosiers et al. presented a large series of 443 patients with critical limb ischemia and infrapopliteal disease where PTA was used as primary treatment obtaining a 1-year primary patency of 74% and a limb salvage rate of 96%. The authors concluded that endovascular treatment will become the primary treatment for critical limb ischemia in infragenicular disease.16 Primary stenting seems to provide better results than simple PTA, as demonstrated by a multicenter prospective, blinded randomized study comparing PTA to balloonexpandable carbofilm-coated stents. In this study, 6-month primary patency was 84% with stenting and 61% without stenting (p < 0.05).17 Self-expanding nitinol stents with a low profile (4-French compatible sheath) has been successfully used in bailing out failed infrapopliteal PTAs with high 6-month patency rates.18 Elderly patients over 80 are at high risk when undergoing surgical procedures especially in view of the fact that they have multilevel arterial obstruction requiring extensive procedures. Atar et al., in their series of patients with a mean age of 83 (range: 80–94), obtained a 1-year limb salvage rate of 74% with wound healing achieved in 80% and rest pain improvement in 57%. These results were obtained in spite of the fact that only 15% of PTAs were clinically patent at 1-year follow-up. These results seem to support the view of aggressing endovascular treatment for infrainguinal and infrapopliteal disease in elderly patients in spite of poor patency rates.19 Salas et al. reported high limb salvage rates in a similar population of elderly patients, albeit noticing a relatively high peri-procedural mortality rate and a low 24-month survival rate due to severe associated co-morbidities in this group of patients.20 End stage renal disease (ESRD) is a most challenging co-morbidity when treating infra-popliteal disease. Aulivola et al. observed a lower success rate in wound healing in patients with ESRD when compared to patients without ESRD in the
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Infrapopliteal arterial diseases: angioplasty and stenting same series. ESRD patients had a three times higher major amputation rate (43 vs. 15% of non-ESRD patients).21 Drug-eluting stents are being investigated by several authors22,23 but definitive evidence of a superior performance in the long term, when compared to bare stents, has yet to be demonstrated by prospective randomized double blind studies. With increasing experience and refinements in the technique, infrapopliteal PTA with and without stenting has been used with success in treating claudication. In a prospective study published in 2005, Krankenberg et al. showed encouraging 12-month patency rates of 63% (primary), 82% (assisted), and 91.5% (secondary). The IWD (initial walking distance) increased from a baseline of 49 ± 34 up to 107 ± 67 meters. AWD (absolute walking distance) increased from a baseline 102 ± 88 meters up to 167 ± 74 meters (p < 0.0001 vs. baseline each). Twenty-five percent of patients in this study had stents implanted and 18% had excimer laser-assisted PTA.24
Technique Four different yet interlacing techniques are available for below-the-knee PTA. These are outline below. Transluminal simple PTA The patient is properly prepared with 250 mg ticlopidine twice a day starting at least 3 days prior to the procedure, plus coated aspirin 160 mg once a day. A complete selective diagnostic angiogram is performed. Under road-mapping, the ipsilateral common femoral artery or the superficial femoral artery is punctured antegrade, and a 4-French introducer is inserted. Heparin 5000 UI are given. Accurate magnified diagnostic angiograms are repeated in-current through this access. Stenoses are crossed with a 0.014-inch coronary straight high support guide (Choice PT Grafix), and are dilated with either short coronary balloons or longer, low-profile peripheral balloons (Invatec’s Submarine, Jomed’s Opera, BS’s Bijoux, Cordis’ Savvy, or Guidant’s Viatrak). Overstretching and excessive balloon diameters are avoided. The balloons are inflated at 6–14 atmospheres. When using coronary balloons, dilatation up to 24 atmospheres may help with resistant calcific lesions, and the most recalcitrant stenosis may require a low-pressure cutting balloon. Long occlusions can sometimes be reopened, thus obtaining direct flow to the foot. It is our policy to generally open only one out of three infragenicular vessels to avoid the risk of generalized thrombosis should complications occur: a leeway for emergency distal bypass should always be left open just in case things go very wrong. To advance a Choice PT Grafix through a long occlusion, the guide should never be pushed alone because it would coil and become useless. The guide is kept inside a rapid-exchange coronary balloon, usually 2 mm in diameter, and must be pushed just a few millimeters ahead of the tip of the balloon, which in turn must be advanced progressively. Coronary balloons have the lowest profile, and are the most useful in crossing difficult lesions. Longer low-profile peripheral balloons may later smoothen the inner wall of the vessel with a more homogeneous pressure over a long stretch. Balloons as long as 12 cm are used to obtain a smooth surface and to reduce the operator’s exposure to x-rays, because they require a smaller
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number of sequential inflations. Upon completion of the procedure, the introducers are immediately removed and 50 mg protamine are given to reverse heparin. Antiplatelet drugs are given for a long time: ticlopidine for the first 6 months at a dose of 250 mg QD and aspirin permenantly. In no case is post-op heparin given, either IV or subcutaneously (unless needed for other reasons: implanted heart mechanical valve, previous embolism, etc.). In terms of limb salvage, early clinical results with this technique are quite good, with prompt healing of the lesions and time to develop new collaterals and more resilient granulation tissue before the vessel reoccludes. Reocclusion is a problem, but doesn’t necessarily produce recurrence of symptoms. Published studies are generally unreliable when they consider a vessel as open by means of direct Doppler or improved distal ABPI: such data is not very reliable when evaluating post-PTA infragenicular vessels. Angiograms are the gold standard, and the reocclusion rate of simple, non-stented infragenicular PTA is very high in the treatment of completely occluded vessels, especially when the obstructed segment is long. Subintimal angioplasty Dr. Bolia, in Leicester, accidentally developed and then perfected a technique for subintimal angioplasty of the femoral artery, which he later applied to infragenicular vessels yielding positive clinical success. In a paper from 1994, he reported excellent early results in the recanalization of long occluded segments of tibioperoneal vessels using this technique.25,26 While the transluminal PTA requires a straight 0.014 guide which the operator attempts to keep centered in the vessel, in subintimal PTA a loop technique is used, and after exiting the lumen of the vessel above the obstruction, it is re-entered below it when feasible. Various techniques and specific endovascular instruments have been made available to facilitate re-entering the lumen distally, and recently Cordis has proposed a specifically designed catheter. In good hands, and with proper training and experience, this technique may reopen even the longest occlusions: long-term patency in most published studies has been evaluated with non-invasive means and, possibly, a long-term follow-up study employing arteriogram in order to demonstrate flow and lumen patency with certainty may provide more precise patency data. Limb salvage rates, however, are very encouraging, while initial failure rate remains high at 16%.27 An AV fistula may hiatrogenically develop during this procedure and a 0.8% incidence has been reported by Ananthakrishnan et al. and was successfully treated in 80% of cases with alternative dissection and stent placement, balloon tamponade, and coil embolization.28 Spot stenting While effective in presence of stenosis, simple PTAs show good clinical results but poorer anatomical ones in long-term follow-up of complete occlusions of tibioperoneal vessels. Spot stenting of complete occlusions seems to provide better results in terms both of patency and of limb salvage. There is the need for low French size stents, which must be selfexpandable because external compression is always possible in the calf and ankle. Nitinol stents, such as the 4-French Abbott
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XPERT and the 3-French SciMed RADIUS (now out of production), are quite suitable for this purpose. When necessary, even the dorsalis pedis can be successfully reached by positioning a 3mm stent. Stents should probably be inserted when cutting balloons are used, because when practiced alone this technique is generally followed by complete reocclusion of the vessel. A further possibility consist of inserting stents in a Y fashion at the tibioperoneal bifurcation (Figures 72.1 a and b). Long segment retro and infragenicular stenting This is an extreme limb salvage technique, once performed only when surgery was not feasible but recently being considered as primary procedure in limb salvage. Patients included in this group usually have long calcified occlusions, unsuitable for simple PTA because of recoil, dissection and unstability of plaque during flexion. The procedure should be performed by thoroughly trained operators using long, flexible stents. Nitinol appears to be the best material currently available, provided that stents with flexible cell strut design and with three interlinks are used. The Cordis SMART, while being an outstanding stent in rectilinear structures, bends unnaturally under flexion, due to its six-interlink system, which makes it very rigid and prone to early fracture under transversal
(a)
(b)
Figure 72.1 (a) Complete thrombosis of stenotic lesions in the infrapopliteal trifurcation; (b) thrombolysis, PTA and Y stenting.
flexion stress. Besides, six-interlink systems significantly reduce flow during knee flexion. Recent modifications made on the new 150 mm extra-long SMART stent made this device more flexible and apt to be inserted in proximity of the knee line. When multiple stents are used, they should be slightly overlapped and, upon completion of the procedure, a flexion angiogram should be performed to assure proper positioning and absence of kinks. Long-term results of over two years have angiographically demonstrated that primary patency is highest in non-diabetic patients, and lowest in diabetic women. Unlike surgical bypass, it appears that distal run-off is less determinant in causing early closure of sequential stenting, making this procedure a reasonable alternative when the most distal vessels are severely diseased. The retrogenicular segment of the popliteal artery is a very critical area where both PTA and stented PTA have often failed. Studies of the behavior of the popliteal artery during knee movement has shown a better way to choose and position stents in this area.29 Balloon-expandable stents are obviously excluded here, because they are liable to flexion, external compression, and deformation. Even self-expanding stents, to be delivered in the popliteal artery, need to be highly flexible. Boston Scientific’s Symphony and Bard’s Memotherm kink when flexed, and they are not appropriate for popliteal stenting. Cordis’s SMART, in its current version, has up to six interlacing links in its parallel rings structure. This partially limits the flexibility of the stent and produces excessive rigidity of the stented artery and a tendency to a premature fracture of the struts undergoing repeated flexion. Patients with retrogenicular implantation of the Cordis SMART stent have maintained patency for well over a year; in spite of strut fractures and temporary deformation of the stent under flexion. It is in any case preferable to utilize more flexible stents in this position, unless the newer extra-long and modified version of the SMART stent structure are used and their fatigue studies are made available for popliteal stenting. Abbott Xpert and Absolut, EV3 Protegé or Edward’s nitinol stent have less interring links, which make these devices extremely flexible and fit to being positioned behind the knee. These stents may still fracture, due to the long term fatigue that continuous knee flexion produces: however, they lend a better shape to the stented artery and they do not usually deform and kink unduly under flexion, maintaining a patent lumen throughout the movement cycle of the knee joint. Correct positioning of the stents, both in the proximal and distal part of the popliteal artery, will determine early and late patency. Positioning must be checked both in straight and flexed posture of the knee. This is needed because stents, looking perfect when seen on a straight knee angiography, may produce arterial distortion during flexion of the knee. This will cause kinking and obstruction of flow or damage to the intima followed by a rapidly progressing stenosis. A flexion angiography that, by reaching 90∞ angulations, shows eventual deformation of the arteries and kinking of the nitinol struts, will assess the correct positioning of the stent in each patient. Positioning of stents in the popliteal area has a high failure rate unless flexion angiography is done and ruled satisfactory (Figure 72.2a–e). Also, flexion angiography performed prior to the stenting procedure may help assess the natural bending of the vessel already impaired by the presence of heavily calcified plaques.
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(a)
(b)
(c)
(d)
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(e)
Figure 72.2 Demonstration of the need for a flexion angiogram when stenting behind the knee: (a) one stent above and one stent below the knee to treat two spot lesions; (b) perfect angiogram on a straight leg; (c) angiogram under flexion shows complete obstruction to flow; (d) insertion of two more stents to obtain sequential continuity; and, (e) final angiogram under flexion shows a satisfactory flow.
In a series of retrogenicular stents (popliteal and infrapopliteal) reported by Calabrese, early stent failure rate was as high as 50% when no flexion angiography had been done during the stenting procedure but a much better 5% when stents had been controlled under flexion. Thus flexion angiography becomes imperative when performing PTA or stenting in proximity of the knee line or whenever a long segment of femoropopliteal or infrapopliteal vessels are being stented.29 Infragenicular PTA is progressively replacing surgical bypass for limb salvage in selected patients and granted the application of strict criteria, results are very encouraging. Proper antiplatelet treatment, impeccable atraumatic coronary-type techniques, strict patient follow-up, and additional medical (control of diabetes, microbiologic workup and treat-
ment) and wound treatment (debridement, minor amputations, skin transplants), produce excellent limb salvage. The insertion of properly placed self-expanding nitinol stents promises to significantly improve patency in complete occlusions and may win a significant place in the treatment of recurrent stenotic lesions. Aggressive invasive studies of coronary, renal, and cerebrovascular circulation, along with the treatment of severe, if asymptomatic, arterial lesions, seem to promise an improvement of the current long-term dismal survival rates of patients with severe foot ischemia. In terms of survival, patency, and limb salvage, patients with chronic terminal renal failure provide the least encouraging results with the use of below-the-knee PTA.
REFERENCES 1. 2. 3. 4.
5. 6.
7.
Friedman SG, Safa TK. Pedal branches arterial bypass for limb salvage. Am Surg 2002; 68(5): 446–8 Brown K, Schoenberg N, Moore E, Saddekni A. Percutaneous transluminal angioplasty of infrapopliteal vessels: preliminary results and technical considerations. Radiology, 1988; 169(1): 75–8 Sivananthan U, Browne T, Thorley P, Rees M. Percutaneous transluminal angioplasty of the tibial arteries. Br J Surg 1994; 81(9): 1282–5 Treiman G, Treiman R, Ichikawa L, Van Allan R. Should percutaneous transluminal angioplasty be recommended for treatment of infrageniculate popliteal artery or tibioperoneal trunk stenosis ? J Vasc Surg 1995; 22(4): 457–65 1995 Bull PG, Mendel H, Hold M, Denck H. Distal popliteal and tibioperoneal transluminal angioplasty: long term follow-up. J Vasc Interv Radiol 1992; 3(1): 45–53 Löfberg AM, Lörelius LE, Karacagil S et al. The use of below-knee percutaneous transluminal angioplasty in arterial occlusive disease causing chronic critical limb ischemia. Cardiovasc Interv Radiology 1996; 19(5): 317–22 Brown KT, Moore ED, Getrajdman GI, Saddekni S. Infrapopliteal angioplasty: long-term follow-up. J Vasc Interv Radiol 1993; 4(1): 139–44
8. 9. 10. 11.
12. 13.
14.
Veith F, Gupta SK, Wengerter KR. Changing arteriosclerotic disease patterns and management strategies in lower-limb-threatening ischaemia. Ann Surg 1990; 212(4): 278–83 Fraser S, Al-Kutoubi A, Wolfe J. Percutaneous transluminal angioplasty of the infrapopliteal vessels: the evidence. Radiology 1996; 200(1): 33–6 Bakal CW, Cynaman J, Sprayregen S. Infrapopliteal percutaneous transluminal angioplasty: what we know. Radiology 1996; 200(1): 36–43 Dorros G, Jaff MR, Dorros AM, Mathiak LM, He T. Tibioperoneal (outflow lesion) angioplasty can be used as primary treatment in 235 patients with critical limb ischemia – five-year follow-up. Circulation 2001; 104(17) 2057–62 Boyer L, Therre T, Garcier JM et al. Infrapopliteal percutaneous transluminal angioplasty for limb salvage. Acta Radiol 2000; 41(1): 73–7 Söder H, Manninen H, Jaakkola P et al. Prospective trial of infrapopliteal artery balloon angioplasty for critical limb ischemia: angiographic and clinical results. J Vasc Interv Radiol 2000; 11(8): 1021–31 Faglia E, Mantero M, Caminiti M et al. Extensive use of peripheral angioplasty, particularly infrapopliteal, in the treatment of
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17. 18. 19. 20.
21.
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Textbook of peripheral vascular interventions ischemic diabetic foot ulcers: clinical results of a multicentrico study of 221 consecutive diabetic subjects. J Intern Med 2002; 252(3): 225–32 Nasr MK, McCarthy RJ, Hardman J, Chalmers A, Horrocks M. The increasing role of percutaneous transluminal angioplasty in the primary management of critical limb ischaemia. Eur J Vasc Endovasc Surg 2002; 23(5): 298–403 Bosiers M, Hart JP, Deloose K, Verbist J, Peeters P. Endovascular therapy as the primary approach for limb salvage in patients with critical limb ischemia: experience with 443 infrapopliteal procedures. Vascular 2006; 14(2): 63–9 Rand T, Basile A, Cejna M et al. PTA versus carbofilm-coated stents in infrapopliteal arteries: pilot study. Cardiovasc Intervent Radiol 2006; 29(1): 29–38 Tepe G, Zeller T, Heller S et al. Self-expanding nitinol stents for treatment of infragenicular arteries following unsuccessful balloon angioplasty. Eur Radiol 2007; 17(8): 2088–95 Atar E, Siegel Y, Avrahami R et al. Balloon angioplasty of popliteal and crural arteries in elderly with critical chronic limb ischemia. Eur J Radiol 2005; 53(2): 287–92 Salas CA, Adam DJ, Papavassiliou VG, London NJ. Percutaneous transluminal angioplasty for critical limb ischaemia in octogenarians and nonagenarians. Eur J Vasc Endovasc Surg 2004; 28(2): 142–5 Aulivola B, Gargiulo M, Bessoni M, Rumolo A, Stella A. Infrapopliteal angioplasty for limb salvage in the setting of renal failure: do results justify its use? Ann Vasc Surg 2005; 19(6): 762–8
22. 23.
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25. 26. 27. 28.
29.
Commeau P, Barragan P, Roquebert PO. Sirolimus for below the knee lesions: mid-term results of SiroBTK study. Catheter Cardiovasc Interv 2006; 68(5): 793–8 Siablis D, Kraniotis P, Karnabatidis D, Kagadis GC, Katsanos K, Tsolakis J. Sirolimus-eluting versus bare stents for bailout after suboptimal infrapopliteal angioplasty for critical limb ischemia: 6-month angiographic results from a nonrandomized prospective single-center study. J Endovasc Ther 2005; 12(6): 685–95 Krankenberg H, Sorge I, Zeller T, Tabler T. Percutaneous transluminal angioplasty of infrapopliteal arteries in patients with intermittent claudication: acute and one-year results. Catheter Cardiovasc Interv 2005; 64(1): 12–7 Bolia A, Sayers RD, Thompson MM, Bell PR. Subintimal and intraluminal recanalization of occluded crural arteries by percutaneous balloon angioplasty. Eur J Vasc Surg 1994; 8(2): 214–9 Varty K, Bolia A, Naylor A, Bell P, London N. Infrapopliteal percutaneous transluminal angioplasty: a safe and successful procedure. Eur J Vasc Endovasc Surg 1995; 9(3): 341–5 Markose G, Bolia A. Subintimal angioplasty in the management of lower limb ischaemia. J Cardiovasc Surg (Torino) 2006; 47(4): 399–406 Ananthakrishnan G, DeNunzio M, Bungay P et al. The occurrence of arterio-venous fistula during lower limb subintimal angioplasty: treatment and outcome. Eur J Vasc Endovasc Surg 2006; 32(6): 675–9 Calabrese E. Stenting below the knee in limb salvage: Long-term results. Am J Cardiol 2004; suppl. V 94: 7E
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Critical limb ischemia DE Allie, CJ Hebert, EV Mitran, CM Walker, and RR Patlola
Introduction Critical limb ischemia (CLI) is the end stage of lower extremity peripheral arterial disease (PAD). The recent guidelines define CLI as limb pain that occurs at rest or impending limb loss that is caused by severe compromise of blood flow to the affected extremity.1 The patients present with lower extremity rest pain, ulceration, or gangrene and a significant risk for limb loss. The wealth of knowledge on CLI as an integral part of the big chapter of PAD could be divided chronologically into two periods; namely (1) the accumulation of literature from the beginning until 1998 contributing to the TransAtlantic Inter Society Consensus (TASC) report published in 2000;2 and (2) the Guidelines for the Management of Patients With Peripheral Arterial Disease (Lower Extremity, Renal, Mesenteric, and Abdominal Aortic): A Collaborative Report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines covering the literature up to 2004 and published in March 2006.1 The names “critical limb ischemia,” “chronic critical limb ischemia,” and “chronic limb ischemia” have been used for this disease to date.1–5 In spite of the large volume of published data, CLI remains poorly characterized in the clinical literature due to a wide range of patient-to-patient variability. The Guidelines recommendations are all at the level of evidencebased medicine B and C, translating the lack of randomized clinical trials on CLI.1 In the last two years few such studies were initiated but hopefully their results will contribute to a level A evidence-based medicine for the CLI management.
Epidemiology The statistics revealed that at the beginning of the twentieth century, cardiovascular diseases (CVD) accounted for less than 10% of all death worldwide while at the beginning of the twenty-first century CVD accounts for nearly half of all deaths in the developed world, and 25% in the developing world.6 In this context, CVD needs to be treated as an “epidemic” and consequently PAD and CLI, intrinsic to CVD, could become global health problems. The recent literature on CLI shows great awareness. CLI has started to be defined as a global epidemic and to be discussed not only as a medical problem but as a public health problem at large medical gatherings
such as the Charing Cross Symposium and the first international multidisciplinary CLI Summit.7–10 CLI has a significant dimension in medical practice being bilateral and incurable. Unfortunately, there is a lack of data regarding CLI incidence and prevalence. The literature reports a CLI incidence between 500–1000 cases per million per year.11 The prevalence in the US is 1% in the population older than 50 years and approximately 2% in the population older than 70 years.12 In patients with PAD, when lesion obstruction exceeds 50% it may cause intermittent claudication; estimates of the prevalence of intermittent claudication vary by population, from 0.6% to nearly 10%. Approximately 20–25% of patients will require revascularization, while fewer than 5% will progress to CLI.13 The reports on amputations due to CLI reveal a number of greater than 150,000–200,0000 major and minor lower extremity amputations in the US and Europe yearly.14 The amputation rate in the US has increased from 19 to 30 per 100,000 persons over the last two decades, primarily due to diabetes and an ageing population.14 In the population over 85 years of age the amputation rate is 140 per 100,000 persons per year with a mortality rate of 13–17%.14 When referring to CLI in diabetics, statistics show that one out of every four diabetics will face CLI within their lifetime, and those with CLI will have a 7–40 times greater risk of amputation.15 An amputation is a marker for death as the 3–4 year mortality post-amputation is > 50–60%.2,12
Clinical presentation The clinical categories of CLI indicating the progress from asymptomatic PAD to CLI are presented by Creager and Libby16 as recommended by Rutherford et al. (Table 73.1). Rutherford’s 1997 “standards for reports” are today used in clinical practice.4 The pathophysiology of CLI is determined by the abnormal microcirculation. As was hypothesized by Creager and Libby, based on the literature, several factors could be contributory to CLI, for example a reduced number of skin capillaries, decreased capillary perfusion, reduced blood cell deformability, increased leucocytes adhesivity, platelet aggregation and fibrinogen, microthrombosis, excessive vasoconstriction, and interstitial edema.16 Infrainguinal arterial blockages are the most common etiology of claudication and critical limb ischemia (CLI). The superficial femoral (SFA) and popliteal arteries (PA) pose interventional challenges. Longitudinal occlusions are common. These vessels elongate, foreshorten, bend, torque, and are externally compressible. Lesions are 639
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Table 73.1
Rutherford–Becker classification4
Category Clinical description
Objective criteria
0 1
Normal treadmill* or reactive hyperemia test
3
Asymptomatic – no hemodynamically significant occlusive disease Mild claudication Moderate claudication Severe claudication
4
Ischemic rest pain
5
Minor tissue lossnon-healing ulcer, focal gangrene with diffuse pedal ischemia Major tissue lossextending transmetatarsally; functional foot no longer salvageable
2
6
Completes treadmill exercise; AP after exercise > 50 mmHg but > 20 mmHg lower than resting value Resting AP < 60 mmHg, ankle or metatarsal PVD flat or barely pulsatile; TP < 40 mmHg Resting AP < 60 mmHg, ankle or metatarsal PVD flat or barely pulsatile, TP < 40 mmHg
Surgical bypass techniques are used in the treatment of distal diffuse arterial occlusion. Despite limitations, infrainguinal endovascular intervention has dramatically increased as primary therapy as well as post-failure surgical intervention for claudication and CLI. New endovascular tools are being developed to cross occlusions, remove thrombus, and open vessels. Crossing long total occlusions is challenging. There have been several devices developed for crossing when available guidewires and catheters fail. A guidewire using optical reflectometry for guidance and radiofrequency ablation to cross is being evaluated.18 Excimer laser catheters (CliRpath, Spectranetics, Colorado Springs, CO) advanced via a “step by step” technique are also used for crossing.8,19 Blunt dissection devices (Frontrunner XP CTO Catheter System, LuMed, Johnson & Johnson, Piscataway, NJ) mechanically spread the lumen of the vessel to allow crossing.20 Re-entry tools with or without ultrasonic guidance allow the interventionalist to puncture back into the vessel lumen.21 Devices to mechanically remove the clot alone or in conjunction with thrombolytics are crucial. Some devices actually aspirate thrombus, others macerate then aspirate, and the excimer laser photoablates the thrombus.14,19,22,23 Balloons, atherectomy devices, and stents are the therapeutic cornerstones: ●
AP = ankle pressure; PVR = pulse volume recording; TP = toe pressure. *Treadmill protocol: 2 miles per hour, 12% constant grade. ●
often calcified. Acute and chronic thrombosis are common. The infrapopliteal vessels (IP) are smaller, lesions often involve branch points, and the vessels are much less dynamic. The risk factors for CLI are those of general atherosclerosis: cigarette smoking, diabetes mellitus, dyslipidemia, hypertension, hyperhomocysteinemia, increased fibrinogen and high level of C-reactive protein, obesity, and metabolic syndrome. Symptoms of CLI are pain at rest, non-healing ulcerations, and gangrene. The pain manifests as a burning pain in the ball of the foot and toes, increased in intensity at night when the patients are lying down. Often patients need to dangle the legs over the side of the bed to relieve the pain, this position leading to edema of feet and ankles. One objective sign is pallor of the foot with elevation and rubor on dependency. The nonhealing wounds are found in the areas of foot trauma due to improper fitting shoes or to injury. Gangrene follows necrosis and is usually present on the toes. The battery of tests to establish the diagnosis of CLI as recommended by the Guidelines is presented in Figure 73.1.1 The diagnosis of CLI is based on the following hemodynamic parameters: an ankle–brachial index of 0.4 or less; an ankle systolic pressure of 50 mmHg or less; and a toe systolic pressure of 30 mmHg or less.
Treatment At the present there is no single optimal treatment or “gold standard” for CLI patients.17 Revascularization, either surgical or endovascular, aims to relieve pain, heal the wounds, and prevent amputation. The gold standards: open surgical revascularization, endarterectomy, or surgical infrainguinal bypass, are increasingly replaced at present by endovascular therapy.
●
Balloons: in addition to standard balloons, cutting balloons, and cryoballoons are being evaluated to lessen dissection and future intima hyperplasia.24,25 Atherectomy: directional plaque excision allows directed excision and removal of plaque (up to 6 mm) (SilverHawk® catheter, Fox Hollow Technologies, Redwood City, CA).26,27 Stents: in the SFA and popliteal arteries self-expanding nitinol stents are used. Stents may be bare metal, medicated, or covered. At the time of writing, several FDA-approved stents for PAD in the limbs include the Zilver vascular stent (Cook, Bloomington, IN, 2006), Viabahn endoprosthesis (W.C. Gore & Associates, Newark, DE, 2005), Intrastent stent (EV3, St. Paul, MN, 2004), SMART and SMART Control nitinol stent system (Cordis, Warren, NJ, 2003), Intra Coil self-expanding peripheral stent (Sulzer Intratherapeutics, St Paul, MN, 2002), Wallstent iliac endoprosthesis (Boston Scientific, Natick, MA, 1996), Palmaz balloon-expandable stent (Cordis, Warren, NJ, 1991). Stents that are longer, more flexible, and more fracture-resistant, can achieve better wall apposition, and be more accurately delivered are all being developed. There is great interest in what role medicated stents may have but there are no FDA-approved drug-eluting stents for limb vessels.28,29
The results of three clinical trials published in 2006 (Laser Angioplasty for Critical Limb Ischemia (LACI), Catheter-Based Plaque Excision with SilverHawk® in Critical Limb Ischemia, and Percutaneous Transluminal Angioplasty for Treatment of “Below-the-Knee” Critical Limb Ischemia, all using endovascular therapy in CLI patients, concluded the following. ●
●
The excimer laser angioplasty for CLI offers high technical success and limb salvage rates in patients unfit for traditional surgical revascularization. The catheter-based plaque excision is a safe and effective revascularization method for patients with CLI.
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Legulcer/Restpain/Gangrene Rutherford 4–6
Confirm ischemic etiology (differential diagnosis; noninvasive tests [ABI, duplex, 16–64 slice CTA])
Assess and treat co-existing disease if appropriate: cardiovascular disease, diabetes, anemia, pulmonary disease, local infection, systemic disease, etc. Appropriate limb salvage consultations for revascularization: podiatry, wound care, plastics, reconstruction, etc.
Leg potentially salvageable (> 85–90%)
Leg not salvageable (irreversible gangrene above level of the forefoot, institutionalized and nonmobile, vascular anatomy precludes successful intervention [rare])
Image arterial lesions: Duplex 16–64 slice CTA Angiography
Primary amputation (80 years of age. A meta-analysis of four DBS reports published since 2001 reveals a 5-year LS rate of 65–78.1% in 1619 CLI patients (68–100% diabetic).38–41 In a landmark article, Pomposelli et al. reported a decade’s experience with pedal bypass in 1032 CLI patients (92% diabetic) with excellent 5- and 10-year LS rates of 78.1 and 59.8% respectively.41 It must be noted that these reports were from experienced institutes committed to LS. An analysis by Hunick et al. of 4511 patients treated with DBS revealed a 5-year patency rate of 66% in CLI with
(a)
(b)
(c)
(d)
Figure 73.2 (a) Occluded 2.5 mm posterior tibial artery with “fresh” thrombus. Thrombus extracted using the Fogarty thrombectomy balloon catheter. Note this simple but elegant technology was the first of all endovascular devices; (b) Successful distal anastamosis (autogenous vein); (c) Note the metallic anastomotic graft marker which should always be placed on all anastomosis as this will facilitate future interventions by decreasing fluoroscopic time and contrast use and assist in locating grafts and “graft take-offs”; (d) angiogram demonstrating excellent patency with good posterior tibial runoff to the tarsal branches.
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Critical limb ischemia available venous conduits and 75% 5-year LS (Figure 73.2).42 Samples of other studies with a mixture of conduits reveal 1-year patency rates from 33 to 92% and 5-year patency rates from 38 to 80%.43,44 Clearly considering inconsistencies in these DBS results, the known limitations of DBS, the recent improvement in percutaneous endovascular revascularization (PER) technology/results and the fact that PER does not take away surgical options, it now may be time to debate the issue of the true contemporary “gold standard” or initial treatment for CLI treatment.
PTA only or PTA plus stenting in CLI Improvements in wires, balloons, CTO crossing and re-entry catheters, and stents have resulted in increased PER utilization and improved outcomes in CLI. Subintimal angioplasty has shown high (80–90%) PS rates and LS rates of > 85% but this complex technique has not gained widespread use beyond a few committed centers and the results have not been consistently reproducible. PTA-only data in CLI is sparse and nonstandardized but several conclusions can be drawn. Dorros et al. reported tibial PTA as a primary treatment in 235 CLI patients with a 91% 5-year LS rate with low complications.45 In a metaanalysis of 5 PTA reports treating 702 CLI patients, the LS rates are 79–91% with low complication and acceptable reintervention rates (9–15%) and DBS rates (2–15%).45–49 Faglia et al. recently reported PTA as the first choice in PER in 993 diabetics with CLI. During 26 ± 15-month follow-up, 1.7% underwent major amputation with 87/993 (8.8%) experiencing clinical restenosis. A 5-year primary clinical patency rate of 88% was reported.50 Kudo and Ahn et al. very recently reported a 10-year PTA experience in 111 CLI patients with 0.9% peri-procedural mortality and initial technical and clinical success of 96.4 and 92.8%, respectively.51 The 5-year primary patency, assisted patency, and secondary patency were 31.4, 75.5, and 79.6% respectively. The 5-year LS rate was 89.1% concluding that PTA was safe and effective and potentially the primary treatment for CLI.51 The role of IPA stenting is expanding after poor initial experiences without dedicated tibial stents. Biamino et al. reported a 44.2% primary patency and 80% primary-assisted patency in 51 patients treated with 3–4 mm bare metal (BMS) coronary stents but with > 90% LS.52 The role of dedicated drug-eluting stents (DES) and absorbable metal stents (AMS) are now being explored. Scheinert et al. treated 30 IPA with sacrolimus-coated DES (3.0–3.5 mm) versus 30 BMS and found no difference in 6-month angiographic restenosis (60.9 vs. 56.5%, p = NS).53 More recently, another 60 CLI patients were similarly treated comparing BMS (n = 30) to sirolimus-coated stents (n = 30) with a significant difference in favor of DES.53 Peeters and Bosiers et al. have recently investigated magnesium AMS in the IPA and reported 100% PS in 20 CLI patients with a 6-month clinical patency rate of 78.9% and LS of 94.7%.54 A US phase I study is planned.
Laser application in CLI The pioneering laser work of Professor Giancarlo Biamino has led to an understanding of the unique thrombus and
643
atheroablative properties of pulsed excimer laser angioplasty (ELA) in contrast to earlier (now abandoned) continuous wave thermal lasers. The excimer laser is now a viable option in treating CLI. The landmark Laser Angioplasty for Critical Limb Ischemia (LACI) trial represents one of the only organized multicenter trials addressing the true CLI patient population and even today this trial has not received the true credit it deserves. The LACI trial enrolled 155 CLI limbs with 423 lesions in 15 US and German sites.55 All patients were considered poor or non-surgical candidates with high co-morbidities (Rutherford class 4 = 29%, and 5–6 = 71%). The arteries treated included SFA (41%), PA (15%), and IPA (41%) with ~ 50% requiring multivessel ELA.55 The LACI phase 2 results included a procedural success (PS) of 90%; a 99% rate ELA (and this despite 8% failed wire crossing therefore the “step-by-step technique” was utilized (Figure 73.3a); an adjuvant PTA of 96% and stent rate of 45% overall (SFA = 61%, PA = 38%, and IPA = 16%); straight line flow to the foot of 89%; 6-month LS of 93% with very low peri-procedural complications (10% overall adverse events at 6 months); and a 6-month reintervention rate of 16% with 2% requiring DBS.55 The LACI trial demonstrated that PER in CLI can achieve high PS and 6-month LS rates (93%) in very fragile and complex CLI patients with very low complication and reintervention who had no other surgical option. Similar results have been reported recently in the Belgium LACI and the CIS LACI equivalent studies.56,57
Plaque excision in CLI The SilverHawk® plaque excision (PE) catheter (FoxHollow Technologies, Redwood City, CA) is a device that allows PE and retrieval without barotrauma (Figure 73.3b). The first-generation device was larger profile and better suited for the SFA and PA with a 12-month clinical primary patency of 86.8% and primary-assisted patency of 100% with 94% LS recently reported by Ramaiah et al.58 Adjuvant PTA/stenting was reported in only 8.6%. Similar SFA results are reported by other single centers and in the TALON Registry, which is a multicenter, prospective, non-randomized observation outcomes registry collecting data on PE in treating infrainguinal disease.59 Overall, the early TALON SFA experience can be characterized by safety with low complications (0.7% perforation, dissection A/B = 2.5% and ≥ C = 0.5%, and no thrombosis or embolization), high PS (> 95%), 6-month TLR rate of 11%, and low stent use (4.7%).59 The new lower profile catheters have further expanded PE into CLI and tibial arteries. The 12-month TALON data in 505 patients with 1047 lesions report CLI (Rutherford ≥ 5) in 14% with 25% overall IPA lesions treated. Standalone PE was used in 74% with stenting in 5.3%. Kaplan–Meier analysis demonstrated overall 12-month freedom from TLR of 80%, 90% in IPA lesions.60 The conclusion at a recent PE CLI summit was that PE is safe and is an emerging effective “tool” in treating CLI. As is true with all CLI treatments, the need for a more clinical and objective (DSA-CTA) long-term follow-up was recognized and is being highly anticipated.
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(a)
(b)
(c) Figure 73.3 (a) Excimer laser catheter demonstrating the “step-by-step technique” to cross a total occlusion using laser atheroablative properties; (b) SilverHawk® PE catheter demonstrating plaque apposition and excision which is accomplished by a motorized carbide cutter blade with the plaque collected in the distal nosecone chamber; (c) The PolarCath demonstrating the dual balloon chambers and the four steps of the cryoplasty procedure.
Cryoplasty in CLI Medical cryotherapy has been used since the late 1960s, primarily in cryosurgery where extreme cold (–10∞/20∞ C) eliminated tissue (tumors, etc.) but only since 1997/1998 has a vascular application been considered even though clinically arteries are known to be relatively immune to cold. The PolarCath (Boston Scientific, Natick, MA) is a novel PTA system that simultaneously dilates and rapidly cools from 37∞ C to –10∞ C the immediate tissue within contact to a known depth of only 500 µm therefore avoiding deep wall injury with less dissection. The “freezing” occurs by the controlled inflation (20 seconds) of a duel balloon system with nitrous oxide instead of saline/contrast and this triggers a controlled form of dilation and smooth muscle cell death, apoptosis, that results in less elastic recoil and negative (constrictive) remodeling, and less inflammatory response therefore less cell proliferation (less neointimal hyperplasia). Overall this results in less dissections and less need for stent use in this more controlled plaque fracture–microfracture
environment (8 atmospheres pressure, 25 seconds dwell time, and –10∞ C temperature) (Figure 73.3c). One of the intriguing aspects of cryotherapy is that for the first time we may be delivering a true “biologic” treatment to the vessel wall that may result in positive remodeling and outcomes. The PolarCath received FDA approval for use in the SFA and PA in September 2002 after a 15-site US and German multicenter registry reported results in 102 patients.61 The PS was 96% with 87% receiving standalone therapy and 9% requiring stenting. Only 7% reported dissections > type C. At 9 months, 15% required reintervention with a clinical patency of 85%.61 Fava et al. reported 15 patients with SFA and PA lesions with a PS rate of 93% and 6- and 18-month angiographic primary patency to be 100 and 83% respectively.62 Moran et al. reported cryoplasty in IPA results in 20 CLI patients with 26 lesions. Six of the 26 lesions received adjuvant pretreatment with either PE or laser atherectomy.63 The PS was 95% with a 95% LS and freedom from major amputation rate reported. The recent release of smaller diameter (2.5–4.0 mm) and longer length small balloons (20–60 mm) has facilitated the
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(a)
(b)
(c)
(d)
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(e) Figure 73.4 64-slice CTA demonstrating total occlusion of a calcified SFA and distal PA just distal to a patent bypass graft; (a) Note the patent run-off vessels; (b) DSA demonstrating the flush PA occlusion. The lesion was crossed with an 0.018-inch guidewire and 2.0 mm laser; (c) A PolarCath was then positioned across the remaining lesion; (d) PolarCath balloon inflation; (e) Excellent immediate results combining laser debulking followed by cryoplasty. (See Color plates.)
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PolarCath options in treating CLI. Currently the multidisciplinary, multicenter Below the Knee Chill “Big Chill” trial is prospectively enrolling non-randomized CLI patients in a registry to further evaluate cryoplasty and outcomes with data forthcoming late 2005. Our own CIS early (3-months) data was presented recently at a PolarCath CLI Summit in which 16 patients with 29 IPAs were treated with 8/16 total occlusions requiring lesion pretreatment with laser (6) and PE (2) (Figure 73.4a–e). The PS and 3-month LS was 100% with no complications, no ≥ C dissections, and no stents.
Conclusion Contemporary CLI treatment is in a stage of rapid evolution with several novel devices and strategies now available to physicians. A low threshold for obtaining early, non-invasive CTA imaging for both diagnosis and treatment planning is advised. It has been estimated that < 50% of patients with primary amputations receive preamputation vascular imaging
for revascularization and < 20% DSA.15 Additionally, it has been estimated that < 50% of CLI patients undergoing an amputation are even referred for a consideration of revascularization before primary amputation.15 Assuredly, even less African American patients with CLI get referred for LS. This is simply not acceptable today, especially when considering the availability of various diagnostic modalities, the safety and efficacy of the emerging “tools” to accomplish PVI, and the multiple recent reports of excellent (> 85–90%) 3–5 year LS rates with both DBS and PVI. We are in the midst of a major paradigm shift in which CLI can and should be treated aggressively starting with the diagnosis and novel revascularization strategies, to the multidisciplinary referral and necessary follow up of this complex patient population. Just 3–4 short years ago our “tool box” for treating CLI was relatively bare compared to today. The contemporary CLI “tool box” is armed with multiple novel PVI technologies and strategies that often can and should be used in conjunction, all enabling the clinician to provide the CLI patient with a much higher likelihood of limb salvage.
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Hirsh AT, Haskal ZJ, Hertzer NR et al. ACC/AHA Guidelines for the Management of Patients With Peripheral Arterial Disease (Lower Extremity, Renal, Mesenteric, and Abdominal Aortic): A Collaborative Report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice. J Am Coll Cardiol 2006; 47(6): 1239–312 TransAtlantic Inter-Society Consensus (TASC): Management in peripheral arterial disease (PAD). J Vasc Surg 2000; 3(2) suppl. 1 Dormandy J, Verstraete M, Andreani D et al. Second European consensus document on chronic critical leg ischemia. Circulation 1991; 84 (suppl. 4): 1–26 Rutherford RB, Baker DJ, Ernst C et al. Recommended standards for reports dealing with lower extremity ischemia: Revised version. J Vasc Surg 1997; 26(3): 517–38 Shammas NW, Dippel EJ. Evidence–based management of peripheral vascular disease. Curr Atheroscler Rep 2005; 7: 358–63 Gaziano MI: Global burden of cardiovascular disease. In: Braunwald’s Heart Disease, seventh edition. 2005, 1–26 Allie DE, Hebert CJ, Lirtzman MD et al. Critical limb ischemia: a global epidemic. a critical analysis of current treatment unmasks the clinical and economic costs of CLI. EuroIntervent J 2005; 1(1): 75–84 Allie DE, Hebert CJ, Lirtzman MD et al. Adjunctive bioengineered bi-layered cell therapy (apligraf) with excimer laser revascularization improves wound healing and limb salvage in critical limb ischemia. Vasc Dis Manag 2006; 185–92 Biamino G. Critical limb ischemia “a global epidemic”. Shocking recent data reveal the impact of amputations. First CLI International Summit, Miami, Florida, October 26–27, 2005 <www.newcvhorizons.com/site2.ph> Allie DE. The first international CLI Summit on lower extremity PVD and critical limb ischemia. New cardiovascular horizons and management of the diabetic foot & wound healing. Interview: Meetings Corner, Vascular Disease Management, September/ October, 2005, A30–A33 Novo S, Coppola G, Milio G. Critical limb ischemia: definition and natural history. Curr Drug Targets Cardiovasc Haematol Disord 2004; 4(3): 219–25 Jaff MR, Biamino G. An overview of Critical Limb Ischemia, Endovasc Today 2004: 45–8 Garcia LA. Epidemiology and pathophysiology of lower extremity peripheral arterial disease. J Endovasc Ther 2006; 13(suppl. 2), II3–9 David E. Allie MD, Hebert CJ, Walker CM. Excimer laser-assisted angioplasty in severe infrapopliteal disease and CLI: The CIS “LACI Equivalent” Experience. Vasc Dis Manag 2004; 14–22
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Akbari CM. Diabetes and critical limb ischemia. Endovasc Today 2004: 66–9 Creager MA, Libby P. Peripheral arterial disease. In: Braunwald’s Heart Disease, seventh edition. 2005: 1437–61 Bosiers M, Deloose K, Verbist J et al. Percutaneous transluminal angioplasty for treatment of “below-the-knee” critical limb ischemia: early outcomes following the use of sirolimus-eluting stents. J Cardiovasc Surg (Torino), 2006; 47(2): 171–6 Kirvaitis RJ, Heuser RR, Das TS et al. Usefulness of optical coherent reflectometry with guided radiofrequency energy to treat chronic total occlusions in peripheral arteries (the GRIP trial). Am J Cardiol 2004; 94(8): 1081–4 Biamino G: The excimer laser: science fiction fantasy or practical tool? J Endovasc Ther 2004; 11 (suppl. 2): II207–22 Orlic D, Stankovic G, Sangiorgi et al. Preliminary experience with the Frontrunner coronary catheter: novel device dedicated to mechanical revascularization of chronic total occlusions. Catheter Cardiovasc Interv 2005; 64(2): 146–52 Saketkhoo RR, Razavi MK, Padidar A et al. Percutaneous bypass: subintimal recanalization of peripheral occlusive disease with IVUS guided luminal re-entry. Tech Vasc Interv Radiol 2004; 7(1): 23–7 Zehnder T, Birrer M, Do DD, Baumgartner I et al. Percutaneous catheter thrombus aspiration for acute or subacute arterial occlusion of the legs: how much thrombolysis is needed? Eur J Vasc Endovasc Surg 2000; 20(1): 41–6 Wildberger JE, Haage P, Bovelander J et al. Percutaneous venous thrombectomy using the Arrow-Trerotola percutaneous thrombolytic device (PTD) with temporary caval filtration: in vitro investigations. Cardiovasc Intervent Radiol 2005; 28(2): 221–7 Albiero R, Silber S, Di Mario C et al. RESCUT Investigators. Cutting balloon versus conventional balloon angioplasty for the treatment of in-stent restenosis: results of the restenosis cutting balloon evaluation trial (RESCUT). J Am Coll Cardiol 2004; 43(6): 943–9 Joye JD. Clinical application of CryoPlasty therapy. Chapter 3: CryoPlasty Therapy. In: Cryoplasty Therapy: New Treatment Strategies for Infrainguinal Disease and Critical Limb Ischemia. HMP Communications, March 31, 2006: 24–26 Favero L, Simpson JB, Reimers B. Treatment of an ostial and a bifurcation lesion with a new directional atherectomy device. Heart 2004; 90(8): e46 Pershad A, Stevenson J. Directional atherectomy with the SilverHawk plaque excision device in the treatment of a proximal subclavian-vertebral artery stenosis in coronary-subclavian steal syndrome (CSSS). J Invasive Cardiol 2004; 16(12): 723–4 Duda SH, Bosiers M, Lammer J, Scheinert D et al. Sirolimuseluting versus bare nitinol stent for obstructive superficial femoral artery disease: the SIROCCO II trial. J Vasc Interv Radiol 2005; 16(3): 331–8
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Oliva VL, Soulez G. Sirolimus-eluting stents versus the superficial femoral artery: second round. J Vasc Interv Radiol 2005; 16(3): 313–5 Laird JR, Zeller T, Gray BH et al: LACI Investigators. Limb Salvage following laser-assisted angioplasty for critical limb ischemia: results of the LACI multicenter trial. J Endovasc Ther 2006; 13 (1): 1–11 Kandzari DE, Kiesz RS, Allie DE et al. Procedural and clinical outcomes with catheter-based plaque excision in critical limb ischemia. J Endovasc Ther 2006; 13: 12–22 Bosiers M, Deloose K, Verbist J et al. Percutaneous transluminal angioplasty for treatment of “below-the-knee” critical limb ischemia: early outcomes following the use of sirolimus-eluting stents. J Cardiovasc Surg (Torino) 2006; 47(2): 171–6 Allie DE, Hall PA, Shammas NW et al. Bivalirudin in peripheral interventions. Results of the APPROVE trial and emerging role of “endopharmacology” in treating PVD. Endovasc Today 2005: 27–32 Allie DE, Hebert CJ, Lirtzman MD et al. A safety and feasibility report of combined direct thrombin and GP IIb/IIIa inhibition with bivalirudin and tirofiban in peripheral vascular disease intervention: “treating critical limb ischemia like acute coronary syndrome”. J Invas Cardiol 2005; 17(8): 427–32 Yost, ML. Peripheral Arterial Disease: A Report by The Sage Group, 2004, vol. II Transatlantic Inter-Society Consensus (TASC) on Management of Peripheral Arterial Disease (PAD). J Vasc Surg 2000; 31: S271 Transatlantic Inter-Society Consensus (TASC) on Management of Peripheral Arterial Disease (PAD). J Vasc Surg 2000; 31: 1–296 Kalra M et al. Limb salvage after successful pedal bypass grafting is associated with improved long-term survival. J Vasc Surg 2001; 33: 6–16 Curi MA et al. Long-term results if infrageniculate bypass grafting using all-autogeneous composite vein. Annals Vasc Surg 2002; doi: 10.1007/s10016-001-0266-6 Toursarkissian B et al. Early duplex-delivered hemodynamic parameters after lower extremity bypass in diabetics: implications for mid-term outcomes. Annals Vasc Surg 2002; doi: 10.1007/ s10016-001-0272-8 Pomposelli FB et al. A decade of experience with dorsalis pedis artery bypass: Analysis of outcome in more than 1,000 cases. J Vasc Surg 2003: 37; 307–15 Hunick MG, Wong JB et al. Revascularization for femoropopliteal disease. A decision and cost-effectiveness analysis. JAMA 1995; 274: 165-171 Gonzalez-Fajardo JA, Vaquero C. Femorocrural bypass for limb salvage: real indications and results. In: Branchereau A, Jacobs M, eds. Critical Limb Ischemia. New York: Futura, 1999: 167–72 Krajewski LP, Olin JW. Atherosclerosis of the aorta and lower extremity arteries. In: Young JR, Lin JW, Bartholomew JR, eds. Peripheral Vascular Disease, second edition. St. Louis: Mosby, 1996: 227 Dorros G, Jaff MR. Tibioperoneal (outflow lesion) angioplasty can be used as primary treatment in 235 patients with critical limb ischemia. Circulation 2001; 104: 2057–62 Soder HK et al. Prospective trial if infrapopliteal artery balloon angioplasty for critical limb ischemia: Angiographic and Clinical Results. JVIR 2000; 11: 1021–31 Danielsson G et al. Percutaneous transluminal angioplasty of crural arteries: diabetes and other factors influencing outcome. Eur J Vasc Surg 2001; 21: 432–6
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Lofberg AM et al. The use of below-knee percutaneous transluminal angioplasty in arterial occlusive disease causing chronic critical limb ischemia. Cardiovasc Intervent Radiol 1996; 19: 317–22 Matsi JJ et al. Impact of risk factors on limb salvage after angioplasty in chronic critical lower limb ischemia. Angiol 1994; 45: 797–804 Faglia E, Dalla Paola, L Clerici G et al. Peripheral angioplasty as the first-choice revascularization procedure in diabetic patients with critical limb ischemia: prospective study of 993 consecutive patients hospitalized and followed between 1999–2003. Euro J Vasc Endovasc Surg 2005; 29(6): 620–7 Kudo T, Chandra FA, Ahn SS. The effectiveness of percutaneous transluminal angioplasty for the treatment of critical limb ischemia: a 10-year experience. J Vasc Surg 2005; 41(3): 423–35 Biamino, G. Tibioperoneal stenting: new recanalization tools and techniques, including debulking and stenting, allow for the treatment of very complex lesions in the challenging infrageniculate region. Endovasc Today 2004; 3(2): 58–60 Scheinert D, Schmidt A, Biamino G. Are drug-eluting stents better in tibial stenting? Presented at the International Congress XVIII Annual Meeting, February 2005; <www.endovascularcongress.org> Peeters P, Bosiers M, Verbist J. The answer for infrapopliteal lesions is absorbable metal stents. Presented at the International Congress XVIII Annual Meeting, February 2005; <www.endovascularcongress.org> Laird JR, Laser angioplasty for critical limb ischemia (LACI): Results of the LACI phase 2 clinical trial. Presented at the ISET Annual Meeting, January 2003; <www.iset.com> Bosiers M, Peeters P, Elset FV. Excimer laser-assisted angioplasty for critical limb ischemia: results of the LACI Belgium Study. Eur J Vasc Endovasc Surg 2005; 29(6): 613–9 Allie, DE, Hebert, CJ, Walker, CM. Excimer laser-assisted angioplasty in severe infrapopliteal disease and CLI: The CIS “LACI Equivalent” Experience. Vasc Dis Man 2004: 14–22 Ramaiah V. One-year results of SilverHawk atherectomy of the SFA: Have we tamed the SFA? Presented at International Congress XVIII Annual Meeting, February 2005; <www.endovascularcongress.org> Gammon R, Fail PS, Walker CM et al. Early results from the treating peripherals with SilverHawk: Outcomes Collection (TALON) Registry. Am J Cardiol 2004; 94 (suppl. 6A): 184E Ramaiah VG, Gammon RS, Kiesz S et al. Mid-term results from TALON: A Prospective, multi-center registry on infrainguinal plaque excision. Presented at the Society of Vascular Surgery Annual Meeting, June 2005; <www.vascularweb.org> Laird JR. Interim results of the Cryovascular peripheral balloon catheter system safety registry. Presented at the Annual Meeting of the Society of Radiology. April 2003 Fava M, Loyola S, Polydorou A et al. Cryoplasty for femoropopliteal arterial disease: late angiographic results in initial human experience. J Vasc Interv Radiol 2004; 15: 1239–43 Moran M, Joye J. Cryoplasty for critical limb ischemia: initial below-the-knee results. Am J Cardiol 2004; 94(6): suppl. 7E Allie DE, Hebert CJ, Lirtzman, MD et al. Critical limb ischemia: a global epidemic. A critical analysis of current treatment unmasks the clinical and economic costs of CLI. Eur Interv 2005: 1(1): 75–84
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Acute limb ischemia DE Allie, CJ Hebert, EV Mitran, CM Walker, and RR Patlola
Introduction Defined as most challenging, catastrophic, threatening, or extremely serious vascular event, acute limb ischemia (ALI) is a vascular emergency requiring careful evaluation and prompt intervention, either thrombolytic, surgical, or endovascular. ALI may be the first manifestation in a previously asymptomatic patient or could be an acute event in a patient with critical limb ischemia (CLI). According to the TransAtlantic Inter Society Consensus (TASC): “Acute limb ischemia is any sudden decrease or worsening in limb perfusion causing a potential threat to extremity viability.”1 Regardless of the fact that there was protean published data on peripheral arterial diseases (PAD), acute limb ischemia, as an intrinsic part of this topic, was not well organized in the specialized medical literature until January 2000, when the TASC document was published. Due to the working group who elaborated this scientific document, the literature on PAD up to 1998 was evaluated and structured on a consensus process. From that point on the literature under the PAD umbrella was mostly oriented on three big chapters, namely intermittent claudication (IC), ALI, and CLI. Recently, in December 2005, for the first time ever the “Guidelines for the Management of Patients With Peripheral Arterial Disease (Lower Extremity, Renal, Mesenteric, and Abdominal Aortic): A Collaborative Report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines” were provided to the vascular medicine world.2 In this paper, the wealth of medical literature on PAD, including ALI, was reviewed up to 2004. In the present chapter we focus on the evidence-based medicine for the global management of this illness based on the recommendations of the guidelines and the result of a recent search of the published literature on acute limb ischemia conducted on Medline, the Cochrane Library, Biosis, manual searches of journals, meetings, proceedings, clinical trials from the National Center Watch and World Center Watch, the Center of Drug Evaluation and Research, the World Wide Web, and the pharmaceutical and device industries, from 2004 to date.1,2 The new search revealed a good number of published original studies but the number of randomized clinical trials is still sparse. PAD is a manifestation of the generalized atherosclerosis reflecting aggressive atherosclerosis and atherothrombosis in multiple vascular beds. The most involved arteries in order of occurrence are the 648
femoropopliteal–tibial, aortoiliac, carotid, vertebral, splachnic, renal, and brachiocephalic. Hiatt et al. stated that PAD is most common in the lower extremities.3,4 Typically the vessels involved are large, the lesions are often long, and the blood flow is slow. Few factors are specific for PAD: it is often associated with a high incidence of coronary artery disease (CAD) and cerebrovascular disease and the main risk factors for PAD are the same as those for cardiovascular disease, namely cigarette smoking, diabetes mellitus, hypertension, hyperlipidemia, diet high in saturated fats, hyperhomocysteinemia, raised Lp(a) lipoprotein concentrations, obesity, and physical inactivity. The pathophysiology of PAD begins with atherosclerotic plaques in one or multiple peripheral arteries; the plaques become unstable and the thrombus develops. ALI is caused by acute arterial occlusion secondary to thrombus, or to embolus generated at a distant site or due to trauma generated by accidents. Emboli usually originate from existing cardiac disease (atrial fibrillation, myocardial infarction, rheumatic heart disease, prosthetic heart valve, bacterial endocarditis, or atrial myxoma) and by the arterial disease (atherosclerosis, aneurysm, intra-arterial procedures, foreignbody embolism). Thrombosis is generated by atherosclerosis, arterial dissection, aneurysm, and trauma. Thrombus formation relates to the following events: vessel injury, platelet adhesion, activation, and aggregation. The result is a platelet plug, the nucleus of the arterial thrombus.4 On the key thrombogenic factors, Rauch et al. stated that the degree of plaque disruption (erosion, fissure, or ulceration) and the amount of stenosis caused by disrupted plaque and overall mural thrombus are the key factors for determining thrombogenicity at the local arterial site.5 Another key factor is the blood rheology. Lowe et al. presented a comprehensive view on hemorheology, reporting that interactions between blood and vessel wall, which are important in hemostasis, thrombosis, and atherogenesis (platelet adhesion and aggregation; coagulation and fibrinolysis; protein and leucocytes infiltration) occur under conditions of minimal flow velocity and maximal flow force.6 The rheological risk factors (plasma viscosity, fibrinogen, hematocrit and white cell count) are the promoters of platelet adhesion and aggregation. Acute limb ischemia is associated with limb loss and can be life-threatening if reperfusion of the ischemic limb is not accomplished in a timely and safe manner. The guidelines stated that this form of CLI may be the first manifestation of arterial disease in a previously asymptomatic patient or may occur as an acute event in a patient with lower limb PAD.2 The name acute limb ischemia (ALI) refers to patients presenting with vascular ischemic disease of < 24 hours–14 days
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Acute limb ischemia at a critical stage when an abrupt change, amputation, or death was expected. As little as 4–6 hours of limb ischemia may lead to irreversible tissue loss in a previously normal extremity; several days of ischemia may be tolerated by a patient with chronic atherosclerotic disease.
Epidemiology At the present there are no clear-cut epidemiological studies on ALI. As stated by Dormandy et al. data on ALI epidemiology is scarce.8 This group of authors cited from the literature the following data: ALI represented 10–16% of the vascular workload and had an incidence of 4–12 cases per 100,000 population per year. Ouriel also cited from literature an ALI incidence of 1.7 cases per 10,000 population per year, a mortality of 26%, and an amputation rate of 37%.9 According to Bryne the incidence of ALI was 14 cases per 100,000 population per year, and ALI accounted for 12% of operations in an average vascular unit; the life expectancy indicated that at 5 years only 17–44% of ALI patients were still alive.10 As Ansel et al. assert, there is a good evidence that ALI incidence is increasing due to aging of the population and to the increased use of endovascular procedures for the treatment of arterial obstructive lesions generating the iatrogenic cases (from the thrombus from a sheath or debris embolization during balloon angioplasty).11 Also, they mentioned that the increase in ALI incidence in males was due to more arterial thrombosis as a consequence of male predilection for atherosclerotic disease. In a recent published monography on ALI, Yost hypothesized that a prevalence of 140,000 to 175,000 cases of ALI per year could be estimated in US.12 This chapter’s authors postulate that due to a global increase in PAD incidence, the incidence and prevalence of ALI might be more serious than that reported in the literature; for example, Razavi reported that 20–25% of CLI patients develop ALI.13 The implication of these figures could be very important in ALI’s incidence, since CLI cases are increasing and becoming a global public health problem. Therefore, PAD and its components, IC, ALI, and CLI warrant randomized clinical trials and epidemiological studies to elucidate ALI’s incidence and prevalence, which is still an obscure problem. Another problem of unknown dimension and under-reported, but definitely increasing daily, is the incidence of ALI originating from vascular trauma, in the context of traffic and industrial accidents.
Clinical presentation ALI is an acute occlusion of an artery in the limb as a result of embolus or thrombosis. When the cause of ALI is an arterial embolism the clinical diagnosis is based on the sudden onset or sudden worsening of symptoms, a known embolic source, the absence of other manifestation of PAD, the presence of normal arterial pulses, and Doppler systolic blood pressures in the contralateral limb. When arterial thrombosis is the cause, then the origin of thrombosis could be either an atherosclerotic plaque rupture from the aorta to the digital arteries, or the thrombosis of a lower extremity bypass graft. The blunt trauma (fractures, dislocations),
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the popliteal entrapment, or cystic adventitial disease could be the other causes of thrombosis; iatrogenic vascular trauma from diagnostic or therapeutic catheter placement (including guidewire manipulation) could also cause arterial occlusion.14 The symptoms in ALI depend on the location, the extent of arterial obstruction, and the capacity of collateral vessels to perfuse the ischemic territory. The hallmarks of ALI symptoms are the 6 p’s: pain, paresthesias, pulselessness, pallor, poikilothermia, and paralysis.15 The assessment of these symptoms should be done by comparing the contralateral limb. Pain is usually the first symptom presented by the ALI patients. It is the expression of hypoxia due to lack of blood supply, depending on the site of obstruction and the presence of collateral circulation. A less severe hypoxia will translate as a pain localized to the most distal portion of the extremity, toes, and plantar surface. When the ischemia increases, the pain progresses proximally involving the entire extremity. Paresthesia is present and may progress from a burning sensation to complete anesthesia. Associated with this are absent pulses, cool foot, and pallor progressing to cyanosis. If the disease is not properly treated, the last stage includes paralysis, thrombosed superficial veins, and necrosis. Irreversible damage to the limb muscles can occur within 4–6 hours. The urgent investigation should include Doppler blood flow to establish the presence or absence of arterial flow. If the signals are audible in the limb and segmental pressure at ankle exceeds 40 mmHg, the extremity will survive from hours to a few days. Absent blood flow at the ankle or no flow in the popliteal artery represents an extreme emergency and needs intervention to prevent the limb loss. The clinical classification of ischemia levels in ALI is still debated because, as the guidelines state, “It is frequently not possible to precisely delineate the status of the patients with an acutely ischemic limb.”2 There are four clinical categories of ALI: viable, threatened marginally, threatened immediately, and irreversible.7 In Table 74.1 the clinical classification scheme recommended by SVS/ISCVS is displayed.7 The clinical recommendations for ALI according to criteria of evidence-based medicine are: 2 1. “Class I: patients with acute limb ischemia and a salvageable extremity should undergo an emergent evaluation that defines the anatomic level of occlusion and that leads to prompt endovascular or surgical revascularization (level of evidence: B).” 2. “Class III: patients with acute limb ischemia and a nonviable extremity should not undergo an evaluation to define vascular anatomy or efforts to attempt revascularization (level of evidence: B).” The diagnostic tests are conditioned by the limited time and the indication for urgent revascularization. The history, physical examination, ankle–brachial index (ABI), Doppler ultrasound, color-assisted duplex ultrasonography, contrast arteriography, magnetic resonance, and computed tomography are the ALI diagnostic tests. The differential diagnosis of ALI must be made with vasospasm, arteritis, hypercoagulable states, compartment syndromes, arterial dissection, and external arterial compression (popliteal cyst).
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Table 74.1
Clinical categories of acute limb ischemia
Category
Description/prognosis
Sensory loss
Muscle weakness
Arterial Doppler signals
Venous Doppler signals
Viable
Not immediately threatened
None
None
Audible
Audible
Salvageable if promptly treated Salvageable with immediate revascularization Major tissue loss or permanent nerve damage inevitable
Minimal (toes) None or none More than toes Mild, moderate associated with rest pain Profound, anesthetic Profound paralysis (rigor)
Often inaudible Usually inaudible
Audible
Threatened Marginally Immediately Irreversible
Treatment The emergent treatment of ALI is a challenge. TASC defined the management of ALI as immediate, surgical (open surgical thrombectomy (OST)) and endovascular (catheter-directed thrombolysis (CT), rheolytic thrombectomy (RT), percutaneous aspiration thrombectomy (PAT), percutaneous mechanical thrombectomy (PMT)).1 Catheter-directed thrombolysis is recommended in levels I and IIa patients, if thrombolysis is not contraindicated; the revascularization (surgical, endovascular) is recommended to category IIb and early category III; and amputation in irreversible category III. From our experience in treating ALI it could be acknowledged that no single available therapy for ALI has become the gold standard and a successful outcome often requires several thrombolytic/thrombectomy strategies or combination therapy including antiplatelet therapy with GP IIb/IIIa agents.16 The immediate measures for patient survival consist of anticoagulation via heparin (a sufficient dose to increase partial thromboplastin time by 1.5–2.5 times control values to prevent thrombus propagation or recurrent embolism), oxygen inhalation, treatment of cardiac failure, or atrial or ventricular arrhythmias. Simple methods to improve existing perfusion (keeping the foot dependent, avoiding extrinsic pressure over the heel or bony prominence, avoiding temperature extremes, maximizing tissue oxygenation, and correcting hypotension) are required. Open surgical techniques for ALI comprise: balloon catheter thromboembolectomy, bypass procedures to direct blood flow beyond occlusion, and endarterectomy with or without patch angioplasty. Open surgical thrombectomy (OST) and revascularization was introduced in the late 1960s by Fogarty et al.17 OST improved limb salvage rates dramatically with amputation rates in the range 6–18% but the mortality rates have remained alarmingly high (15–20%), primarily due to the high association of cardiopulmonary co-morbidities.18–20 Chemical thrombolysis (CT) treatment for acute limb ischemia (ALI) has become integral to achieving limb salvage since the early 1980s. The thrombolytic agents, urokinase (UK) (Abbokinase, Abbott Laboratories, Chicago, IL), streptokinase (Streptase, Astra Pharmaceutical, Eatontown, NJ) alteplase (rtPA, Genentech, San Francisco, CA), tenecteplase
Inaudible
Audible Inaudible
(TNK), (Genentech) are the thrombolytics used in ALI treatment. Potential advantages of CT include: ●
●
● ●
non-surgical therapy which allows medical stabilization avoiding emergent OST in these medically compromised patients potentially reducing high peri-operative mortality and morbidity; improved microvascular thrombolysis not accessible to OST, mechanical thrombectomy, or PTA; produces minimal endothelial or intimal injury; reduces the magnitude of definitive surgical or endovascular procedures.
Potential disadvantages of CT include: ● ● ● ● ● ●
long infusion times; relative contraindication in the threatened limb; increased bleeding risks; thromboembolic complications; increased ICU stays and hospital resource utilization; 15–20% rate of CT contraindications (recent surgery, stroke, high risk of bleeding, etc).
incomplete thrombolysis often requiring additional therapy (OST or mechanical thrombectomy). Several multicentered randomized trials comparing OST to CT have shown a significant decrease mortality rate with CT.21–23 A method of overcoming the disadvantages of open surgery and pharmacologic lysis in ALI is the rheolytic thrombectomy (RT); it implies the use of the percutaneous mechanical device AngioJet (Possis, Minneapolis, MN), a recirculating rheolityc mechanical thrombectomy catheter, to clear thrombus. The AngioJet has shown to be safe and effective.24,25 As an alternative treatment, mechanical trombectomy techniques are used in ALI. In recent years hydrodynamic or rotational thrombectomy systems are replacing thrombolysis. Clot aspiration (percutaneous arterial embolectomy), hydrodynamic catheters, and devices for mechanical clot destruction, are all percutaneous mechanical thrombectomy methods accepted for ALI. Their advantage is the straightforward removal of clot and rapid revascularization, avoiding lengthy procedures.26–30 As a consequence of the treatment with
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Acute limb ischemia percutaneous mechanical thrombectomy devices, between 1995–2000 the amputation rates were reported at 5–18% and mortality rate 8–14%.31–34 Several algorithms were suggested regarding the treatment of ALI.14 At the Cardiovascular Institute of the South, the protocol for ALI treatment includes: ●
●
●
the use of bivalirudin as anticoagulation strategy encompassing effective direct thrombin inhibition without increasing or possibly reducing the risk of hemorrhagic events; peri-procedural antiplatelet therapy via glycoprotein receptor inhibitors GPIIb/IIIa; the novel “power-pulse spray”(P-PS) technique to simultaneously maximize the advantages and benefits of RT and CT.16, 35–40
Shammas presented an algorithm for ALI built upon the platform of mechanical thrombectomy utilizing the AngioJet System with or without the P-PS technique.41
The CIS power-pulse spray (P-PS) technique The novel P-PS technique (Table 74.2) was developed at CIS to: (1) address the limitations of monotherapy; and (2) simultaneously maximize the advantages and benefits of both RT and CT while minimizing their disadvantages and limitations in an effort to rapidly reperfuse the ischemic limb, rapidly remove acute and subacute thrombus, lessen risks and complications, decrease ICU and hospital resource utilization, and improve clinical outcomes. The P-PS technique has recently received FDA market clearance for the use of AngioJet for power-pulse spray delivery of a physician-specified fluid such as a thrombolytic agent via the AngioJet catheter. As outlined in Table 74.2 the total or subtotal iliofemoral or bypass graft thrombotic occlusion is crossed using standard techniques with a 0.035-inch guidewire. This step is often facilitated with a 5-French Terumo glide-catheter (Boston Scientific, Minneapolis, MN). Initially, the 6-French AngioJet catheter and RT system is set up and primed in its “thrombectomy mode” with normal saline. A “lytic bag” is then created by adding either 1,000,000 IU UK or 10 mg TNK to 50 cm3 of normal saline, which is then exchanged for the saline prime while a stopcock is added and closed to the outflow port RT catheter manifold, thus converting the RT system to its P-PS mode. It is important to advance the RT catheter slowly at 0.5–1.0 mm increments through the entire thrombosed segment using a single foot pedal pump/pulse per advanced increment. The RT system is set to deliver 0.6 ml volume of lytic solution per pedal pump/pulse. The infused volume meter on the device unit console is set at zero at the initiation of the P-PS mode, allowing calculation of the total lytic volume and dose. A single antegrade and retrograde RT pass in the P-PS mode is recommended: the RT catheter is then removed. The concentrated pulsed lytic is allowed to “lyse” for 30 minutes as the RT system is converted back to its thrombectomy mode. It is important to evacuate the residual 12 ml of lytic outside the patient to avoid infusing additional lytic. The AngioJet RT catheter is then reintroduced with a single antegrade and retrograde pass followed by immediate
Table 74.2
651
The CIS “power-pulse spray” protocol
1. Cross thrombotic occlusion with 0.035-inch Glidewire Preparation of the AngioJet Catheter 2. Set-up and prime 6-French AngioJet Xpeedior RT catheter in its “Thrombectomy Mode” as per instructions for use. Prime system using 12 ml of normal saline 3. Exchange saline priming bag for 10 mg TNK or 1,000,000 IU UK in 50 cm3 NS (“lytic bag”) 4. Activate the RT catheter to prime with lytic (infuse 12 ml) 5. Reset Infused Volume meter to Zero on AngioJet Drive Unit console 6. Attach 3-way stopcock to outflow port AngioJet catheter manifold 7. CLOSE THE STOPCOCK to occlude outflow PPS Technique 8. Advance AngioJet catheter slowly at 0.5–1.0 mm increments through the entire thrombosed segment, using one foot pedal pump/pulse per advanced increment 9. Each foot pedal pump/pulse delivers 0.6ml lytic solution 10. Continue advancing and pulsing lytic until entire occlusion has been crossed 11. Repeat power-pulsing in retrograde direction and remove catheter (1 pedal tap/1.0 mm withdrawal). The Infused Volume meter calculates total solution (convertible to total lytic dose) 12. Allow pulsed lytic to “lyse” for 30 minutes Normal “Thrombectomy” Mode 13. OPEN STOPCOCK 14. Exchange lytic bag with priming NS bag 15. Evacuate 12 ml lytic residual. (OUTSIDE the patient) 16. Reintroduce AngioJet catheter in “Thrombectomy Mode” 17. Make a single antegrade and retrograde pass with AngioJet 18. Obtain post-thrombectomy angiogram 19. Further treatment at discretion of clinician (unmasked “culprit lesion”- PTA/stent)
angiography. Recently Possis has developed a prepackaged system simplifying the P-PS technique and facilitating setup and delivery of this therapy. Case presentation #1 An 81-year-old white male with a history of diabetes, stroke, MI, PVD, hypertension, and a prior CABG presented with an acute onset of right leg and foot pain, coolness, and weakness of 6-hour duration. Physical examination revealed a cold, pulseless, ischemic right foot (Figure 74.1). An urgent contralateral approach peripheral angiogram revealed a total occlusion of the proximal right common iliac artery below the aortic bifurcation (Figure 74.2a). The thrombotic occlusion was crossed using a 0.035-inch glidewire and the CIS P-PS was used for revascularization. A discrete “culprit lesion” was unmasked after the pulsed thrombolytic was allowed to “lyse” for 30 minutes (Figure 74.2b). A single balloon-expandable stent and short self-expanding stent was deployed providing revascularization in a total procedural time of 65 minutes (Figure 74.2c).
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Textbook of peripheral vascular interventions Case presentation #2: A 69-year-old white male with a history of diabetes, MI, PVD, CABG, and previous left femoral-popliteal bypass graft (FBG) presented with 6-hour onset of acute left leg pain and weakness. Physical examination revealed a cold, pulseless, ischemic left foot (Figure 74.3a). An emergent contralateral angiogram revealed a total occlusion of the left common femoral artery and the previous FBG, which was identified by a previously placed metal “anastomotic graft marker” (AGM) (Figure 74.3b). The occluded graft was crossed using a 0.035-inch Glidewire and the CIS P-PS protocol was used for successful revascularization (Figure 74.3c–f). The AGM facilitated intubating and crossing the graft after failure to cross the occluded native SFA.
Figure 74.1 This 81-year-old white male presented with pale, painful, pulseless, paresthetic, paretic right foot, demonstrating the six p’s of acute limb ischemia.
ICU monitoring was not required, limb salvage was achieved, and the patient was asymptomatic at 36-hour discharge and at 30-day follow-up. A 30-day post-procedural angiogram revealed excellent results (Figure 74.2d).
P-PS technique in a group of patients with ALI Forty-nine CLI patients presented with ALI. Forty-nine arteries (15 iliac, 22 SFA, 12 bypass graft) were treated with the P-PS technique: 1. Using a 6 Fr RT catheter, NS prime was exchanged for thrombolytic solution (Group I: 10–20 mg TNK/50 cm3 NS, n = 25; Group II: 1,000,000 UK/50 cm NS, n = 24);
(a)
(b)
(c)
(d)
Figure 74.2 Series of angiograms demonstrating the CIS P-PS technique: (a) subacute proximal common iliac artery occlusion; (b) immediate post-P-PS angiogram after 30 minutes TNK lysis unmasking a discrete “culprit” lesion; (c) post-PTA/stent results; (d) 30-day follow-up angiogram.
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(a)
653
(b)
(c)
(d)
Figure 74.3 (a) A cold, pulseless, ischemic left foot 2 years after FBG. (b) Angiogram shows 100% of left CFA, FPBG, SFA and profunda artery. Note the circular metal AGM; (c, d) The double marker tip of the new AngioJet is seen in the proximal and distal FBG in the P-PS mode.
2. The outflow port was closed, then the catheter was advanced at 1 mm increments while pulsing lytic agent; 3. After 30 minutes of local thrombolysis, RT and definitive treatment of the underlying stenosis were performed. Procedure success was 23/25 (92%) and 22/24 (91.6%) for group I and II respectively. The mean total procedure time was 72 minutes and 75 minutes in group I and II respectively. Thirty-day limb salvage was 91% in both groups. There were no major surgical complications in either group and equivalent minor complications (8%). Procedure time ranged from 40–110 minutes (mean = 72) in group I and from 45–116 minutes (mean = 75) in group II and was thus
essentially equivalent in both dosage groups (overall mean = 73.5). The iliac artery procedure times were generally shorter (mean = 59 minutes, range = 40–78) as compared to the SFA and FBG procedures (mean = 79 minutes, range = 54–115). There were no major or vascular complications requiring surgery in either group and two minor hematomas (< 5 cm) occurred in each group (group I: 2/25 (8%) and group II: 2/24 (8.4%)). No patients experienced significant fibrinogen drop of more than 25% (mean drop = 12.4%). The FBG subset responded exceptionally well with 100% success rate and mean total procedure time of 61 minutes. There were no clinically or angiographically apparent embolic complications and only two patients in each group
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(e)
(f)
Figure 74.3, cont’d (e) Angiogram 30-minutes post P-PS shows almost complete graft thrombus removal; (f) Final angiogram after a distal anastomotic site stenosis was identified (note AGM) and underwent PTA/stenting (note a previously placed popliteal stent).
required ICU care monitoring primarily for pre-existing coronary artery disease and ventricular dysrhythmias. The ABI mean improvement was 0.31 ± 0.16 with a range of 0.14–0.41. Forty of 49 (81.6%) were available for 30-day duplex ultrasound, 37/40 (92.5%) limbs had < 50% restenosis, and 3/40 (7.5%) had > 50% restenosis at the PTA/stent site by duplex ultrasound velocity and waveform analysis. Two out of three underwent repeat angiography and repeat PTA/stenting, both of the superficial femoral artery, and the third patient was treated medically. All patients experienced clinical improvement after completion of lysis and revascularization.
Four procedural failures due to an inability to cross the lesion and 2/4 (50%) underwent surgical revascularization. Both procedural failures not undergoing surgical revascularization required major amputations during that admission. In conclusion, the P-PS technique offers several potential advantages compared to more traditional monotherapy thrombectomy or thrombolytic strategies for patients with a wide variety of ALI patients. The technique is a tool that will potentially allow clinicians to achieve rapid arterial thrombolysis and thrombectomy in minutes, not hours or days, and “treat ALI like the acute coronary syndrome (ACS)”.
REFERENCES 1. 2.
3. 4. 5. 6. 7.
TransAtlantic Inter-Society Consensus (TASC): Management in Peripheral Arterial Disease (PAD). J Vasc Surg 2000; 3(2): suppl. 1 Hirsh AT, Haskal ZJ, Hertzer NR et al. ACC/AHA Guidelines for the Management of Patients With Peripheral Arterial Disease (Lower Extremity, Renal, Mesenteric, and Abdominal Aortic): A Collaborative Report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of Interventional Radiology, and the ACC/AHA Task Force on Practice. J Am Coll Cardiol 2006; 47(6):1239–312 Jackson MR, Clagett PG. Antithrombotic therapy in peripheral arterial occlusive disease. Chest 2001; 119(suppl.1): S283–299 Hiatt WR. Preventing atherothrombotic events in peripheral arterial disease: the use of antiplatelet therapy. J Intern Med 2002; 251: 193–206 Rauch U, Osende JI, Fuster V et al. Thrombus formation on atherosclerotic plaques: pathogenesis and clinical consequences. Ann Intern Med 2001; 134(3): 224–38 Lowe GDO. Rheological influences on thrombosis. Bailliere Clin Hematol 1999; 12(3): 435–49 Katzen BT. Clinical diagnosis and prognosis of acute limb ischemia. Rev Cardiovasc Med 2002; 3(suppl. 2): S2–6
8. 9. 10.
11. 12. 13. 14. 15.
Dormandy J, Heek L, Vig S. Acute limb ischemia. Sem Vasc Surg 1999; 12(2): 148–53 Ouriel K. Acute limb ischemia. In: Rutherford, RB, ed. Vascular Surgery, fifth edition. WB Saunders, 2000: 813–21 Bryne J. Etiology and natural history: diagnosis and evaluation. Acute limb ischemia. In: Hallett JW, Mills JL, Earnshaw J, Reekers JA, eds. Comprehensive Vascular and Endovascular Surgery. Mosby, 2003: 197–212 Ansel GM, Botti CF, Silver MJ. Mechanical devices and acute limb ischemia. Endovasc Today 2003: 46–8 Yost ML. Acute limb ischemia. The Sage Group #404-816-0746, September 2005. Razavi MK. Thrombolysis in acute limb ischemia. What’s new on the horizon. Presented at New Cardiovascular Horizons, New Orleans, October 15, 2004. Allie DE. Dethrombosing strategies and endopharmacotherapy: an emerging role in our cli “toolbox”. Commentary. Vasc Dis Man 2006; 3(3): 277–78 Kasirajan K, Ouriel K. Current options in the diagnosis and management of acute limb ischemia. Prog Cardiovasc Nurs 2002; 17(1): 26–34
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17. 18. 19. 20. 21.
22. 23. 24. 25.
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28.
Allie DE, Hebert CJ, Lirtzman MD et al. Continuous tenecteplase (TNK) infusion combined with peri/postprocedural platelet glycoprotein IIb/IIIa inhibition in peripheral arterial thrombolysis: initial safety and feasibility experience. J Endovasc Ther 2004; 11(4): 427–35 Fogarty TJ, Cranley JJ, Krause RJ et al. A method for extraction of arterial emboli and thrombi. Surg Gynecol Obstet 1963; 116: 241–244 Cambria RP, Abbott WM. Acute arterial thrombosis of the lower extremity: Its natural history contrasted with arterial embolism. Arch Surg 1984; 119: 784–7 Blaisdell FW, Steele M, Allen RE. Management of active lower extremity arterial ischemia due to embolism and thrombus. Surgery 1978; 84: 822–34 Yeager RA, Moneta GL, Porter JM. Surgical management of severe acute lower extremity ischemia. J Vasc Surg 1992; 15: 385–91 Ouriel K, Shortell CK, DeWeese JA et al. A comparison of thrombolytic therapy with operative revascularization in the initial treatment of acute peripheral arterial ischemia. J Vasc Surg 1994; 19: 1021–30 The STILE Investigators. Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischemia of the lower extremity. Ann Surg 1994; 220: 251–66 Ouriel K, Veith FJ, Sarahara AA. For the TOPAS Investigators. Thrombolysis or peripheral arterial surgery: phase I results. J Vasc Surg 1996; 23: 64–73 Kasirajan K, Gray B, Beavers FP et al. Rheolytic trombectomy in the management of acute and subacute limb-threatening ischemia. J Vasc Interv Radiol 2001; 12: 413–21 Hanover TM, Kalbaugh CA, Gray BH et al. Safety and efficacy of reteplase for the treatment of acute arterial occlusion: complexity of underlying lesion predicts outcome. Ann Vasc Surg 2005; 19(6): 817–22 Vorwerk D. Mechanical thrombectomy is an alternative way to go: the European experience commentary on: quality improvement guidelines for percutaneous management of acute limb ischemia. Cardiovasc Intervent Radiol 2006; 29(1): 7–10 Rajan DK, Patel NH, Valji K et al. CIRSE and SIR Standards of Practice Committees. Quality improvement guidelines for percutaneous management of acute limb ischemia. J Vasc Interv Radiol 2005; 16(5): 585–95 Ouriel K. Endovascular techniques in the treatment of acute limb ischemia: thrombolytic agents, trials, and percutaneous mechanical thrombectomy techniques. Semin Vasc Surg 2003; 16(4): 270–9
29. 30. 31. 32.
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Vorwerk D. Mechanical thrombectomy in acute and subacute leg ischemia. Acta Chir Belg 2003; 103(6): 548–54 Laird JR: The management of acute limb ischemia: techniques for dealing with thrombus. J Interv Cardiol 2001; 14(5): 539–46 Kasirajan K, Ouriel K. Management of acute lower extremity ischemia: treatment strategies and outcome. Curr Interven Card Reports 2000; 2: 119–29 Ramee SR, Lansky AJ, Money SR et al. Randomized trial comparing Rheolytic thrombectomy to surgical embolectomy for thrombosed hemodialysis grafts and peripheral arteries: an interim report. Circulation 1995; 92(8): Ramee SR, Kuntz RE, Schatz RA et al. Preliminary experience with the POSSIS coronary AngioJet Rheolytic thrombectomy catheter in the VeGas I Pilot Study. J Am Coll Cardiol 1996; 27(suppl. A): 69A Silva JA, Ramee SR, Collins TJ et al. Rheolytic thrombectomy in the treatment of acute limb threatening ischemia: Immediate result and six-month follow-up of the multicenter AngioJet registry. Cathet Cardiovasc Diagn 1998; 45: 386–93 Allie DE. Patients with peripheral artery disease undergoing percutaneous peripheral interventions are at increased risk for complications without adequate anticoagulation. J Invas Cardiol 2004; 16(suppl. G): 18–21 Allie DE. Optimal antiplatelet therapy: lessons learned from PCI applicable to PAD and PPI. Commentary to: Interventional Pharmacology. Vasc Dis Man 2005; 63–4 Allie DE, Hall PA, Shammas NW et al. Bivalirudin in peripheral interventions. Results of the APPROVE trial and emerging role of “endopharmacology” in treating PVD. Endovasc Today 2005: 27–32 Allie DE, Hebert CJ, Walker CM. The CIS “power-pulse spray” technique. novel simultaneous combination therapy for rapid revascularization in critical limb ischemia. Endovasc Today 2003; 2(2): 25–30 Allie DE, Hebert CJ, Walker CM: The CIS “power-pulse spray” technique. Vasc Dis Man 2004; 12–16 Allie DE, Craig M Walker CM. The CIS “power-pulse spray” technique. Vascular & Endovascular Challenges, 26th International Symposium Charing Cross Controversies, Challenges, Consensus, BIBA Medical, London, 2004, 312–30 Shammas N. Dethrombosis of lower extremities: Pharmacologic and mechanical techniques. Vasc Dis Man 2006; 3(3): 272–6
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Endovascular treatment for infrainguinal failing graft A de Carvalho Lobato and DF Colli Jr
Background Peripheral artery disease (PAD) is a highly prevalent disorder, affecting approximately 1% of women and 2% of men with ages of between 45 and 69 years and raising to 9.4 and 11.6%, respectively, at 65–74 years of age. PAD is usually an under-recognized problem as approximately half of patients are asymptomatic, despite having abnormal physical examination. Poor rehabilitation rates and the high costs associated with management of post-amputation patients justify aggressive revascularization policy in critical limb ischemia (CLI). According to the National Institute of Health, PAD accounts for 60,000 hospitalizations per year with a mean length of stay of 11 days. Approximately 15% of the infrainguinal vein bypass grafts performed need revision.1 A single revision is usually necessary in 69% of cases and subsequent additional revisions in 31%.2 Observations of the PREVENT III multicenter trial on demographics and co-morbidities suggested limb salvage patients reflect a population with diffused, advanced atherosclerosis. Preoperative mortality was 2.7%, major morbidity included myocardial infarction in 4.7%, and stroke/transient ischemic attack in 1.4%.3 Risk factors interfering with primary and assisted primary patency include race (African Americans worse than Caucasians), hypertension, diabetes, hypercholesterolemia, saphenous grafts of thicker wall, early flow disturbances, level of bypass graft, need for revision within 6 months of index surgery, number of segments treated, the most distal artery treated, and grade D TASC classification.2,4–9 Reported overall limb salvage rates are over 80% in the majority of series.2,5
Diagnosis and surveillance Early diagnosis is the key to ensure graft patency maintenance through a minimally invasive procedure and prevent major surgery or tissue loss. Symptom relapse or changes in local physical examination are usually the first clues and should raise immediate suspicion of infrainguinal failing graft and prompt investigation. Sudden, spontaneous onset of ipsilateral blue-toe syndrome has been reported as a clinical presentation in 1% of cases in a large series. Episodes occurred at intervals of 4–11 months and resulted from atypical distal microembolization originating from focal preocclusive intraluminal 656
vein graft stenosis.10 Clinical findings have been reported to underestimate incidence of problem grafts when compared to duplex scanning.11 Duplex ultrasound Patients undergoing infrainguinal vein graft must be followedup on a strict color-flow duplex ultrasound surveillance program due to the high incidence of vein graft stenosis and occlusion occurring either in the bypass graft or in the adjacent inflow or outflow arteries. The use of duplex ultrasound as the primary imaging method for vein graft surveillance is well established and widely accepted.11,12 The use of duplex scanning as part of the surveillance program for prosthetic grafts, however, is still controversial. Results of the recently published Vein Graft Surveillance Randomized Trial (VGST) failed to demonstrate any additional benefit in terms of limb salvage rates or health-related quality of life when intensive surveillance with duplex scanning was compared to clinical surveillance. In addition, the former was associated with a mean £495 cost per patient.13 The surveillance program, undertaken at our institution, includes a color-flow duplex scan of the bypass conduit and adjacent inflow and outflow arteries and Doppler-derived ankle–brachial indices (ABI) 1 month after the procedure and every 3 months during the first year, accordingly to the obtained results. From the second year on, the duplex should be performed every 6 months to check for disease progression. The reported interval incidence of event causing de novo stenoses varies from 8 to 22% of the total number of duplex tests performed at 3 months and from 8 to 33% at 6 months after the operation. A drop in this incidence is usually seen at 9 and 12 months (2–7 and 1%, respectively) and thereafter (14%) in those who had a normal bypass during the first 6 months surveillance.14 The optimal duration of post-operative duplex surveillance of infrainguinal vein grafts is controversial. Previous reports have suggested nearly all vein graft stenoses appear within the first post-operative year and that normal duplex scan findings during this period would eliminate the need for ongoing surveillance. According to the results of a large series conducted by Passman et al., only 25% of cases had mid-graft PSVs • 45 cm/second or focal velocities • 200 cm/second identified on the initial examination; 75% were found during subsequent surveillance, with 31% detected after 6 months.14
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Endovascular treatment for infrainguinal failing graft The following parameters should be studied during the duplex scan: 1. graft peak systolic velocity (PSVgraft); 2. the maximum peak systolic velocity (at the site of a stenosis or in normal grafts at the narrowest segment of the bypass) (PSVmax); 3. the ratio between PSVgraft and PSVmax, (PSVindex); 4. end-diastolic velocity (EDV) at a stenosis or from narrowest graft segment; 5. color-flow image diameter measurements. Diameter reductions best identify all stenotic lesions greater than 29% (sensitivity 88%, specificity 99%) while peak systolic velocity-index is good for the identification of stenoses greater than 49% (sensitivity 89%, specificity 92%). Increased EDV, on the other hand, indicates high grade stenoses (70–99%) (sensitivity 91%, specificity 100%).15 The currently accepted threshold criteria for further evaluation and intervention to prevent graft occlusion was thoroughly validated and comprises high-velocity criteria (HVC), defined as peak systolic velocity (PSV) > 300 cm/second and velocity ratio (Vr) > 3.5; and low-velocity criteria (LVC), defined as PSV < 45 cm/second and an ABI decrease > 0.15. Infrainguinal vein grafts with normal serial color-flow duplex scan and ABI are at minimal risk of spontaneous graft occlusion. A PSV > 180 cm/second and Vr > 1.5 indicates over 50% of grafts will ultimately require revision or progress to occlusion. Grafts with such lesions can be safely monitored by color-flow duplex scanning until progression to lesions meeting HVC occurs, with minimal risk of graft occlusion. A decrease in ABI > 0.15 with normal duplex scanning mandates arteriography to identify inflow and outflow lesions or a missed graft stenosis.16,17 Duplex ultrasound versus angiography Angiography should be performed routinely at the beginning of the intervention to confirm ultrasound findings. Duplex ultrasound has been reported as a reliable test for revising failing infrainguinal grafts and avoiding morbidity, discomfort, and cost of confirmatory arteriography in two-thirds of cases.15 The degree of diameter stenosis on ultrasound has been compared with angiography findings to determine concordance. Overall accuracy of duplex ultrasound was
Table 75.1
88% (κ value of 0.80). In discordant cases, ultrasound correctly identified a stenosis, but overestimated the degree of stenosis compared with angiography. Idu et al.11 demonstrated that PSV ratio provides the best correlation with angiographic stenoses in more than 70% of cases (PSV ratio cutoff 3.0: sensitivity 80%, specificity 84%).18,19 The value of routine angiography before graft revision has been evaluated in diabetics and revealed additional findings in 76% of cases, with a resultant alteration of the operative plan in 71% of cases. The most frequent additional angiographic finding was the identification or localization of a lesion in the inflow or outflow tracts (6.6% cases).4 Incidence rates The reported incidence rates of restenosis after infrainguinal bypass are summarized in Table 75.1.
Treatment Previous reports of the natural history of infrainguinal vein grafts has demonstrated the incidence of post-operative graft stenosis and the need for revision to vary accordingly to the bypass grafting technique adopted. Three-year primary and secondary graft patency rates were higher (p < 0.001) for in situ bypass grafts (85/97%) compared with reversed (57/83%), non-reversed translocated (62/78%), or alternative (51/76%) vein bypass grafts. During a mean follow-up interval of 19 months, the incidence of graft revision was higher for reversed saphenous (23%) and alternative (28%) vein bypass grafts compared with in situ (10%) or nonreversed (16%) saphenous vein bypass grafts. Despite a normal intraoperative graft duplex scan, the revision/failure rate of reversed vein grafts was 2.5 times greater than in situ/non-reversed translocated vein conduits (primary patency rate at 3 years, 60 vs. 87%, p = 0.009). Bypass grafts modified at operation on the basis of duplex scanning were two times more likely to require post-operative revision than grafts with normal intraoperative scans.20 Antithrombotic and antiplatelet therapy In order to avoid graft occlusion, patients are usually treated with either an antiplatelet or antithrombotic drug,
Reported incidence rates for infrainguinal failing graft
Ref
Year
Author
29 14 19 16 20 6 30 2 13
1993 1995 1996 1997 1997 1999 2000 2004 2005
Mills J et al. Passman MA et al. Calligaro Westband et al. Gupta AK et al. Inhat AM et al. Goh RH et al. Nguyen LL et al. Davies AH et al.
No. grafts 227 447 85 101 338 341 352 1260 594
657
Mean follow-up (months) 22 — 11 — 19 35 — 51 18
Restenoses (%) 21% 8% 24.7% 22.7% 10–28% 26% 24.4% 14.9% 12–19%
Inflow/outflow lesions 12.8%/8.5% — — — — 7% — — —
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or a combination of both. Little is known, however, about the optimal dose and/or efficacy of both drugs on the prevention of this complication. The benefits of the long-term administration of oral anticoagulant therapy remain unclear in patients with lower extremity arterial bypass surgery. A prospective study conducted by Jackson et al.,21 in 402 patients, examined whether oral anticoagulation therapy reduced the degree of ischemia after occlusion of PTFE and vein femoropopliteal bypass grafts. The patients with PTFE who were undergoing warfarin plus aspirin therapy (WASA therapy) at the time of graft occlusion had less grade II ischemia than those patients who were undergoing ASA therapy (aspirin therapy) alone (28 vs. 55%; p = 0.057). However, the incidence rate of severe ischemia after graft occlusion remained greater with PTFE grafts and WASA therapy as compared with all the vein grafts (28 vs. 18%). The vein graft occlusions had the same incidence rate of grade II ischemia in WASA therapy as with ASA therapy (20 vs. 17%; p = 1.0). Similar results were reported by Johnson et al.22 in a large multicenter, prospective, non-masked clinical trial including 831 patients who underwent peripheral arterial bypass surgery. In the prosthetic bypass group, there was no significant difference in patency rate in the 8-mm bypass subgroup, but there was a significant difference in patency rate in the 6-mm bypass subgroup (femoral–popliteal; 71.4% in the WASA group vs. 57.9% in the ASA group; p = 0.02). In the vein bypass group, patency rate was unaffected (75.3% in the WASA group vs. 74.9% in the ASA group). Two recent meta-analyses performed by Dorffler-Melly et al.1,23 for the Cochrane Database evaluated the effect of antithrombotic and antiplatelet drugs. The first one, conducted in 2003,1 evaluated vitamine K antagonists (VKA) and aspirine/dipiridamole, concluding that patients operated for an infrainguinal venous graft might benefit from treatment with VKA, whereas patients receiving an artificial graft might profit more from platelet inhibitors (aspirin). However, the evidence was not conclusive and the need for randomized controlled trials with larger patient numbers was emphasized. The second study, published in 2005,23 observed a 60% reduction of recurrent obstruction with 330 mg aspirin (ASA) combined with dipyridamol (DIP) as compared to placebo at 12 months follow-up. At 6 months following endovascular treatment, a positive effect on patency was found with 50–100 mg ASA combined with DIP (n = 356). However, this was not significant. ASA/DIP tended towards showing a superior effect on patency after femoropopliteal angioplasty compared with VKA at 3, 6, and 12 months. Peri-interventional treatment with LMWH in femoropopliteal obstructions resulted in significantly lower restenosis/reocclusion rates than with unfractionated heparin. The author concluded that aspirin (50–300 mg) started prior to femoropopliteal endovascular treatment appears to be the most effective and is safe. Clopidogrel might be an alternative, but data are lacking. Abciximab might be a useful adjunctive for high-risk patients with long segmental femoropopliteal interventions. Low molecular weight heparin seems to be more effective in preventing reocclusion or restenosis than unfractionated heparin. It is our routine to prescribe clopidogrel (75 mg) and aspirin (200 mg/day) for 8 weeks in these patients.
Thrombolytic therapy Vein graft thrombolysis is unlikely to yield durable patency overall. Diffuse graft disease, limited outflow, and a high recurrence rate of anastomotic stenoses after balloon angioplasty explain poor long-term results after thrombolysis of failed grafts. Most successfully lysed grafts (> 80%) required adjunctive surgery or percutaneous transluminal angioplasty after thrombolysis. Overall, failure rates have been reported from 19–25% of cases and the primary graft patency rate varied from 19 to 34% at 1 year and 25% at 2 years after thrombolysis.24–28 Among the benefits of thrombolysis are the significant immediate limb salvage rates and uncovering of the anatomic defects responsible for thrombosis. This is more successful in autogenous grafts (90%) as compared to non-autogenous conduits (41%). The most common lesions underlying autogenous graft failure comprised stenoses within the body of the graft (37%), while the most common lesions in failed non-autogenous grafts appeared to be stenoses at the anastomosis (27%).25 It is, however, characterized by a high procedure-related morbidity with high costs. Complications have been reported in up to 29% in native artery occlusions, to 42% in vein grafts, and 53% in prosthetic or composite grafts. Bleeding is the most common complication (major bleeding 16%, minor bleeding 22%), followed by distal embolization in 24% of cases, arterial dissection in 4%, and amputation and death in 2%.28
Surgical/endovascular therapy Critical limb ischemia has been considered as a primary indication for bypass surgery. This opinion however is being revised with the continued enhancement of endovascular techniques and expertise, new advances in imaging techniques, and new developments in angioplasty equipment. Besides, current lower morbidity, cost and results of percutaneous transluminal angioplasty support the increasing indication of this procedure in CLI patients. Graft revision by endovascular means has been proposed as a suitable alternative to more invasive surgery. Factors considered when choosing balloon angioplasty include significant co-morbidities that precluded operative intervention, the lack of adequate conduit for surgical revision, and poor accessibility of the stenotic lesion.30 The results of a long-term series conducted by Kudo et al.5 concluded PTA is a feasible, safe, and effective procedure for the treatment of CLI. Initial technical success rates were high and procedural mortality and complication rates were low. Primary assisted patency rate was 76%, secondary patency rate 80%, and 5 years limb salvage rate 89%. Risk factor analysis indicated hypertension, multiple segment lesions, more distal lesions, and TASC type D as significant independent predictors of worse long-term results. This opinion is also shared by other authors.30,31
Endovascular tactics The selection of the endovascular approach should take into consideration its distance to the lesion as well as the existence of previous surgical incisions. The closest access allows for
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Figure 75.3 Distal anterior femorotibial venous graft stenosis angioplasty angiograms demonstrating a severe focal stenosis probably caused by intimal hyperplasia (black arrows). The final result is signaled by the white arrow. Figure 75.1 60∞ RAO angiography of an obese patient demonstrating a flexible structured introducer positioned by a right common femoral artery antegrade access. Note the wideangle angulation of the device, without lumen derangement.
better torquability and should therefore be preferred, unless local conditions preclude its usage. In such cases, the physician should opt either for another access (contralateral, brachial, or popliteal) or to make a small dissection and punch the arterial graft directly. We recommend the use of flexible and structured introducers to avoid kinking when performing antegrade femoral punctures in obese patients (Figure 75.1). A 0.014-inch
floppy-end guidewire under roap-map guidance should be chosen to overcome stenotic lesions (Figure 75.2). When experiencing difficulties placing the 0.014-inch guidewire through occlusive lesions, the use of a 0.035-inch stiff angulated hydrophilic guidewire should be attempted and replaced with a 0.014-inch one. The balloon catheter selection is based on the aimed diameter and non-complacent high-pressure balloons should be preferentially employed. The cutting
Figure 75.2 Roadmap acquisition demonstrating a 0.014-inch guidewire positioning through the stenotic lesion.
Figure 75.4 Balloon angioplasty of a venous posterior femorotibial graft. The black arrow demonstrates the focal stenosis and the white one the final result.
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Textbook of peripheral vascular interventions balloon is an interesting proposal for short focal lesions with intimal hyperplasia. Stent deployment should be reserved for selected cases, when recoil, gradient pressure across the lesion (> 10 mmHg), thrombosis, dissection with limited flow, or rupture occurs after angioplasty. In these cases, either a balloonexpandable, a self-expandable, or a covered stent may be chosen (Figures 75.3–75.5).
Summary Balloon angioplasty of failing infrainguinal vein bypass grafts can be successfully performed with a low complication rate. Acceptable short-term patency can be achieved. This procedure should be considered as an initial option in failing IVB grafts. Figure 75.5 Balloon-expandable stent angioplasty of a focal stenosis probably caused by intimal hyperplasia in a venous femoropopliteal graft (black arrow). The final result is demonstrated by the white arrow.
REFERENCES 1. 2. 3. 4. 5. 6.
7.
8. 9.
10. 11. 12. 13.
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15. 16.
Dorffler-Melly J, Buller HR, Koopman MM et al. Antithrombotic agents for preventing thrombosis after infrainguinal arterial bypass surgery. Cochrane Database Syst Rev 2003; (4): CD000536 Nguyen LL, Conte MS, Menard MT et al. Infrainguinal vein bypass graft revision: factors affecting long-term outcome. J Vasc Surg 2004; 40(5): 916–23 Conte MS, Bandyk DF, Clowes AW et al. Risk factors, medical therapies and perioperative events in limb salvage surgery: observations from the PREVENT III multicenter trial. J Vasc Surg 2005; 42: 456–64 Toursarkissian B, D’Ayala M, Shireman PK, Schoolfield J, Sykes MT. Lower extremity bypass graft revision in diabetics. Vasc Surg 2001; 35(5): 369–77 Kudo T, Chandra FA, Ahn SS. The effectiveness of percutaneous transluminal angioplasty for the treatment of critical limb ischemia: 10-year experience. J Vasc Surg 2005; 41: 423–35 Ihnat DM, Mills JL, Dawson DL et al. The correlation of early flow disturbances with the development of infrainguinal graft stenosis: a 10 year study of 341 autogenous vein grafts. J Vasc Surg 1999; 30: 8–15 Chew DK, Nguyen LL, Owens CD et al. Comparative analysis of autogenous infrainguinal bypass grafts in African Americans and Caucasians: the association of race with graft function and limb salvage. J Vasc Surg 2005; 42: 695–701 Marin ML, Veith FJ, Panetta TF et al. Saphenous vein biopsy: a predictor of vein graft failure. J Vasc Surg 1993; 18: 407–14 Beattie DK, Sian M, Greenhalgh RM et al. Influence of systemic factors on pre-existing intimal hyperplasia and their effect on the outcome of infrainguinal arterial reconstruction with vein. Br J Surg 1999; 86: 1441–7 Fujitani RM, Mills JL and Taylor SM. The “blue-toe” syndrome as a harbinger of impending infrainguinal vein graft failure: a report of three cases. Ann Vasc Surg 1993; 7: 330–5 Idu MM, Blankenstein JD, de Gier P et al. Impact of a color-flow duplex surveillance program on infrainguinal vein graft patency: a five-year experience. J Vasc Surg 1993; 17: 42–52 Hill SL. Duplex scan graft surveillance: how often and in whom? Am Surg 1995; 61(6): 507–12 Davies AH, Hawdon AJ, Sydes MR et al. Is duplex surveillance of value after leg vein bypass grafting? Principal results of the Vein Graft Surveillance Randomised Trial (VGST). Circulation 2005; 112: 1985–91 Passman MA, Moneta GL, Nehler MR et al. Do normal early color-flow duplex surveillance examination results of infrainguinal vein grafts preclude the need for late graft revision? J Vasc Surg 1995; 22: 476–81 Buth J, Disselhoff B, Sommeling C et al. Color-flow duplex criteria for grading stenosis in infrainguinal vein grafts. J Vasc Surg. 1991; 14: 716–26 Westerband A, Mills JL, Kistler S et al. Prospective validation of threshold criteria for intervention in infrainguinal vein
17. 18. 19. 20. 21.
22.
23.
24. 25.
26. 27. 28. 29. 30.
31.
grafts undergoing duplex surveillance. Ann Vasc Surg 1997; 11(1): 44–8 Buth J, Disselhoff B, Sommeling C et al. Color-flow duplex criteria for grading stenosis in infrainguinal vein grafts. J Vasc Surg 1991; 14(6): 716–26 Idu MM, Buth J, Hop WC. Vein graft surveillance: is graft revision without angiography justified and what criteria should be used? J Vasc Surg 1998; 27(3): 399–411 Calligaro KD, Syrek JR, Dougherty MJ. Selective use of duplex ultrasound to replace preoperative arteriography for failing arterial vein grafts. J Vasc Surg 1998; 27(1): 89–94 Gupta AK, Bandyk DF et al Cheanvechai D. Natural history of infrainguinal vein graft stenosis relative to bypass grafting technique. J Vasc Surg 1997; 25(2): 211–20 Jackson MR, Johnson WC, Williford WO. The effect of anticoagulation therapy and graft selection on the ischemic consequences of femoropopliteal bypass graft occlusion: results from a multicenter randomized clinical trial. J Vasc Surg 2002; 35(2): 292–8 Johnson WC, Williford WO. Benefits, morbidity, and mortality associated with long-term administration of oral anticoagulant therapy to patients with peripheral arterial bypass procedures: a prospective randomized study. J Vasc Surg 2002; 35(3): 413–21 Dorffler-Melly J, Koopman MM, Prins MH, Antiplatelet and anticoagulant drugs for prevention of restenosis/reocclusion following peripheral endovascular treatment. Cochrane Database Syst Rev 2005; (1): CD002071 Conrad MF, Shepard AD, Rubinfeld IS et al. Long-term results of catheter-directed thrombolysis to treat infrainguinal bypass graft occlusion: the urokinase era. J Vasc Surg 2003; 37(5): 1009–16 Ouriel K, Shortell CK, Green RM et al. Differential mechanisms of failure of autogenous and non-autogenous bypass conduits: an assessment following successful graft thrombolysis. Cardiovasc Surg 1995; 3(5): 469–73 Berridge DC, al-Kutoubi A, Mansfield AO et al. Thrombolysis in arterial graft thrombosis. Eur J Vasc Endovasc Surg 1995; 9(2): 129–32 Nackman GB, Walsh DB, Fillinger MF et al. Thrombolysis of occluded infrainguinal vein grafts: predictors of outcome. J Vasc Surg 1997; 25(6): 1023–31 Rickard MJ, Fisher CM, Soong CV et al. Limitations of intra-arterial thrombolysis. Cardiovasc Surg 1997; 5(6): 634–40 Mills JL, Fujitani RM, Taylor SM. The characteristics and anatomic distribution of lesions that cause reversed vein graft failure: a five-year prospective study. J Vasc Surg 1993; 17(1): 195–204 Goh RH, Sniderman KW, Kalman PG. Long-term follow-up of management of failing in situ saphenous vein bypass grafts using endovascular intervention techniques. J Vasc Interv Radiol 2000; 11(6): 705–12 Carlson GA, Hoballah JJ, Sharp WJ et al. Balloon angioplasty as a treatment of failing infrainguinal autologous vein bypass grafts. J Vasc Surg 2004; 39(2): 421–6
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Thromboangiitis obliterans (Buerger’s disease) A Pokrovsky and AV Chupin
Introduction The nature of occlusive arterial lesions in young smokers has remained an object of constant debate since 1879, when Von Winiwarter first described a vascular syndrome and called it “obliterative endarteritis.” In 1908, Leo Buerger published his seminal manuscript and then a book (in 1924) devoted to this disease which he called “thromboangiitis obliterans” (TAO). This term has since become widely accepted. TAO was a commonly stated diagnosis in the past. Today this disease occurs far less frequently then two or three decades ago. It must be stressed that TAO is a distinct disease which differs from atherothrombosis and atherosclerosis, and unlike these diseases has a significantly lower prevalence.
Definition Thromboangiitis obliterans (TAO) is a segmental occlusive inflammatory disease of arterial and venous walls with subsequent thrombosis. It occurs primarily in young male smokers1,2 and affects small and medium-sized vessels of upper and lower extremities.
Epidemiology TAO has a worldwide distribution, but the highest incidence is registered in the Middle East and Far East.3,4 The prevalence rate of the disease in the general population of Japan is 5 per 100,000.5 TAO prevalence among patients with peripheral arterial disease varies from 0.5–5.6% in Western Europe to 45–63% in India; 16–66% in Korea and Japan, and 80% in Israel among Jews of Ashkenazi ancestry. This variance may be attributed partly to differences in diagnostic criteria.6,7
Etiology and pathogenesis Hereditary preponderance or genetic disposition is thought to be a primary factor in etiopathogenesis of TAO. In recent years a new concept has been proposed concerning the crucial role of host histocompatibility antigens in several major immunological functions, giving a key for understanding of interaction mechanisms between HLA-antigens and pathological processes. HLA genes are involved in the regulation of
immune responses and/or can mediate immunological reactions.9 It was found that A1, B5, B7, B8, B9, and DRW2 antigens are more common in patients with TAO than in healthy subjects. For example, antigen HLA-B5 increases the risk of TAO by 78.2%. Nevertheless, genetic disposition may never come into effect in the absence of external promoting factors, including tobacco use. Smoking is known to aggravate the disease and attenuate treatment effectiveness. TAO is often defined as “the disease of young tobacco smokers” – 98% of patients are heavy smokers; some authors reports 100% of tobacco use among TAO patients.9 Tobacco smoke affects humans in different ways. The most deleterious components of smoke are carbon monoxide, conitine (the main metabolite of nicotine), and glycoprotein antigen, which plays a primary role in triggering autoimmune responses. These smoke components can serve as antigens and enhance hypersensitiveness. This fact is proved by the increased IgE level in plasma of people with prolonged smoking history. It has been shown that nicotine and carboxyhemoglobin elicit functional and structural changes in endothelial cells. Tobacco use affects thromboxan A2 and prostacyclin biosynthesis with subsequent impairment of blood rheology and endothelial function. Besides, some authors do not exclude deviations of antigen structure in vascular intima due to tobacco hypersensitivity. Thus smoking should be viewed as a risk factor of TAO, which can trigger the delayed hyperergic reaction in patients with respective genetic disposition. Recent literature has suggested an autoimmune nature of TAO genesis. The pathological process begins with multiple tears of the internal elastic membrane. Histological examination reveals granulomas with giant cells in sites of internal elastic membrane ruptures, containing IgG, anaphylotoxins C3a, C5a, and circulating immune complexes. Antigens (changed endothelial cells) that appear due to vascular wall lesions activate T- and B-components of the immune reaction.10 Activated T-cells, bioactive amines, antivascular antibodies, circulating immune complexes, and anaphylotoxins elicit proliferative inflammation of the vascular wall; increasing its permeability, platelet and neutrophil aggregation, and causing vasoconstriction. Hence immune inflammation, as a form of immediate and delayed hypersensitivity, appears to be the background of vascular pathology in TAO. Productive arteritises with cellular immune lesions of vascular wall predominate 661
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in TAO. Necrotic (destructive-infiltrative and destructive-proliferative) arteritises are less common and also have a cellular immune mechanism of vascular damage. Vascular wall inflammation causes local impairment of blood flow and tissue ischemia. This in turn leads to a significant regional decrease of the main components of the anticoagulation system (antithrombin III, antithrombin reserve), drastic slowing of Hageman-factor-dependent fibrinolysis and euglobulin lysis. Local lesion of arterial and venous walls is accompanied by a significant increase in Willebrand factor level and both spontaneous and ADP-induced platelet aggregation. Activation of local hemostatic mechanisms (both vascular and platelet) and increased blood coagulation parameters due to progressive pathological process in the vascular wall, and depletion and inhibition of anticoagulatory and plasmin paths all lead to a constant locally prethrombotic situation in vessels of affected extremity. Immune inflammation in TAO takes place not only in arteries, but also in veins and microcirculation vessels (arterioles, capillaries, and venules) (Figure 76.1). Immune complexes can be found in the walls of these vessels during destructive processes. Immunological changes in vascular walls are accompanied by mucoid swelling of the intima and adventitia, destruction and dystrophy of endothelium, inflammatory infiltration, and – as a result – thrombosis of the
(a)
affected vessel.11 Thus, immune reactions causing the damage of vascular endothelium can be considered primary in TAO pathogenesis. Blood hypercoagulation plays a secondary but very important role. Immune complexes were found in vascular tissues in 100% of cases; autoimmune antibodies to the vascular wall in 86%.12 The schematic sequence of events in TAO pathogenesis can be described as follows: genetic disposition, smoking, triggering of the autoimmune reaction, vascular wall swelling and damage, and local thrombosis. The clear understanding of this pattern is essential for the development of a treatment strategy for TAO patients. Peripheral endothelium-dependent vasodilatation was shown to slow down in patients with TAO, while non-endothelial mechanisms of vasodilatation remain unchanged.13 The role of hyperhomocysteinemia in TAO pathogenesis is unclear.14 One cannot exclude the interaction between such thrombophilic states as antiphospholipid syndrome and TAO.15
Clinical features TAO is most prevalent in young male adults (18–40 years) and affects distal segments of major arteries of upper and lower extremities. In 25–65% of cases pathological process is localized
(b)
(c) Figure 76.1 Electronic microscopy showing thromboangiitis obliterans of: (a) arteries; (b) veins; and (c) arterioles and venules. (See Color plates.)
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Thromboangiitis obliterans (Buerger’s disease) in major arteries of the upper limbs.16 In our study, angiographic investigation of upper limbs has revealed arterial lesions in more then 60% of 125 patients, while clinical symptoms were present only in 23% of them. In rare cases lesions are localized in visceral, coronary, and brachiocephalic arteries. The most severe lesions involve visceral arteries, primarily the celiac trunk17 and upper mesenterial artery.18 Mesenterial arterial lesions occur in 5–7% of cases.16 Sometimes “abdominal complaints” appear prior to clinical symptoms in lower limbs and embarrass differential diagnosis.19 According to the literature, mortality rate in the intestinal form of TAO is as high as 25 versus 4% in peripheral forms of the disease. This fact stresses the importance of early diagnosis of intestinal TAO. Doppler ultrasonography of mesenterial arteries may enhance early diagnosis.20 Three variants of the disease progression are known: acute malignant generalized course, prevalent in young patients (18–25 years) which becomes systemic in 3 months to 1 year; 2. subacute oscillatory course with recurrent relapses and remissions of different duration; 3. chronic gradually progressive course – the disease develops for several years with long period of compensated regional circulation, in the absence of pronounced aggravations.
Figure 76.2
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Toe gangrene in thromboangiitis obliterans.
1
The last variant is the most favorable. The chronic course is more prevalent in patients 30–35 years old and is often accompanied by atherosclerosis later on. Clinical progression of TAO can be principally divided into two stages – functional/spastic and obliterative/organic. Spastic stage has poor symptomatology (numbness, paresthesia, undulating coldness). These complaints are transient and patients are deprived of physician’s attention and appropriate health care. The obliteration stage of distal arterial vasculature is characterized by the development of regional ischemia and stabilization of clinical signs. Increased perception of coldness, limb fatigability, numbness, dyshidrosis, and paresthesia manifest first, followed by intermittent claudication and pain in the foot arch and toes. Trophic disturbances gradually aggravate: diminished skin tonus and elasticity, hypothermia, impaired hidrosis, discoloration, and altered growth of nails and hair. Paronychia and panaritium are quite common, along with atrophy of the leg and foot skin, subcutaneous tissues, and muscles. Trophic alterations can also involve foot bones. Further progression of the disease can lead to irreversible trophic disturbances: superficial and then deep ulcers and gangrene (Figure 76.2). Ulcers are resistant to conservative treatment, prone to infection, painful even at rest, and force the patient to set the extremity in an involuntary position. Late stages of TAO are characterized by paralysis of capillaries, lymphangitis and phlebitis with thermal reaction, foot and leg cyanosis, and moist gangrene. Along with severe regional ischemia the patient usually demonstrates symptoms of general intoxication and sepsis. The standard Fontaine four-graded classification of limb ischemia is used for clinical characterization of TAO: ●
grade I – subclinical signs (corresponding to spastic stage of the disease);
● ● ●
grade II – symptoms of intermittent claudication; grade III – development of rest pain; grade IV – foot ulcerative and necrotic defects.
Diagnostic criteria Today TAO diagnosis is usually based on two main sets of diagnostic criteria: ●
●
Shionoya’s21 diagnostic criteria include: 䊊 history of smoking; 䊊 onset before the age of 50 years; 䊊 infrapopliteal arterial occlusions; 䊊 either arm involvement or phlebitis migrans; 䊊 the absence of risk factors for atherosclerosis other than smoking. Olin’s22 diagnostic criteria include: 䊊 age of less than 45 years; 䊊 current (or recent) history of tobacco use; 䊊 the presence of distal-extremity ischemia (indicated by claudication, rest pain, ischemic ulcers, or gangrene) documented by non-invasive vascular testing; 䊊 exclusion of autoimmune diseases, hypercoagulable states, and diabetes mellitus by laboratory tests; 䊊 exclusion of a proximal source of emboli by echocardiography and arteriography; 䊊 consistent arteriographic findings in the clinically involved and non-involved limbs.
Diagnostic investigation Usually TAO does not involve aortic branches. Thus there are no sounds above the femoral arteries, abdominal aorta, and aortic branches, typical for atherosclerotic lesions. Characteristic involvement of distal arteries is diagnosed by palpation of the dorsal foot arteries, posterior tibial artery, popliteal artery, radial, and ulnar arteries. Significant decrease or the absence of pulsation is evidence of organic arterial damage.
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Diagnostic imaging is used for the assessment of macro- and microcirculation in the affected extremity. Complex ultrasonography can visualize regional macrohemodynamics, measure segmental arterial pressure at the level of upper and lower third of the thigh and leg, with calculation of ankle–brachial index (ABI), as well as enabling spectral analysis of the Doppler signal to determine the type of blood flow in affected arterial segments. TAO patients have higher ankle blood pressure and ABI than patients with corresponding clinical ischemic stages of atherosclerotic origin. This is due to increased rigidity of affected tibial arteries and their resistance to compression in TAO patients. It must be stressed that ABI measurement is important for treatment monitoring and follow-up of patients. Duplex scanning is an obligatory component of complex ultrasonic investigation and is fulfilled at every level of the extremity, from femoral to foot arteries. This investigation gives a complete picture of affected vasculature and helps to evaluate the possibility of saphenous vein use for grafting during the surgery planning. Duplex scanning can also control the patency of an arterial prosthesis after reconstructive interventions. Modern modalities of diagnostic imaging, such as multislice CT and MR-angiography, are of a certain value for diagnosis and differential diagnosis of TAO. MRA can be actively used for the diagnosis of other vascular beds when multifocal TAL is suspected. The final method of diagnostic assessment of distal arterial lesions is selective angiography through transfemoral (contralateral extremity) or transaxillary access. Angiography often reveals lesions in a “healthy” extremity. Multiple segmental occlusions of limb distal arteries are characteristic of TAO; each occlusion can have one of two features: obliqueness or abruptness. The arterial wall proximal to an occlusion is usually smooth. The “wrinkled” appearance of femoral or tibial arteries often reflects the very TAO lesion and occasional arterial spasm. Extensive collateral vasculature surrounding occlusion is quite common. It can maintain blood supply in the extremity despite the occlusion of all major arteries of the leg. These collaterals have a characteristic spiral or root-shaped appearance (Figure 76.3). The angiographic picture of upper limb arterial lesions is similar to that of lower limbs. Unlike atherosclerosis obliterans, TAO lesions lack calcinosis of the vascular wall and mosaic defects of arterial outline. Although clinically evident cases of TAO can be successfully diagnosed and managed without angiography, this diagnostic modality is strongly recommended for unclear cases and planning of surgical reconstructions. The most informative method of diagnostic assessment of microcirculation in the affected limb is transcutaneous oxygen tension measurement (TCOM) in the foot. TCOM is carried out with the patient in a sitting or supine position. Aggressive intravenous infusion therapy is indicated when oxygen tension is less then 30 mmHg in the supine position. If oxygen tension does not exceed 10 mmHg, it is unreasonable to expect a positive effect from conservative treatment. If appropriate, vascular reconstructive intervention is indicated in this case, considering unfavorable prognosis of the disease. Laboratory findings There are no specific laboratory tests to aid in the diagnosis of TAO. Increase in Westergren sedimentation rate or leucocytosis
are practically absent. In our 282 patients with TAO (clinical signs of critical ischemia) these parameters were in the normal range; the rise was found only in patients with foot moist necrosis. At the same time, elevation of C-reactive protein (CRP) level was evident in more than 60% and correlated with the clinical activity index of vasculitis. Attention must be paid to parameters of cellular and humoral immunity, though they usually reflect an exhaustion of immune reaction to active autoimmune processes. Indicative of true TAO activity are humoral immunity parameters, including circulating immune complexes (CIC), IgG, and IgM. Their rise can serve as an indication for anti-inflammatory therapy. Increased humoral immunity parameters were found in 59 from 66 patients treated in our clinic (2.6-fold increase of CIC, 4.1-fold increase of IgG, and 2.3-fold increase of IgM). All of them received non-specific anti-inflammatory therapy. Differential diagnosis The distal nature of TAO and the involvement of the legs and arms help to differentiate it from atherosclerosis (specific angiographic picture). To differentiate from vasculitis it is important to consider the results of morphological investigation. In cases of TAO the internal elastic membrane and media are intact, unlike the usual destruction of these layers in systemic vasculitis.23 An abnormal result in the Allen test24 in young smokers with leg ulcerations is highly suggestive of TAO. This test demonstrates small-vessel involvement in both arms and legs, which is absent in atherosclerosis. But an abnormal result can also be present in other types of small-vessel occlusive disease of hands, such as scleroderma, the CREST syndrome, repetitive trauma, emboli, hypercoagulable states, and vasculitis.
Treatment The main effective strategy of TAO therapy is smoking cessation. Thus patients with TAO diagnosis must completely discontinue the use of tobacco to prevent progression of the disease and avoid amputation.25,26 Even smoking one or two cigarettes a day, using nicotine replacement, or chewing tobacco may keep the disease active.27,28 If there was no gangrene when the patient discontinued smoking, amputation did not occur. Without cessation of tobacco use patients are at a high risk of finger, toe or limb amputation Patients must avoid thermal, chemical and mechanical trauma, especially caused by unsuitable shoes or with minor surgery of toes and fungal infection. They must avoid vasospastic reactions provoked by prolonged cold exposition. Complex drug therapy includes microcirculationnormalizing agents (pentoxifylline, cylostazol) and anticoagulants (aspirin, ticlopidine, and clopidogrel in therapeutic doses). The course of intravenous infusions with lowmolecular dextrans (rheopolyglucinum) can be recommended in doses of 400 ml/day for 10 days. Patients with TAO stages III and IV (critical limb ischemia), rest pain, and trophic disturbances are treated in hospital. Prolonged epidural blockades can be indicated, since they were shown to improve effectively regional circulation. Blockades are fulfilled through a constant microirrigator
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(b)
(c) Figure 76.3
Typical lesion of leg and foot arteries in thromboangiitis obliterans.
inserted into the epidural space at level LI–II with 2% solution of trimecaine (10 ml, 3–6 times per day for 7–10 days) as an anesthetic. Despite a leading role of inflammation in the pathogenesis of TAO, anti-inflammatory agents (such as steroids) are used extremely rarely. Nevertheless, in our opinion, the acute inflammatory process, demonstrated by a rise of humoral immunity parameters (CIC, IgG, IgM) and CRP, can be an indication for anti-inflammatory treatment such as loading pulse therapy (depo-prednisolon, cytostatics). It can significantly increase the effectiveness of treatment, especially for patients with critical ischemia. We use the following protocol of pulse therapy: day 1 – depo-prednisolon (1 g) + cytostatics (1 g); days 2 and 3 – depo-prednisolon (1 g); day 7 – cytostatics (1 g). One course of pulse therapy was effective in 47 of 59 (79.7%) patients treated in our clinic, according to IgM and
CRP levels as control parameters of drug therapy effectiveness. If patients did not respond to the first course, they received the second one with a week interval. Intravenous therapy with prostaglandins (E1 and E2) was shown to improve microcirculation and enhance complete healing of trophic lesions. A prostaglandin analogue iloprost is also used for critical ischemia. It was effective in pain syndrome resolution for 63% of patients and for trophic ulcer healing in 35% of cases. Iloprost elicits more adverse reactions then prostaglandin E1, including hypertension, headache, and numbness.29,30 Prostaglandin E1 is used as monotherapy or in combination with revascularization procedures. As monotherapy it appears effective for critical ischemia in 55–70% of cases.31,32 We used prostaglandin E1 (vazaprostan) in 78 TAO patients with lower limb critical ischemia and achieved elimination of correspondent symptoms in 51
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(65.4%) of them. Another 20 patients (25.6%) demonstrated improvement – attenuation of pain, decrease in limb coldness, and cleaning of necrotic suppurative wound. Although acetylsalicylic acid (aspirin) is widely prescribed for patients with TAO, controlled studies did not prove the effectiveness of this agent and other anticoagulants. Transluminal angioplasty is feasible for TAO when major or medium-sized vessels are involved while distal vasculature remains intact. Such cases occur extremely rarely. Arterial reconstructions are impossible in most cases due to the diffuse nature of lesions and their distal localization.25 Reconstruction of distal arteries has arguable usefulness as the risk of failure remains high.33 Nevertheless the appropriateness of bypass procedures with autovein grafting should be discussed for patients with severe ischemia and patent distal circulation. Sasajima et al. retrospectively reviewed the results of 71 infrainguinal bypasses in 61 patients with TAO.34 There were 38 graft failures, the main causes including anastomosis to a diseased artery, disease progression (which occurred in smokers after surgery), and vein graft stenosis. Of 38, 10 were restored to patency by revision surgery. Primary and secondary patency rates were 48.8 and 62.5% at 5 years, respectively. The patency rate in the non-smoking group was significantly higher than in those who continued to smoke (66.8 vs. 34.7%, respectively). The authors conclude that bypass to the distal arteries is an effective treatment for TAO patients, and the long-term patency is quite satisfactory as long as patients stop smoking.34 When the standard reconstructive interventions are unfeasible in the absence of patent leg and foot arteries, the only alternative for limb amputation can be non-standard methods of distal revascularization – omental transplantation to the leg and recanalization with venous flow reversion. Omental grafts can be free or pedicled. Talwar et al.35 compared clinical outcomes of free omental graft transfer (15 patients, first group) and pedicled omental transplantation (28 patients, second group). Two groups demonstrated similar results: the relief of intermittent claudication (80 vs. 82% in the first and second groups, respectively), rest pain (82 vs. 91%), coldness (83 vs. 87%), discoloration (80 vs. 82%), ulcer epithelization (75 vs. 78%), and post-amputation ulcer healing (75 vs. 86%). But the time taken for symptom relief was significantly less in the second group. These findings are evidence of the similar effectiveness of both methods and support a possible local action of the omentum. Similar results were demonstrated in another study on pedicled omental transfer for ischemic limbs.36 Bhargava et al. treated 56 patients (78 limbs) suffering from chronic occlusive arterial disease. Improvement in intermittent claudication was achieved in about 85% of patients, relief from rest pain in 86%, and healing of chronic ulcers in 73% of patients. Objective control was carried out with plethysmography. Relief from ischemia was more prominent in cases of TAO than in cases of atherosclerosis obliterans.36 Lower limb critical ischemia was coped in 67% of patients with TAO, trophic ulcers healed in 2–4 weeks in cases of successful procedures. Outcomes were followed-up after 4 years; recurrent ischemia only developed in 5% of patients. So, the omental graft transplantation to leg can achieve the resolution of critical ischemia in 67–86% of cases with a
prolonged and stable positive effect. The 5-year rate of ischemia recurrence is as low as 5–10%. Thus, omental transfer can be considered a method of choice for limb salvage in cases of critical ischemia when standard reconstructive interventions are impossible. But the positive effect of the procedure develops only 3–4 weeks after the operation. Arterialization of foot venous circulation is another type of surgical treatment of critical ischemia in patients with TAO. This method was suggested by Sheil in 197737 and was further improved and actively used in the Department of Vascular Surgery, AV Vishnevsky Institute of Surgery in Moscow (Figure 76.4). More then 130 procedures of venous flow arterialization were fulfilled there, including 69 patients with TAO and critical ischemia. Critical ischemia was eliminated in the early post-operative period in 80% of cases (Figure 76.5). Five years post-operatively, functional capacity was preserved in 75–80% of limbs.38 Sympathectomy can be fulfilled without preliminary tests with nitroglycerin to check arterial spasm in patients with TAO. Preference should be given to laparoscopic or thoracoscopic sympathectomy.39,40 This method yields more benefits in patients with infrapopliteal lesions (direct improvement was achieved in 88% of cases) than with femoropopliteal disease (the rate of success was only 35.4%). Sympathectomy has a good early effect on pain relief and trophic ulcer healing in some patients with TAO, but fails to provide long-term benefits.39 Results of spinal cord stimulation and intramuscular administration of vascular epithelial growth factors gene therapy in patients with TAO have been published and promised good perspectives.41,42 Limb amputation is indicated for patients with stage IV critical ischemia, when all types of complex therapy were tried and failed. Correct level of amputation is crucial for adequate post-operative healing of the limb stump. The choice of amputation level should be guided by transcutaneous oxygen tension values, measured at different levels of the affected limb. An oxygen level exceeding 40 mmHg is necessary for adequate healing of the surgical wound (Figure 76.6).
Conclusion – prognosis TAO is characterized by the occlusion of peripheral arteries in young smokers. Despite a low prevalence of the disease in Europe and the US, its therapy remains a major challenge for vascular surgeons. The cause of TAO is unknown, but there is an extremely strong association between the heavy use of tobacco, and TAO onset and progression. When patients stop smoking, the natural history of the disease is beneficial. Despite a high rate of toe gangrene and foot ulcers, leg function can be preserved almost always, given a good potential of spontaneous healing of trophic changes. Clearer understanding of real TAO progression not only has a predictive significance, but is important for determining the place of surgical and conservative methods in treatment planning. The analysis of our own results (52 arterial reconstructions) has shown that in patients, who completely quit smoking, a 5-year cumulative patency of arterial reconstructions was 71.6%, compared with 21.1% in those who continued smoking. Further more, in 43.3% of patients, who preserved the
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(a) Figure 76.4
The scheme of deep venous system arterialization of foot in a patient with thromboangiitis obliterans.
(a) Figure 76.5
(b)
(b)
Foot angiogram of a patient with thromboangiitis obliterans before and after venous blood flow arterialization.
667
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Textbook of peripheral vascular interventions dose of tobacco after treating critical ischemia, recurrence occurred in 1 year and led to limb amputation in 38.5% of cases. In a group of patients with total smoking cessation, the 1-year rate of recurrent critical ischemia was 6.9% with a favorable outcome in all cases. This fact proves the necessity of complete discontinuation of tobacco use in patients with TAO.
Figure 76.6 Determination of amputation level in a patient with thromboangiitis obliterans according to transcutaneous oxygen tension data.
REFERENCES 1. 2. 3. 4. 5. 6.
7. 8. 9. 10. 11. 12. 13.
14. 15. 16.
Buerger L. Thromboangiitis obliterans: a study of the vascular lesions leading to presenile gangrene. Am J Med Sci 1908; 136: 567–80 Buerger L. The Circulatory Disturbance of the Extremities: Including Gangrene, Vasomotor and Trophic Disorders. Philadelphia: Saunders, 1924 Lie JT. Thromboangiitis obliterans (Buerger’s disease) revisited. Pathol Annu 1988; 23: 257–91 Lie JT. The rise and fall and resurgence of thromboangiitis obliterans (Buerger’s disease). Acta Pathol Jpn 1989; 39: 153–8 Shionoya S. Buerger’s disease (thromboangiitis obliterans). In: Rutherford, Vascular Surgery, fourth edition. Philadelphia: WB Saunders, 1994: 235–45 Cachovan M. Epidemiologic und geographisches Verteilungsmuster der Thromboangiitis obliterans. In: Thromboangiitis obliterans Morbus Winiwarter-Buerger. Heidrich H, ed. Stuttgart: Georg Thieme, 1988: 31–6 Matsushita M, Nishikimi N, Sakurai T, Nimura Y. Decrease in prevalence of Buerger’s disease in Japan. Surgery 1998; 124: 498–502 Aerbajinai W, Tsuchiya T, Kimura A, Yasukochi Y, Numano F. HLA class II DNA typing in Buerger’s disease. Int J Cardiol 1997; 54 (suppl.): S197–202 Sayin A, Bozkurt AK, Tuzun H et al. Surgical treatment of Buerger’s disease: experience with 216 patients. Cardiovasc Surg 1993; 1(4): 377–80 Ledford DK. Immunologic aspects of cardiovascular disease. JAMA 1992; 268(20): 2923–9 Lie JT. Buerger’s disease and inflammatory aspects of atherosclerosis. Curr Opin Rheumatol 1990; 2(1): 76–80 Li L. Preliminary application of the immunogold-silver staining technique in diagnosing thromboangiitis obliterans. Chung Hua Wai Ko Tsa Chih 1989; 27(4): 233–5 Makita S, Nakamura M, Murakami H et al. Impaired endotheliumdependent vasorelaxation in peripheral vasculature of patients with thromboangiitis obliterans (Buerger’s disease). Circulation 1996; 94: 211–5 Diehm C, Stammler F. Thromboangiitis obliterans (Buerger’s disease). N Engl J Med 2001; 344: 230–1 Adar R, Papa MZ, Schneiderman J. Thromboangiitis obliterans: an old disease in need of a new look. Int J Cardiol 2000; 75: 167–70 Fernandez-Miranda C, Rubio R, Vicario JL et al. Tromboangitis obliterante (enfermedad de Buerger). Estudio de 41 casos. Med Clin Barc 1993; 101(9): 321–6
17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31. 32. 33.
Durand JM, Lefevre P, Kaplanski G. et al. Thromboangiitis obliterans associated with coeliac disease. Cardiovasc Surg 1993; 1(3); 273–5 Kempczinski RF, Clark SM, Blebea J, Koelliker DD, FenoglioPreiser C. Intestinal ischemia secondary to thromboangiitis obliterans. Ann Vasc Surg 1993; 7(4): 354–8 Sauvaget F, Debray M, Herve-de-Sigalony JP et al. Colonic ischemia reveals thromboangiitis obliterans (Buerger’s disease). Gastroenterology 1996; 110(3): 900–3 Nyuyen TB, Quere S, Galezowski N, Brisset D. Maladie de Buerger revelee par une perforation digestive. A propos d’un cas et revue de la litterature. Rev Med Interne 1996; 17(1): 70–5 Shionoya S. Diagnostic criteria of Buerger’s disease. Int J Cardiol 1998; 1: 243–45 Olin JW. Thromboangiitis obliterans (Buerger’s disease). N Engl J Med 2000; 343: 864–9 Olin JW, Lie JT. Thromboangiitis obliterans (Buerger’s disease). In: Loscalzo J, Creager MA, Dzau VJ, eds. Vascular Medicine, second edition. Boston: Little Brown; 1996: 1033–49 Olin JM, Lie JT. Thromboangiitis obliterans (Buerger’s disease). In: Current Management of Hypertensive and Vascular Diseases. Cooke JP, Frohlich ED, eds. St Louis: Mosby, 1992: 265–71 Olin JW, Young JR, Graor RA, Ruschhaupt WF, Bartholomew JR. The changing clinical spectrum of thromboangiitis obliterans (Buerger’s disease). Circulation 1990; 82: IV3–8 Shionoya S. What is the Buerger’s disease? World J Surg 1983; 7: 544–51 Joyce JW. Buerger’s disease (Thromboangiitis obliterans). Rheum Dis Clin North Am 1990; 16: 463–70 Lie JT. Thromboangiitis obliterans (Buerger’s disease) and smokeless tobacco. Arthritis Rheum 1988; 31: 812–3 Diehm C, Stammler F. Thrombangiitis obliterans (Buerger-Syndrom). Klinik, Diagnostik und Theraple. Dtsch Med Wochenschr 1996; 121(49): 1543–8 Hildebrand M. Pharmacokinetics and tolerability of oral iloprost in thromboangiitis obliterans patients. Eur J Clin Pharmacol 1997; 53(1): 51–6 Kowal-Gierczak B, Kurzawska-Mielecka M, Czarnacki M. Prostaglandyna E1 w leczeniu przewleklego niedokrwienia konczyn. Pol Arch Med Wewn 1990; 84(5): 321–7 Miyauchi Y. Treatment of the peripheral vascular diseases with prostaglandin. Nippon Rinsho 1994; 52(8): 2182–6 Inada K, Iwashima Y, Okada A, Matsumoto K. Nonatherosclerotic segmental arterial occlusion of the extremity. Arch Surg 1974; 108: 663–7
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Sasajima T, Kubo Y, Inaba M, Goh K, Azuma N. Role of infrainguinal bypass in Buerger’s disease: an eighteen-year experience. Eur J Vasc Endovasc Surg 1997; 13: 186–92 Talwar S, Jain S, Porwal R, Laddha BL, Prasad P. Free versus pedicled omental grafts for limb salvage in Buerger’s disease. Aust NZ J Surg 1998; 68(1): 38–40 Bhargava JS, Makker A, Bhargava K et al. Pedicled omental transfer for ischaemic limbs – a 5-year experience. J Indian Med Assoc 1997; 95(4): 100–2 Sheil AGR. Treatment of critical ischemia of the lower limb by venous arterialization: an interim report. Br J Surg 1977; 64: 197–9 Pokrovsky AV, Dan VN, Chupin AV, Khorovets AG. Arterialization of the foot venous system in the treatment of the critical lower limb
39. 40. 41. 42.
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ischemia and distal arterial bed occlusion. J Cardiovasc Surg 1998; 39(suppl.1): 171-8 Chander J, Singh L, Lal P et al. Retroperitoneoscopic lumbar sympathectomy for Buerger’s disease: a novel technique. JSLS 2004; 8: 291–6 Lau H, Cheng SW. Buerger’s disease in Hong Kong: a review of 89 cases. Aust NZ J Surg 1997; 67: 264–9 Swigris JJ, Olin JW, Mekhail NA. Implantable spinal cord stimulator to treat the ischemic manifestations of thromboangiitis obliterans (Buerger’s disease). J Vasc Surg 1999; 29: 928–35 Isner JM, Baumgartner I, Rauh G et al. Treatment of thromboangiitis obliterans (Buerger’s disease) by intramuscular gene transfer of vascular endothelial growth factor: preliminary clinical results. J Vasc Surg 1998; 28: 964–73
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Percutaneous endovascular treatment of peripheral aneurysms M Henry, I Henry, and M Hugel
Introduction Peripheral arterial aneurysms are relatively uncommon diseases.1,2 They may present incidentally and asymptomatic (discovery for example on echography or on a computed tomography (CT) scan carried out for another disease), or following complications such as rupture, compression, or thromboembolism. These aneurysms have traditionally been treated surgically but the operative risks are high, particularly when surgery is required on an emergency basis.3,4 An endovascular treatment has been recently proposed involving the following two techniques: ●
●
placement of a stent-graft following arteriotomy due to the large size of the prosthesis;5,6 percutaneous implantation of an endoprosthesis (mostly covered).7–14
This minimally invasive technique avoids surgical incision and should reduce morbidity and mortality associated with surgical repair of peripheral aneurysms. We report our experience of percutaneous endoluminal treatment of 52 peripheral aneurysms (50 patients) using covered stents in the majority of the cases.
Patients and methods Fifty patients underwent elective percutaneous endovascular treatment of 52 peripheral aneurysms. Two patients had bilateral aneurysms (1 femoral and 1 iliac). Forty-three patients were males, 7 were females, with a mean age of 65.8 ± 10 years (range 47–85 years). The risk factors were smoking in 37 patients, hypertension in 29, dyslipidemia in 29 and diabetes in 12. Twenty-four patients also had concomitant coronary artery disease; 7 presented with severe respiratory insufficiency; and 2
Table 77.1
Location
had renal failure. All patients presented with clinical arterial defects of the lower limbs (mean arterial brachial pressure index 0.62 ± 0.16). According to Rutherford’s classification, 17 patients were in category 1, 25 were in category 2/3 and 8 in category 4. With regards to the distal run-off, 7 patients had one, 24 had two, and 21 had three distal patent arteries. Nine patients also had an associated aneurysm of the abdominal aorta, but these aneurysms were not large enough to be referred to surgery. In all patients the clinical assessment consisted of an arterial duplex scan examination, a front and profile arteriography of the abdominal aorta and distal arteries, and a computed tomography (CT) scan. This was to determine the precise localization of the aneurysm, its size (length, diameter), shape, the presence of a major arterial branch within the aneurysm (problem of the internal iliac artery for the iliac localizations), and position as compared to the healthy artery (important for fixation of the prosthesis in the healthy artery). The aneurysms involved the following arteries: ●
● ●
iliac: 25 cases involved the common iliac artery and 1 involved the internal iliac artery; femoral: 13 cases; popliteal: 13 cases.
The lesion characteristics are summarized in Table 77.1. The aneurysms were atheromatous in 48 cases. Two were false aneurysms that developed at the distal extremity of a Cragg Endoprop System I stent, which had been placed after recanalization of the femoral artery (n = 1) and popliteal artery (n = 1). Two aneurysms were of infectious origin (post-angioplasty and stenting of common iliac arteries). The endovascular therapy was decided 3 months after a prolonged treatment with antibiotics and disappearance of the infection. Indication for treatment of the aneurysm depended on clinical criteria (severity of intermittent claudication due to associated
IFPA lesion characteristics
No.
Mean lesion length (mm)
Iliac 26 55.6 ± 28.8 (10–150) Femoral 13 95.6 ± 95.3 (20–290) Popliteal 13 73 ± 71.8 (20–260) IFPA = Iliofemoro popliteal aneurysms
670
Mean lesion diameter (mm) 30 ± 13.4 (13–80) 20 ± 9.7 (8–40) 19.8 ± 8 (12–35)
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IFPA – type of stents
Stents Covered stents Cragg/Passager Corvita Endotex Wallgraft Viabahn Stent graft Non-covered stents Palmaz Optimed Expander Wallstent Total
Iliac
Femoral
Popliteal
Total
32 9 20 1 1 1 1 2
19 13 5 — 1 — — —
16 12 3 — — 1 — 3
67 34 28 1 2 2 2 5
1 1 — — 34
— — — — 19
— — 2 1 19
1 1 2 1 72
stenoses), or on anatomical criteria (diameter of the aneurysm, estimated on angiography or on CT scan, with risks of rupture). Different prostheses were used to treat these aneurysms. Table 77.2 summarizes the different prostheses and the sites of their implantation. The first aneurysm we treated was located in the common iliac artery. It was treated with a stent-graft consisting of a polytetrafluorethylene (PTFE) prosthesis (IMPRA) sutured on two P204 Palmaz stents (Cordis/J&J, Warren, NJ), placed by the percutaneous approach through a 12-French introducer sheath. Four aneurysms were treated with non-covered stents: ●
●
●
●
671
One pseudoaneurysm, associated with a stenosis, developed in the distal part of a Cragg Endopro System I stent, which had been implanted 2 years earlier for treatment of a popliteal occlusion. A Wallstent stent (7 mm in diameter, 3 cm in length) was then implanted with an excellent result. One isolated aneurysm was situated in the internal iliac artery. The ostium of this artery presented a very tight stenosis. Adjacent to it, there was a tight stenosis in the external iliac artery. A selective catheterization of the internal iliac artery was performed by a contralateral approach, and embolization was done using several coils (Cook, Bloomington, IN). The angioplasty of the initial part of the external iliac artery led to total occlusion of the internal iliac artery, thereby excluding the aneurysm. A P304 Palmaz stent was then placed, covering the ostium of the internal iliac artery and the initial part of the external iliac artery, providing an excellent result. The exclusion of the aneurysm was confirmed on the CT scan. One aneurysm in the common iliac artery, adjacent to a tight stenosis, was treated with a self-expandable nitinol stent (Optimed, Medcare, Franconville, France) with a very good result. One aneurysm in the popliteal artery was treated with a self-expandable nitinol Expander stent (Bolton Medical) with a very good result.
All the other aneurysms were treated with covered stents. To avoid migration, the size of the stents used was 10–20% larger
than the normal size of the artery. We used six types of prostheses, as outline below. The Cragg Endopro System 1 or Passager (Boston Scientific, Natik, MA) The technical characteristics of this prosthesis have been described.7,9–13 It was often used in the treatment of occlusive iliofemoropopliteal lesions.11–13 Twenty-two aneurysms were treated with this endoprosthesis (eight at the iliac level, seven at the femoral level, and seven at the popliteal level). The origin of the internal iliac artery was involved in one patient presenting with an iliac aneurysm. To prevent retrograde filling of the aneurysm, transcatheter coil embolization of the internal iliac artery was performed prior to the placement of the covered stent. The Corvita prosthesis (formerly developed by Schneider/Boston Scientific) This prosthesis consists of two main components: a selfexpanding cylindrical wire structure and a highly porous and elastic coating consisting of polycarbonate urethane. It exists in various lengths and sizes and can be cut to the required length by the user. Twenty-one aneurysms were treated by Corvita prosthesis implantation using either the percutaneous retrograde approach (n = 13), the antegrade approach (n = 6) or the contralateral approach (n = 1). The popliteal approach was used in one case. The introducer size ranged between 7 and 12 French. The Wallgraft (Boston Scientific) This prosthesis was used to treat an aneurysm in the common iliac artery and one aneurysm in femoral artery, with success. A new Endotex prosthesis (in experiment) This prosthesis was used once to treat a common iliac aneurysm with immediate success. This stent consists of a flat sheet of nitinol covered with polyester.
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IFPA – Immediate results: length of prosthesis
Location
No.
Iliac Femoral Popliteal
26 13 13
Mean lesion length (mm) 55.6 ± 28.8 (10–150) 95.6 ± 95.3 (20–290) 76 ± 72.2 (20–260)
The Jostent covered stent (Jomed AB, Helsingborg, Sweden) This balloon-expandable prosthesis is available in lengths ranging from 28 to 58 mm and its expansion diameter ranges from 5 to 10 mm. It consists of two thin stainless-steel prostheses. There is a PTFE coating between the two prostheses. It may be used to treat peripheral aneurysms but a flexion area such as the popliteal artery should be avoided due to potential compression. The Viabahn endoprosthesis (Gore, Flagstaff, AZ) This prosthesis was used once to treat a popliteal aneurysm. It is a self-expanding endoprosthesis constructed with an expanded PTFE liner attached to the external nitinol stent structure, and is very flexible with a good radial strength. Radio-opaque markers enhance visualization to facilitate accurate placement. For the SFA this prosthesis is available in diameters ranging from 6 to 8 mm and in lengths of 25, 50, 100, and 150 cm. Table 77. 3 shows the number of stents used to treat the 52 aneurysms. Seventy-two prostheses were used. In certain cases, several prostheses were implanted in the same artery in order to completely cover the aneurysm. Any associated stenosis is dilated with a balloon that has a diameter equal to that of the artery. During the entire procedure, repeated angiographies are performed to make sure that the positioning of the prosthesis is correct and there is no residual leakage.
(a) Figure 77.1
Mean length of prosthesis (mm) 68.7 ± 28.4 (13–80) 118 ± 95.6 (25–300) 105.9 ± 94.2 (30–300)
An intravascular ultrasound examination (IVUS) was performed in four patients and confirmed a good intravascular result. The procedures were performed under local anesthesia and mild neuroleptanalgesia. At the beginning of the procedure, 1 g of aspirin and 5000 units of intravenous heparin were given as bolus. Heparin was then given for 24 hours and the patient’s coagulation was checked regularly. Thereafter, the patient received ticlopidine (500 mg/day) or clopidogrel (75 mg/day) and aspirin (100 mg/day) for 1 month. Aspirin (250 mg/day) was then continued thereafter. Patients also routinely received 3 mg of Kefadol (cefamandole) following the procedure, as prophylaxis against infection. Strict follow-up of these patients was performed as follows: ●
●
●
Duplex scan, echo-Doppler, and CT scan were performed the day after the procedure. At 6 months, the patients were followed-up by duplex scan, angiography. and CT scan. Thereafter, a duplex scan was performed every 6 months. Arteriography and a CT scan were performed only if a problem was suspected.
Immediate results Results are shown in Figures 77.1–77.4. An immediate technical success with total exclusion of the aneurysm was obtained
(b)
(a) Bilateral iliac aneurysm; (b) treatment with a Corvita endoprosthesis. Angioplasty at 6 months.
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(a)
(b)
(c)
(d)
(e)
(f)
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(g) Figure 77.2 (a) Large aneurysm of the right iliac artery – front view; (b) coil embolization inside the internal iliac artery; (c) result after implantation of two Corvita endoprostheses; (d) persistent leak inside the aneurysm; (e) result after coil embolization of the aneurysmal sac by contralateral approach; (f) spiral CT scan – large iliac aneurysm; (g) immediate post-procedure result. Total exclusion of the aneurysm after coils embolization inside the sac.
in all cases except two (96%). In one case of a long, tortuous and calcified femoropopliteal aneurysm, which was associated with a severe stenosis, it was impossible to cover its lower part due to the stiffness of the introduction device of the Cragg Endoprop System I, and a mild leakage persisted at the lower part. In the second case of a large iliac aneurysm (8 cm in diameter), we had an incomplete exclusion of the aneurysmal sac despite placement of a Corvita endoprosthesis. Placement of coils in the aneurysmal sac, using the contralateral approach, allowed a total exclusion of the aneurysm, and this was confirmed on angiogram and CT scan. All other aneurysms were perfectly excluded, and the results were confirmed by a follow-up echo-Doppler and/or CT scan performed after the procedure. Table 77.3 indicates the mean
length of prostheses as compared to the mean length of the lesions at the different levels. It indicates a good coverage of the lesions. Table 77.4 shows the mean arterial diameter obtained as compared to the mean diameter of the aneurysms at the different sites.
Complications Thrombosis of the prosthesis: 8/52 (15%) ●
Four early thromboses between day 1 and day 15: 2 at the iliac level (1 with a Corvita prosthesis, successfully treated using Fogarty’s technique, 1 with an Endotex prosthesis
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(b)
(a)
(b)
Figure 77.3 (a) Long femoro-popliteal aneurysm; (b) result after implantation of a Corvita endoprosthesis.
Figure 77.4 (a) Aneurysm of the upper part of the popliteal artery. Treatment with Cragg Endopro System I prosthesis (or Passager); (b) result after treatment.
requiring a bypass); 2 at the popliteal level (1 with a Corvita prosthesis, successfully treated by repeat angioplasty, and 1 with a Cragg Endopro System I/Passager stent requiring a bypass). Three thromboses which appeared between 3 and 6 months; 1 at the femoral level (Cragg Endopro System I/Passager), requiring bypass surgery; 2 at the popliteal level (1 Cragg Endopro System I/Passager, 1 Corvita endoluminal graft), treated medically (the patients had refused surgery). One thrombosis appeared at 2 years at the popliteal level (Corvita prosthesis). The prosthesis was recanalized by the percutaneous approach.
Fever and pain syndrome This syndrome was observed in four patients following implantation of Cragg stents at the femoral level. We found no infectious etiology. Everything returned to normal within a few days.
●
●
The thrombosis rate seems more frequent in the popliteal artery, but it is worth mentioning that no serious problem arose after stent thrombosis and there was no need for amputation. Distal embolism A distal embolism occurred at the deep femoral artery level, following exclusion of an iliac aneurysm. It was successfully treated by surgical embolectomy.
Table 77.4
One hematoma at the puncture site This did not require surgery. Two deaths One patient died at 6 days and the other one at 6 months (patients who have been treated for bilateral femoral aneurysms) of myocardial infarction.
Follow-up A strict follow-up of these patients is important to detect any problem, restenosis, or leakage, and to evaluate the patency rate of these prostheses.
IFPA – Immediate results: diameter
Location
No.
Mean lesion diameter before stent (mm)
Mean arterial diameter after stent (mm)
Iliac Femoral Popliteal
26 13 13
30.9 ± 13.3 (13–80) 20.0 ± 9.5 (8–40) 19.9 ± 7.9 (12–35)
9.1 ± 2.0 (6–14) 7.5 ± 1.6 (6–10) 7.8 ± 2.0 (6–14)
The mean Doppler index at 24 hours was 0.92 ± 0.10.
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Percutaneous endovascular treatment of peripheral aneurysms 100
100 88.8%
90 80
90
81.3%
80
82.6%
70 (%)
675
70
60
(%)
50
50
40
40
30
30
20
72.5%
60
20 PII PII
10 0 0
6
12
18
24
30
36
42
48
54
60
PII PII
10 0 0
66
6
12 18
24
Figure 77.5
Figure 77.6
IFPA: all lesions.
Restenosis At 6 months follow-up the mean ankle–brachial index (ABI) was 0.87 ± 0.11. Two restenoses appeared outside the stent: one at the iliac level (Cragg stent) associated with a small leakage successfully treated by angioplasty and implantation of another Cragg stent; and one at the popliteal level (Corvita stent) treated by angioplasty and implantation of a Intracoil Stent (EV3, Plymouth MN). Long-term follow-up The mean follow-up was 20.6 ± 13.2 months. Our maximum follow-up was 61 months. Figures 77.5–77.9 summarize the different primary (PI) and secondary (PII) patency rates at the different level. In our series, the patencies were very good at the iliac level (PI = 92.1%, PII = 96%) and not so good, but still satisfactory, at the femoropopliteal level (PI = 78.3%, PII = 86.9%).
96.0%
100 90
(%) 50
(%) 50
40
40
30
30
20
0 42
48
54
60
91.6%
20
PII PII
10
91.6%
80
60
36
PII PII
10 66
0
0
6
12 18
24
Months
Figure 77.7
IFPA: femoropopliteal.
60 66
IFPA: iliac.
90
60
30
54
The most common etiology of iliofemoropopliteal aneurysms is atherosclerosis. Other causes included infection, dissection, trauma, post-operative injury, and collagen diseases such as Marfan syndrome. Among our patients, the etiology was atherosclerosis in 48 cases, infection in 2 cases, and anastomosis in 2 cases. These aneurysms are easily identified by ultrasonography, contrast-enhanced CT scanning, MRI, and angiography. Popliteal artery aneurysms are the most common peripheral aneurysm (70%)15–18 and they are very often bilateral. They occur with a frequency that is second only to that of aneurysms of the abdominal aorta. A review19 of a large series of popliteal aneurysms showed that they are associated with abdominal aortic aneurysms in 28% and with iliac and femoral aneurysms in 35% of cases.20 They have a high incidence of thromboembolic and limb-threatening complications (36–69% of the cases).21–30 They are sometimes diagnosed by
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Figure 77.8
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symptoms produced by neurological compression or venous compression with phlebitis. Rupture at this level is rare. An aneurysmal diameter of 15 mm or more should be an indication for intervention. Femoral aneurysms are the second most common form of peripheral artery aneurysms. They are also usually bilateral. Eighty-five percent of them are associated with aortoiliac aneurysms and 44% with popliteal aneurysms.31 They are usually asymptomatic and they can be diagnosed by palpation of a pulsatile mass in the groin. However, sometimes they present with a distal embolization or an acute thrombosis threatening the limb. Pseudoaneurysms are frequent at this level, secondary to a trauma, arterial rupture, or rupture at the level of an anastomosis of a bypass graft. An arterial diameter of more than 20 mm should be an indication of intervention. Isolated aneurysms of the iliac arteries are rather uncommon, accounting for only 2–7% of atherosclerotic aneurysms of the aortoiliac segment.32–35 They may rupture, embolize, thrombose, or produce pressure symptoms. The natural course of an iliac aneurysm is one of progressive expansion which eventually leads to rupture. The rate of rupture, which increases with aneurysm size, has been estimated to be 31%.3 Other clinicians estimate the rate to be 14–70%.4,28,36–40 The mean diameter of ruptured iliac aneurysms was 5.6 cm,3 but ruptures of 3-cm aneurysms have been reported.2 The signs and symptoms of iliac aneurysms are produced by the mass effect or erosion into adjacent organs.3 Symptoms are usually related to gastrointestinal, genitourinary, neurological, or venous structures.8 Internal iliac artery aneurysms have a very poor prognosis. The largest surgical series by Brin and Busuttil41 reported a 67% incidence of rupture with a 90% mortality in untreated patients. Treatment is recommended for iliac aneurysms larger than 3 cm in diameter.41,42 Until recently, peripheral aneurysms were treated surgically. At the popliteal level, the risk of untreated disease is high (30% risk of amputation) but operative repair in patients without symptoms is relatively safe.18,21,23,43 Good long-term patency rates have been achieved, especially when the run-off vessels have not been occluded by embolization.44 Exclusion of the aneurysm and bypass or resection bypass can be performed17,18 but morbidity and risks of amputation in patients
undergoing elective repair have been reported.15,25,43,45 The mortality was 3–5% and the risk of amputation was 7–15% in patients without symptoms and 80% in the patients presenting with thrombosis. The patency rate at 5 years has been reported to be 91% in asymptomatic patients and 54% in symptomatic patients.29 At the femoral level, the same technique of exclusion of the aneurysm can be performed with excellent results. The mortality rate was 2%, the risk of amputation 2–5% but 30% in the case of an extensive femoropopliteal thrombosis.46 For iliac aneurysms, the current recommended treatment is surgical repair but this is associated with a mortality rate of 7–11% for elective operations and 33–50% when surgery is required on an emergency basis.3 The technical complexities of operating on vessels deep within the pelvis, especially after previous aortic surgery, have made standard elective surgical management of iliac aneurysms more difficult than for aortic aneurysms.5 Exclusion of the aneurysm or alternative therapies using simple aneurysm ligation and coil embolization have therefore been attempted to treat these aneurysms.47–49 Whereas radiographic exclusion of flow in the aneurysms has been successfully achieved with these techniques, continued growth and rupture of the apparently excluded lesions is well documented.50–53 The lower extremity arterial flow may also be compromised.5 With an internal iliac artery aneurysm, the origin of the aneurysm may be easily oversewn, but the anterior and posterior divisions of the internal iliac artery usually arise deep in the pelvis and may be difficult or impossible to ligate or oversew from within. Without occlusion of these vessels, the aneurysm can remain patent by filling itself from contralateral pelvic collateral branches and the potential for aneurysm rupture remains.6 Hollis et al.54 described a technique of percutaneous occlusion of the entire iliac system and cross-femoral bypass to revascularize the lower extremity on the affected site. With this technique, proximal ligation is not performed and, theoretically, the iliac system could recanalize and rupture of the internal iliac artery aneurysm can occur.6 Endoluminal graft placement is an alternative approach to conventional surgical repair of peripheral aneurysms. This new technique is less invasive and avoids the need for incision, general anesthesia and prolonged hospitalization; also, there is minimal blood loss. These advantages are particularly important in patients who are high-risk surgical candidates because of associated co-morbid medical conditions. This concept was initially proposed by Dotter.55 In 1985, Cragg et al.56 reported the first percutaneous graft placement procedure with the use of a nitinol stent. The experimental feasibility of treating aneurysms with Dacron or PTFE grafts was demonstrated by several authors.57–60 Parodi et al. performed the first percutaneous treatment of an aortoiliac aneurysm.28 Since then, endovascular stented grafts have been used effectively to treat aneurysms of the thoracic and abdominal aorta as well as other vessel, pseudoaneurysms, and arteriovenous fistulas.28,36,38,59,61–65 This technique of stent-graft placement was also developed to treat peripheral aneurysms. Marin et al.5,44 used a stent composed of PTFE grafts combined with balloonexpandable Palmaz stents at both extremities. Although this technique fosters good results, it also has certain drawbacks: since the stent is in a 14-French introducer, it requires a
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Percutaneous endovascular treatment of peripheral aneurysms surgical arteriotomy; and there is a possibility of a narrowing or kinking of the uncovered midgraft segment because of the absence of metallic reinforcement. Marin et al. observed one case of kinking after treatment of an iliac aneurysm with this technique.5 Laborde et al59 also observed a kinking of the prosthesis in six out eight cases and two acute thromboses in an experimental model. Dorros et al.66 reported 11 isolated iliac artery aneurysms treated by the same stent graft as described by Marin. The devices were delivered percutaneously through standard 14-French sheaths and deployed by balloon dilation. Non-covered stents have also been proposed for the treatment of peripheral aneurysms. Vorwerk et al.49 used noncovered self-expanding stents to treat ulcerated plaques and focal aneurysms involving the iliac arteries. Blais and Bonneau67 successfully used a non-covered stent to thrombose an iliac pseudoaneurysm next to a stenotic lesion. We treated four aneurysms with this type of non-covered stent. These non-covered stents may only be used in a limited number of small aneurysms with a narrow neck, in the lower third of the femoral artery, and in the popliteal artery in the case of focal lesions; these prostheses are more flexible and better adapted to these locations. Some interventionists have treated largeneck iliac aneurysms percutaneously by placing stents across the neck, followed by coil embolization through the struts of the stent.68 However, the use of covered stents seems to be the easiest technique since it allows the treatment of most of the lesions using a percutaneous approach. Razavi et al.8 reported a series of seven iliac aneurysms treated with Z-covered stents, coated either with polyester material (three cases) or ultrathin PTFE graft material (four cases). These stent grafts were introduced through 12–16-F angiographic sheaths placed percutaneously, but a surgical suture of the artery was necessary in four cases after withdrawal of the introducer. Therefore, this limits the interest in these stents. Covered stents, such as Cragg Endopro System I/Passager, Corvita Wallgraft, and Viabahn have the advantage of being implantable percutaneously through introducers that usually range from 7 to 9 French. Several limited series have been published7,9,10–14 and have reported promising results. These covered stents have a metallic self-expandable support on their entire length. This avoids external compression or kinking of the prosthesis that could reduce arterial flow, as has been seen with stent grafts. Some stents like Viabahn are very flexible and can be placed by a contralateral approach. Curti et al.12 reported a series of 13 procedures for 11 iliac pseudoaneurysms and 2 true iliac aneurysms with a 92% technical success and found the self-expanding Passager stent more useful in treating these patients, due to its good radial strength. Beregi et al.13 reported a series of 19 aneurysms (7 iliac, 5 subclavian, 3 femoral, 3 popliteal, 1 carotid) treated with Cragg Endopro System I or Passager with a 95% technical success. The 1-year patencies for iliac, head and neck, femoral, and popliteal arteries were 86%, 50%, 33%, and 100% respectively. The authors describe local puncture site complications (thrombosis or hemorrhage) due to the large introducer size (12 French) needed to implant a stent of 10 mm in diameter. The brachial access is a potential point of access for this technique. Scheinert et al.69 reported a series of 48 iliac aneurysms treated by percutaneous implantation of stent-grafts.
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The Cragg Endopro prosthesis was used in 37 cases, Passager in 6 and Wallgraft in 5 cases. A technical success of 97.9% was obtained. Primary patency rate were 100% after 1 year, 97.9% after 2 years, 94.9% after 3 years and 87.6% after 4 years. No secondary leaks were observed. Furthermore, the aneurysm diameter had reduced from 24.8 ± 8 mm to 23.1 ± 6.6 mm at the last follow-up. Boules et al.70 reported a series of 45 patients with 61 isolated iliac aneurysms. Thirty-four patients were treated with unilateral iliac stent grafts, eight with bifurcated aortic stent grafts and three with coil embolization alone. On post-operative CT scan obtained at 1, 6, 12, 24, and 36 months, aneurysm shrinkage was noted in 18, 29, 57, 67, and 83% of the cases, respectively, compared with the baseline diameter. One hypogastric aneurysm enlarged in the presence of a type II endoleak. Five endoleaks were noted at 1 month, with four other endoleaks identified on later CT scans. At 2 years, primary patency was 95% and freedom from secondary interventions was 88%. Calvet et al.71 published a series of 25 aneurysms treated with Cragg Endopro/Passager, Hemobahn (17 iliac, 4 popliteal, 1 femoral, 1 subclavian, 1 carotid). Technical success was obtained in all patients. At 1 year, 94.4% stents were patent, at 2 years 90.2%. Howell et al.72 treated 17 femoropopliteal aneurysms using the Wallgraft. Technical success was 100%. Six-month and 1-year aneurysm exclusion rates were 100% for both location but four (31%) popliteal stent grafts thrombosed at follow-up. Recently, Lagana et al.73 reported a series of 17 femoropopliteal aneurysms: 14 treated with Wallgraft, 2 with Hemobahn and 1 with an Excluder. Technical success was 100%. During a mean follow-up of 26.9 months (3–60), 6 (38%) thrombosed. The primary patency was 63% and the assisted primary patency 73%. To treat aneurysms originating near a major collateral vessel, the embolization of that vessel seems essential prior to stent placement to prevent retrograde filling of the aneurysm and to reduce the risk of rupture of this aneurysm. Special care should be given for the treatment of internal iliac aneurysms. Indeed, it should first be excluded with a stent placed in the iliac artery, usually using the retrograde ipsilateral approach. However, embolization of such vessels excludes a bilateral procedure that avoids complications such as pelvis ischemia7 (bowel or urinary tract). At the popliteal level, good results have been reported with endovascular therapy.28,39,44,55–60,74–81 However, it seems that the treatment of such aneurysms leads to a higher thrombosis rate. Movements of the knee may lead to kinking of the prosthesis, which may be responsible for thromboses. It is worth mentioning that in our series, even after thrombosis of the prosthesis, the limb never had threatening ischemia and did not require amputation. Rousseau et al.7 believe that this procedure should not be performed for aneurysmal lesions extending distally to the origin of the anterior tibial artery to avoid obstruction of this vessel by the prosthesis. Dorffner et al.9 suggest that implantation in vessels subject to mechanical stress such as the popliteal segments 2 (from the branches of the superior genicular arteries to the branches of the inferior genicular arteries) and 3 (from the branches of the inferior genicular arteries to the arcus tendineus m. solei) is not recommended because disintegration of stent filaments may occur. However, implantation of covered stents to treat
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aneurysms of the distal femoral artery and popliteal segment 1 can be performed safely. When treating long aneurysms, it is safer to place the distal stent first and then the proximal stent(s), overlapping each other by at least 1 cm, to avoid the stents separating from each other and falling into the aneurysmal sac, leading to leakage. Several types of complications may arise in treating these aneurysms: ●
●
●
●
●
The initial arteriogram obtained after placement of the stent-graft may reveal small leaks into the aneurysms from proximal and distal communication. The leaks can be corrected by placement of additional identical stent graft or by transcatheter embolization with coils.8 One patient in our series presented a stent leak that was successfully corrected by the placement of coils in the aneurysmal sac. Leaks may appear later, thus indicating the importance of a strict follow-up with echo-Doppler and CT scan.70 Early thrombosis may be observed, particularly at the popliteal level.7 A fibrinolytic drug treatment may then be implemented. It is difficult to know if an anticoagulant therapy would have been better than antiaggregant drugs, as in our protocol. Restenosis is described at the extremities of the prostheses (two cases in our series), similar to the bypass stenoses observed by the surgeons. This justifies a regular surveillance of these prostheses so as to detect and treat them with an angioplasty or placement of another prosthesis.7,11 Distal embolizations may occur during the treatment of these aneurysms.5 This may require other interventional procedures (thromboaspiration, mechanical thrombectomy) or surgical embolectomy. Appearance of a leakage can occur during the follow-up (one case in our series) demonstrating the importance of follow-up.
The indications for the interventional treatment of peripheral aneurysms are still being debated. The interventional treatment seems to be an alternative to surgery for iliac and femoral lesions. Iliac aneurysms are often associated with distended arteries that are too large for currently available stents. Forcing the indications for endovascular repair entails the risk of converting to operation or using a large number of stents to obtain complete exclusion of the aneurysm. The state of the
abdominal aorta should also be considered if it shows signs of aneurysmal disease; treating the isolated iliac aneurysm may be only a temporary measure, since subsequent aortic repair will become necessary.66 For popliteal aneurysms an interventional treatment may be proposed for patients with high surgical risks. The thrombosis rate seems to be higher with covered stents and may limit the indications at this level. There were no guidelines for choosing one stent rather than another: choice mainly depends on the operator’s decision. In our experience we observed no difference in terms of complications between the different covered stents. These stents seem also equivalent in terms of mid- and long-term patencies. The Corvita prosthesis was easier to implant in long lesions using the contralateral approach (these prostheses were available in longer lengths than the other stents and they could be cut to the desired length). Unfortunately these prostheses are no longer available. The Viabahn seems the easiest stent to use to treat at least femoropopliteal aneurysm due to its flexibility and easiness to implant. Compressive forms of aneurysms, particularly in the iliac artery, are still treated surgically. The signs of compression usually persist after the interventional treatment. Only very high surgical risk patients should undergo an endoluminal treatment. This technique could also be useful in the case of aneurysmal ruptures that have high operative mortality, such as aneurysmal ruptures of traumatic origins.38,74
Conclusion Percutaneous interventional treatment of peripheral aneurysms currently seems to be an alternative to surgery. The implantation of covered stents using the percutaneous approach is easy and efficient, and immediate success is obtained in most cases. And yet, the thrombosis rate obtained with these prostheses is high, and it may limit their indications, particularly in the popliteal artery. The mid-term patency in the iliac and femoral arteries is good. The popliteal artery is still a surgical indication, except for high-risk patients. Technical improvements are awaited to make it a safer and more efficient treatment. A new technology is in experiment, the multilayer stent (without any covering), which could totally change the interventional treatment of peripheral aneurysms.
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Razavi MK, Dake MD, Semba CP et al. Percutaneous endoluminal placement of stent-grafts for the treatment of isolated iliac artery aneurysms. Radiology 1995; 197: 801–4 Dorffner R, Winkelbauer F, Kettenbach J et al. Successful exclusion of a large femoropopliteal aneurysm with a covered nitinol stent. Cardiovasc Intervent Radiol 1996; 19: 117–9 Gieskes L, Rousseau H, Otal P et al. Traitement percutané par endoprothèse couverte des anévrismes poplités: expérience clinique préliminaire. J Mal Vasc 1995; 20: 264–7 Henry M, Amor M, Cragg A et al. Occlusive and aneurysmal peripheral arterial disease: assessment of a stent-graft system. Radiology 1996; 201: 717–24 Curti T, Stella A, Rossi C. Endovascular repair as first choice treatment for anastomatic and true iliac aneurysms. J Endovasc Ther 2001; 8: 139–43
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Bereji JP, Prat A, Willoteaux S. Covered stents in the treatment of peripheral aneurysms: procedural results and midterm follow up. Cardiovasc Intervent Radiol 1999; 22: 13–9 Krajcer Z, Khoshnevis R, Leachman DR. Endoluminal exclusion of an iliac artery aneurysm by wallstent endoprosthesis and PTFE vascular graft. Tex Heart Inst J 1997; 24: 11–4 Halliday AW, Wolfe JH, Taylor PR et al. The management of popliteal aneurysm: the importance of early surgical repair. Ann R Coll Surg 1991; 73: 253–7 MacGowan GW, Saif MF, O’Neil G et al. Ultrasound examination in the diagnosis of popliteal artery aneurysms. Br J Surg 1985; 72: 528–9 Lowell R, Gloviczki P. Anévrismes de l’artère poplitée, les risques de l’abstention chirurgicale. Ann Chir Vasc 1994; 8: 14–23 Szilagyi DE, Schwartz RL, Reddy HD. Popliteal arterial aneurysms: their natural history and management. Arch Surg 1981; 116: 724–8 Cole CW, Thijssen AM, Barber GG et al. Popliteal aneurysms: an index of generalized vascular disease. Can J Surg 1989; 32: 65–8 Breslin DJ, Jewell ER. Peripheral aneurysms. Cardiol Clin 1991; 9: 489–96 Vermilion BD, Kimmins SA, Pace WG et al. A review of 147 popliteal aneurysms with long-term follow-up. Surgery 1981; 90: 1009–14 Baird JR, Sivasankar R, Hayward R et al. Popliteal aneurysm: a review and analysis of sixty-one cases. Surgery 1966; 59: 911–7 Whitehouse WM Jr, Wakefield TW, Graham LM et al. Limb-threatening potential of atherosclerotic popliteal artery aneurysms. Surgery 1983; 93: 694–9 Evans WE, Hayes JP. Popliteal and femoral aneurysms. In: Rutherford RB, ed. Vascular Surgery, vol 2, third, edition. Philadelphia: WB Saunders, 1989: 951; 957 Anton GE, Hertzer NR, Beven EG et al. Surgical management of popliteal aneurysms: trends in presentation treatment, and results from 1952 to 1984. J Vasc Surg 1986; 3: 125–34 Evans WE, Bernhard VM, Kauffman HM. Femorotibial bypass in patients with popliteal aneurysms. Am J Surg 1971; 122: 555–7 Linton RR. The arteriosclerotic popliteal aneurysm: report of fourteen patients treated by preliminary lumbar sympathetic ganglionectomy and aneurysmectomy. Surgery 1949; 26: 41–58 Parodi JC, Palmaz MD, Barone HD. Transfemoral intraluminal graft implantation for abdominal aortic aneurysm. Ann Vasc Surg 1991; 5: 491–9 Shortell CK, DeWeese JA, Ouriel K et al. Popliteal artery aneurysms: a twenty-five year surgical experience. J Vasc Surg 1991; 14: 771–9 Bouhouros J, Martin P. Popliteal aneurysm: a review of 116 cases. Br J Surg 1974; 61: 469–75 Graham LM, Zelenock GB, Whitehouse WM Jr et al. Clinical significance of arteriosclerotic femoral artery aneurysms. Arch Surg 1980; 115: 502–7 Nachbur BH, Inderbitzi RG, Bar W. Isolated iliac aneurysms. Eur J Vasc Surg 1991; 5: 375–81 McCready RA, Pairolero PC, Gilmore JC et al. Isolated iliac artery aneurysms. Surgery 1983; 93: 688–93 Lowry SF, Kraft RO. Isolated aneurysms of the iliac artery. Arch Surg 1978; 113: 1289–93 Sacks NPM, Huddy SPJ, Wegner T et al. Management of solitary iliac aneurysms. J Cardiovasc Surg 1992; 33: 679–383 Dake MD, Miller C, Semba CP et al. Transluminal placement of endovascular stent-grafts for the treatment of descending thoracic aortic aneurysms. N Engl J Med 1994; 331: 1729–34 May J, White G, Waugh R et al. Transluminal placement of a prosthetic graft-stent device for treatment of subclavian artery aneurysm. J Vasc Surg 1993; 18: 1056–59 Marin ML, Veith FJ, Panetta TF et al. Transluminally placed endovascular stented graft repair for arterial trauma. J Vasc Surg 1994; 20: 466–73 Cragg AH, Dake MD. Percutaneous femoropopliteal graft placement. Radiology 1993; 187: 643–8 Schuler JJ, Flanigan DP. Iliac artery aneurysms. In: Bergan JJ, Yao JST, eds. Aneurysms: Diagnosis and Treatment. New York: Grune & Stratton, 1982: 469–85 Brin B, Busuttil R. Isolated hypogastric artery aneurysms. Arch Surg 1982; 117: 1329–33 Kasulke RJ, Clifford A, Nichols W et al. Isolated atherosclerotic aneurysms of the internal iliac arteries. Arch Surg 1982; 117: 73–7 Reilly MK, Abbott WM, Darling RC. Aggressive surgical management of popliteal artery aneurysms. Am J Surg 1983; 145: 498–502 Marin ML, Veith FJ, Panetta TF et al. Transfemoral endoluminal stented graft repair of a popliteal artery aneurysm. J Vasc Surg 1994; 19: 754–7
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Schellack J, Smith RB III, Perdue GD. Nonoperative management of selected popliteal aneurysms. Arch Surg 1987; 122: 372–5 Morris GC, Edwards W, Cooley DA et al. Surgical importance of profunda femoris artery: analysis of 102 cases with combined aorto-iliac and femoro-popliteal occlusive disease treated by revascularization of deep femoral artery. Arch Surg 1961; 82: 52–7 Reuter SR, Carson SN. Thrombosis of a common iliac artery aneurysm by selective embolization and entraanatomic bypass. Am J Roentgenol 1980; 134: 1248–50 Michaels JA, McWhinnie D, Hands LJ et al. Iliac aneurysm treated by percutaneous occlusion and femorofemoral crossover grafting. Fr J Surg 1994; 81: 37–8 Vorwerk D, Gunther RW, Wendt G et al. Ulcerated plaques and focal aneurysms of iliac arteries: treatment with noncovered, selfexpanding stents. Am J Roentgenol 1994; 162: 1421–4 Deb B, Benjamin M, Comerota AJ. Delayed rupture of an internal iliac artery aneurysm following proximal ligation for abdominal aortic aneurysm repair. Ann Vasc Surg 1992; 6: 537–40 Kwaan JHM, Dahl RK. Fatal rupture after successful surgical thrombosis of an abdominal aortic aneurysm. Surgery 1984; 95: 235–7 Schanzer H, Papa MC, Miller CM. Rupture of surgically thrombosed abdominal aortic aneurysm. J Vasc Surg 1985; 2: 278–80 Cho SI, Johnson WC, Bush HL Jr et al. Lethal complications associated with non-restrictive treatment of abdominal aortic aneurysms. Arch Surg 1982; 117: 1214–7 Hollis HW Jr, Luethke JM, Yakes WF et al. Percutaneous embolization of an internal iliac artery aneurysm: technical considerations and literature review. JVIR 1994; 5: 449–51 Dotter CT. Transluminally placed coil spring endarterial tube grafts: long term patency in canine popliteal artery. Invest Radiol 1969; 4: 329–32 Cragg AH, Lund G, Rysavy JA et al. Percutaneous arterial grafting. Radiology 1985; 150: 45–9 Balko B, Piasceck GJ, Dhirai MS et al. Transfemoral placement of intraluminal polyurethane prosthesis for abdominal aneurysm. J Surg Res 1986; 40: 305–9 Lawrence DD, Charnsangevej C, Wright KC et al. Percutaneous endovascular graft: experimental evaluation. Radiology 1987; 163: 357–60 Laborde JC, Parodi JC, Clem MF et al. Intraluminal bypass of abdominal aortic aneurysm: feasibility study. Radiology 1992; 157: 185–90 Boudghene F, Anidjar S, Allaire E et al. Endovascular grafting in elastase-induced experimental aortic aneurysms in dogs: feasibility and preliminary results. JVIR 1993; 4: 497–504 Mirich D, Wright KC, Wallace S et al. Percutaneously placed endovascular grafts for aortic aneurysms: feasibility study. Radiology 1989; 170: 1033–7 Parodi JC. Endovascular repair of abdominal aortic aneurysms. Adv Vasc Surg 1993; 1: 85–106 Chuter TAM, Green RM, Ouriel K et al. Transfemoral endovascular aortic graft placement. J Vasc Surg 1993; 18: 185–97 Marin ML, Veith FJ. Transfemoral repair of abdominal aortic aneurysms. N Engl J Med 1994; 331: 1751 Marin ML, Veith FJ, Panetta TF et al. Percutaneous transfemoral stented graft repair of a traumatic femoral arterioveinous fistula. J Vasc Surg 1993; 18: 298–301 Dorros G, Cohn JM, Jaff M. Percutaneous endovascular stent graft repair of iliac artery aneurysms. J Endovasc Surg 1997; 4: 370–5 Blais C, Bonneau D. Post angioplasty pseudoaneurysm treated with a vascular stent. Am J Roentgenol 1994; 162: 238–9 O’Brien CJM, Rankin RN. Percutaneous management of largeneck aneurysms with arterial stent placement and coils embolization. JVIR 1994; 5: 443–8 Scheinert D, Schroder M, Steinkamp H et al. Treatment of iliac artery aneurysms by percutaneous implantation of stent grafts. Circulation 2000; 102: III-253 Boules TN, Settler F, Stanziale SF et al. Endovascular management of isolated iliac artery aneurysms. J Vasc Surg 2006; 44: 29–37 Calvet P, Chabbert V, Chemia P et al. Endoluminal treatment of peripheral aneurysm with covered endoprosthesis. J Mal Vasc 2001; 26: 299–306 Howell M, Kracjer Z, Diethrich EB et al. Wallgraft endoprosthesis for the percutaneous treatment of femoral and popliteal artery aneurysms. J Endovasc Ther 2002; 9: 76–81 Lagana D, Carrafiello G, Mangini M et al. Endovascular treatment of femoropoliteal aneurysms: a five-year experience. Cardiovasc Intervent Radiol 2006; 29: 819–25 Parodi JC. Endovascular repair of abdominal aortic aneurysms and other arterial lesions. J Vasc Surg 1995; 21: 549–57
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79. 80. 81.
Henry M, Amor M, Ethevenot G et al. Initial experience with the Cragg Endopro System I for intraluminal treatment of peripheral vascular disease. J Endovasc Surg 1994; 1: 31–43 Becker GJ, Benenati FJ, Zemel G et al. Percutaneous placement of a balloon-expandable intraluminal graft for life threatening subclavian arterial haemorrhage. JVIR 1991; 2: 225–9 Marin ML, Veith FJ, Cynamon J et al. Transfemoral endovascular stented graft treatment of aortoiliac and femoropopliteal occlusive disease for limb salvage. Am J Surg 1994; 168: 156–262
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SECTION XI Other localizations
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Embolization in peripheral territory CJ Schönholz, E Mendaro, and K Ehrens
Introduction The continuous development and improvement of materials and techniques in recent years has led to a wide spectrum of methods for transcatheter occlusive therapy. Since the 1970s the percutaneous treatment of multiple and varied pathologies with detachable balloons, big particles, and rudimentary coils has been introduced.1–3 Advances in agents for embolization and in catheter and guidewire technology have increased the reach of the interventional radiologist in treating a variety of pathologic conditions that were traditionally treated by surgery. The proper use of embolization techniques requires an understanding of the vascular anatomy and pathology, the tools used to deliver embolic agents, and the embolic agents themselves.
Embolic agents An ideal embolic agent would be precisely sized, nonclumping, highly radio-opaque, non-toxic, non-allergenic, and inexpensive.4 It would allow easily controlled delivery through conventional or microcatheter systems to a specific vascular territory, and would provide reliable occlusion for the desired length of time. It is the task of the interventional radiologist to find the appropriate embolic agent to match the clinical indication. Methods for embolization can be categorized by the duration of the effect and the type of agent. Resorbable agents generally give temporary occlusion, although permanent occlusion may result, especially when there is poor collateral flow and necrosis occurs. Non-resorbable agents usually give permanent occlusion. The types of agents include liquids, particulates, and mechanical devices. Liquid and particulate agents tend to give distal occlusion, whereas mechanical agents are generally larger and tend to give proximal vessel occlusion.4,5
Commonly used embolization materials These materials can be divided into the following groups; details of some of these are given below. ●
Biodegradable particles: 䊊 gelatin sponge (Gelfoam); 䊊 microfibrillar collagen (Avitene); 䊊 starch microspheres (Spherex).
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Permanent particles: 䊊 polyvinyl alcohol sponge (Ivalon, Contour); 䊊 acrylic microspheres (Embospheres). Liquids: 䊊 ethanol; 䊊 iodized oil (lipiodol); 䊊 glue (n-butyl-cyanoacrylate – histoacryl); 䊊 Ethiblock; 䊊 hypertonic glucose; 䊊 Onyx. Mechanical agents: 䊊 metallic coils, fibered coils, GDC; 䊊 detachable balloons; 䊊 vascular occlusors.
Biodegradable particles Gelfoam Gelfoam is a gelatin sponge that causes vascular occlusion by mechanical obstruction, induction of thrombosis, and inflammation of the vessel wall. The gelatin dissolves and permits recanalization of the artery within days to weeks.6 Since it does not cause permanent occlusion, Gelfoam is useful in treating benign sources of bleeding such as trauma, or for temporary devascularization of masses immediately before resection to minimize blood loss. Gelfoam powder is 40–60 µm and causes occlusion of vessels 100–200 µm in diameter. Gelfoam powder is good for preoperative embolization of tumors or organs. Microfibrillar collagen Avitene is a preparation of collagen fibers.7 The fibers are 5 µm in diameter by 70–100 µm in length, and cause vascular occlusion at the 25–250 µm level. Avitene causes a granulomatous reaction. Recanalization of the vessels begins at about a week and continues over 1–2 months. Collagen is useful for tumor embolization, either preoperatively or palliatively, and has been used for chemoembolization in the liver. It can be used mixed with Gelfoam and Ivalon. Permanent particles Polyvinyl alcohol (PVA – Ivalon) Polyvinyl alcohol (PVA) is an inert plastic sponge that is ground into coarsely shaped particles of graded dimensions from 100 to 1000 µm. It causes permanent mechanical occlusion of the vessel lumen with subsequent ingrowth of thrombus and fibrin. The irregular, cratered surface of the particles makes them prone to clump into aggregates, so that occlusion 683
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occurs at the level of vessels larger than the nominal size of the particles used. Like Gelfoam, PVA particles tend to float in contrast, so the syringe must be pointed upward during injection to avoid clumping at the back of the barrel. It is used in cases of distal devascularization, such as preoperative tumors, or in cases of hemoptysis in bronchial embolization.
Ethanol Ethanol is a very powerful sclerosing agent that causes tissue necrosis and vessel thrombosis. It is used for organ ablation or tumor devascularization.14 The distribution of the ethanol is difficult to control, and it is important to avoid reflux at the moment of embolization.
Microspheres (embospheres) This permanent embolic agent has the advantage of a regular shape and precise targeted level occlusion due to its calibrated size. This agent is used as the other permanent particle, with similar indications.
Onyx Onyx, or ethylene vinyl alcohol copolymer, is a non-adhesive radio-opaque liquid embolic agent used in combination with DMSO (dimethyl sulfoxide) and tantalum powder in varying concentrations. The tantalum powder is added for radioopacity and the DMSO rapidly diffuses out of solution and causes embolization upon contact with aqueous media such as blood. The solidification and rate of embolization is dependent on the concentration of ethylene in the polymer.15 It has most often been used successfully in the treatment of AVMs and tumor embolization. Studies have shown faster and more effective embolization with easier fluoroscopic monitoring and less vascular recanalization as compared to the most commonly used embolic agent, PVA.16 In addition, surgical removal of vascular malformations seems to be associated with less morbidity than with NBCA.17,18 Risk of pulmonary embolism appears to be much lower with Onyx than with PVA particles or NBCA, but DMSO injection is associated with pain and vasospasm so general anesthesia is often warranted.15 In addition, it is far more expensive and the price increases for higher concentrations of ethylene copolymer.19
Mechanical agents Coils These permanent occlusive agents are available in varying wire sizes, lengths, coil diameters, and shapes. The conventional steel coil embolus consists of a short length of guidewire with multiple polyester strands attached transversely along most of its length between the turns of the wire. These devices come prepackaged and stretched out in metal cartridges, eliminating the need for a special mandrel introducer and permitting their delivery through conventional 5-French, 0.035- and 0.038-inch tapered catheters using conventional, floppy guidewires. They are used, for instance, in cases of pseudoaneurysms or arteriovenous fistulae (AVFs), leading to the occlusion of the afferent feeding channel. The 0.018- or 0.010-inch platinum Guglielmi detachable coils (GDC) coils are recommended for use with 1.118–0.010-inch inner lumen catheters, such as the Tracker 18 or Excel 014. These modern microcoils are used in the treatment of cerebral aneurysms. There are many reports of its use in peripheral territory too.8,9 Liquid agents Unlike particles, which by virtue of their size are arrested at a precapillary level, liquid sclerosants can pass to the capillary level and through to the venous circulation.10 This feature makes them desirable agents in the treatment of vascular malformations. Vascular occlusion occurs from a combination of thrombosis and destruction of the vessel endothelium, which is usually permanent. Liquid sclerosants (e.g. ethanol) are more challenging to use than particulates due to their deeper penetration into tissue, making their distribution harder to control and increasing the risk of non-target embolization. NBCA (n-isobutyl cyanocrylate) This is a liquid, rapidly plastic adhesive agent that polymerizes immediately upon contact with any ionic surface (blood, endothelium), which makes necessary the use of a coaxial technique with microcatheters.11 It is a permanent occlusive agent, and is not radio-opaque, so it needs ethiodized oils or tantalum powder to be opacified.12,13 Due to its precision delivery, NBCA is used for arteriovenous malformations (AVMs) in cerebral or peripheral territories. Much experience of the operator in the management of the agent and in endovascular microcatheter techniques is required to avoid complications, because of the rapid action and strong adhesive quality of the agent.
Transcatheter peripheral embolization: some clinical indications Pelvis and extremities transcatheter embolizations Trauma Before undertaking transcatheter therapy for arterial lesions, it is important to understand the surgical alternatives for treatment and their risks and benefits. Radiologic management is primarily limited to embolotherapy, the intentional occlusion of a vessel. The technique of embolization depends on the type and location of the vascular lesions. In trauma, a temporary occluding agent such as the gelatin sponge is theoretically advantageous because many of these lesions will heal.20,21 Alternatively, fibered coils and platinum microcoils, although permanent, offer the advantage of speed and precise positioning. The success rate for transcatheter embolization has been reported to be between 85 and 100%. Uterine fibroid embolization Uterine fibroid embolization is a promising procedure in the treatment of uterine leiomyomata with good clinical results.22–26 This alternative treatment is a minimally invasive technique with low complication rates, very good clinical efficacy, and a significant reduction in fibroid size and, consequently, in symptoms.27–35 The bilateral uterine artery embolization is performed with permanent particulated agents (PVA, 300–500 µm) or Gelfoam (Figure 78.1).28 Recent studies have shown embolic treatment to have similar efficacy
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Figure 78.1 Uterine fibroid embolization: (a) pelvic angiogram showing bilateral uterine arteries enlargement; (b, c) selective left internal iliac artery and right uterine artery angiogram showing hypervascular fibroids; (d) completion pelvic angiogram after uterine fibroid embolization with PVA particles.
in relieving symptoms, but a lower rate of complications when compared to hysterectomy (50 vs. 27.5%; p = 0.01).24
inflammatory origin. In general, the long-term control rate of hemoptysis is approximately 70–94% (Figure 78.2).39
Bronchial embolization in the treatment of hemoptysis Once the site of hemorrhage is known, attention can be confined to embolization of bronchial arteries and collaterals supplying that area.36 Transcatheter embolization requires a stable catheter position. When a stable catheter position cannot be obtained with these catheters, coaxial catheterization can be performed. Distal embolization should be performed whenever possible. Special attention must be paid to detect the presence of a spinal artery for avoiding neurologic complication. The most commonly used embolic materials for bronchial artery embolization include Gelfoam and PVA particles.37,38 Bronchial artery embolization has been shown to be a very effective technique for the immediate control of hemoptysis of
Splenic embolization Trauma The goal of embolization in splenic trauma is to stop active bleeding while preserving as much splenic tissue as possible. This is achieved with the use of coils (stainless steel coils) as occlusive agents, embolizing the splenic artery of one of its branches.40,41 They are relatively safe, fast, easy to use, and inexpensive, with good clinical and angiographic results. Gelfoam can also be used in association with coils to assure the complete vessel occlusion (Figure 78.3).42 Hypersplenism The more conventional technique of splenic embolization; that is, particulate embolization of the spleen, is employed
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Figure 78.2 Bronchial embolization for bleeding control: (a) pre-embolization selective bronchial angiogram in a patient with massive hemoptysis due to tuberculosis; (b) post-embolization with PVA angiogram demonstrates distal occlusion. Hemorrhage control was achieved.
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Figure 78.3 Splenic embolization in a patient with trauma: (a) splenic artery angiogram showing contrast extravasation at the upper pole; (b) superselective branch angiogram using a microcatheter placed near to the area of vessel rupture; (c) follow-up angiogram after embolization with PVA particles; (d) completion splenic angiogram showing small avascular area in the upper pole where embolization was preformed.
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Embolization in peripheral territory in hypersplenism.44–46 The goal is permanent reduction of splenic substance. The technique is performed with particulated permanent agents such as PVA or microspheres.47 Hypervascular tumor embolization Embolization of a variety of tumors has been performed, preoperatively or as an isolated therapy.48,49 Embolization of tumors is done for preoperative vascular control and to palliate unresectable lesions.50 In general, the isolated use of mechanical agents to occlude proximal vessels has a limited role, especially if the organ is to remain in the patient, since collateral flow will quickly result in reperfusion. Even in organs with end arteries, such as the kidney, agents traveling to the distal, small-vessel level give a more definitive occlusion, which is achieved with particulate agents (Figure 78.4).51,52
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Hepatic malignancies: chemoembolization Many pharmacological agents have been used for hepatic artery infusion.53 The most frequently used drugs for chemoembolization are doxorubicin, cisplatin, and mitomycin. A number of embolic agents have been used to treat liver tumors. The agents are broadly categorized into mechanical and particulate (further subdivided into permanent and temporary). Mechanical agents such as coils, differing little from proximal surgical ligation of a vessel, have little role in the primary management of liver tumors. In these cancer patients, the most experience has been accumulated with the embolic agents Gelfoam, PVA, and lipiodol.55 Proponents of embolization alone advocate PVA particles because they provide permanent occlusion. Since the hepatic artery is to be intentionally embolized, confirmation of portal vein patency is essential.56 In the presence of portal vein
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Figure 78.4 Kidney angiomyolipoma embolization: (a, b) early and late phase angiogram showing hypervascular tumors; (c) superselective angiogram of the inferior pole branch prior to embolization; (d) post-embolization renal artery angiogram showing only opacification of the normal vessels.
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(c) (d) Figure 78.5 Hepatocellular carcinoma embolization: (a, b) Selective celiac artery angiogram in early and late arterial phase showing a large hypervascular tumor in the right lobe of the liver; (c) superselective angiogram performed through a microcatheter obtained prior to chemoembolization; (d) final hepatic artery angiogram showing complete occlusion of the abnormal vessels.
thrombus, hepatic chemoembolization can be safely performed if collateral flow is adequate. Fever and abdominal pain (“post-embolization syndrome”) occur commonly after such procedures and can be effectively treated with nonsteroidal anti-inflammatory agents (Figure 78.5).
they may create difficulties due to the mass effect on adjacent structures (of greater concern intracranially). Percutaneous occlusion is effective when the sac and origin of the aneurysm is securely closed. For aneurysmatic lesions, mechanical agents can provide occlusion for all of these methods: ●
Peripheral aneurysms, pseudoaneurysms, and arteriovenous malformations Aneurysms and pseudoaneurysms The major indications for treating aneurysms are to prevent hemorrhagic or thromboembolic complications. Less frequently,
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placing a stent or endovascular graft and closing the orifice of an aneurysm, is an alternative method of occlusion while preserving the vessel; fibered coils and microcoils are also a good indication for this kind of lesion, filling the aneurysm sac or occluding the afferent vessel.
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Figure 78.6 (a) Selective right superficial femoral artery angiogram showing a congenital arteriovenous malformation (AVM) at the level of the thigh, arterial phase; (b) venous phase; (c) superselective injection with a 3-French microcatheter placed in one of the feeding arteries; (d) post-embolization angiogram after injection of 0.8 cm3 of histoacryl. No filling of the AVM is noted.
Arteriovenous malformations These lesions may cause complications due to hemorrhage, mass effect, high-output heart failure, or local ischemia due to vascular steal. They are best treated by eradicating the nidus, so the isolated occlusion of feeding vessels with mechanical devices frequently only results in at best temporary benefit as collateral vessels enlarge to supply the malformation. The smaller mechanical agents, such as 0.018 microcoils, have a role because they can be placed closer to the nidus. Liquid agents such as NBCA (histoacryl),
which occlude the malformation nidus, have demonstrated excellent results with very low recurrency rates (Figure 78.6).57 Malformations that are simple AVFs or in which eradication of the nidus is not essential, such as pulmonary arteriovenous malformations, are well treated by mechanical embolization devices. In such cases, depending on the branching pattern, the length of the artery supplying the malformation, and the size of the artery, the decision is made to either embolize the feeding artery with coils or with detachable balloons for occlusion (Figure 78.7).
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(c) Figure 78.7 Coil embolization in a child with pulmonary arteriovenous malformation: (a) selective lower lobe branch angiogram showing the AVM; (b) multiple coils were deployed at the feeding vessels; (c) post-embolization right pulmonary angiogram showing complete occlusion of the AVM.
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Dawbain G, Lussenhop AJ, Spence WT. Artificial embolization of cerebral arteries: report of use in a case of arteriovenous malformation. JAMA 1960; 172: 1153–5 Tadavarthy SM, Moller JH. Amplatz K. Polyvinyl alcohol (Ivalon): a new embolic material. AJR 1975: 125: 609–16 Gianturco C, Anderson JH, Wallace S. Mechanical devices for arterial occlusion. AJR 1975; 154: 428–35 Castañeda-Zuñiga WR, Tadavarthy SM. Interventional Radiology. Baltimore: Williams & Wilkins, 1992 Greenfield AJ, Athanasoulis CA, Waltman AC. Transcatheter vessel occlusion: selection of methods and material. Cardiovasc Intervent Radiol 1980; 3: 222–8 Jander HP, Russinovich NAE. Transcatheter Gelfoam embolization in abdominal, retroperitoneal, and pelvic hemorrhage. Radiology 1980; 136: Diamond NG, Casarella WJ, Bachman DM, Wolff M. Microfibrillar collagen hemostat: a new transcatheter embolization agent. Radiology 1979; 133: 775–9 Morse SS, Clark RA, Puffenbarger A. Plantinum microcoils for therapeutic embolization: nonneuroradiologic applications. Technical note. AJR 1990; 155: 401–3 Tisnado J, Beachley MC, Cho SR. Peripheral embolization of a stainless steel coil. AJR 1979; 133: 324–6 Goldman ML, Philip PL, Sarrafizadeh MS. Bucrylate, a liquid tissue adhesive for transcatheter embolization. Appl Radiol 1984: 89–94 Dotter CT, Goldman ML, Rosch J. Instant selective arterial occlusion with isobutyl-2-cyanoacrylate. Radiology 1975; 114: 227–30 Frenny PC, Bush WH, Kidd R. Transcatheter occlusive therapy of genitourinary abnormalities using isobutyl-2-cyanoacrylate. AJR 1979; 133: 647–56 Cromwell LD, Kerber CW. Modification of cyanoacrylate for therapeutic embolization: preliminary experience. AJR 1981; 137: 781–5 Ellman BA, Parkhill BJ, Curry TS et al. Ablation of renal tumors with absolute ethanol: a new technique. Radiology 1981; 141: 619–26 Cantasdemir M, Kantarci F, Mihmanli I, Numan F. Embolization of profunda femoris artery branch pseudoaneurysms with ethylene vinyl alcohol copolymer (Onyx). J Vasc Interv Radiol 2002; 13: 725–8 Wright KC, Greff RJ, Price RE. Experimental evaluation of cellulose acetate NF and ethylene-vinyl alcohol copolymer for selective arterial embolization. J Vasc Interv Radiol; 10(9): 1207–18 Jahan R, Murayama Y, Gobin YP et al. Embolization of arteriovenous malformations with Onyx: clinicopathological experience in 23 patients. Neurosurgery 2001; 48: 984–95 Taki W, Yonekawa Y, Iwata H et al. A new liquid material for embolization of arteriovenous malformations. AJNR Am J Neuroradiol 1990; 11: 163–8 Numan F, Ömeroglu A, Kara B et al. Embolization of peripheral vascular malformations with ethylene vinyl alcohol copolymer (Onyx). J Vasc Interv Radiol; 10(9): 1207–18 Matalon T, Athanasoulis CA, Margolies MN et al. Hemorrhage with pelvic fractures: efficacy of transcatheter embolization. AJR 1979; 133: 859–67 Ben-Menachem Y, Handel SF, Ray RD, Child TL III. Embolization procedures in trauma: a matter of urgency. Semin Intervent Radiol 1985; 2: 107–17 Uterine artery embolization in a 10-week cervical pregnancy with coexisting fibroids. Int J Gynaecol Obstet 2001; 72(3): 253–8 Ravina JH. Fibroma: surgical myomectomy or embolization or GnRH analogs? Embolization of uterine fibroma: a new treatment. Gynecol Obstet Fertil 2001; 29(1): 66–7 Spies J, Niedzwiecki G, Goodwin S et al. Training standards for physicians performing uterine artery embolization for leiomyomata: consensus statement developed by the Task Force on Uterine Artery Embolization and the Standards Division of the Society of Cardiovascular & Interventional Radiology – August 2000. J Vasc Interv Radiol 2001; 12(1): 19–21 McLucas B, Adler L, Perrella R. Uterine fibroid embolization: nonsurgical treatment for symptomatic fibroids. J Am Coll Surg 2001; 192(1): 95–105 Pelage J, Le Dref O, Jacob D et al. Uterine artery embolization: anatomical and technical considerations, indications, results and complications. J Radiol 2000; 81(12-Fmc): 1863–72 Worthington-Kirsch RL, Fueredi GA, Goodwin SC et al. Polyvinyl alcohol particle size for uterine artery embolization. Radiology 2001; 218(2): 605–6 Braude P, Reidy J, Nott V et al. Embolization of uterine leiomyomata: current concepts in management. Hum Reprod Update 2000; 6(6): 603–8
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Golfieri R, Muzzi C, De laco P et al. The percutaneous treatment of uterine fibromas by means of transcatheter arterial embolization. Radiol Med (Torino) 2000; 100(1–2): 48–55 Lund N, Justesen P, Elle B et al. Fibroids treated by uterine artery embolization. A review. Acta Obstet Gynecol Scand 2000; 79(11): 905–10 Dubel GJ, Ferland RJ, Murphy TP, Frishman G. The emerging role of uterine artery embolization in the management of symptomatic uterine fibroids. Med Health R I 2000; 83(10): 305–11 Brunereau L, Herbreteau D, Gallas S et al. Uterine artery embolization in the primary treatment of uterine leiomyomas: technical features and prospective follow-up with clinical and sonographic examinations in 58 patients. Am J Roentgenol 2000; 175(5): 1267–72 McLucas B, Adler L, Perrella R. Uterine fibroid embolization: nonsurgical treatment for symptomatic fibroids. J Am Coll Surg 2001; 192(1): 95–105 Pelage J, Le Dref O, Jacob D et al. Uterine artery embolization: anatomical and technical considerations, indications, results and complications. J Radiol 2000; 81(12-Fmc): 1863–72 Reidy JF, Spies JB, Walker WJ. Polyvinyl alcohol particle size for uterine artery embolization. Radiology 2001: 218(2): 605–6 Remy J, Arnaud A, Fardou H et al. Treatment of hemoptysis by embolization of bronchial arteries. Radiology 1977; 122: 33–7 Cohen AM, Doershuk CF, Stern RC. Bronchial artery embolization to control hemoptysis in cystic fibrosis. Radiology 1990; 175: 401–5 Vujic I, Pyle R, Parker E, Mithoefer J. Control of massive hemoptysis by embolization of intercostals arteries. Radiology 1980; 137: 617–20 Fisher RG, Ben-Menachen Y. Embolization procedures in trauma: the abdomen – extraperitoneal. Semin Intervent Radiol 1985; 2: 148–57 Richman SD, Green WW, Kroll R, Casarella WJ. Superselective transcatheter embolization of traumatic renal hemorrhage. AJR 1977; 128: 843–4 Yoon W, Kim JK, Kim YH, Chung TW, Kang HK. Bronchial and nonbronchial systemic artery embolization for life-threatening hemoptysis: a comprehensive review. Radiographics; 22(6): 1395–8 Castañeda-Zuñiga WR, Hammerschmidt DE, Sanchez R, Amplatz K. Nonsurgical splenectomy. AJR 1977; 129: 805–11 Hagiwara A et al. Nonsurgical management of patients with blunt splenic injury: efficacy of transcatheter arterial embolization. AJR 1996; 167: 159–66 Chuang VO, Reuter SR. Experimental diminution of splenic function by selective embolization of the esplenic artery. Surg Gynecol Obstet 1975; 140: 715–20 Alwmark A, Bengmark S, Gullstrand P et al. Evaluation of splenic embolization in patient with portal hypertension and hyperesplenism. Ann Surg 1982; 196: 518–24 Owman T, Lunderquist A, Alwmark A, Borjesson B. Embolization of the spleen for treatment of splenomegaly and hypersplenism in patients with portal hypertension. Invest Radiol 1979; 14: 457–64 Castañeda-Zuñiga WR, Hammerschmidt DE, Sanchez R, Amplatz K. Nonsurgical splenectomy. AJR 1977; 129: 805–11 Chuang VP. Superselective hepatic tumor embolization with tracker-18 catheter. J Intervent Radiol 1988; 3: 69–71 Coldwell DM. Hepatic arterial embolization utilizing a coaxial catheter system technical note. Cardiovasc Intervent Radiol 1990; 13: 53–4 Ruan DT. Warren RS. Palliative techniques for hepatic cancer. Surg Oncol Clin North Am 2004; 13(3): 505–16 Almgard LE, Fernstrom I, Haverling M. Treatment of renal adenocarcinoma by embolic occlusion of the renal circulation. Br J Urol 1973; 45: 474–9 Kaisary AV, Williams G, Riddle PR. The role of preo-perative embolization in renal cell carcinoma. J Urol 1984; 131: 641–6 Chuang VP, Wallace S. Hepatic arterial redistribution for intraarterial infusion of hepatic neoplasms. Radiology 1980; 135: 295–9 Carr BI. Hepatocellular carcinoma: current management and future trends. Gastroenterology 2004; 127(5 suppl. 1): S218–24 Shimizu T, Sako M, Hirota S. Intraarterial infusion therapy with polysaccharide solution as a carrier of anticancer agents. Nippon Acta Radiol 1988; 48: 702 Lee KH. Sung KB. Lee DY. Park SJ. Kim KW. Yu JS. Transcatheter arterial chemoembolization for hepatocellular carcinoma: anatomic and hemodynamic considerations in the hepatic artery and portal vein. Radiographics 2002; 22: 1077 Lookstein RA, Guller J. Embolization of Complex Vascular Lesions. Mount Sinai J Med 2004; 71(1): 17–28
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Uterine artery embolization for fibroids J Pisco and M Duarte
Uterine fibroids Uterine fibroids are the most common solid tumors of the female tract and the most frequent benign tumors of adult women. They develop in 20–40% of women of reproductive age,1 but the true prevalence is unknown because more than 50% are asymptomatic.2 They are a source of morbidity and a common indication for surgery, with healthcare costs and impact on quality of life. These benign tumors arise from the uterine smooth muscle cells and are classified into three types: submucosal, intramural, and subserosal. Submucosal fibroids, the least common type, protrude into the uterine cavity and distort the underlying endometrium. They can cause abnormal uterine bleeding and reproductive dysfunction. Intramural, the most common, grow within the muscle. Subserosal are under the serosa and give the uterus an irregular contour. If large enough they may cause pressure symptoms. Pedunculated fibroids grow from a stalk and can be submucosal or subserosal.
Pathophysiology Estrogens have an important role in the fibroid pathophysiology. Fibroids arise after menarche, are common during reproductive years, and can increase in size during pregnancy, but after delivery they usually shrink back to their prepregnancy size. They regress with gonadotropin-releasing hormone (GnRH) agonist therapy3 and improve after menopause, when the level of estrogen decreases dramatically. However, menopausal women who are taking supplemental estrogen (hormone replacement therapy) may not experience symptom relief. Progesterone is also important, because antiprogestins can cause myoma regression.4 Growth factors also have a role in fibroid pathology, but this is not fully understood.5–7 There is evidence supporting a genetic basis for fibroids.8 There are 2–6-fold more fibroids in the first-degree relatives of affected women than in controls. African women have twice the incidence of fibroids compared to Caucasian women, develop the disease at an earlier age with increased severity, and have a greater risk of anemia.9,10 Reproductive characteristics also affect the risk of fibroids, because parity appears to be protective.
Diagnosis and patients evaluation The most common symptom is abnormal menstrual bleeding, and is the main indication for therapy. It presents as 692
menorrhagia (heavy menses) or polymenorrhea (frequent menstrual bleeding every 21 days or less). Abnormal uterine bleeding may lead to iron deficiency (anemia). Submucosal fibroids produce more bleeding. Pelvic pain and severe dysmenorrheal during a menstrual cycle can occur either with fibroids alone or more commonly when they coexist with endometriosis, pelvic inflammatory disease, or adhesions. As the fibroids grow, pressure effects increase, producing urinary symptoms from anterior fibroids, constipation from posterior fibroids, and dyspareunia. The endometrial cavity distortion by submucosal fibroids can increase the risk of infertility, but other factors of infertility should be assessed before considering the role of uterine fibroids.11 Fibroids can cause pregnancy complications such as spontaneous abortion, preterm labor, placental previa, malpresentation or dystocia.12 Giant fibroids can produce pressure symptoms, distortion of the pelvic anatomy, pelvic or lower limb thrombosis, dyspneia, or sciatic neuropathy. Gynecologic examination, imaging, and other tests complete the evaluation and the differential diagnosis of symptoms. The diagnosis of fibroids is suspected by the palpation of an enlarged uterus with an irregular contour. Ultrasound (US) is highly accurate for the diagnosis, excludes the possibility of ovarian neoplasm, and maps the size and fibroid location, but magnetic resonance imaging (MRI) provides a better resolution.
Fibroid imaging Imaging is essential to the evaluation, treatment, and postprocedural management of patients undergoing embolization. At US, when the muscular component predominates, the fibroid appears as a hypoechoic solid mass.13 If it undergoes degeneration, cystic or hemorrhagic necrosis results in an anechoic mass with acoustic enhancement. Calcifications in older women present as echogenic foci with shadowing. Sonohysterography is a technique more sensitive for submucosal fibroids. Color Doppler sonography can be used to assess fibroids and uterine vascularity and flow patterns. Fibroids have marked peripheral blood flow with decreased central flow or an avascular core.14 The imaging goals in uterine artery embolization (UAE) candidates are: to assess the presence, number, size, and location of fibroids and the myometrial vascularity, and exclude concomitant pathology, where the symptoms may mimic fibroids. Adenomyosis, endometrial or cervical polyps, endometrial hyperplasia, and cancer can mimic the bleeding patterns associated with fibroids. Adnexal masses can also
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Uterine artery embolization for fibroids mimic serosal fibroids. The diagnosis must be confirmed with preoperative imaging, either US (transabdominal or endovaginal scanning) or magnetic resonance (MR), the most accurate modality to study potential UAE patients. The volume of the uterus and the dominant (i.e. largest) fibroid are measured by using the formula of a prolate ellipsoid (length × width × height × 0.5233). MR provides information on the outcome of the embolization. A fibroid that has high signal intensity on T1-weighted images and shows no signal of enhancement after gadolinium administration is likely to have undergone hemorrhagic degeneration and uterine artery embolization (UAE) is unlikely to improve. The preinterventional contrast-enhanced MR angiographic findings can identify the probability of an ovarian artery supplying the uterine fibroids.15–17 The frequency of this type of collateral supply ranges from 5 to 8% in the literature.18,19 Conventional aortography after UAE can be restricted to those cases in which MR angiography depicts an ovarian artery with a high probability of fibroid supply. But the majority of these ovarian arteries are not shown on angiograms after embolization.20 Possible explanations are a reduction in the “sump effect” of the fibroids with reduced demand through the uterus–ovarian anastomosis or a retrograde embolic occlusion of the anastomosis after UAE. Dilated ovarian arteries discovered on pre-UAE aortograms, may not be visible in up to 63% of cases on post-UAE aortograms.21
Therapies The decision to treat women depends on various factors: the presence of symptoms, uterine size, fibroid number and location, patient age, how close the patient is to menopause, and pregnancy desire. Asymptomatic fibroids usually do not require treatment, just follow-up with gynecologic examination or ultrasound (US). In post-menopausal women, generally the tumor size and the associated symptoms gradually reduce. GnRH agonists are the most effective medical therapy, but discontinuation results in recurrence of symptoms and increases in tumor size. GnRh agonists lead to long-time suppression of the hormonal system. They are expensive and cause significant side-effects like post-menopausal symptoms and osteoporosis if used for longer than 6 months. Surgical therapy, in the form of abdominal hysterectomy or myomectomy, has been the traditional treatment for symptomatic fibroids. Hysterectomy provides the only cure, however fertility is lost. Hysterectomy can be performed by abdominal or vaginal approach. Abdominal myomectomy (removal of fibroids while preserving the uterus) is an alternative surgery. The main advantage is the preservation of reproductive function, but there is a risk of subsequent surgery, from 11 to 26%, due to recurrence or to new fibroids.22,23 The traditional surgery treatment entails general anesthesia, a long hospital stay, and long recovery periods. Concerns about quality of life, uterine-sparing alternatives and cost effectiveness have given rise to the development of several treatment alternatives to hysterectomy. The less invasive forms of therapy are laparoscopic myomectomy, hysteroscopic fibroid resection, myolysis, and UAE. Laparoscopic
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myomectomy is ideal for women with a small number of subserosal or intramural fibroids and a small uterus. By hysteroscopic myomectomy the fibroids are resected with an endoscope placed through the cervix and indicated for submucosal fibroids. Myolysis targets the destruction of fibroids using energy delivery systems. The first embolization for fibroids was performed in 1974, on a woman with intractable fibroid-related menorrhagia in whom the surgery and general anesthesia were considered too risky. The bleeding was successfully controlled. Some years later, Ravina performed UAE in patients with uterine fibroids previously to hysterectomy in 1994.24 Later, in 1995, they presented the method as an alternative treatment to hysterectomy.25 Since then, a number of series involving patients with uterine fibroids who were treated with UAE have been reported in the literature. These studies suggest that this procedure is an effective treatment and well tolerated. UAE is an angiographic procedure that occludes the blood supply to the fibroids, which results in their ischemic infarction and subsequent degeneration. This leads to a reduction in the fibroid’s size and a decrease or resolution of the symptoms.26–29
Patient selection and preprocedure evaluation The decision to treat should be based on symptoms. The fibroids that require therapy present heavy uterine bleeding leading to anemia or symptoms that affect the patient’s quality of life. Crucial to a successful outcome is the appropriate selection of patients. Because the symptoms associated with fibroids are not specific, it is important to determine if they can be explained by the fibroids. Preprocedural evaluation should include a gynecologic and general medical history. A gynecologic history includes the symptoms, menstrual history, and reproductive history. The general medical history should include prior surgeries, allergies, and medication use. After a gynecologic examination that reveals an enlarged or nodular uterus, an ultrasound scan is requested to confirm the presence of fibroids. Imaging plays a vital role in the preprocedural planning for UAE, as it allows assessment of fibroids and of the associated conditions that may imitate or exacerbate the symptoms. Pelvic MR can provide details of size, location, and viability. MR changes the treatment planned prior to UAE in 15% of patients.30 The two most common conditions that produce similar symptoms are adenomyosis and endometriosis; they may change the successful outcome, or even predispose to complications. Adenomyosis appears associated with fibroids in 10–20% of patients.31 The only definitive treatment to adenomyosis is hysterectomy. However, if adenomyosis is associated with fibroids, UAE may have an important role. Tumor size is not a limitation for UAE. Successful outcomes can be obtained with UAE to treat large fibroids, without increased risk to patients.32 A pedunculated submucosal or an intramural fibroid that intrudes sufficiently into the endometrial cavity may slough after embolization. In most cases dilatation of the cervix occurs and allows fibroid expulsion, without any additional manipulation. If the fibroid has not passed spontaneously
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within 48–72 hours of observation, resection of the fibroid by the gynecologist is necessary. In subserosal pedunculated fibroids the point of attachment may disintegrate after UAE, and the fibroid may become free in the abdominal cavity. Some studies showed that there is no serious complications after embolization for pedunculated subserosal fibroids with stalk diameters of 2 cm or larger. Pedunculated subserosal fibroids are defined as those in which the diameter of the stalk is 50% narrower than the diameter of the fibroid. No significant difference in stalk diameters was noted 4 months or 1 year after embolization compared with the diameters before the treatment33 and no serious complications such as separation of the tumors from the uterus, torsion of the tumors, or infection occurred after embolization. One group of patients particularly suited to UAE treatment are those who have not responded to conventional treatments. Hormonal therapy (GnRh agonists) must be discontinued 3 months prior to UAE to allow the arteries to resume their normal size and physiologic response to embolotherapy. When patients are properly screened and advised, UAE has been shown to be a safe and effective means of managing fibroid-related symptoms.
Contraindications An absolute contraindication is a viable intrauterine pregnancy and an active infection of the uterus or adnexa. A suspected pelvic malignancy is also a contraindication, unless embolization is used as a palliative or adjunctive role. Chronic endometritis is a relative contraindication, because antibiotic coverage during and after UAE may be adequate to suppress any serious infectious complications and to allow full recovery.
Peri-procedural care UAE can be an extremely tolerable procedure when the technique is optimal and when there is a well-defined postembolization therapy. UAE can be performed under intravenous conscious sedation (with anxiolytics and
(a)
(b)
sedatives), analgesics for pain, antiemetics for nausea and antibiotics to prevent infectious complications (1 g of cefazolin or vancomycin if the patient is allergic to penicillin). Additional doses of oral antibiotics for up to 5 days after UAE can be used.10–12 An intravenous access is essential during and after UAE while the patient is hospitalized, to allow administration of medications and fluids, and can also be used for resuscitation if needed.
Fibroid embolization procedure UAE can be performed as an outpatient34 and as an elective procedure, with a few hours admission, in a standard angiographic unit, under conscious sedation, and with local anesthesia.35 Using a transfemoral approach, UAE is performed with bilateral selective uterine artery catheterization36–38 using 5-French catheters and fluoroscopic control. For patients with very small uterine arteries, tortuous or flow-restricting spasm, a coaxial 0.025-inch microcatheter can be inserted through the 5-French catheter, with the outer catheter retracted into the hypogastric artery. An initial hypogastric arteriogram is obtained using the road-map technique and superselective catheterization of both uterine arteries is performed. In most cases, the catheter tips are placed in the transverse portions of the uterine arteries, distal to its cervicovaginal branch and an arteriogram is performed. This preembolization angiogram shows the large abnormal fibroids vessels. Embolization is achieved by deploying polyvinyl alcohol particles (350–500, 500–710 µm diameter) or gelatin-coated tris-acryl microspheres (500–900 µm), that are injected slowly under fluoroscopic control. These particles wedge in the fibroid vessels and occlude them. Both uterine arteries are occluded but normal myometrial branches are spared. After each artery has been embolized, a final uterine arteriogram is performed. The angiographic end point of embolization is the devascularization of the perifibroid plexus and sluggish antegrade flow in both uterine arteries (Figure 79.1). At the end of the procedure, patients are transferred to an observation unit for post-procedural care. Technical success is achieved when both uterine arteries are selectively catheterized and the embolic agent occludes the fibroid vascular bed (Figure 79.2).
(c)
(d)
Figure 79.1 35-year-old woman with menorrhagia of 2 weeks: (a) left uterine angiography showing hypervascularization in a round area corresponding to the fibroid; (b) after embolization the hypervascularization is gone; (c) right uterine angiography showing hypervascularization; (d) after embolization the hypervascularization is gone but the uterine artery is patent.
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Figure 79.2 41-year-old woman with urinary urgency due to a large fibroid: (a) left uterine angiography showing hypervascularization in a round zone due to fibroid; (b) following embolization the hypervascularization is gone; (c) right uterine angiography showing hypervascularization; (d) following embolization the hypervascularization is gone, but the uterine artery is patent; (e) after both uterine arteries embolization contrast stays in the fibroid.
UAE requires great familiarity with the pelvic arterial anatomy to ensure the safety and success of the procedure. Variations of the vascularization of uterine fibroid tumors may account for treatment failures and complications. The uterine artery classically arises as a first or second branch of the anterior division of the internal iliac artery (from the inferior gluteal artery) in 51% of cases.39–41 The origin of the uterine artery is well identified on the contralateral oblique projection in most patients. In 6% of cases, the uterine artery is the first branch of the internal iliac artery above the level of the inferior gluteal and superior gluteal arteries. In this anatomic variant, or when the internal iliac artery terminates in trifurcation (15–40%), ipsilateral anterior oblique projection should be performed for better visualization. The presence of fibroids will distort the anatomy of the dilated uterine arteries. This discrepancy, in size and degree of flow to the fibroid compared to normal, allows uterine embolization to be safe and effective. The embolic agents used for embolization are sized to occlude the fibroid branches, and the normal branches usually have a smaller diameter than the embolic agent. The ovarian artery can provide blood supply. This can explain failed procedures despite proper embolization of the uterine artery and also some reported ovarian failure after UAE. If there is a question about the need for ovarian embolization, the procedure should be deferred and the patient re-evaluated 3 months after treatment
Post-procedural side effects Most patients will experience 2–5 days of post-procedural symptoms, including pelvic pain, nausea, anorexia, low-grade fever, and fatigue, known as post-embolization syndrome. These symptoms can be controlled with non-steroidal anti-inflammatories, analgesics and antiemetics in the perioperative period.
Follow-up protocols UAE is a procedure with a low major complication rate and reduced length of hospital stay compared to hysterectomy,42 but higher readmission rates after UAE stress the need for careful post-procedural follow-up. Each patient must be prospectively followed up. Control follow-up is performed by clinical examination performed in the first 10 days, 3 and 6 months, and 1 and 2 years after the procedure. MR imaging evaluation and blood testing should be undertaken 3 and 6 months, and 1 and 2 years after UAE. For better evaluation the patients should answer a standard questionnaire with a scale for grading symptom status. At each follow-up control that information is compared with the baseline one. The patients also are interviewed by telephone after the procedure to evaluate events such as pelvic pain, groin hematoma, abnormal bleeding, or infection, as well as changes in their symptoms.
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(a)
(b)
(c)
Figure 79.3 Contrast-enhanced sagittal MRI: (a) three fibroids are shown; (b) 2 weeks after embolization the fibroids show low intensity due to ischemia; (c) 1 year after embolization: fibroids with ischemia and decreased size.
Because the technical goal of fibroid embolization is infarction, it is important to assess the rate of the infarction. The MR imaging appearance of fibroids after embolization has been described. Post-UAE MR shows significant decrease in size of the uterus and fibroids43 and signal intensity changes that are consistent with hemorrhagic infarction, including increased signal intensity on T1-weighted images and homogeneous decreased signal intensity on T2-weighted images. Following UAE, fibroid vascularity is significantly diminished due to ischemia, but the myometrial perfusion is maintained (Figure 79.3). At the follow-up examinations the percentage of tissue perfused in the dominant fibroid (from 0 to 100%) is evaluated. The degree of fibroid infarction immediately after UAE based on gadolinium-enhanced MR may be predictive of subsequent fibroid volume reduction,44 determining complete versus incomplete infarction, predicting the success of the procedure. The usual appearance of a successful infarcted fibroid is a complete absence of vascularity. If it is not completely avascular, with areas of perfusion on the initial postprocedural imaging, the residual viable tissue may regrow. Recent studies have linked early and late clinical failure to incomplete infarction of fibroids.45–47 Besides technical causes (difficulty in catheterization), collateral ovarian artery supply of fibroids has been reported as a cause of incomplete infarction of targeted fibroids and subsequent clinical failure of the procedure. Spasm may also result in incomplete occlusion of fibroid vessels, and this may result in residual areas of fibroid perfusion.
Results UAE is a method with a high technical success rate. The treatment has good effect on fibroid volume reduction (from 48.8 to 83%) and on clinical symptoms reduction (from 61 to 96%).36,48–51 From the 342 patients that we treated there was an initial clinical success in 331/342 (96.8%). The medium-term success between 3 and 27 months was obtained in 309/342 (90.4%).
Following embolization of 18 failures there were good results in 15, therefore the secondary clinical success was shown in 324 (94.7%).
UAE in adenomyosis UAE as a treatment of adenomyosis with coexisting fibroids has shown mixed results in the studies to date. Adenomyosis is a benign uterine disease characterized by ectopic endometrial glands and stroma within the myometrium. It commonly affects premenopausal women and the clinical manifestations are similar to those of uterine fibroids.52,53 Midterm results of UAE to treat adenomyosis show clinical improvement in 55% of treated patients, with a 2-year follow-up.54 The results of this study may indicate that UAE can be a treatment option successful in 50% of patients with symptomatic adenomyosis refractory to medical therapy, allowing a substantial number to avoid hysterectomy. UAE for adenomyosis may be especially valuable in the subset of patients desiring future fertility, those who have increased surgical risk, or in those absolutely desiring uterine preservation.
Complications Major procedural complications have been reported in less than 4% of patients. A severe ischemic injury to the uterus with required hysterectomy occurs only in 0.05% of patients. Pyometrium has also been reported, which may necessitate a hysterectomy. Less severe infections are treated with intravenous antibiotics. Injuries to other pelvic organs have not occurred. Another rare complication is pulmonary embolus in 0.2%. One possible side-effect of UAE treatment is vaginal discharge. MR may show the necrotic tissue displaced into the endometrial/ endocervical canal. Another potential side-effect is diminished ovarian function. One to five percent of women older than 45 years are reported to have lost their menstrual periods after this procedure. Another study of basal FSH levels pre- and post-procedure to determine if there is a change in
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ovarian function or whether this effect is limited to those perimenopausal showed changes in basal FSH in 15% of patients over the age of 45.
myomectomy is no longer feasible, UAE may be the best alternative. Patients can try to get pregnant 6-months following UAE.
Pregnancy after UAE
Conclusion
A main concern regarding selection of UAE candidates is the issue of fertility. Successful pregnancies with no obvious sideeffects have been reported;55,56 however, whether there are any negative impacts of UAE on either the uterus or ovaries that will interfere with the ability to conceive is unknown. If there are one or two dominant fibroids causing an anatomic deformity of the uterine cavity, myomectomy is the treatment of choice. If there are so many fibroids that
UAE is a minimally invasive procedure, safe and effective as a treatment alternative to surgery in patients with symptomatic fibroids,48,49,57–59 with a low complication rate, and reduced hospital stay and recovery time.60,61 UAE leads to an impressive mid- and long-term improvement of all investigated physical and psychological fibroid-related and fibroidassociated symptoms and significantly improves women’s health-related quality of life.62
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Goodwin S, McLucas B, Lee M et al. Uterine artery embolization for the treatment of uterine leiomyomata: midterm results. J Vasc Interv Radiol 1999; 10: 1159–65 Andersen PE, Lund N, Justesen P et al. Uterine artery embolization for symptomatic uterine fibroids: initial success and short-term results. Acta Radiol 2001; 42: 234–8 Azziz R. Adenomyosis: current perspectives. Obstet Gynecol Clin North Am 1989; 16: 221–35 Vercellini P, Ragni G, Trespidi L et al. Adenomyosis: a déjà vu? Obstet Gynecol Surv 1993; 48: 789–94 Pelage JP, Jacob D, Fazel A. Midterm results of uterine artery embolization for symptomatic adenomyosis: initial experience. Radiology 2005; 234: 948–53 Ciraru VN, Ravina J. Pregnancy after embolization of uterine myomata. Min Invas Ther Allied Tecnolg 1999; 8: 407–10 McLucas B, Goodwin S. Pregnancy following uterine fibroid embolization. Int J Gynecol Obstet 2001; 74: 1–7 Pelage JP, Le Dref O, Soyer P et al. Fibroid related menorrhagia: treatment with superselective embolization of the uterine arteries and midterm follow-up. Radiology 2000; 215: 428–31 Pinto I, Chimeno P, Romo A et al. Uterine fibroids: Uterine artery embolization versus abdominal hysterectomy for treatment – a prospective, randomized, and controlled clinical trial. Radiology 2003; 226: 425–31 Pron G, Bennett J, Common A et al. The Ontario Uterine Fibroid Embolization Trial II. Uterine fibroid reduction and symptom relief after uterine artery embolization for fibroids. Fertil Steril 2003; 79: 120–7 Spies JB, Ascher SA, Roth AR et al. Uterine artery embolization for leiomyomata. Obstet Gynecol 2001; 98: 29–34 Beinfeld MT, Bosch JL, Isaacson KB. Cost-effectiveness of uterine artery embolization and hysterectomy for uterine fibroids. Radiology 2004; 230: 207–13 Bucek R, Puchner S, Lammer J. Mid- and long-term quality-of-life assessment in patients undergoing uterine fibroid embolization. AJR 2006; 186: 877–82
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Hemodialysis access intervention E Calabrese and B Yasin
Patients with chronic renal failure need to have arteriovenous (AV) fistulas or grafts patent and with adequate flow to undergo effective dialysis. Long-term patency of AV fistulas has limitations and more than 85% of AV fistulas thrombose or malfunction during the entire period when a patient is dependent on dialysis. AV fistulas with direct arteriovenous anastomosis have a longer primary patency than PTFE graft (3 years vs. 1 year) while secondary patency, affected by multiple interventions, can last as long as 7 years in a CiminoBrescia shunt in the wrist, 3-5 years in the arm, and just 2 years for PTFE. Following irreversible recurrent failure of the initial AV fistula in spite of several revisions, new fistulas and grafts are inserted. There are several signs that suggest the need for a consultation by a surgeon and an interventional radiologist. These signs include: decreased pulsatility in the fistula, failure of maturation, insufficient inflow or outflow, vacuum phenomenon, abnormally high venous pressures, suboptimal blood flow through the shunt (700–800 ml/minute in PTFE graft and 500 ml/minute in native fistulas), edema of the arm, forearm or hand. Complications of AV shunts can be early or late and can produce malfunction due to thrombosis, low flow, too high a flow, aneurysm formation, or peripheral ischemia. Most of them can be approached by an endovascular technique.
Early complications The most common cause of early malfunction is a technical problem during the surgical procedure when the AV fistula is built. Early causes of low-flow malfunction include technical problems at the site of anastomosis, kinking of the vein or artery that has been mobilized, choice of too small a vein for the anastomosis (often due to the unavailability of suitable veins), inflow obstruction due to proximal arterial stenosis, outflow obstruction due to distal venous stenosis or thrombosis, or premature use of the AV fistula for dialysis before it has matured. Kink The artery and/or the vein should be freed enough to be joined without any undue kink. If a kink develops this will severely interfere with flow and eventually produce thrombosis, often within a few hours. Kinking can be solved at the operation table by freeing up a longer length of the vessel and driving it through a smoother curve or by releasing hardened
tissue that may act as a band. Interventional approach to solving a kink discovered after operative wound closure would require insertion of a flexible, self-expandable stent but this may not suffice to counteract the strength of a tissue band and it may still produce kinks elsewhere by straightening the vein. For early kinks appearing immediately after wound closure, surgery is a better recommendation than stenting in most cases. Anastomosis problems A technical problem in constructing the anastomosis between artery and vein can produce early stenosis or can completely stop the flow. The microsurgical technique, helped by magnifying loops, utilizes 7-0 or even 8-0 prolene and helps reduce problems in suturing. A slow and more expensive interrupted suture should have no significant advantage over a properly made continuous suture. Some operators prefer to perform a side-to-side AV anastomosis at the wrist but it should be remembered that the segment of vein on the side of the hand should be better ligated to limit venous hypertension to the hand. Occasionally, when the distal segment of the artery is not ligated or divided, inversion of flow can ensue with a steal syndrome and consequent ischemia (the approach to this problem will be discussed later in this chapter). Fluted incisions of the ends of both the vein and the artery, with termino-terminal anastomosis, will help obtain better flow and a wider anastomosis provided that the operator is able to obtain a smooth curve in joining the two vessels. Side-to-side laterolateral anastomosis in inexperienced hands, or with poor technique, can be marred by encroachment of a suture in the opposite wall of the vessel, thus producing obstruction to flow. If recognized at surgery, this problem can be solved by redoing the whole anastomosis but, if not immediately seen, thrombosis will ensue. Attempts at treating this problem immediately with interventional techniques should be discouraged with surgical exploration being a better option. Interventional procedures involving the anastomosis should be delayed for a month if possible and situations that require a more immediate approach should give preference to an open surgical technique. Balloon dilatation, with or without stenting, may easily produce disruption of a fresh anastomosis and cause bleeding. Small covered stents could be of help but self-expandable ones are only currently available for larger vessels and would be impossible to use in the tiny vessels of the forearm. Balloon-expandable stent-grafts are always prone to external compression and should be avoided if possible. 699
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Outflow problems Central vein stenosis or occlusion due to prior use of central vein hemodialysis catheters, causes severe peripheral edema, reduces the outflow of a fistula and produces early or late occlusion. Simultaneous creation of an AV fistula and angioplasty, with our without stenting, of the central vein outflow, is a reasonable approach. The rationale of a simultaneous PTA and surgical approach derives from the fact that the increased flow produced by the newly created AV fistula increases the chances of success of the venous PTA and, in turn, opening the central vein by PTA will reduce the risk of thrombosis of the AV fistula.1 It seems that PTA with venous stenting is a safe and effective procedure in treating central vein stenosis2 and a transjugular approach can be used if needed.3 Outflow veins that are extremely small may interfere with effective maturation of the fistula and an early endovascular dilatation of multiple small vein stenoses may help salvage the fistula.4 Angiographic studies within 3 months in non-maturing
fistulas showed significant stenosis in 88% of cases. Angioplasty was attempted in 96% of patients with stenosis, achieving a technical success of 92% after angioplasty. Mean primary patency at 6 months and 1 year was respectively 45 and 34%. Mean secondary patency was 79% at 6 months and 75% at 1 year. In Clark’s study, patients without a thrill following angioplasty were more than twice as likely to lose patency as patients with a thrill. Inflow problems Dujim et al.5 evaluated with contrast-enhanced magnetic resonance the inflow and outflow tract of 66 dysfunctional AV fistulas and 35 AV grafts. MRI showed 19 arterial stenoses in 14 patients (14%); digital subtraction angiography confirmed 18 of these lesions in 13 patients and showed no additional inflow lesion. Of the 13 patients, 7 had arterial inflow lesions only while 6 had an additional stenosis in the outflow or in the
(a)
(c)
(b)
(d)
(e) Figure 80.1 (a) Malfunctioning Cimino-Brescia AVF at the wrist with severe stenosis at the anastomosis site; (b) macro image of the stenosis; (c) PTA with cutting balloon; (d) insertion of self-expandable Abbott’s Xpert stent because of severe recoil after PTA; (e) final result with stent in place and mild residual recoil.
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Hemodialysis access intervention shunt itself. Angioplasty proved effective in improving flow in all but 3 patients (77%).
Late complications Late causes of low-flow malfunction include progressing arterial stenosis, neointimal overgrowth at the anastomosis, neointimal overgrowth in the venous outflow tract, damage and progressing thrombosis of the veins due to repeated punctures, progressive stenosis inside the prosthetic graft and, rarely, acute thrombosis due to excessive and prolonged local compression. Other causes of malfunction that may also require intervention are aneurysm formation, bleeding, arteriovenous steal syndrome with ischemia of the hand, ischemia of the hand due to progressing arterial occlusive disease, cardiac failure and pulmonary edema, or pulmonary hypertension due to high-flow AV fistulas. Outflow problems Increased outflow resistance may severely impair the flow of the AV fistula, producing venous hypertension I and severe edema in the limb and neck and eventually lead to inefficient hemodialysis flow or even failure of the fistula. Endovascular treatment relays on PTA is supported by stenting of the vein. Thrombosis of the anonima, especially if bilateral, will result in reduction of venous drainage from the head and neck with ensuing severe swelling of the face and occasionally headaches. Draining of one of the anonymous veins may suffice to improve symptoms, due to the extensive collateral flow between the right and left venous systems draining the neck. Large self-expandable or balloon-expandable stents will help achieve long-term patency, protected by the increased flow supplied by an open AV fistula. Repeated angioplasty and additional stenting are generally needed, and they will often maintain a secondary patency over long periods. A small series of central vein stenoses treated with Wallstent implantation6 reported a 6-month primary patency rate of 66% at 6 months, 25% at 1 year, and 0% at 2 years with Wallstent implantation in the central veins. In the same series the secondary patency was 100% at 6 months, 75% at 1 year, and 57% at 2 years, thus pointing out to the need for close follow-up and repeated interventional procedures to maintain patency. Stent migration is a possibility and is seen both in central vein and peripheral vein positioning of stents: accurate choice of the dimension, length, and position of the stent is required. Also, delayed shortening of implanted Wallstents have been reported in the large central veins. In exceptional situations, Dacron grafts have been surgically implanted between the subclavian vein and the right atrium to treat severe venous hypertension. Stenosis in the proximity of the AV anastomosis is a common occurrence both in fistulas and graft implantation and PTA. Self-expandable stent implantation is an effective treatment (see Figure 80.1). Primary stenting of anastomotic or venous stenosis in the proximity of the anastomosis should be discouraged because some of these lesions are extremely hard to dilate. The insertion of a stent should immediately follow a satisfactory balloon dilatation without significant
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residual stenosis, to avoid an hourglass-shaped profile of the stent with severe residual stenosis. Satisfactory dilatation of the lesion should be obtained prior to stent implantation, often utilizing extremely high balloon inflation pressures, exceeding 20 atmospheres. Tenacious stenoses may respond to the cutting balloon technique. A prospective randomized study7 comparing cutting balloon against conventional PTA in 173 patients showed identical 61% patency results at 6 months follow-up in the two groups. While there were no device-related complications in the PTA group, while nine device-related complications, including vein rupture, dissection, and thrombosis, were observed in the cutting balloon group, thus highlighting the dangers when using cutting balloons with no ensuing improvement in long-term results. Implantation of self-expandable stents when treating a failing PTFE AV graft is superior to PTA alone. When treating a distal graft-to-vein anastomosis, this is the most common reported lesion responsible for a failing graft. In a series of 60 patients treated for a dysfunctional PTFE grafts, stenosis after intervention was 7% in the stent group and 16% with PTA alone (p = 0.001). Mean primary graft patency was 5.6 months after PTA alone and 8.2 months after stent placement and, notably, when stents were placed across the elbow joint, mean primary graft patency was 8.9 months. Only one stent fracture was reported in this series that utilized SMART stents.8 When PTA fails, surgical revision is indicated if possible, before considering the construction of a new fistula elsewhere. Surgical thrombectomy and revisions do prolong the life of the AV fistula but they can often be cumbersome and may render prompt use of the fistula difficult. Thrombolysis, more specifically pulsed-spray thrombolysis, followed by PTA and stenting, increases the useful life of AV fistulas. These procedures do not require prolonged hospitalization and can be completed in a couple of hours as day-hospital procedures. Pulsed-spray pharmacomechanical thrombolysis was proposed in 1989 by Bookstein9 who used small pulses of highly concentrated urokinase forcefully sprayed throughout the thrombus of an AV graft during system heparinization. Later studies involving the same author using both pulsed-spray thrombolysis and clot fragmentation of residual thrombus with mechanical devices and PTA with stenting of residual stenosis. This multi-approach technique helped reduce the mean thrombotic agent infusion time and increased clinical success.10,11 In countries such as the US, where urokinase is not any longer available, RTPA has been used as thrombolytic agent. The technique has been described as follows: a 21-gauge needle is inserted in the graft pointing toward the venous outflow. Once in the lumen of the graft, a 0.018 guide is inserted and the needle is replaced by a thin catheter with multiple side-holes. An adequate venous outflow is documented prior to initiation of pulsed-spray thrombolysis and then urokinase is initiated. A second puncture is then performed with a similar technique but this time the needle points toward the arterial end of the PTFE graft and, with the help of a guide, a multihole catheter is inserted. On this side of the graft attention is needed to avoid the guidewire of the catheter itself to reach the arterial anastomosis, thus risking arterial embolization of thrombus fragments. Venous thrombolysis is first completed, with venography identifying outflow stenosis that, if present, must be treated with PTA and possibly stenting.
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Only after the venous part of the procedure is completed, pulsed-spray and mechanical dislodgement of the thrombus on the arterial side of the graft is performed. The plug, usually present at the arterial to graft anastomosis is dislodged with mechanical devices such as a small Fogarty or an Oasis thromboaspiration and fragmentation device. An effective thrill and documented Doppler flow should be evident immediately after a successful declotting procedure that usually last less than 1 hour. Distal ischemia of the hand and fingers has been frequently reported after building AV fistulas and several causes can be responsible for this event. Building an AV fistula in a patient without an appropriate Allen test to check for patency and efficiency of ulnar artery circulation may produce ischemia of the hand in those patients where the radial artery is the only vessel supplying the palmar arch. Arterial steal syndrome is another cause of ischemia, seen when the distal end of the radial artery is not ligated and flow from the compensating ulnar artery goes back into the fistula, due to lower resistance, instead of reaching the digital arteries. Ligation of the radial artery distal to the fistula usually improves the situation if the ulnar artery has an efficient flow. Advancement of arterial disease with severe calcifications and stenosis of the ulnar and radial artery in the proximity of the wrist may cause severe ischemia of the hand and the rigidity of the vessels may often impair any attempt at PTA or any successful surgical bypass. Most of the time though, high pressure balloons or even cutting balloons may help improve distal flow to the hand and, in some cases, ligation of the radial artery distal to the AV fistula followed by a brachial–radial distal bypass with an inverted vein will greatly improve the flow. Brachial artery stenosis or stenosis of the proximal segment of the radial, ulnar, or interosseous artery may be treated with PTA. In any case, in the presence of ischemia of the hand a thorough selective upper limb arteriography will help diagnose and treat the problem.12 In diabetic patients with chronic renal failure in dialysis, severe infections of the hand may occur and this may lead to
gangrene of the fingers or the entire hand. Part of the problem is due to low blood flow, arterial steal, or multiple arterial stenosis. More often the gangrene is due to bacterial infection from anaerobes, proteus, enterobacteriaceae, or methicillinresistant staph: these require prompt diagnosis and specific treatment. Increasing blood flow to the hand is only part of the solution: drainage of phlegmons and abscesses plus properly chosen antibiotics and local open wound treatment are essential to save the hand and fingers. Large proximal fistulas or short, straight AV grafts may produce a very high-output AV shunt that may induce heart failure and pulmonary hypertension. Occasionally, pulmonary hypertension develops shortly after the construction of an AV fistula even before starting the patient on hemodialysis. A reduced basal and stimulatory nitric oxide level is the laboratory hallmark of this syndrome and is probably induced by the endothelial dysfunction that reduces the ability of the pulmonary bed to adapt to the increased pulmonary flow produced by AV fistulas in patients with chronic renal failure. So far no interventional procedure has been extensively tested to effectively reduce flow in AV fistulas and grafts but embolization with spirals or plugs and endovascular occlusion of the fistula or graft is a reasonable approach. The patient is switched to an alternate mean of dialysis (peritoneal or central venous cannula) and is usually referred to renal transplant with a high priority.13
Conclusion Patency of AV fistulas and grafts depend on an effective and accurate surgical technique when they are constructed. A careful use of the access by the dialysis team, a constant attentive monitoring of flows, pressures and pulses at frequent intervals and a prompt action whenever interventional or surgical procedures are needed will prolong the life of the fistula and its usability. Quality improvement programs monitoring access flow in dialysis centers improve long-term efficiency of AV dialysis accesses.14,15
REFERENCES 1. 2. 3. 4. 5. 6.
7. 8.
Shemesh D, Olsha O, Berelowitz D et al. Integrated approach to construction and maintenance of prosthetic arteriovenous access for emodialysis. Vascular 2004; 12(4): 243–55 Bornak A, Wicky S, Ris HB et al. Endovascular treatment of stenoses in the superior vena cava syndrome caused by non-tumoral lesions. Eur Radiol 2003; 13(5): 950–6 Basile A, Medina JG, Lupattelli T, Medina VG, Leal R. Internal jugular vein access for the interventional management of nonfunctioning artero-venous haemodialysis fistulas. Eur J Radiol 2004; 52(3): 288–92 Clark TW, Cohen RA, Kwak A et al. Salvage of nonmaturing native fistulas by using angioplasty. Radiology 2007; 242(1): 286–92 Duijm LE, Liem YS, van der Rijt RH, Nobrega FJ, van der Bosch HC et al. Inflow stenoses in dysfunctional hemodialysis access fistulae and grafts. Am J Kidney Dis 2006; 48(1): 98–105 Verstandig AG, Bloom AI, Sasson T, Haviv YS, Rubinger D. Shortening and migration of wallstents after stenting of central venous stenoses in hemodialysis patients. Cardiovasc Intervent Radiol 2003; 26(1): 58–64 Vesely TM, Siegel JB. Use of the peripheral cutting balloon to treat hemodialysis-related stenosis. J Vasc Interv Radiol 2005; 16(12): 1593–603 Vogel PM, Parise C. Comparison of SMART stent placement for arteriovenous graft salvage versus successful graft PTA. J Vasc Interv Radiol 2005; 16(12): 1619–26
9. 10.
11.
12. 13. 14.
15.
Bookstein JJ, Fellmeth B, Roberts A et al. Pulsed-spray pharmacomechanical thrombolysis: preliminary clinical results. Am J Roentgenol 1989; 152(5): 1097–100 Valji K, Bookstein JJ, Roberts AC et al. Pulse spray pharmacomechanical thrombolysis of thrombosed hemodialysis access grafts: long term experience and comparison of original and current techniques. Am J Roentgenol 1995; 164(6): 1495–500 Cho SK, Han H, Kim SS et al. Percutaneous treatment of failed native dialysis fistulas: use of pulse-spray pharmacomechanical thrombolysis as the primary mode of therapy. Korean J Radiol 2006; 7(3): 180–6 Asif A, Leon C, Merrill D et al. Arterial steal syndrome: a modest proposal for an old paradigm. Am J Kidney Dis 2006; 48(1): 88–97 Yigla M, Abassi Z, Reisner SA, Nakhoul. Pulmonary hypertension in hemodialysis patients: an unrecognized threat. Semin Dial 2006; 19(5): 353–7 Wijnen E, Planken N, Keuter X et al. Impact of a quality improvement programme based on vascular access flow monitoring on costs, access occlusion and access failure. Nephrol Dial Transplant 2006; 21(12): 3514–9 Plantinga LC, Jaar BG, Astor B et al. Association of clinic vascular access monitoring practices with clinical outcomes in hemodialysis patients. Nephron Clin Pract 2006; 104(4): 151–9
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Endovascular surgery in treatment of some congenital heart defects BG Alekyan, VP Podzolkov, VA Garibyan, MG Pursanov, KE Kardenas, and E Yu Danilov
Transluminal balloon angioplasty for coarctation and recoarctation of the aorta Material and methods From 1985 to 2006, 208 transluminal balloon angioplasties (TLBAPs) were carried out in 194 patients with coarctation syndrome. There were 136 (70.1%) patients with aortic coarctation and 58 (29.8%) with recoarctation. The patients were assigned to two groups: group 1 – 93 (70%) patients with membranous type of coarctation, and group 2 – 41 (30%) patients with hypoplastic type of coarctation. Results Immediate good results of TLBAP in patients with membranous coarctation were noted in 74 (79%) cases. Systolic pressure gradient (SPG) between the ascending and the descending aorta decreased from 41.0 ± 16.3 to 7.3 ± 6.7 mmHg. Good results of TLBAP in patients with hypoplasticcoarctation were noted in 24 (63%) cases. SPG between the ascending and the descending aorta decreased from 40.0 ± 15.3 to 9.7 ± 8.2 mmHg. Among patients with aortic recoarctation good results were noted in 41 (70%) cases. Long-term results of TLBAP were studied in the follow-up, ranging from 6 months to 20 years in 69 (35.5%) patients. Thirtyfive (50.7%) of them had membranous coarctation; 17 (24.6%) had hypoplastic coarctation, and 17 (24.6%) had recoarctation of the aorta. Good and satisfactory results in membranous coarctation were noted in 31 (88.5%) patients. Unsatisfactory results were noted in 25.5% of patients with hypoplastic restriction and in 23.5% of patients with recoarctation. No serious complications were noted during or after TLBAP, with the exception of left axillary artery thrombosis in 3 patients aged under 36 months and 3 cases of femoral artery thrombosis. Five patients needed thrombectomy, the sixth patient underwent conservative treatment.
Conclusions Balloon angioplasty permits good and satisfactory long-term results in 89.7% of patients. The results of TLBAP are better in patients with membranous aortic coarctation.
Stenting of aortic coarctation and recoarctation Material and methods From 1995 to 2006 we have performed stenting of aortic coarctation in 22 (64.7%) patients and of aortic recoarctation in 12 (35.2%) patients in whom TLBAP proved ineffective. Results Immediate post-stenting results were judged to be good in 32 (94.1%) patients. SPG between the ascending and the descending aorta decreased from 47.0 ± 15.3 to 2.7 ± 3.2 mmHg. Long-term results were studied at 6 months–11 years in 20 patients (58.8%). Good results of stenting were noted in 19 (95%) cases. Mean SPG between the ascending and the descending aorta did not exceed 5 mmHg. Satisfactory results were noted in one (5%) patient whose SPG-systolic gradient pressure was 25 mmHg In one (3%) case, 13 months after stenting, a false aortic aneurysm developed. This complication was successfully treated using endovascular methods, with stent-graft implantation (Valiant, Medtronic) (Figure 81.1 and 81.2). Conclusions Good immediate and long-term results of stenting in cases of aortic coarctation and recoarctation allowed us to recommend this method for wider use in patients of the older age group.
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(a)
(b)
Figure 81.1 Stenting of aortic coarctation: (a) AC (the arrow shows the site of restriction); (b) the stent is completely deployed, AC is corrected.
Stenting of pulmonary arteries in patients with congenital heart diseases Material and methods We have implanted 87 stents in order to eliminate the obstruction of 77 segments of the pulmonary arteries in 66 patients.
(a)
The patients’ age varied from 2 to 27 years (mean 11.7 ± 7.8 years). Over one-half of patients (35/66) were over 10 years of age. The patients’ weight varied from 9.5 to 74 kg (mean 28.5 ± 27.3 kg). Twenty-seven patients had radical correction of Fallot’s tetralogy (TF) and pulmonary artery atresia (PAA); 20 had reconstruction of RV outflow tract for TF and PAA; 7 patients had cyanotic CHD; 10 had Fontan operation and bidirectional
(b)
(d)
(c)
(e)
Figure 81.2 False aneurysm in a patient after stenting of aortic coarctation: (a) preprocedural CT angiography (the arrow shows the aneurysm exceeding the stent’s edges); (b, c) preprocedural angiography; (d) after stent-graft implantation in the aorta; (e) CT angiography after stent-graft implantation in the thoracic aorta.
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Figure 81.3 Stenting of the left pulmonary artery stenosis caused by previously created Blalock-Taussig anastomosis in a patient with Fallot’s tetralogy: (a) severe stenosis of the left PA (arrow); (b) absent stenosis after PA stenting; (c, d) stages of stenting.
cava–pulmonary anastomosis for complex CHD; and 2 had peripheral stenoses of the pulmonary artery with intact ventricular septum. No serious procedure-related complications were seen. Results After stenting, the vessel diameter increased by an average of 4.9 ± 4.5 mm to 12.45 ± 2.8 mm, and systolic pressure gradient
(a) Figure 81.4
decreased by an average of 55.6 ± 38.8 mmHg to 19.6 ± 18.5 mmHg. The ratio between RV systolic pressure and systemic arterial pressure decreased on average by 0.82 ± 0.09 to 0.46 ± 0.05 in patients with intact ventricular septum. The effectiveness of pulmonary artery stenting was 95.0% (72 of 77 segments). No serious procedure-related complications were seen. Long-term results of pulmonary artery stenting were studied in 42 (63.6%) patients (47 stents) at 6–65 months (mean 19.8 ± 16.6 months) after the procedure. Control catheterization and
(b)
Recanalization with stenting of Gore-Tex anastomosis.
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(a)
(b)
Figure 81.5 Stenting of stenotic LAPCA supplying the right lung: (a); before stenting – stenosis in the proximal segment (arrow); (b) after stenting (Palmaz stent) there is no stenosis.
angiography showed that all stents were patent, and no stent migration or reposition were noted. Only in two cases (4.2%) was in-stent restenosis due to intimal hyperplasia revealed. Repeated balloon dilatations of the implanted stents were performed in seven patients (nine stents). In two cases this was related to restenosis and in six cases with the child’s growth. Conclusions Stenting is effective and rather complicated from the technical standpoint procedure in patients with obstructive pathology of the pulmonary artery. The rate of immediate success of pulmonary artery stenting was 95.0%. The frequency of late post-stenting restenosis was 4.2%. Our results suggest the feasibility of repeated dilatation in long-term follow-up after the procedure (Figure 81.3).
Stenting of the conduits and the right ventricular outflow tract Material and methods Nine patients aged 3–12 years underwent stent placement for the restriction of the restricted conduits between the RV
Figure 81.6
and the RA (seven cases) and the RV outflow tract (two cases). Among seven in whom conduits were stented, two had had radical correction of the PAA with the use of valved xenopericardial conduit, one had had Rastelli operation for TGA with the use of aortic allograft and four had had PAA after the reconstruction of RV outflow tract without VSD closure and with the formation of xenopericardial valveless conduit. In two cases we stented the RB outflow tract in a patient with primary TF and a patient with TF and iatrogenic atresia of the left pulmonary artery. Results Ten stents were used in nine patients for the correction of conduit restriction. In patients with radical correction of the defect the stenting resulted in a decrease in systolic pressure gradient between the right ventricle and the pulmonary artery, on average from 76.3 ± 16.7 mmHg to 39.5 ± 22.2 mmHg. The ratio between TV systolic pressure and arterial systolic pressure decreased from 0.81 ± 0.04 to 0.63 ± 0.07. The diameter of the stenotic conduit’s segment increased on average from 13.7 ± 2.3 mm to 16.8 ± 2.8 mm. In four patients, after the reconstruction of the tight ventricular outflow tract, the stenting contributed to a significant
Angiogram of a patient with left heart hypoplasia syndrome: (a) before stenting; (b) after stenting.
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Endovascular surgery in treatment of some congenital heart defects increase of the stenotic segment diameter from 2.5 ± 0.5 mm to 7.3 ± 0.6 mm; at the same time pulmonary arterial systolic pressure increased on the average from 14.6 ± 4.7 mmHg to 41.3 ± 21.6 mmHg. Conduit stenting proved effective in the immediate post-procedural period. The stenting of a conduit in patients after RV outflow tract reconstruction was considered as a palliative procedure, allowing the increase of antegrade blood flow to the pulmonary artery, which contributed to the development of the hypoplastic pulmonary arteries. Arterial blood saturation with oxygen in these patients increased from 73.6 ± 3.5% to 82.0 ± 2.0%. The stenting of the RV outflow tract resulted in an increase of arterial blood saturation with oxygen in two patients with TF from 45 to 74% and from 71 to 84%, respectively. In these cases stenting was considered as a palliative procedure aimed at the improvement of the clinical state of patient in one case and at the development of hypoplastic pulmonary arteries in the other. Conclusions Thus, stenting allows to extend the conduits’ durability and to delay the operations for their replacement. The stenting of the reconstructed RV outflow tract in patients with PAA without VSD closure and RV outflow tract in patients with TF is a palliative procedure, aimed at the increase of arterial blood saturation with oxygen and at the development of the hypoplastic pulmonary arteries.
Transluminal balloon angioplasty of the stenotic systemic–pulmonary and cava–pulmonary anastomoses in patients with cyanotic congenital heart diseases Material and methods Balloon angioplasty for the restrictions of systemic– pulmonary and cava–pulmonary anastomoses was performed in 107 patients aged 1.5 months–19 years. In 87, dilatation was
Figure 81.7
Embolization of a coronary–cardiac fistula.
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performed for the obstruction of Blalock–Taussig; in 11, Gore-Tex; in 1 (1%), Vishnevsky–Donetzky; in 2 (2%), of central anastomosis; and in 6, for the restriction of cava– pulmonary anastomosis. In two patients it was necessary to perform stenting in order to correct anastomotic obstruction. The patients were assigned to three groups: with discrete obstruction, with extended obstruction, and with thrombosis. Most patients were assigned to the first group. While performing balloon angioplasty of the Blalock– Taussig anastomosis we used balloons with a diameter corresponding to the diameter of the subclavian artery proximal to the stenotic segment; for the dilatation of the Gore–Tex anastomosis the balloons corresponded to the prosthesis diameter. Results After balloon dilatation of the stenotic segment arterial blood saturation with oxygen increased from 64.6 ± 1.8% to 82.1 ± 1.7%. Systolic pressure in the PA increased from 15.5 ± 0.9 to 24.2 ± 1.9 mmHg. Angiometric data showed that the diameter of the stenotic segment of the anastomosis increased from 2.5 ± 2.8 to 5.8 ± 3.5 mm. The results of balloon angioplasty were judged to be good in 74 (69.1%) patients, satisfactory in 29 (27.1%), and unsatisfactory in 4 (3.8%). The best results were obtained in patients with discrete stenosis and in patients with thrombosed anastomoses. Peri-and post-procedural complications were noted in 3 (2.8%) patients: pulmonary edema in 2 and pre-edema state in 1 patient due to anastomosis hyperfunction. In 2 cases these complications were terminated with drugs, and in 1 patient with pulmonary edema successful radical correction of the defect was performed. Conclusions Balloon angioplasty of the stenotic anastomoses is an effective method of treatment in this group of patients and can serve as an alternative to the repeated surgical intervention for second anastomosis creation.
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Figure 81.8
Successful closure of a VSD using Amplatzer ventricular septal occluder.
Stenting of large aorto–pulmonary collateral arteries in patients with pulmonary artery atresia Material and methods The stenting of large aorto-pulmonary collateral arteries (LAPCA) was carried out in 6 patients with pulmonary artery atresia (PAA). The patients were aged from 5 to 19 years (12 ± 4.9 years on average). Four patients had type IV PAA and two had type II. The clinical state was considered as extremely severe in 1 patient (after surgical unifocalization of a collateral artery complicated by thrombosis of the anastomosis), severe in 2, and satisfactory in 3 patients. Arterial blood saturation with oxygen varied from 40 to 76% (mean 66 ± 13.2%). In four cases the stenting of the stenotic segment was preceded by balloon dilatation. In three cases peripheral Palmaz stents were used; in the remaining cases, coronary stents. Results After stenting of the LAPCA the diameter of the stenotic segment increased on average from 2.3 ± 0.9 mm to 4.5 ± 1.3 mm. Arterial blood saturation with oxygen increased on average from 66 ± 13.2 to 77.8 ± 3.6% (values scatter from 73 to 84%). No procedure-related complications were noted, neither during the procedure nor in the immediate postprocedural period. Somatic state improved, cyanosis decreased, and working capacity increased in all patients. No repeat interventions were performed. Conclusions Despite the small number of cases we can confirm that TLBAP and stenting of the LAPCA in patients with cyanotic CHD
result in pulmonary blood flow improvement. It is necessary to take into account the rigid character of LAPCA, making it necessary to use high-pressure balloons for dilatation and stenting.
Embolization of large aortopulmonary collateral arteries in patients with pulmonary artery atresia Material and methods We have performed embolization of 122 collateral arteries in 52 patients using 202 Gianturco coils and 2 Amplatzer occluders. Twenty patients had PAA after the reconstruction of RV outflow tract, 6 had PAA after the creation of systemic– pulmonary anastomosis, 10 had had Fontan operations and creation of a bidirectional cava–pulmonary anastomosis, and 16 patients had different cyanotic CHD. Results The diameters of the coils varied from 3 to 10 mm, 3.4 ± 1.3 coils on average were used for the embolization of one collateral artery. Complete closure of collaterals was achieved in 78.0% of cases. In two cases LAPCA were closed using Amplatzer occluders. The indication for occluder implantation was large diameter of the collateral artery in the absence of stenosis. Conclusions Embolization closure of LAPCA in patients with cyanotic CHD (pulmonary artery atresia, TF, etc.) is one of the stages of complex treatment, allowing the preparation of patients for radical correction of the defect. In post-Fontan operation
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Figure 81.9
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Closure of two ASDs using two Amplatzer occluders.
patients and bidirectional cava–pulmonary anastomosis, the embolization of collaterals allows the prevention of early postoperative complications.
Stenting of patent ductus arteriosus in patients with ductus-dependent systemic and pulmonary blood flow The outcome of a Norwood operation in left heart hypoplasia depends primarily on the success of the first stage of treatment, however a lot of patients with this defect die before the second stage could be undertaken. The stenting of patent ductus arteriosus in combination with bilateral ligation of the pulmonary artery branches is a new approach to the treatment of left heart hypoplasia. The stenting of PDA in congenital heart diseases with ductus-dependent pulmonary blood flow improves the clinical state of patients, stabilizes their hemodynamics, decreases the level of hypoxemia and leads to the development of hypoplastic pulmonary arteries, thus creating a basis for further surgical correction. Material and methods The stenting of PDA was performed in 27 patients with different ductus-dependent CHD. The age of patients varied from 6 hours to 3 months, and their body weight varied from 1800 to 4400 grams. There were 26 newborn patients. Twenty-three patients were in critical state. There were 12 patients with ductus-dependent systemic and 15 patients with ductusdependent pulmonary blood flow. Direct stenting of the PDA was performed in 19 cases. In 5 cases it was preceded by balloon angioplasty of the duct. Coronary and peripheral stents were used. Results The procedure was technically successful in 24 (88.8%) cases. Seven patients in an initially severe state died during the immediate post-procedural period. Acute stent thrombosis noted in one case necessitated emergency creation of
systemic–pulmonary anastomosis. Ten (37.1%) patients with ductus-dependent pulmonary blood flow were discharged in a satisfactory state. Seven (25.9%) patients with ductus-dependent systemic blood flow underwent surgery aimed at bilateral restriction of the pulmonary arteries after the stenting procedure. One patient with left heart hypoplasia syndrome underwent a hybrid operation, namely bilateral restriction of a PA with simultaneous PDA stenting, performed from the main PA approach. Conclusions Stenting of PDA in patients with severely decreased pulmonary blood flow is an effective palliative procedure, allowing the improvement of the clinical state of patients. Stenting of the PDA in patients with ductus-dependent systemic blood flow is the first step towards subsequent surgical correction of the defect.
Transcatheter closure of patent ductus arteriosus By September 2006, transcatheter coil closure of primary patent ductus arteriosus (PDA) and PDA recanalized after surgical ligation was attempted in 591 patients. In 497 cases we used Gianturco coils (Cook, Denmark); in 8, the Buttoned device “Custom Medical Device” Grecce; in 85, the Amplatzer duct occluder; and in 1, the Amplatzer muscular ventricular septal occluder (AGA Med Corp.). The patients’ age varied from 1.5 months to 74 years. The PDA diameter varied from 1.1 to 14 mm. Results Immediate Intraprocedural complete PDA occlusion was achieved in 547 (97.3%) patients. In 7 cases coil implantation was unsuccessful due to ductus kinking or large diameter. Coil migration into the pulmonary artery occurred in 10 cases, the coils were retrieved with a trap. In all cases of Amplatzer and Buttoned device use, complete occlusion was achieved.
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Long-term The results were studied in 430 patients in the follow-up ranging from 1 month to 11 years. In 424 cases complete PDA closure was confirmed. In 5 patients with small residual shunt after coil embolization we repeated the procedure with the implantation of additional coils, which led to complete occlusion of the duct. In 1 patient an additional Buttoned device was implanted. Conclusion The use of coils is preferable while closing PDAs with a diameter up to 3.0 mm, while larger ducts have to be closed with mechanical Amplatzer occluders and Buttoned devices.
Transcatheter closure of congenital coronary-cardiac fistulae Material and methods By September 2006, 22 patients underwent transcatheter closure of coronary–cardiac fistulae. In 21 cases Gianturco were used, and in 1 patient, besides the coils, we used the Amplatzer duct occluder and Amplatzer plug occluder. The age of patients varied from 11 months to 44 years, and weight from 9 to 74 kg. In 6 cases there were fistulae between the right coronary artery (RCA) and the right ventricle (RB); in 1, between the posterior interventricular branch of the RCA and the RV; in 3, between the RCA and the right atrium (RA); in 1, between the RCA branch and the pulmonary arterial trunk (PA); in 2, between the left anterior descending branch (LAD) of the left coronary artery (LCA) and the PA; in 5, between the LAD and the RV; in 2, between the circumflex branch (CxB) and the RV; and in 2 cases, between the CxB and the RA. Results Complete intraocclusion of the fistulae was achieved in 21 patients. In 1 patient with a huge aneurysm of the right coronary artery (RCA), small residual permeability of the
Figure 81.10
Stenting of the right ventricular outflow tract.
fistula persisted. The following complications were encountered: femoral artery thrombosis in 1 patient (thrombectomy was performed); coil migration in the PA in 1 patient (the coil was retrieved with a “trap”); and in 2 cases severely tortuous coronary artery was damaged by the guidewire during catheterization, which led to immediate fistulae thrombosis without any complications. Late results were studied in all patients in the follow-up, which ranged from 6 months to 15 years. A patient with incomplete fistulae closure underwent the implantation of two additional coils 1 year after the procedure; complete fistula occlusion was achieved. In all remaining cases complete closure of the fistulae was confirmed. Conclusions Coronary fistulae closure with coils in some cases is an effective alternative to surgical intervention. In large fistulae it is reasonable to use special mechanical occluders.
Use of occluders for the treatment of patients with ventricular septal defect Aim The aim was to show our experience with Amplatzer and Sideris occluder implantation for the treatment of patients with ventricular septal defect. Material and methods Two types of occluders were used for defect closure: Amplatzer membranous ventricular septal occluder, (APVSO, AGA-Med, USA), Amplatzer muscular ventricular septal occluder (AMVSO, AGA-Med) and Patch occluder (PO, Sideris, Greece). VSD closure was performed in 35 patients. In 23 cases the defect was membranous; in 4, muscular; in 7 patients there was membranous defect recanalization after previously performed correction (in 5 cases after isolated defect plasty and in 2 cases after radical correction of a defect: Fallot’s tetralogy, double outlet ventricle with common open AV channel); and in 1 case the defect was closed in a patient with transposition
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Endovascular surgery in treatment of some congenital heart defects of the great arteries after atrial switch operation (Mustard operation). In 27 cases we have used an APVSO occluder; in 4, AMVSO; in 4, the Sideris patch occluder. The size of Amplatzer occluders varied from 4 to 16 mm. Results The use of APVSO and AMVSO led to successful closure of all defects. The regurgitation at the upper edge of the occluder with the diameter of 0.5–1.0 mm was seen in three patients. At followup study (up to 12 months) regurgitation was absent in all patients. The use of the patch occluder led to defect closure in three cases. In one case after proximal balloon inflation AV block occurred. After balloon removal normal heart rhythm resumed. Conclusions The use of occluders for the treatment of congenital ventricular septal defects is an effective and safe technique, and in some cases it can be considered as the alternative to surgical correction.
Endovascular closure of secondary atrial septal defects using the Amplatzer septal occluder From February 1997 to September 2006 endovascular closure of ASD-II was performed in 150 patients. The age of patients ranged from 11 months to 69 years; the weight, from 8.4 to 114 kg. Transthoracic ECG showed the following localization of ASDs in 150 patients: central defect in 61 (40.6%) patients; defect with deficient or absent anterior (aortic) rim in 58 (38.2%); defect in the atrial septum aneurysm in 7 (5.2%) patients; 18 patients (12%) had 2 atrial septal defects; and in 6 cases recanalization of ASD was found. The procedure of ASD closure in 130 patients was carried out under TTE, in 20 (14.8%) under TEE control. The average diameter of implanted occluders was 18.1 ± 8.4 mm (range: 5–38 mm). In the group of 18 patients with 2 defects, in 12 cases both ASDs were closed with 1 occluder and in 6 cases 2 occluders were used (the distance between the defects being over 6 mm). Immediately after the implantation, complete closure of ASD with the Amplatzer septal occluder was achieved in 143 (95.3%) patients, at 1 day after the implantation in 145 (96,6%), at 1 month in 146 (97%), and at 3 months in 149 (99.3%) patients. In 1 patient (0.7%), occluder implantation proved unsuccessful due to the presence of an 5 mm residual shunt. Complete closure of atrial septal defects at 1-year follow-up was achieved in 99.3% of cases. No complications occurred during the procedure of occluder implantation and
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in the long-term follow-up. Thus endovascular closure of ASD is a safe and effective method of treatment.
Endovascular closure of different pathological communications using Amplatzer occluders Aim The aim was to show the feasibility of Amplatzer occluders use in the treatment of different pathological communications. Material and methods Ten patients underwent endovascular closure of different pathological communications. Three of them had antegrade pulmonary arterial blood flow after hemodynamic Fontan correction, two had a fistula between the left ventricle and the right atrium after mitral (in one case) and tricuspid (in another case) valve replacement. In two other cases we had to close a recanalized defect of the aorto-pulmonary septum. Three remaining patients presented with giant aneurysm of the right vertebral artery (n = 1); rupture of the sinus of Valsalva aneurysm into the right ventricle after the correction of Fallot’s tetralogy (n = 1), and a patent Cooley anastomosis after radical correction of Fallot’s tetralogy (n = 1). In all patients we used Amplatzer occluders for closure of the atrial septal defect (three cases) and large PDA (seven cases). The patients’ age varied from 3 to 33 years. Results The occluder was successfully implanted in all patients. In eight cases angiography performed in the operating room showed the absence of shunt. In two cases small residual shunt through the occluder’s struts was revealed, but after 24 hours it resumed completely. In all cases we noted a decrease in pressure in the right cardiac cavities, and in a patient with right vertebral artery aneurysm, clinical regress of cerebral insufficiency. No occluder-related complications (migration or breakage of the device, thrombi formation) were noted in any of our patients. Conclusions Amplatzer occluders, well reputed in the treatment of congenital septal defects and large PDAs, can be used for the treatment of other pathological communications. Thus, at the present time the spectrum of use of endovascular techniques is quite large. This spectrum can be further enlarged with the development of modern medical technologies, thus allowing them to occupy a well-deserved place in complex treatment of congenital heart diseases.
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Endovascular treatment of some congenital diseases: hemangiomas and vascular malformations BB Lee, J Laredo, DH Deaton, and RF Neville
Introduction Infantile/neonatal hemangioma and congenital vascular malformation are usually classified into a single vascular anomaly group. They are separate clinical entities where each behaves differently and has a very different clinical course. Because of this distinction, the diagnosis and management of each are entirely different.1 Infantile/neonatal hemangioma, in general, represents a “vascular tumor” with self-limiting growth,1,2 while congenital vascular malformation (CVM) represents a chronic, embryologically derived vascular lesion.3 Proper diagnosis is therefore essential for the appropriate management of both conditions. The management of hemangioma is generally medical (e.g. steroid, interferon) with limited addition and/or application of non-medical treatment modalities (e.g. laser therapy, surgical excision) when indicated.4,5 The natural history of hemangioma is characterized by self-limited growth with spontaneous tumor regression. Therefore, aggressive management is generally reserved for treatment of complications (e.g. bleeding) and threatened vital function (e.g. visual function). In contrast, the management of CVMs is more complex due to the various origins of the three different circulatory systems (arterial, venous, and lymphatic) and its embryological subtypes producing extratruncular and truncular lesions.6,7 Proper identification of CVM lesion(s) and subtype, based on the Hamburg classification6,7 is essential for the accurate management of the various types of CVMs: venous malformation (VM),8–11 lymphatic malformation (LM),12,13 arteriovenous malformation (AVM),14–16 arterial malformation (AM),17 and the CVM containing all three components, the hemolymphatic malformation (HLM).18–20 Initial diagnosis of CVMs can be made utilizing combinations of various non-invasive and minimally invasive studies: Duplex ultrasonography,21 MR imaging/CT scanning,22 Whole-body blood pool scintigraphy (WBBPS),23 transarterial lung perfusion scintigraphy (TLPS),24 and lymphoscintigraphy.25,26 More invasive studies (e.g. arteriography, phlebography, direct puncture angiography) are occasionally needed in the differential diagnosis of CVMs, but are generally reserved for situations where intervention and treatment is indicated.27 Complete diagnosis of CVM should include classification of its embryological subtype (truncular or extratruncular), 712
since its response to therapy and its natural history depend heavily on embryologic subtypes.28 The extratruncular lesion represents an embryologic tissue remnant that is the result of premature developmental arrest that has occurred in its “earlier” stage of embryogenesis (e.g. the reticular stage).29–31 Extratruncular lesions therefore retain their mesenchymal cell characteristics and potential to proliferate when required (e.g. due to trauma, surgery, hormones, or pregnancy). The extratruncular lesion remains dormant in the vicinity of named (truncular) vessels. When activated, depending upon its location and severity, it becomes a limb threatening if not life-threatening condition. Therefore, its management should address both the embryologic and hemodynamic characteristics. In contrast to the extratruncular lesion, the truncular lesion is the result of a developmental defect that occurs in a “later” stage of embryogenesis, resulting in a lesion that no longer has the potential to proliferate.29–31 Because truncular lesions have no potential for proliferation, the management of these lesions is only dependent on its hemodynamic impact (e.g. arterial ischemia, venous insufficiency). Truncular lesions also produce various anatomical defects; for example, sometimes the whole embryonic vein persists (e.g. marginal or lateral embryonic vein) producing significant hemodynamic effects. Other anatomical defects affecting the named vessel itself include webs and spurs (e.g. vein webs and spurs). In addition, truncular lesions may also produce aplastic, hypoplastic, and hyperplastic lesions (e.g. absence of iliac vein, iliac vein stenosis). Once treatment is indicated, an endovascular approach with angioplasty and/or stenting is often useful; otherwise surgical correction or bypass can be performed to address the hemodynamic abnormality, which will be discussed in other chapters accordingly. The final decision for treatment, as well as selection of the treatment modalities, should be made by a multidisciplinary team approach, based on various indications32,33 (Table 82.1). The treatment strategy should be based on the consensus by the many different specialists involved in the patient’s care (e.g. vascular surgeon, orthopedic surgeon, plastic surgeon, head and neck surgeon, interventional radiologist, physiatrist). Periodic follow-up evaluation and assessment of treatment results should be made based on Duplex scan, WBBPS, TLPS, CT, and/or MRI in the majority of cases. This is especially important during therapy requiring multiple treatment sessions.
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Endovascular therapy – indication (general)
Hemorrhage High output heart failure (AV shunting malformation) Secondary ischemic complications (AV shunting malformation) Secondary complications of chronic venous hypertension (venous malformation) Lesions located in a life threatening region (e.g. proximity to the airway), or located in an area threatening vital functions (e.g. seeing, eating, hearing, or breathing) Disabling pain Functional impairment Cosmetically severe deformity Vascular bone syndrome Lesions located in an area with potentially high risk of complication (e.g. hemarthrosis, deep vein thrombosis and/or pulmonary embolism) Lymph leak with or without infection (lymphatic malformation) Recurrent sepsis, local and/or systemic (lymphatic malformation)
For the evaluation of the majority of CVMs, arteriography has been the gold standard for confirmation of treatment results.34
Indication for endovascular management Surgical therapy remains the only solution for “cure” by complete excision. Complete surgical excision generally requires radical resection, which often carries a high rate of morbidity. On the other hand, incomplete surgical resection of the lesion nidus is intolerable. High recurrence rates following surgical excision of diffusely infiltrating lesions in particular have been problematic. Over the last two decades, a new, more contemporary concept of CVM management has gained acceptance as a treatment modality based on endovascular (embolotherapy and sclerotherapy) therapy as a component of total care management. Complete integration with surgical therapy has been adopted on the basis of a multidisciplinary team approach.32,35–41 Endovascular therapy based on advanced technology has become feasible to deliver various embolic agents and sclerosants with acceptable outcomes over the last two decades. This new approach is now fully accepted as an alternative to traditional surgical resection, even though it cannot cure but only control the lesion effectively for a limited period of time. Endovascular therapy has two modes of therapy: independent and adjunctive. Independent therapy This is indicated when the CVM lesion extends beyond the deep fascia with involvement of muscle, tendon, and bone, as is seen in the diffuse infiltrating type of the extratruncular form. Independent therapy is now considered the primary therapy and treatment of choice in the non-surgical and poor surgical candidate, and should be considered in the “surgically inaccessible” lesion as the primary option. In situations where independent endovascular therapy carries less risk over surgery,
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the endovascular therapy is preferred over surgical therapy, especially for treatment of the less virulent types of CVM (e.g. LM). In other situations where the CVM lesion is surgically curable with equivalent risk to endovascular therapy, the latter therapy is still preferred.34 Independent endovascular therapy should be performed over multiple sessions, whenever possible, in order to reduce the potential risk of acute and chronic morbidity, and complications associated with the embolo/ sclerotherapy agents (e.g. ethanol).11,42 Adjunctive therapy Endovascular therapy has a new extended role in the treatment of the “surgically accessible” lesion, as supplemental therapy to surgical resection. Through a combined approach utilizing preoperative sclerotherapy, the safety and efficacy of subsequent surgical therapy can be enhanced with significant reduction of the associated morbidity and complications (e.g. intraoperative bleeding). Adjunctive endovascular therapy also plays a role as post-operative supplemental therapy to aid in local control, and may help prevent overzealous surgical excision.34
Selection of endovascular management Numerous embolic and sclerosing agents have been used to control CVM lesions with variable results.43–53 Among them, absolute ethanol, n-butyl cyanoacrylate (NBCA), coils, and contour particles (e.g. Ivalon) remain the most frequently used agents for CVM management.34 These agents have been used successfully in various combinations, simultaneously, or in multiple stages. This is especially true in situations to control the high-flow, fistulous type of AVM. The recent introduction of foam sclerotherapy using detergent-based sclerosing agents (e.g. polidocanol, sotradecol), has demonstrated more efficacious results while reducing the total amount of sclerosant used. Early trials have demonstrated encouraging results, particularly in the management of VM and LM lesions. The risk of paradoxical air embolization to the brain (through a potential atrial or ventricular septal defect) along with its potential long-term effects, has not been clearly defined. However, to date there have been no reports of significant brain injury due to paradoxical air embolization during foam sclerotherapy. Its use should be limited to localized lesions with extreme caution in order to reduce the risk of paradoxical air embolization. The long-term outcome and efficacy of foam slcerotherapy still remains to be demonstrated. Absolute ethanol still remains the sclerosing agent of choice for treatment of primitive extratruncular lesions, especially in situations where the lesion is surgically unresectable such as in the diffuse infiltrating type.34 NBCA glue is an endovascular embolic agent primarily used preoperatively for treatment of surgically excisable lesions. Preoperative embolization of CVM lesions has been shown to reduce morbidity associated with surgical resection. It has also been utilized with acceptable results as sole, independent therapy in certain conditions (e.g. inoperable pelvic CVMs). There are three approaches to obtain access the “nidus” of the CVM lesion for endovascular treatment: transarterial,
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transvenous, and direct puncture. All three can be utilized simultaneously in order to maximize the efficacy of the treatment. The percutaneous direct puncture approach to the lesion is generally preferred and carries minimal risk. The transarterial approach can be used effectively with an appropriate guiding catheter (5–6-French) and guidewire. Use of a microcatheter allows superselection of various areas of the lesion/nidus for the proper treatment. The transarterial approach carries a higher risk of complication, therefore its use should be limited to situations where the direct puncture approach is not possible due to small lesion size (e.g. facial AVM). The traditional, old-fashioned approach to the treatment of AVM lesions was to simply shut off the feeding artery. This practice should be condemned and abandoned because it leaves the nidus of the lesion intact, resulting in a more aggressive response of neovascular recruitment by this primitive lesion. This aggressive response ultimately results in a significantly worse condition without exception.
Ethanol sclerotherapy Lesion recurrence is an inherent problem associated with any extratruncular CVM lesion possessing mesenchymal cell characteristics. Invariably, initial endovascular treatment using embolic and sclerosing agents other than pure ethanol often results in long-term failure. Ethanol sclerotherapy has been shown to be efficacious with minimal lesion recurrence, in the treatment of CVMs. Ethanol sclerotherapy is also associated with numerous complications and significant morbidity, therefore its use has never been accepted with much enthusiasm. On the other hand, ethanol sclerotherapy has been shown repeatedly to be the most effective sclerosing agent where treatment results in the complete destruction of endothelial cells and permanent injury of the lesion, with the least likelihood of recurrence.54,55 Despite the controversy surrounding the use of ethanol sclerotherapy, it still remains an extremely valuable endovascular sclerosing agent that is useful in the treatment of CVMs, mainly VMs and AVMs.34 The importance of vigilant cardiopulmonary monitoring during the sclerotherapy procedure cannot be overemphasized. During ethanol sclerotherapy, there is a risk of ethanol entering the venous system after injection into the CVM lesion. Ethanol entering the pulmonary vascular bed would result in an increase in pulmonary arterial pressure due to a direct chemical toxicity. Pulmonary hypertension is a potentially fatal complication of ethanol sclerotherapy. If evidence of pulmonary hypertension is detected during therapy, ethanol injection should be immediately discontinued to prevent further progression to pulmonary artery spasm and subsequent cardiopulmonary arrest.42
Coil and glue embolotherapy Coil embolic therapy produces a mechanical disruption of blood flow resulting in lesion thrombosis. Coil embolic therapy does not have any direct effect on the endothelium to induce permanent damage/injury. The absence of endothelial injury allows the eventual recanalization of the feeding vessel and recurrence of the CVM lesion. Treatment of an extratruncular
lesion via coil embolic therapy therefore requires additional endovascular therapy with absolute ethanol and/or NBCA, in order to obtain complete ablation of the lesion nidus. Coil embolization is most effective in controlling large, high-flow AVM lesions. Coil embolization of the draining vein of a large, high-flow AVM lesion will convert the lesion to a low-flow lesion, thus making subsequent sclerotherapy safer. Platinum spiral coils, tornado coils, and detachable coils have been used with success in the treatment of AVMs prior to ethanol sclerotherapy. Glue (n-butyl cyanoacrylate) embolization therapy is limited to the surgical resection candidate and can be carried out with a 30–50% concentrated solution that minimizes the foreign body reaction. Access to the lesion should be obtained as close as possible to the AV connection nidus in order to make a glue cast from the lesion nidus to the proximal draining vein. Glue embolization in this manner facilitates surgical resection and minimizes the risk of bleeding. Onyx is a new glue embolic agent that remains to be assessed more appropriately.
Clinical experiences – endovascular treatment These experiences are from a retrospective analysis of SMC (Samsung Medical Center, Seoul, Korea) data. Venous malformation (VM) Among a total of 1203 CVM patients, 453 were identified as predominantly VM (37.7%) (male: 202; female: 251; mean age of 19.5 years); 166 out of a total of 453 VM patients were candidates for endovascular treatment; sclerotherapy alone to 137, and combined surgical and endovascular therapy to 29 patients. Sclerotherapy mostly with ethanol (434/512) was given to 166 patients (152 with extratruncular lesions) through 512 sessions. Embolotherapy with NBCA (n-butyl cyanoacrylate) was given independently as preoperative adjunct therapy for subsequent surgical excision (42 sessions to 22 extratruncular lesions) or in conjunction with ethanol sclerotherapy. Immediate success rate following each session of ethanol sclerotherapy was 98.8% (504 sessions among 512 sessions on 186 patients); failure rate was 1.6 % (8/512 sessions). Acute complications were mostly minor skin complications except one permanent peroneal nerve palsy. All the skin complcations were resolved spontaneously with or without additional wound care in limited extent. Late results following completion of multisession therapy (average 3.8 sessions per patient) have shown excellent results with no evidence of recurrence (average follow-up period 42.2 months). Twentytwo patients that underwent preoperative embolo/sclerotherapy with various combinations of NBCA and ethanol achieved 100% success rate with minimal morbidity and no recurrence (41.2 months follow-up) (Figure 82.1). Lymphatic malformation (LM) Ninety-seven patients with extratruncular lesions received endovascular treatments: sclerotherapy with OK-432 (a lyophilized mixture of a low virulence strain of streptococcus pyogenes of human origin incubated with benzylpenicillin)
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(a)
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(b) Transarterial lung perfusion scintigraphy (TLPS)
Whole body blood pool scintigraphy (WBBPS)
(c)
(d)
Figure 82.1 (a) Clinical appearance of diffusely infiltrating venous malformation (VM) lesions affecting the entire right thigh; clinically, it mimics ordinary varicose veins but is often associated with various complications (e.g. bleeding, ecchymosis) in addition to pain. (b) Coronal view of T2 weighted MRI shows extensive VM lesions affecting right upper thigh. This finding is compatible with the clinical findings. (c) Whole body blood pool scintigraphy (WBBPS) showing abnormal blood pool along the upper and lower thigh region as a positive finding for the VM lesions. WBBPS can provide qualitative as well as quantitative data. (d) Transarterial lung perfusion scintigraphy (TLPS) showing negative finding of AV shunting to rule out potential risk of combined (micro) AV shunting condition. Continued
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(e)
(f)
(g)
Figure 82.1, Cont’d (e) Right femoral arteriography finding confirming the independent VM lesions with no AV malformation. It is extremely important to rule out the presence of an AVM if there is any suspicion clinically. (f) Percutaneous direct puncture phlebography of the VM lesion which confirmed diffusely infiltrating “extratruncular” type lesions which are surgically inaccessible. This invasive study can often be deferred until needed as a road map for the further treatment. (g) Angiographic finding shows percutaneous ethanol sclerotherapy to the extratruncular VM lesions. Lesion B was successfully controlled with total 14 ml of 80% ethanol.
(89/97) or ethanol (8/97) as independent therapy (82/97) or adjunct therapy (15/97). Fifteen received preoperative OK-432 and/or ethanol sclerotherapy for subsequent surgical excision. Independent OK-432 sclerotherapy delivered through 169 sessions gave excellent results in the majority with cystic type lesions (51/61) and limited success with cavernous type (5/10) at 32 months minimum follow-up. Independent absolute ethanol sclerotherapy also gave excellent results through 12 sessions on 8 patients with recurrent lesions (6/8) but with significant complications (4/8). Preoperative OK-432 sclerotherapy and subsequent surgical excision (15/35) has shown good to excellent results in 12 out of 15 patients at 49 months of minimum follow-up period (Figure 82.2). AV shunting malformation (AVM) One hundred and forty-five patients (12.1%) were confirmed as having AVM, mostly (91/145) of the diffuse infiltrating extratruncular form with macro-AV shunting nidus. Ninety (82-extratruncular; 8-truncular) out of 145, selected for the treatment with various indications, underwent endovascular embolo/sclerotherapy with various combinations of absolute ethanol, NBCA, glue, contour particles (Ivalon) and coils either as independent therapy or as adjunct therapy prior to surgical therapy. Twenty patients with surgically accessible lesions completed a total of 27 multisessions of preoperative endovascular therapy with various combinations of the embolo/scleroagents and subsequent surgical excisions. All 20 patients have shown excellent interim results with the combined approach of surgical and endovascular therapy with
no evidence of recurrence during the limited follow-up periods of 41.0 months on average following surgery (Figure 82.3). Sixty-nine patients with surgically inaccessible lesions underwent a total of 334 sessions of multisession independent endovascular therapy with various combinations of the agents (with failure on 16 sessions). Interim results following the completion of multisession therapy (average duration of 18.6 months) were excellent in the majority (48/69) and fair to good among the rest (12/69), with recurrence from poorly controlled lesions (9/69) during the limited follow-up period of 32.2 months on average. One hundred twenty-nine complications developed out of total of 334 sessions (38.6%) in 57 patients; mostly minor skin and soft tissue related complications (89/129) and transient pulmonary hypertension. Major complications included 2 pulmonary embolism, 1 retinal artery occlusion, 2 transient/ permanent facial nerve palsy, 2 deep vein thrombosis, 1 rhabdomyolysis with acute renal failure, and 2 cartilage necrosis. Most of the major complications developed in patients with the AV fistula type of truncular form with a high-flow condition; 1 of 3 patients with high flow AV fistula who abandoned continuous treatment eventually required amputation as life-saving procedure.
Discussion Endovascular therapy aims to address the underlying primary pathology and correct the hemodynamic disturbances produced
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Endovascular treatment of some congenital diseases: hemangiomas and vascular malformations by a CVM lesion. The traditional conservative approach to the young, pediatric population is still valid, especially for management of common venous malformations (without bone involvement). This approach involves waiting until the child reaches the age of 2 years in order to be mature enough to tolerate the various endovascular and surgical procedures required for proper diagnosis and treatment.56 An earlier more aggressive approach is preferred over the traditional approach in situations where the CVM lesion is AVM, a VM combined with vascular-bone syndrome,57–59 or a lesion found at a life- or limbthreatening location. Severe CVM lesions that render a limb completely non-functional, with significant limb growth discrepancy, should be considered for the early amputation.
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Early amputation will allow quicker recovery and faster rehabilitation.
Conclusion Endovascular therapy of surgically inaccessible CVMs is essential as a new independent therapy. The additional role of endovascular therapy as supplemental therapy to surgical resection of surgically accessible lesions is one that results in significantly improved treatment results compared with traditional surgical therapy. This combined approach also results in reduced complications and morbidity.
(b)
(c) (d) Figure 82.2 (a) Clinical appearance of lymphatic malformation (LM) affecting the right face. It appears as a diffuse swelling over the right cheek bone area (arrow). (b) MR-T2 weighted image of the skull shows multicystic LM lesions affecting the entire right temporal region, which is compatible with the clinical finding. (c) Whole body blood pool scintigraphy (WBBPS) has shown no abnormal blood pool along the lesions. It confirms the LM indirectly and also rules out the VM by the absence of abnormal pool along the lesions. (d) Duplex US study shows a macrocystic type extratruncular LM lesion (black arrow) which can be a candidate for the OK-432/ethanol sclerotherapy. Continued
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(f)
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Figure 82.2, Cont’d (e) Duplex US study shows mixed condition of microcystic LM lesions (white arrow) which can be treated with OK-432 (picibanil) with less risk. (f) Percutaneous direct puncture angiography shows ethanol sclerotherapy to the “recurrent” LM lesion which failed to respond to OK-432 previously. A total of 4.0 ml of 50% ethanol controlled the lesion successfully with no complication. (g) Duplex US study shows US-guided sclerotherapy to superficially located macrocystic LM lesion (arrow). OK-432 (picibanil) was used on this de novo lesion as the treatment of choice. (h) Duplex US study shows excellent response to OK-432 by the macrocystic LM lesion. There is no residual lesion following the therapy (arrow).
Figure 82.3 (a) Clinical appearance of a massive AVM involving the left forearm and hand as a potentially limb/life threatening condition. The patient had massive recurrent bleeding from the lesion. (b) MRI findings confirm an AVM lesion affecting the entire left forearm and hand. (c) Transarterial lung perfusion scintigraphy (TLPS) shows this massive AVM lesion accompanies the shunting percentage over 99.0% through the lesion, with high risk of limb loss as well as high cardiac failure. (d) Whole body blood pool scintigraphy (WBBPS) also shows a hemodynamically active AVM lesion affecting the entire left upper extremity. (e) Brachial arteriography shows massively dilated tortuous veins draining extensive AVM lesions involving the hand. The lesions were confirmed to be a mixed lesion of non-fistulous lesions with the niduses and fistulous lesions with no sizable niduses. (f) Angiography during the first/initial ethanol sclerotherapy (28 ml) shows successful control of major fistulas as well as non-fistulous AVM lesions affecting the hand. (g) Additional/second therapy with 31 ml of pure ethanol was able to provide further control of residual AVM lesions in the wrist region with no complication.
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Transtarterial Lung Perfusion Scintigraphy (TLPS)
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Whole-Body-Blood-Pool Scintigraphy
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(g) (a) For legend see opposite page.
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Mulliken JB, Glowacki J. Hemangiomas and vascular malformations in infants and children: a classification based on endothelial characteristics. Plast Reconstr Surg 1982; 69: 412–20 Mulliken JB. Treatment of hemangiomas. In: Mulliken JB, Young AE, eds. Vascular Birthmarks, Hemangiomas and Malformations. Philadelphia: WB Saunders, 1988: 88–90 Malan E, Puglionisi A. Congenital angiodysplasias of the extremities, note II: arterial, arterial and venous, and hemolymphatic dysplasias. J Cardiovasc Surg (Torino) 1965; 6: 255–345 Ehringhaus C. Corticosteroid treatment of infantile cutaneous hemangiomas. In: Belov S, Loose DA, Weber J, eds. Vascular Malformations. Reinbek: Einhorn-Presse, 1989: 197–9 Ezekowitz RAB, Mulliken JB, Folkman J. Interferon alpha-2a therapy for life-threatening hemangiomas of infancy. N Engl J Med 1992; 326: 1456–63 Belov St. Classification of congenital vascular defects. Int Angiol 1990; 9: 141–6 Belov St. Anatomopathological classification of congenital vascular defects. Sem Vasc Surg 1993; 6: 219–24 Lee BB. Current concept of venous malformation (VM). Phlebolymphology 2003; 43: 197–203 Lee BB. Congenital venous malformation: changing concept on the current diagnosis and management. Asian J Surgery 1999; 22(2): 152–4 Lee BB, Kim DI, Huh S et al. New experiences with absolute ethanol sclerotherapy in the management of a complex form of congenital venous malformation. J Vasc Surg 2001; 33: 764–72 Lee BB, Do YS, Byun HS et al. Advanced management of venous malformation with ethanol sclerotherapy: mid-term results. J Vasc Surg 2003; 37(3): 533–8 Lee BB, Kim YW, Seo JM et al. Current concepts in lymphatic malformation (LM). J Vasc Endovasc Surg 2005; 39(1): 67–81 Lee BB: Lymphedema–angiodysplasia syndrome: a prodigal form of lymphatic malformation (LM). Phlebolymphology 2005; 47: 324–32 Loose DA, Müller E. Problems in surgery of congenital vascular malformations with arteriovenous shunts. In: de Castro Silva M, ed. Atualizacao em Angiologia. Belo Horizonte: Brazilian Society of Angiology, 1978: 121–41 Lee BB, Do YS, Yakes W et al. Management of arterial–venous shunting malformations (AVM) by surgery and embolosclerotherapy. A multidisciplinary approach. J Vasc Surg 2004; 39(3): 590–600 Mattassi R. Surgical treatment of congenital arteriovenous defects. Int Angiol 1990; 9: 196–202 Loose DA, Wang Z. Surgical treatment of predominantly arterial defects. Int Angiol 1990; 9: 183–8 Jacob AG, Driscoll DJ, Shaughnessy WJ et al. Klippel–Trenaunay syndrome: spectrum and management. Mayo Clin Proc 1998; 73(1): 28–36 Lee BB: Klippel–Trenaunay syndrome and pregnancy. Int Angiol 2003; 22(3): 328 Gloviczki P, Stanson AW, Stickler GB et al. Klippel–Trenaunay syndrome: the risks and benefits of vascular interventions. Surgery 1991; 110(3): 469–79 Lee BB, Mattassi R, Choe YH et al. Critical role of duplex ultrasonography for the advanced management of a venous malformation (VM). Phlebology 2005; 20: 28–37 Lee BB, Choe YH, Ahn JM et al. The new role of MRI (magnetic resonance imaging) in the contemporary diagnosis of venous malformation: can it replace angiography? J Am Coll Surg 2004; 198(4): 549–58 Lee BB, Mattassi R, Kim BT et al. Contemporary diagnosis and management of venous and AV shunting malformation by whole body blood pool scintigraphy (WBBPS). Int Angiol 2004; 23(4): 355–67 Lee BB, Mattassi R, Kim BT, Park JM. Advanced management of arteriovenous shunting malformation with transarterial lung perfusion scintigraphy (TLPS) for follow up assessment. Int Angiol 2005; 24(2) 173–84 Lee BB, Bergan, JJ. New clinical and laboratory staging systems to improve management of chronic lymphedema. Lymphology 2005; 38(3): 122–9 Lee BB. Current issue in management of chronic lymphedema; personal reflection on an experience with 1065 patients. Commentary. Lymphology 2005; 38: 28–31 Lee BB, Kim HH, Mattassi R et al. A new approach to the congenital vascular malformation with new concept–Seoul Consensus. Int J Angiol 2003; 12: 248–51
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Lee BB. Critical issues on the management of congenital vascular malformation. Annals Vasc Surg 2004; 18(3): 380–92 Bastide G, Lefebvre D. Anatomy and organogenesis and vascular malformations. In: Belov St, Loose DA, Weber J, eds. Vascular Malformations. Reinbek: Einhorn-Presse Verlag GmbH, 1989: 20–2 Woolard HH. The development of the principal arterial stems in the forelimb of the pig. Contrib Embryol 1922; 14: 139–54 DeTakats G. Vascular anomalies of the extremities. Surg Gynecol Obstet 1932; 55: 227–37 Lee BB, Bergan JJ. Advanced management of congenital vascular malformations: a multidisciplinary approach. Cardiovasc Surg 2002; 10(6): 523–33 Lee BB. Advanced management of congenital vascular malformation (CVM). Int Angiol 2002; 21(3): 209–13 Lee BB. Statues of new approaches to the treatment of congenital vascular malformations (CVMs) – single center experiences – (Editorial Review). Eur J Vasc Endovasc Surg 2005; 30(2): 184–97 Belov S. Congenital agenesia of the deep veins of the lower extremities: surgical treatment. J Cardiovasc Surg (Torino) 1972; 13: 594–8 Vollmar JF, Stalker CG. The surgical treatment of congenital arterio-venous fistulas in the extremities. J Cardiovasc Surg 1976; 17: 340 Loose DA, Weber J. Indications and tactics for a combined treatment of congenital vascular malformations. In: P. Balas, ed. Progress in Angiology. Chapt Miscellanea. Torino: Minerva Medica, 1992: 373–8 Mattassi R. Individual indications for surgical and combined treatment in so-called inoperable cases of congenital vascular defects. In: Balas P, ed. Progress in Angiology 1991. Proceedings of the 7th European Congress of the International Union of Angiology and 3rd Mediterranean Congress of Angiology. Torino, Italy: Minerva Medica; 1992: 383–6 Loose DA. Combined treatment of congenital vascular defects: Indications and tactics. Sem Vasc Surg 1993; 6: 279–96 White RI Jr, Pollak J, Persing J et al. Long-term outcome of embolotherapy and surgery for high-flow extremity arteriovenous malformations. J Vasc Interv Radiol 2000; 11(10): 1285–95 Lee BB. Advanced management of congenital vascular malformation (CVM). Int Angiol 2002; 21(3): 209–13 Shin BS, Do YS, Lee BB et al. Multistage ethanol sclerotherapy of soft-tissue aretriovenous malformations: effect on pulmonary arterial pressure. Radiology 2005; 235: 1072–77 Yakes WF, Parker SH. Diagnosis and management of vascular anomalies. Int Radiol 1992; 1: 152–89 Jackson JE, Allison DJ. Combined therapeutic embolization and surgery. In: Jamieson CW, Yao JT, eds. Vascular Surgery, fifth ed. London: Chapman & Hall Medical, 1995: 435–50 Philipp C, Berlien H-P, Poetke M, Waldschmidt J. Ten years of laser treatment of congenital vascular disorders: techniques and results. Medical Applications of Laser. SPIE Proceedings 1994; 2327 Landthaler M, Hoherleutner U. Laser treatment of congenital vascular malformations. Int Angiol 1990; 9: 208–13 Berenstein A, Kricheff II. Catheter and material selection for transarterial embolization. Technical considerations: catheters. Radiology 1979; 132: 619 Zanetti PH. Cyanoacrylate/iophenylate mixtures: modification and in vitro evaluation as embolic agents. J Intervent Radiol 1987; 2: 65–8 Novak D. Embolization materials. In: Dondelinger RF, Rossi P, Kurdziel JC, Wallace S, eds. Interventional Radiology. New York: Thieme, 1990 Cromwell LD, Kerber CW. Modification of cyano-acrylate for therapeutic embolization: preliminary experience. AJR Am J Roentgenol 1979; 132: 799 Natali J, Merland JJ. Superselective arteriography and therapeutic embolization for vascular malformations (angiodysplasias). J Cardiovasc Surg 1976; 17: 465–72 Weber J. Technique and results of therapeutic catheter embolization of congenital vascular defects. Int Angiol 1990; 9: 214 Weber JH. Vaso-occlusive angiotherapy (VAT) in congenital vascular malformations. Sem Vasc Surg 1993; 6: 279–96 Yakes WF, Luethke JM, Merland JJ et al. Ethanol embolization of arteriovenous fistulas: a primary mode of therapy. Journal of Vascular and Interventional Radiology 1990; 1: 89–96
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Yakes WF, Pevsner PH, Reed MD, Donohu HJ, Ghaed N. Serial embolizations of an extremity arteriovenous malformation with alcohol via direct percutaneous puncture. American Journal of Roentgenology 1986; 146: 1038–40 Lee BB, Mattassi R, Loose D et al. Consensus on controversial issues in contemporary diagnosis and management of congenital vascular malformation– Seoul Communication. Int J Angiol 2004; 13(4): 182–92
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Belov S. Hemodynamic pathogenesis of vascular-bone syndromes in congenital vascular defects. Int Angiol 1990; 9: 155–62 Belov St. Correction of lower limbs length discrepancy in congenital vascular-bone disease by vascular surgery performed during childhood. Sem Vasc Surg 1993; 6: 245–51 Mattassi R. Differential diagnosis in congenital vascular-bone syndromes. Sem Vasc Surg 1993; 6: 233–44
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SECTION XII Unusual vascular diseases of the extremities
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Endovascular management of Budd-Chiari syndrome – suprahepatic inferior vena cava occlusive disease BB Lee, J Laredo, DH Deaton, and RF Neville
Introduction Budd-Chiari syndrome (BCS) is a very rare condition characterized by hepatic venous outflow obstruction at the level of the suprahepatic inferior vena cava (IVC). This obstruction is caused by an IVC lesion/occlusion and/or occlusion of the hepatic veins (HVs) (Figure 83.1).1–3 There are several types of BCS, based on its etiology (e.g. primary and secondary) and underlying pathogenesis (e.g. congenital, inflammatory and/or infectious origin).4–9 The primary/idiopathic BCS has great geographic and racial variance with regard to its underlying etiology: the membranous obstruction of vena cava (MOVC)5,7 or hepatic vein thrombosis due to the hypercoagulable state.6,9 There is a striking difference between Asian/African patients and Caucasian patients,4–9 where MOVC is the most frequent cause of primary BCS among the Asian/African populations and the hypercoagulable state is the most frequent cause of BCS among the Caucasian population. The developmental/congenital anomaly theory is therefore considered the most compatible pathogenic mechanism with Asian/African patients while the thrombosis theory is most compatible with Caucasian patients. BCS is, however, more often secondary due to vascular compression by the intrahepatic or extrahepatic malignancy. Secondary BCS will not be discussed in this chapter. Regardless of its etiology and underyling pathogenesis, primary BCS has received special attention due to the clinical significance and development of portal hypertension/ liver congestion, the progressive nature of this condition and its consequences, and the ultimate risk of hepatocellular carcinoma among Asian/African patients in particular.
Diagnosis The diagnosis of BCS is mandated for accurate assessment of its anatomical and pathophysiological characteristics and severity/extent, for the safe/proper selection of various treatment options.3 When the IVC occlusion occurs at the suprahepatic level, its hemodynamic consequences will impact not only on the systemic venous circulation, but also the portal venous circulation. Therefore, the hemodynamic investigation should aim to appropriately evaluate both systems: the
extent/severity of chronic venous insufficiency of the lower extremities and the extent/severity of hepatic congestion. Assessment should be made with the appropriate combination of laboratory/chemical tests and non-invasive tests. Duplex ultrasonographic (US) study10–12 and contrast-enhanced CT scanning13 of the IVC and HVs are first-line studies in the assessment of the intrahepatic venous collaterals and the portal venous system, the hepatic venous outflow, and the IVC status. Hepatic venous outflow obstruction, abnormalities in the direction of flow in the hepatic vein, and the presence of communicating vessels between hepatic veins, can all be evaluated with real-time imaging by the pulsed Doppler analysis. Duplex ultrasonography remains the basic modality to evaluate the progression of the disease and the response to therapy, as well as providing a guide for the treatment strategy (Figure 83.2). MRI and/or MR angiography14 may be added selectively when indicated. In addition to functional and anatomical status of the IVC and/or hepatic vein occlusion, basic hematologic/coagulation evaluation should be performed. In addition to liver function tests, a coagulation profile should be obtained to rule out coagulopathy as a predisposing factor for BCS, especially for Caucasian patients.3 Full screening for hypercoagulability and collagenous vascular disease is warranted in every primary BCS investigation. Careful assessment of all other possible causes (e.g. bacterial infection, Behcet’s disease)15,16 as predisposing factors should be included. Baseline liver biopsy should be considered in all BCS patients to assess liver parenchymal status (degree of congestion and cirrhosis) appropriately before medical/surgical/ endovascular therapy is initiated. A follow-up biopsy is also strongly recommended as a part of the outcome assessment. Full and repeated assessment of BCS at regular intervals is generally recommended before consideration/selection of additional treatment to the medical regimen.3 Endovascular treatment17–21 should be considered in patients who have failed to respond to conservative medical therapy and have evidence of progression of the disease over a minimum 2-year period. Surgical treatment22–25 options should be considered at the same time for adequate comparison of the risk and benefit of both therapies.3 IVC angiography is required in all patients to establish a road map for further endovascular treatment procedures (Figure 83.3). Selective portal vein study with direct splenoportography, celiac–hepatic angiography, 725
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Figure 83.1 (a) Clinical appearance of the abdominal wall in a patient with primary BCS. Extensive abdominal wall varices (arrows) and ascites are the hallmarks of suprahepatic IVC obstruction by primary BCS. (b) Coronal oblique 3D volume rendered CT image demonstrating suprahepatic IVC obstruction (black arrow) with massively dilated and tortuous collateral vessels of the hemiazygous and azygous venous systems (two white arrows).
and/or percutaneous transhepatic hepatic venography can be added to the evaluation of the BCS candidate for transjugular intrahepatic portosystemic shunt (TIPS).20,23
Management The extent of management strategy remains a critical issue from simple decompression procedure (surgical bypass, angioplasty/ stent) to curative radical procedure (liver transplantation).17–27
(a)
An early aggressive approach is generally preferred for adequate decompression of hepatic congestion. This is especially important in view of BCS as a precancerous lesion28–30 among the Asian/African population in order to reduce its long-term risk. The endovascular management of IVC/HV occlusion with angioplasty and/or stents is generally preferred over surgical management, and carries less risk/morbidity3 since most cases of primary BCS are caused by membranous/ focal/segmental occlusion of the IVC to varying degrees. They will rarely require a mesoatrial bypass26,27 from the superior mesenteric
(b)
Figure 83.2 Duplex ultrasonographic findings of various intrahepatic conditions due to primary BCS. (a) Typical finding of an IVC lesion with focal stenosis (arrows) by MOVC (membraneous obstruction of vena cava); this represents the most common cause of hepatic venous outflow obstruction among patients with primary BCS. (b) Intrahepatic collateral vein depicted as typical “ring” shape connection (block arrow) between right and left hepatic veins; it is present in patients with hepatic venous outflow obstruction.
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Figure 83.3 Angiographic appearance of compensatory collateral venous circulation that develops in response to suprahepatic IVC occlusion. Both patients have extensive compensatory circulation to relieve venous hypertension via intercostals, retroperitoneal, and azygous venous systems.
vein directly to the right atrial appendage for effective decompression of the hepatic outflow occlusion. Early/immediate as well as interim (less than 4 years) results of endovascular therapy are generally known to be excellent,3 especially in patients with focal/membranous occlusion, although there is significant recurrence even after effective control of the obstructing lesions, especially segmental occlusions.3 Depending upon the nature and extent/severity of the occlusion of IVC/HVs, the response to angioplasty and/or stenting procedures are different. Focal/membranous lesions of the IVC remain excellent following balloon angioplasty alone in the majority of cases; excellent anatomical correction of the lesion/occlusion generally results in equivalent functional/hemodynamic recovery with minimum residual pressure gradient following the single or double balloon technique (Figure 83.4). Stenting is seldom required to correct most focal lesions and is reserved for lesions with poor initial response to angioplasty alone or recurrence. Segmental lesions in general require a combination of angioplasty and stenting in order to obtain maximum treatment of the occlusion; these lesions seldom require repeated procedures to maintain patency. Lesions and occlusions limited to the hepatic veins are ideal for treatment with TIPS (transjugular intrahepatic porto-systemic shunt) to effectively relieve intrahepatic congestion. Endovascular management of complete occlusion of the IVC along its long segment with massive thrombus, is generally contraindicated due to the
high risk of pulmonary embolism. Follow-up assessment3 is essential for the long-term management and should be made with duplex US scanning to evaluate IVC/HV patency. Liver function tests are helpful in assessing liver congestion status. Such follow-up should be made at 6-month intervals for a minimum of a 4-year period. Additional tests (e.g. MR angiography, liver biopsy) can be added as indicated. Liver parenchymal status should be assessed separately by duplex US scanning along with the appropriate grading of parenchymal congestion as “remained,” “relieved,” “improved,” or “progressive.” Liver biopsy in patients with known cirrhosis is also essential to evaluate the treatment response with the appropriate grading of cirrhosis as “improved,” “stable,” or “progressive.”
Clinical experience Among 28 patients (13 male, 15 female; mean age: 43.2 years) diagnosed with “primary” type of BCS, etiology was due to suprahepatic IVC stenosis/occlusion (n = 26) and HV outlet obstructive lesions (n = 2) on US study. All the IVC lesions were either focal stenoses or occlusions with/without membraneous lesions (n = 14) or segmental stenoses or occlusions (n = 12). All IVC lesions had at least one patent hepatic vein (HV), usually the right HV (n = 22), which drained into the IVC below the site of occlusion. The right HV usually had
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(b)
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Figure 83.4 Angiographic appearance of balloon angioplasty as part of the endovascular management of an IVC lesion. Various (single or double balloon) techniques are used to achieve adequate dilatation of the obstructing lesion depending on the nature of the lesion, whether it is focal or segmental. Angioplasty is often performed with stenting when indicated.
extensive collateral channels of intrahepatic veins communicating with the left and middle HVs. Other etiologic and predisposing factors, including hypercoagulopathy were completely ruled out among our 28 patients. Patients had an average of 3.6 years (2.8–4.1 years) of clinical history consistent with “chronic” portal hypertension before the diagnosis of primary BCS was made. Liver profiles showed remarkably well-preserved liver function, except in patients with moderate to severe hepatic congestion. Seventeen patients were candidates for endovascular therapy. In these patients, IVC balloon angioplasty with and without stenting was performed via a transfemoral approach, except in cases which required the “kissing balloon technique” via a concomitant, simultaneous transjugular approach. Various angioplasty balloon sizes (5–18 mm balloon, Cook, Bloomington, IN) were used for both preliminary and final dilatation along with conventional spring-coil and laminated hydrophilic guidewires with floppy tips or stiff ends. Wallstents (Boston Scientific, Natick, MA) were used for the stenting procedures. Endovascular post-procedure results were assessed using anatomical and hemodynamic criteria, and were classified as follows: excellent – anatomically complete to near complete dilatation of the stenosis with a hemodynamically comparable reduction of a preprocedure pressure gradient; good – substantial correction of stenosis with no more than a 25–30% residual stenosis and residual pressure gradient; fair – less than 50% residual lesion with an improved pressure gradient; and poor – more than 50% residual lesion. Clinical assessment of relief of portal hypertension following endovascular treatment was classified as follows: excellent – complete to near complete relief of ascites and/or hepatomegaly with compatible laboratory findings (e.g. disappearance of hepatic parenchymal congestion on US evaluation);
good – substantial relief of symptoms of portal hypertension with compatible laboratory improvement; and fair – noticeable clinical response with minimal clinical improvement. Heparin was used only during the endovascular procedure. In cases where simultaneous thrombolysis was required, heparin was then continued for 1 week followed by anticoagulation with sodium warfarin for one month (INR: 2.0). All routine endovascularly treated patients were continued on antiplatelet agents for 1 month post-procedure. The majority of patients treated in the endovascular group (n = 14, out of a total of n = 17 patients), experienced technical success with a good to excellent clinical response and subsequent relief of portal hypertension (Figure 83.5). Angioplasty alone to the focal stenosis (n = 7, 78%), angioplasty plus stent to the segmental stenosis (n = 5, 83%), and TIPS to the hepatic vein outlet obstruction (n = 2, 100%) were performed in this group of patients In the group treated with angioplasty alone (n = 9), 8 focal lesions showed immediate technical success: excellent (n = 7) to good (n = 1) results while 1 segmental lesion had a fair result. In the group treated with angioplasty plus stent (n = 6), 2 focal lesions showed excellent technical results. Three out of 4 segmental lesions also had good to excellent results. One segmental lesion had a poor to minimum result. The average pressure gradient of 28.2 mmHg decreases to 10.6 mmHg with these procedures. In the group treated with TIPS using Wallstents (10 mm diameter, Boston Scientific, Natick, MA) all (n = 2) had excellent results with immediate relief of hepatic vein outlet obstruction. The pressure gradient decreased from 29.1 mmHg to 10.2 mmHg (case 1) and from 23.8 mmHg to 9.2 mmHg (case 2). All 14 patients (angioplasty alone (n = 7), angioplasty plus stent (n = 5), and TIPS (n = 2)) who had excellent results with the endovascular procedures, subsequently achieved excellent
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Figure 83.5 Balloon angioplasty of an occlusive IVC lesion. (a) Preangioplasty appearance of the IVC lesion. (b) Post-angioplasty appearance with a satisfactory result. The lesion was a focal stenosis with MOVC, easily treated with angioplasty alone.
relief of portal hypertension within 6 months as evidenced by clinical improvement (e.g. ascites and hepatomegaly) and improvement on laboratory findings (e.g. liver profiles, hepatic congestion finding on US study). Among the endovascular group (n = 17), restenosis and progression of residual stenosis (n = 4) developed within 2 years, along the region previously treated (failure rate was 23.5%). Among the patients treated with angioplasty alone, one segmental lesion with a fair result showed subsequent deterioration within 6 months and underwent additional stenting later. Another patient with a focal lesion which had a good result initially was also found to have a recurrent high-grade stenosis after she missed her regular 1-year follow-up assessment. Two patients treated with angioplasty plus stent for segmental lesions including one who had a poor result initially, were found to have further progression of their lesions after being lost to follow-up for 2 years. Three of the four patients experienced an excellent result with subsequent stenting of the occluded or stenotic IVC. Two of these patients required combined thrombolytic therapy in addition to stenting. The fourth patient did not improve after this second endovascular procedure and refused bypass surgery despite steady deterioration. Therefore, during a minimum of 4-year follow-up (average 4.5 years), the primary patency rate of endovascular procedures (n = 17) was 76.5% and primary-assisted patency rate was 94.1%. There was no mortality among this endovascular group during the follow-up period.
Angiography has been the gold standard for diagnosing BCS. Real time ultrasonography10–12 has showed an excellent ability to deliver unique intrahepatic hemodynamic and pathophysiologic data (Figure 83.1). We were able to identify abnormalities of the right, middle, and left HVs and abnormal flow patterns in the majority of patients. Monophasic flow was the most common abnormality found with abnormal waveforms present in one or more HVs in the majority of patients. Intrahepatic collaterals and hepatopetal flow in the portal vein were also frequent findings. Ultrasonographic evaluation of patients with liver parenchymal congestion showed 15 relieved, 3 improved and 1 progressed, all of which were directly proportional to the anatomical and hemodynamic response to therapy. Liver biopsies performed in ten cirrhotic patients showed that five remained stable, two improved,31 and three deteriorated, despite successful decompression of the portal hypertension. The three patients that had evidence of deterioration showed no evidence of co-infection with hepatitis B and C viruses. Two of these patients subsequently developed de novo hepatocellular carcinoma (HCC) during the follow-up period (4.7 years). Our experience once again confirms the presence of MOVC-related IVC and/or HV lesions in the majority of patients, which is consistent with other reports from Asia.7,17,21 This anomalous condition of the suprahepatic IVC frequently extends into the hepatic venous system resulting in portal hypertension with or without hepatic insufficiency and
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chronic venous insufficiency of the lower extremities. The congenital/developmental anomaly theory of primary BCS is well supported by these findings.4,5,7 This congenital vascular theory suggests that the formation of the IVC and HVs occurs through a complicated embryonic developmental process.32–38 This hypothesis suggests that aberrations in the embryonic development of the IVC and HVs may result in an increased risk of developing MOVC. Endovascular intervention appears to offer acceptable results and clinical improvement to most patients with primary BCS lesions. However, if venous outflow patency cannot be restored or maintained via an endovascular approach, and if liver function continues to deteriorate resulting in the development of cirrhosis, surgical decompression via bypass surgery or liver transplantation should be seriously considered. Chronic liver congestion, caused by outflow obstruction of the hepatic veins, along with its subsequent histopathologic changes, is believed to lead to the development of hepatocellular carcinoma (HCC).28–30 Our rate of HCC development among primary BCS cases (4 out of 28 patients, 14.3%) is consistent with those reported by other groups reporting a relatively high incidence of HCC development among African and Asian patients. This finding demonstrates the striking differences observed among the different races.29,30 In view of the progressive nature of primary BCS as a precancerous lesion with high incidence of HCC among African and Asian patients, an aggressive approach with liver transplantation may be indicated as a pre-emptive intervention. This is especially true when all other available treatments, including endovascular therapy, fail to halt the progression of the disease.
Clinical evaluation based solely on the patient’s clinical response may be inadequate. Vigilant surveillance using liver US with appropriate HCC screening during follow-up examinations, is mandated, especially in the African/Asian population, where patients with MOVC fall into the high-risk group for HCC development.
Conclusion In primary BCS, both endovascular and surgical interventions provide excellent results with clinical improvement, potentially halting liver parenchymal deterioration caused by the underlying portal hypertension. Endovascular therapy should be considered first-line therapy in the treatment of BCS. It is safe, less invasive, more cost-effective, and has fewer complications compared with surgery. Surgery on the other hand, should be reserved for those BCS cases where endovascular therapy has failed or is not an option.
Acknowledgment SamSung Medical Center and SungKyunKwan University School of Medicine Vascular Center: Kim YW, Kim DI, Kim ES, Moon JY, Han MA Vascular Laboratory: Lee CH, Kim DY Radiology Department: Choe YH, Ahn JM, Do YS, Choo IW Vascular Medicine Department: Kim DK Special thanks for the editing to Cho EK & Yoona Lee
REFERENCES 1. 2. 3. 4. 5.
6. 7.
8. 9. 10. 11. 12.
Wang ZG, Jones RS. Budd-Chiari syndrome. In: Wang ZG, Jones RS. Current Problems in Surgery. New York: Mosby, 1996: 83–211 Slakey DP, Klein AS, Venbrux AC, Cameron JL. Budd-Chiari syndrome: current management options. Ann Surg 2001; 233(4): 522–7 Lee BB, Villavicencio L, Kim YW et al. Primary Budd-Chiari syndrome: outcome of endovascular management for suprahepatic venous obstruction. J Vasc Surg 2006; 43(1): 101–8 De BK, De KK, Sen S et al. Etiology based prevalence of BuddChiari syndrome in eastern India. J Assoc Physicians India 2000; 48(8): 800–3 Croquet V, Aube C, Pilette C et al. Budd-Chiari syndrome due to membranous obstruction of the inferior vena cava of congenital origin. Ten-year follow-up after radiologic treatment. Gastroenterol Clin Biol 1999; 23(2): 259–63 Jagtap A, Shanbag P, Vaidya M. Budd-Chiari syndrome due to antithrombin III deficiency. Indian J Pediatr 2003; 70(12): 1003–5 Rao KS, Gupta BK, Banerjee A, Srivastava KK. Chronic BuddChiari syndrome due to congenital membranous obstruction of the inferior vena cava: clinical experience. Aust N Z J Surg 1989; 59(4): 335–8 Ruh J, Malago M, Busch Y et al. Management of Budd-Chiari syndrome. Dig Dis Sci 2005; 50(3): 540–6 Sugano S, Suzuki T, Makino H et al. Budd-Chiari syndrome attributed to protein C deficiency. Am J Gastroenterol 1996; 91(4): 777–9 Ohnishi K, Terabayashi H, Tsunoda T, Nomura F. Budd-Chiari syndrome: diagnosis with duplex sonography. Am J Gastroenterol 1990; 85(2): 165–9 Chawla Y, Kumar S, Dhiman RK, Suri S, Dilawari JB. Duplex Doppler sonography in patients with Budd-Chiari syndrome. J Gastroenterol Hepatol 1999; 14(9): 904–7 Millener P, Grant EG, Rose S et al. Color Doppler imaging findings in patients with Budd-Chiari syndrome: correlation with venographic findings. AJR Am J Roentgenol 1993; 161(2): 307–12
13. 14. 15. 16. 17. 18.
19. 20. 21. 22.
Lim JH, Park JH, Auh YH. Membranous obstruction of the inferior vena cava: comparison of findings at sonography, CT, and venography. AJR Am J Roentgenol 1992; 159(3): 515–20 Stark DD, Hahn PF, Trey C, Clouse ME, Ferrucci JT Jr. MRI of the Budd-Chiari syndrome. AJR Am J Roentgenol 1986; 146(6): 1141–8 Orloff LA, Orloff MJ. Budd-Chiari syndrome caused by Behcet’s disease: treatment by side-to-side portacaval shunt. J Am Coll Surg 1999; 188(4): 396–407 Bayraktar Y, Balkanci F, Bayraktar M, Calguneri M. Budd-Chiari syndrome: a common complication of Behcet’s disease. Am J Gastroenterol 1997; 92(5): 858–62 Baijal SS, Roy S, Phadke RV et al. Management of idiopathic Budd-Chiari syndrome with primary stent placement: early results. J Vasc Interv Radiol 1996; 7(4): 545–53 Xu K, He FX, Zhang HG, Zhang XT et al. Budd-Chiari syndrome caused by obstruction of the hepatic inferior vena cava: immediate and 2-year treatment results of transluminal angioplasty and metallic stent placement. Cardiovasc Intervent Radiol 1996; 19(1): 32–6 De BK, Biswas PK, Sen S et al. Management of the Budd-Chiari syndrome by balloon cavoplasty. Indian J Gastroenterol 2001; 20(4): 151–4 Rossle M, Olschewski M, Siegerstetter V et al. The Budd-Chiari syndrome: outcome after treatment with the transjugular intrahepatic portosystemic shunt. Surgery 2004; 135(4): 394–403 Wu T, Wang L, Xiao Q, Wang B, Li S, Li X, Zhang J. Percutaneous balloon angioplasty of inferior vena cava in Budd-Chiari syndrome-R1. Int J Cardiol 2002; 83(2): 175–8 Rinckenbach S, Chakfe N, Beaufigeau M et al. Surgical treatment of a Budd-Chiari syndrome secondary to hepatic inferior vena cava agenesia. J Cardiovasc Surg (Torino) 2002; 43(5): 665–9
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Endovascular management of Budd-Chiari syndrome – suprahepatic inferior vena cava occlusive disease 23.
24. 25. 26. 27. 28.
29.
30.
Attwell A, Ludkowski M, Nash R, Kugelmas M. Treatment of BuddChiari syndrome in a liver transplant unit, the role of transjugular intrahepatic porto-systemic shunt and liver transplantation. Aliment Pharmacol Ther 2004; 20(8): 867–73 Shaked A, Goldstein RM, Klintmalm GB et al. Portosystemic shunt versus orthotopic liver transplantation for the Budd-Chiari syndrome. Surg Gynecol Obstet 1992; 174(6): 453–9 Malkowski P, Michalowicz B, Pawlak J et al. Surgical and interventional radiological treatment of Budd-Chiari syndrome: report of nine cases. Hepatogastroenterology 2003; 50(54): 2049–51 Behera A, Menakuru SR, Thingnam S et al. Treatment of BuddChiari syndrome with inferior vena caval occlusion by mesoatrial shunt. Eur J Surg 2002; 168(6): 355–9 Emre A, Kalayci G, Ozden I et al. Mesoatrial shunt in Budd-Chiari syndrome. Am J Surg 2000; 179(4): 304–8 Takamura M, Ichida T, Yokoyama J et al. Recurrence of hepatocellular carcinoma 102 months after successful eradication and removal of membranous obstruction of the inferior vena cava. J Gastroenterol 2004; 39(7): 681–4 Matsui S, Ichida T, Watanabe M et al. Clinical features and etiology of hepatocellular carcinoma arising in patients with membranous obstruction of the inferior vena cava: in reference to hepatitis viral infection. J Gastroenterol Hepatol 2000; 15(10): 1205–11 Bayraktar Y, Egesel T, Saglam F, Balkanci F, Van Thiel DH. Does hepatic vein outflow obstruction contribute to the pathogenesis
31. 32. 33. 34. 35. 36. 37.
38.
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of hepatocellular carcinoma? J Clin Gastroenterol 1998; 27(1): 67–71 Kuniyoshi Y, Koja K, Miyagi K et al. Improvement of liver function after surgery for Budd-Chiari syndrome. Surg Today 2005; 35(2): 122–5 Sen PK, Kinare SG, Kelkar MD et al. Congenital membranous obliteration of the inferior vena cava. J Cardiovasc Surg 1967; 8: 344–52 Anderson RC, Adams P Jr, Burke B. Anomalous inferior vena cava with azygous continuation (infrahepatic interruption of the inferior vena cava): report of 15 new cases. J Pediatr 1961; 59: 370–83 Friedland GW, deVries PA, Nino-Murcia M et al. Congenital anomalies of the inferior vena cava: embryogenesis and MR features. Urol Radiol 1992; 13: 237–48 Alexander ES, Clark RA, Gross BH, Colley DP. CT of congenital anomalies of the inferior vena cava. Comput Radiol 1982; 6(4): 219–26 Rossal RE, Caldwell RA. Obstruction of inferior vena cava by a persistent eustachian valve in a young adult. J Clin Pathol 1957; 10: 40 Beedle RJ, Yeo W, Morcos SK. Congenital absence of the intrahepatic segment of the inferior vena cava with azygos continuation presenting as a mediastinal mass. Postgrad Med J 1989; 65(762): 253–5 McClure CFW, Butler EG. The development of the vena cava inferior in man. Am J Anat 1925; 35: 331–83
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Unusual vascular conditions of the extremities DH Deaton, RF Neville, J Laredo, and BB Lee
Introduction The vast majority of clinically significant vascular disease is the result of atherosclerotic disease and it is for this process that nearly all of the interventional devices available today are designed. Patients with non-atherosclerotic disease generally fall into a category that represents a variety of either congenital or inflammatory conditions that affect blood vessels and a variety of other tissues. The distinction of these syndromes is often difficult and their characterization and treatment are constantly changing. Unlike patients with atherosclerotic disease, these patients are often younger and suffer from a variety of other lesions resulting from their primary diagnosis. These lesions often occur in locations atypical for atherosclerotic lesions and with a different morphologic appearance on angiography. Vascular reconstruction, be it open or endovascular, is performed only when clinical circumstances demand it and when coordinated with the medical therapies that represent the mainstay of treatment for most of these conditions. For the conditions that are inflammatory in nature, vascular intervention is best pursued when the inflammatory process is quiescent and care must be taken to preserve future pathways for open or endovascular construction in this often younger population. This chapter will briefly review the logic and evidence for intervention in: ● ● ● ● ● ● ● ●
fibromuscular dysplasia; giant cell arteritis; polymyalgia rhematica; polyarteritis nodosa (periarteritis nodosa); systemic lupus erythematosus; Kawasaki’s disease; rheumatoid disease with vasculitis; replapsing polychondritis.
Other conditions that would normally be covered in a chapter devoted to this class of vascular disease but are covered elsewhere in this text include: ● ● ● ●
Bechet’s; Takayasu’s arteritis; Burguer’s disease; coarctation of the aorta.
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Heritable diseases of connective tissue that result in aneurysmal disease are covered in chapters devoted to endovascular therapy for aneurysms.
Fibromuscular dysplasia Fibromuscular dysplasia (FMD), or arterial fibrodysplasia, is a non-atherosclerotic and non-inflammatory arterial disease that generally affects women in their fourth and fifth decade. It is generally divided into three specific disease entities, with the questionable existence of a fourth. Intimal fibroplasia represents approximately 5% of this disease classification and affects males and females equally. Medial hyperplasia is a very rare form of this disease and its very existence is debated. Medial fibroplasia is the most common form of FMD representing approximately 85% of patients with this disease process. More than 90% of these patients are female and the vast majority of lesions are found in the renal, extracranial internal carotid, and external iliac arteries. The appearance of these lesions on angiography ranges from a single stenosis to a series of stenoses often referred to as a “string of beads.” The final type of FMD is perimedial dysplasia which represents about 10% of all patients with FMD. Most patients with perimedial dysplasia are female in their fourth or fifth decade of life.1 The type of FMD is rarely, if ever, noted in reports of interventional therapy for this disease. This is largely the result of the minimally invasive nature of endovascular techniques and the resulting lack of pathologic specimens necessary to make a specific diagnosis as to the form of fibromuscular dysplasia. The vast majority of reports concern the most common lesion associated with FMD, renal artery stenosis. FMD affecting the renal arteries generally affects the main renal artery and occasionally the first portion of the segmental branches. All patients with FMD should be examined for evidence of internal carotid and external iliac artery involvement as these vessels are most often involved after the renal arteries. The significance of the lesion is primarily a clinical decision based on the degree of hypertension or renal insufficiency the patient is experiencing as angiographic measurement of stenosis is nearly impossible. The reason angiography is such a poor measure of significance is the morphologic nature of the lesion as a series of intravascular webs and the multiplicity
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Unusual vascular conditions of the extremities of the stenoses acting as resistors in series. For this reason, other objective measures of hemodynamic significance have been employed. Mahmud et al. describe two patients with significant clinical findings but a paucity of angiographic findings that were demonstrated to have severe lesions using a 0.014 pressure wire to measure pressure gradients along the involved renal artery segments. Both patients had an excellent outcome after balloon angioplasty of the affected renal arteries.2 The mainstay of all therapy for renal FMD is now balloon angioplasty. Birrer, et al. describe a prospective 12-month follow-up study of 27 patients with 31 treated renal artery stenoses with follow-up that included monitoring of blood pressure, antihypertensive medication, and creatinine measurements before discharge and at 3, 6, and 12 months. While there was a cumulative 23% restenosis rate at 12 months, arterial hypertension was cured or improved in 93% of patients immediately after the intervention and remained cured/improved in 74% of patients at 12 months of follow-up. More remarkably, renal failure present in five patients before PTRA stabilized or improved in all patients.3 The durability of angioplasty for renal FMD was demonstrated by Surowiec et al. in their report that documented primary patency rates of 81, 69, 69, and 69% at 2, 4, 6, and 8 years, respectively, and assisted primary patency rates of 87, 87, 87, and 87% at 2, 4, 6, and 8 years, respectively. Clinical benefit (improved or cured hypertension) was seen in 79% of patients overall with 65% of patients maintained at 8 years by life-table analysis.4 Several authors have used cutting balloon technology for resistant lesions unresponsive to high pressure conventional balloon angioplasty. Tanemoto et al. reported successful outcome with a cutting balloon after failed conventional balloon angioplasty5 while Oguzkurt et al. reported the rupture of a renal artery after using a 6-mm-diameter cutting balloon in a resistant lesion that eventually required conversion to open surgery.6 This last report emphasizes the adjuncts of careful sizing and hemodynamic assessment necessary to utilize balloon angioplasty successfully for this type of pathology. In the authors’ institution, Georgetown University Hospital, intravascular ultrasound (IVUS) is routinely employed for accurate diameter measurements of both diseased and unaffected segments on all patients with FMD and frequently in all renal artery lesions where the consequences of incorrect balloon or stent diameter can be catastrophic. Kolluri et al. report a case of bilateral brachial artery FMD successfully treated with balloon angioplasty7 and document that while most lesions occur in the renal, carotid, or iliac distribution this disease process can affect a wide variety of vascular beds including upper extremity, lower extremity, and mesenteric vessels.1 Giant cell arteritis Giant cell arteritis is often considered to be synonymous with temporal arteritis but some authors8 also consider Takayasu’s disease to be within the nomenclature of giant cell arteritis as the histology of each is identical in the acute phase and both include the progressive occlusive disease of limb, carotid, and visceral arteries. The primary differentiation between the typical giant cell arteritis patient and the patient with Takayasu’s is one of demographics with the former typically greater than age 50 and with a less predominant female prevalence and the latter the opposite.8
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While Takayasu’s disease frequently requires surgical reconstruction as a result of the age group it affects and the central aortic lesions it produces, giant cell arteritis affecting peripheral vasculature is usually managed medically and only infrequently requires surgical reconstruction. The mainstay of giant cell arteritis therapy is steroid therapy, particularly in its acute phase. Other antiproliferative therapies have also been used to inhibit the acute inflammatory phase of this disease process. Gonzalez-Gay et al. have demonstrated an increased odds ratio of approximately 1.8 for the development of severe ischemic symptoms in patients with traditional risk factors for atherosclerotic disease (i.e. hypertension, hyperlipidemia).9 Giant cell, or temporal, arteritis is most often associated with extracranial vascular occlusive lesions that result in a variety of symptoms including jaw claudication, double vision, blindness, and stroke. There is very little surgical or endovascular intervention for the lesions responsible for these symptoms, although less frequent giant cell arteritis has been reported throughout the rest of the peripheral vasculature where intervention is far more common. Evans et al. reported an 80-yearold female with mesenteric ischemia proven to be giant cell arteritis and emphasize the importance of accurate diagnosis and appropriate medical therapy before any attempt at surgical or endovascular reconstruction is attempted.10 Dellaripa et al. reported on a female patient with bilateral axillary artery stenoses that were unresponsive to corticosteroid therapy successfully treated with balloon angioplasty.11 Amann-Vesti et al. reported on four patients with upper extremity ischemic lesions from giant cell arteritis successfully treated with balloon angioplasty in the setting of prolonged steroid therapy with no recurrence at 2, 5, and 10 years of follow-up.12 Both et al. reported on a total of 29 lesions in 10 patients with a cumulative primary patency rate of 65.2%. Recurrent lesions were noted to develop in the territories of the initial long-segment stenoses resulting in a cumulative secondary patency rate of 82.6% and a cumulative tertiary patency rate of 89.7%.13 Giant cell arteritis is representative of many of the inflammatory arterial disorders in demonstrating the importance of accurate diagnosis and withholding any surgical or interventional therapy until the intensity of the inflammatory process has been tamed with medical therapy. All of the reports cited within emphasize the preoperative and continued postoperative administration of corticosteroids.11–13 Polymyalgia rheumatica Polymyalgia rheumatica is defined as a “significant, often crippling pain and stiffness without local tenderness, involving muscles of the neck, shoulder, and hip” present for at least 1 month in patients over 50 years of age.8 It is nearly four times as prevalent as temporal arteritis and approximately 5–40% of these patients will have an element of arteritis. This clinical syndrome can also be the prodrome of a variety of other inflammatory conditions including rheumatoid arthritis, periarteritis (polyarteritis) nodosa, and systemic lupus ertythematosus.8 Polyarteritis nodosa (periarteritis nodosa) Polyarteritis nodosa has been diagnosed across a wide variety of ages from childhood through the elderly but is most common in males (2:1 male–female ratio) in the fourth
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through sixth decades. The lesions affect small to medium-size arteries with acute inflammation and necrosis and resulting lesions that manifest as either occlusive or aneurysmal. The primary presenting symptom involves aneurysmal degeneration of second or third order branches in the hepatic, renal, and intestinal circulations.8,14 Polyarteritis nodosa is often used to describe any systemic vasculitis and the exact manifestations and clinical presentation of the disease can be variable.15 Interventional therapy in the form of coil embolization for hemobilia and hepatic aneurysm formation has been reported16 and the majority of interventional techniques for this vasculitis is in vessel occlusion to prevent bleeding from aneurysms in the medium vessel circulation. Most occlusive lesions caused by this disease process result in irreversible ischemia and its consequences (e.g. appendicitis, gut perforation, cholecystitis). The primary medical management is with steroids and/or cyclophosphamide8 and these therapies have increased survival from the 15% range to greater than 50%.
Systemic lupus erythematosus Systemic lupus erythematosus (SLE) is an autoimmune disease with a variety of clinical manifestations that include arthritis, nephritis, pericarditis, pleurtitis, cerebritis and lymphadenopathy. Arteritis of small and medium vessels is a component of the disease process in a significant number of cases and manifests itself in the skin, intestinal tract, renal, pulmonary, and coronary circulations with occlusive lesions. Livedo, nodules, and infarcts can be noted on examination of the skin. While the arteritis is not encountered in the larger vessels, the hypercoagulable condition associated with SLE which occurs in 5–10% of cases often presents with deep vein thrombosis or thrombosis of other major arteries. This “lupus anticoagulant” or anti-phospholipid antibody induced hypercoagulability is controlled with chronic anticoagulation.8
Kawasaki’s disease Kawasaki’s disease is unique in its demographic subset of infants and children with few exceptions occurring before the age of 10. Approximately 2% of these patients will die of an intense vasculitis of small and medium vessels. A secondary vasculitic event occurring typically in the first month but sometimes 2 years later are coronary artery aneurysms.8 A variety of interventional techniques for both occlusive and aneurysmal coronary degeneration have been described in this challenging patient subset.17,18 Other authors have noted a Kawasaki-like syndrome of vasculitis in HIV positive patients.19
Rheumatoid disease Two vascular arteriopathies can be associated with rheumatoid arthritis. This first is a non-inflammatory endarteritis that can be responsible for Raynaud’s phenomenon, periungal infarcts, digital pad ulcers, and gangrene. The second form is an active vasculitis that is essentially indistinguishable from polyarteritis nodosa and can result in extensive digital gangrene, lower extremity ulceration and bowel infarction. This second, more active vasculitis occurs late in the course of rheumatoid disease when there are multiple manifestations of that primary disease process.8 While there are no specific reports for interventional therapy in this patient subset, it is important to remember the mechanisms that may be playing a role in a given patient’s clinical presentation when they have both atherosclerotic lesions and a long history of rheumatoid arthritis. Replapsing polychondritis Relapsing polychondritis is a rare disease but is associated with several vascular complications. This disease occurs throughout both sexes from adolescence through the eighth decade. The primary presentation consists of malaise, fever, an elevated sedimentation rate in conjunction with chondritis (i.e. auricular chondritis, nasal condritis, respiratory tract chondritis). Aneurysms of the aorta throughout its course from ascending to infrarenal occur in approximately 10% of patients. Other forms of vasculitis including polyarteritis nodosa, SLE, and Behçet’s overlap, with this disease process in approximately 20–30% of cases.8
Summary Unusual arteriopathies sometimes announce themselves to the clinician as a result of their unusual presentation with respect to the patient’s age and sex as well as the location and characteristic of the lesion. More difficult are the patients that harbor both atherosclerotic changes but have other active pathologic processes that result in vasculitic changes superimposed on the more typical atherosclerotic substrate. Patients with a history of autoimmune disease must be dealt with carefully and any intervention, open surgical or endovascular, must be coordinated with the medical control of the inflammatory process. Close consultation and coordination with other specialists managing the other aspects of what is often a complicated medical picture is of paramount importance in these patients. When done properly, many of the techniques developed for catheter-based arterial reconstruction have as good or better a result in this group of difficult and needy patients.
REFERENCES 1. 2. 3.
Stanley JC and Wakefield TW. Arterial fibrodysplasia. In: Vascular Surgery, Rutherford, RB, ed. Philadelphia: W.B. Saunders, 1989: 245–65 Mahmud E et al. Fibromuscular dysplasia of renal arteries: percutaneous revascularization based on hemodynamic assessment with a pressure measurement guidewire. Catheter Cardiovasc Interv 2006; 67(3): 434–7 Birrer M et al. Treatment of renal artery fibromuscular dysplasia with balloon angioplasty: a prospective follow-up study. Eur J Vasc Endovasc Surg 2002; 23(2): 146–52
4. 5. 6.
Surowiec, SM et al. Percutaneous therapy for renal artery fibromuscular dysplasia. Ann Vasc Surg 2003; 17(6): 650–5 Tanemoto M et al. Cutting balloon angioplasty of resistant renal artery stenosis caused by fibromuscular dysplasia. J Vasc Surg 2005; 41(5): 898–901 Oguzkurt L et al. Rupture of the renal artery after cutting balloon angioplasty in a young woman with fibromuscular dysplasia. Cardiovasc Intervent Radiol, 2005; 28(3): 360–3
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10. 11.
12.
Kolluri R and Ansel G. Fibromuscular dysplasia of bilateral brachial arteries—a case report and literature review. Angiology 2004; 55(6): 685–9 Joyce JW. Uncommon arteriopathies. In: Rutherford, RB, ed. Vascular Surgery. Philadelphia: W.B. Saunders, 1989: 276–86 Gonzalez-Gay MA et al. Influence of traditional risk factors of atherosclerosis in the development of severe ischemic complications in giant cell arteritis. Medicine (Baltimore) 2004; 83(6): 342–7 Evans DC, Murphy MP, Lawson JH. Giant cell arteritis manifesting as mesenteric ischemia. J Vasc Surg 2005; 42(5): 1019–22 Dellaripa PF, Eisenhauer AC. Bilateral percutaneous balloon angioplasty of the axillary arteries in a patient with giant cell arteritis and upper extremity ischemic symptoms not responsive to corticosteroids. J Rheumatol 1998; 25(7): 1429–33 Amann-Vesti BR et al. Immediate and long-term outcome of upper extremity balloon angioplasty in giant cell arteritis. J Endovasc Ther 2003; 10(2): 371–5
13. 14. 15. 16. 17.
18. 19.
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Both M et al. Balloon angioplasty of arteries of the upper extremities in patients with extracranial giant-cell arteritis. Ann Rheum Dis 2006; 65(9): 1124–30 Allanore Y et al. Multiple spontaneous visceral hematomas revealing polyarteritis nodosa. J Rheumatol 2004; 31(9): 1858–60 Segelmark M and Selga D. The challenge of managing patients with polyarteritis nodosa. Curr Opin Rheumatol 2007; 19(1): 33–8 Dutta U et al. Hemobilia as presenting manifestation of polyarteritis nodosa. Indian J Gastroenterol 2004; 23(2): 71–2 Waki K, Baba K. Transcatheter polytetrafluoroethylene-covered stent implantation in a giant coronary artery aneurysm of a child with Kawasaki disease – a potential novel treatment. Catheter Cardiovasc Interv 2006; 68(1): 74–7 Akagi T. Interventions in Kawasaki disease. Pediatr Cardiol 2005; 26(2): 206–12 Johnson RM, Barbarini G, Barbaro G. Kawasaki-like syndromes and other vasculitic syndromes in HIV-infected patients. Aids 2003; 17(suppl. 1): S77–82
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Interventions in inflammatory arterial disease S Rajagopal and L Gopalakrishnan
Inflammatory arteritis
Technical aspects in general
Inflammatory arteritis includes a spectrum of diseases involving large, medium, and small vessels. With rare exceptions, the majority of interventional procedures in inflammatory arteritis are in patients with non-specific aortoarteritis and this chapter will primarily focus on interventions in this condition. Non-specific aortoarteritis (Takayasu’s arteritis) is a chronic inflammatory disease of unknown etiology primarily involving the aorta and its major branches.1 Inflammation leads to stenosis or occlusion and occasionally to aneurysmal dilatation of the vessel involved. Pulmonary artery involvement, coronary artery disease, and valvular heart disease have also been described.2 The disease is seen relatively more frequently in Asia, although cases have been reported worldwide. Clinical features are related to inflammation in the early stages and to the effects of stenotic or occlusive changes in the chronic stage with absent pulses, hypertension, congestive failure, and ischemia in the territory of the involved vessels. Several diagnostic criteria have been proposed to identify this disease.1,3,4 The disease has also been classified into subtypes based on the pattern of involvement.3–7 Several prognostic factors have been identified which influence the natural history.6,8–10 Medical therapy consists of anti-inflammatory agents and immunosuppressants. There are a few reports of surgical treatment,11–14 but catheter-based interventional treatment is increasingly being used with encouraging results.15–40 The pathology is strikingly different from atherosclerosis and influences both interventional and surgical treatment.The pathologic changes involve all three layers of the vessel wall. Histologically, the active phase is characterized by inflammation and granuloma formation while the chronic phase shows extensive intimal and adventitial thickening with scarring of the media. The marked thickening of the adventitia and intima produce lesions which can be extremely resistant to balloon dilatation. The perivascular and mural changes make surgery very difficult. The diffuse involvement of the vessels together with the frequent occurrence of long lesions adds to the therapeutic challenge. Revascularization, whether surgical or interventional, is preferably performed when the disease is not in an active phase (which is usually diagnosed by the presence of systemic signs and a erythrocyte sedimentation rate above 20 mm), as procedures done during the active stage have been associated with a poorer outcome.13,33
Preprocedural evaluation This should include a complete clinical examination with a view to assess the extent of the disease as well as indicate possible approaches for access. Disease activity, manifested by systemic signs and vessel tenderness as well as elevated erythrocyte sedimentation rate, should be ruled out. If activity is detected, the patient is treated with corticosteroids till activity is suppressed, deferring intervention, if possible, until this is achieved. Detailed non-invasive evaluation, particularly with duplex Doppler ultrasonography, and in selected cases computed tomography or magnetic resonance angiography, is useful before proceeding to angiography. Angiography remains the mainstay of investigation to document the extent and severity of disease and decide on the management approach. All patients are pretreated with aspirin and clopidogrel for at least 48 hours prior to the procedure.
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Vascular access The femoral artery is the usually preferred access site as it permits the use of large introducers and also because the subclavian arteries are frequently diseased. In certain cases a brachial approach may be needed, particularly in subclavian artery lesions (in addition to a femoral approach), as the lesion may not be crossable from the femoral approach. If the brachial pulse is not palpable, an arteriotomy may be required. When both subclavians are occluded (as happens not infrequently) and if the aorta is also occluded, a trans-septal approach (with a long kink-resistant sheath) has been described for access to the central aorta and arch vessels.31 Crossing the lesion Stenotic lesions can be crossed with appropriate steerable or hydrophilic wires. Hydrophilic wires (straight or angled) in conjunction with angled or straight catheters also permit crossing of most occlusions. Approaching an occlusion from both ends is sometimes required. Once a wire is through a lesion it can be snared using an appropriate snare and brought to a convenient access site. Subtotal occlusions, particularly in the carotids, may require use of a floppy-tip 0.014-inch coronary wire with an over-the-wire low-profile coronary balloon
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Interventions in inflammatory arterial disease or a microcatheter, to cross the lesion. Once the balloon or catheter is across, it is exchanged for a stiffer wire, preferably a 0.018-inch wire.
●
Angioplasty The use of a long sheath or a guiding catheter (where practicable) is helpful, not only for angiography during the procedure, but also for pressure measurements and during stent deployment. Whenever possible a 0.035-inch extra-stiff wire should be placed across the lesion (exceptions obviously being the carotid or renal arteries). Use of low-profile balloons which are noncompliant and have very high burst pressures is advisable. The last two features are particularly important as often quite high pressures have to be used. Aorto-ostial lesions are usually treated with balloon-expandable stents, particularly those with high radial force. Long lesions in the carotid or subclavian arteries can be treated with self-expanding stents. Higher restenosis rates with stenting compared to data on atherosclerotic lesions suggest that conservative use of stents (especially in relatively smaller diameter vessels like the renal arteries) is prudent. The peripheral cutting balloon, which has four microsurgical blades mounted longitudinally on its surface, has been used in a few cases and has shown promising initial results. The principle of this device is that the blades produce microincisions in the intima and media and the subsequent shear forces of balloon expansion propagate these incisions. Since the fibroelastic continuity of the vessel wall at the lesion site is interrupted by the incisions, resistance to dilatation and recoil are reduced. Joseph et al.38 have reported the use of the peripheral cutting balloon at multiple sites (aorta, renal, subclavian, vertebral, and carotid arteries) in one patient with favorable initial results. Rath et al.39 have reported good immediate results in two patients. One developed a restenosis at four months. The use of the cutting balloon may be associated with complications such as vessel perforation.
Lesions at specific sites
Factors affecting procedure outcome and complications ● Disease activity: Intervention is preferably avoided during the active phase. ● Lesion length: Longer lesions appear to have a worse outcome and higher restenosis rate.16,25 ● High-pressure dilatation: Though often required, this occasionally results in balloon rupture which can be associated with damage to the vessel being treated.33 ● Balloon–artery diameter ratio: Conservative balloon sizing is advisable as overdilatation, particularly with high pressures, can be dangerous. Even with appropriate balloon sizing (that is, not exceeding 1:1) fatal aortic rupture has been reported.36 ● Inadequate stent expansion: Despite use of high pressures, it may occasionally be impossible to expand a stent fully, leading to the angiographic appearance of a deformed stent, due to the vessel being extremely rigid. The use of rotational atherectomy to alter vessel compliance has been reported in this connection,33 though burr size obviously restricts the use to small diameter vessels. Inadequate stent expansion may increase restenosis risk.
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Age of the patient: Children appear to have a higher restenosis rate than adults, at least for renal angioplasty.35
Descending thoracic aorta Lesions at this site commonly present with hypertension and (particularly in children) congestive cardiac failure. The hypertension may be due to both a mechanical component as well as due to renal hypoperfusion as the kidneys are perfused at relatively low pressure. The increased after-load contributes to the failure and may often result in significant systolic dysfunction of the left ventricle. Dramatic reversal of both congestive failure and ventricular dysfunction may be seen after successful angioplasty (see Figures 85.1 and 85.2). Linear dissections are often seen after balloon dilatation, but these often remodel favorably (see Figure 85.3). Stents, either balloon-expandable or self-expanding, have been used to optimize angioplasty results. Abdominal aorta The stenosed segment may be suprarenal, infrarenal or extend across the renal arteries. If the lesion is close to the renal artery, placement of a wire in the renal artery is advisable to preserve access. Large series have been reported with more than 90% procedural success.35 Complications have been relatively rare, and are usually long dissections that can be managed with stents. One case of extravasation with retroperitoneal leak has been reported.35 Both hypertension and claudication are usually significantly improved. Supra-aortic arteries Lesions in the branches of the arch vessels often involve multiple vessels. Occasionally the patient has only one vessel providing cerebral supply and this may also be diseased. Successful treatment of this challenging situation has been reported (see Figure 85.4). 37 Lesions in the carotid are often long and diffuse, and can be technically very challenging. Though intervention should ideally be delayed until disease activity is controlled, one may be confronted with an occasional patient with active disease who also has ongoing and progressive neurologic dysfunction and it may not be possible to defer intervention. The results of interventional procedures appear to compare favorably with surgical procedures in this territory.40 Innominate and carotid arteries The use of coronary wires, long coronary (or other lowprofile) balloons, and long self-expanding stents is required. Care must be taken to ensure that the syndrome of cerebral hyperperfusion is avoided, as these patients often get adapted to cerebral perfusion at very low pressures when multiple vessels are affected (see Figure 85.5). Subclavian artery Subclavian artery lesions are quite common and can be difficult to cross. A bidirectional approach (i.e. a combination of
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(b)
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Figure 85.1 A 5-year-old girl with severe congestive failure and clinical evidence of stenosis of the descending thoracic aorta. (a) Diffuse narrowing of the descending thoracic aorta. (b, c) Aortoplasty and immediate result. (d) Follow-up study after 3 years. There was significant improvement in left ventricular function as a result of reducing afterload (see left ventriculograms in Figure 85.2).
(a)
(b)
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(d)
Figure 85.2 Left ventriculograms: (a, b) before; and (c, d) at follow up, showing marked improvement in left ventricular function on follow-up late after aortoplasty, with reduction of afterload (same patient as in Figure 85.1).
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Figure 85.3 Serial aortograms of a patient who underwent dilatation of the descending thoracic aorta showing favorable remodeling of the aorta: (a) pre-intervention; (b) post-angioplasty; (c) restudy; and (d) follow-up.
an antegrade and a retrograde approach) from both the aorta and the affected brachial artery is often required. Aorto-ostial lesions are usually treated with balloon-expandable stents while distal lesions can be treated with self-expanding stents. Acute stent thrombosis and vessel rupture (requiring the use of a covered stent) have been described.33 Renal arteries The overall success rate was 85% in a large series35 and improved in the later part of the series with the use of a coaxial guiding catheter technique and the use of stents. Average balloon pressure required for angioplasty was 8.1 atmospheres
(a)
(b)
(range: 4–17 atmospheres). Major complications were rare. Restenosis after angioplasty was around 17% in patients restudied at 3–41months. Eighteen patients underwent stent placement, and the procedure was technically successful in all. However restenosis was reported in 36% of 11 patients, including 3 pediatric patients. All were successfully redilated.35 Hypertension was reported cured in 40% and improved in 51%. Ostial lesions can occasionally prove very resistant and incomplete stent expansion may occur despite high pressure dilatation (see Figure 85.6). The use of the cutting balloon to permit dilatation of these resistant ostial lesions may occasionally result in vessel perforation requiring use of a covered stent (see Figure 85.7).
(c)
Figure 85.4 Angioplasty and stenting of tight stenosis of sole supra-aortic artery with aortoplasty in a young boy: (a) pre-intervention; (b) kissing balloon; (c) post-intervention. Note total occlusion of innominate and left common carotid arteries with left vertebral artery providing sole supply to the brain.
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(e)
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(f)
Figure 85.5 (a) Young lady with marked narrowing of the distal innominate, right common carotid, and right and left subclavian arteries and total occlusion of the left common carotid artery. The cerebral flow is mainly through the vertebral arteries. (b, c) Selective left subclavian angiograms before and after angioplasty and stenting of the left subclavian artery. (d) The “string” like narrowing of the right common carotid artery as well as disease of the proximal right subclavian artery. (e) Initial dilatation of the right common carotid artery with a long coronary balloon with a wire in the right subclavian artery. (f) Final result after placement of a long selfexpanding stent in the right common carotid artery with balloon angioplasty of the subclavian artery. The left subclavian artery was dilated first to improve flow through the left vertebral artery and the right common carotid artery was dilated the next day to avoid hyperperfusion syndrome.
Mesenteric arteries Balloon angioplasty and stenting have occasionally been used to provide relief of abdominal angina.29 The technical considerations are similar to other lesions described. Coronary arteries Coronary ostial stenoses may present as myocardial ischemia or infarction. Successful stenting of unprotected left main coronary stenosis has been reported.32 Iliac vessels Balloon angioplasty of iliac arteries with prolonged relief of claudication has been reported in a few cases.35
(a)
(b)
Conclusion Percutaneous transluminal angioplasty with stent implantation in selected situations is a useful mode of treatment in aortoarteritis (Takayasu’s disease) and appears to offer sustained improvement of patient status with an acceptably low complication rate. Future developments will include a better understanding of the pathophysiology of the disease and detection and management of disease activity, better hardware designed to meet the specific technical challenges posed by this disease and more widespread application of interventional techniques.
(c)
Figure 85.6 Resistant renal artery stenosis in a single functioning kidney in a nine year old boy: (a) tight ostial stenosis of the left renal artery; (b) the stent not expanding fully despite the use of a large balloon at high pressure (18 atmospheres); and (c) residual stenosis “waist” on the stent.
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Figure 85.7 Cutting-balloon angioplasty of a tight renal artery ostial stenosis: (a) tight stenosis of the left renal artery ostium; (b) extravasation of contrast due to vessel perforation following use of cutting balloon; (c) result after placement of a covered stent.
REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9. 10. 11. 12. 13. 14. 15. 16.
17.
18.
19.
Arend WP, Michel BA, Bloch DA et al. The American College of Rheumatology 1990 criteria for the classification of Takayasu arteritis. Arthritis Rheum 1990; 33: 1129–34 Kinare S, Gandhi M, Deshpande J. Non-Specific Aorto-Arteritis (Takayasu’s Disease) Pathology and Radiology. Mumbai: Quest, 1998; 17–66 Ishikawa K. Diagnostic approach and proposed criteria for the clinical diagnosis of Takayasu’s arteriopathy. J Am Coll Cardiol 1988; 12: 964–72 Sen PK, Kinare SG, Kelkar MD, Parulkar GB. Nonspecific aortoartoritis. A monography based on a study of 101 cases. Bombay: McGraw-Hill, 1973 Lupi-Herrera E, Sanchez-Torrez G, Marcushamer J et al. Takayasu’s arteritis: clinical study of 107 cases. Am Heart J 1977; 93: 94–103 Ishikawa K. Natural history and classification of occlusive thromboaortopathy (Takayasu’s disease). Circulation 1978; 57: 27–35 Lie JT. The classification and diagnosis of vasculitis in large and medium sized vessels. Pathol Annual 1987; 22(11): 125–62 Ishikawa K. Survival and morbidity after diagnosis of occlusive thromboaortopathy (Takayasu’s disease). Am J Cardiol 1981; 47: 1026–32 Ishikawa K. Patterns of symptoms and prognosis in occlusive thromboaortopathy (Takayasu’s disease). J Am Coll Cardiol 1986; 8: 1041–46 Subramanyam R, Joy J, Balakrishnan KG. Natural history of aortoarteritis (Takayasu’s disease). Circulation 1989; 80: 429–37 Pokrovsky AV. Nonspecific aortoarteritis. In: Rutherford RB, ed. Vascular Surgery, second edition. Philadelphia: WB Saunders, 1989; 217–37 Weaver FA, Yellin AK, Campen DH et al. Surgical procedures in the management of Takayasu’s arteritis. J Vasc Surg 1990; 12: 429–37 Pokrovsky AV, Sultanaliev JA, Spiridonov A. Surgical treatment of vasorenal hypertension in non-specific aortoarteritis (Takayasu’s disease). J Cardiovas Surg 1983; 24: 111–8 Tada Y, Sato O, Ohshima A et al. Surgical treatment of Takayasu’s arteritis. Heart Vessels 1992; 7: 159–67 Fava MP, Foradori GB, Garcia CB et al. Percutaneous transluminal angioplasty in patients with Takayasu arteritis: five year experience. J Vasc Interv Radiol 1993; 4: 649–52 Joseph S, Mandalam KR, Rao VR et al. Percutaneous transluminal angioplasty of the subclavian artery in non specific aortoarteritis: results of long-term follow up. J Vasc Interv Radiol 1994; 5: 573–80 Sharma S, Thatai D, Saxena A et al. Renovascular hypertension resulting from nonspecific aortoarteritis in children: midterm results of percutaneous transluminal renal angioplasty and predictors of restenosis. Am J Roentgenol 1996; 166: 157–62 Tyagi S, Verma PK, Gambhir DS et al. Early and long-term results of subclavian angioplasty in aortoarterieis (Takayasu disease): comparison with atherosclerosis. Cardiovasc Intervent Radiol 1998; 21: 219–24 Rao AS, Ravimandalam K, Rao VRK et al. Takayasu Arteritis: Initial and long-term follow-up in 16 patients after percutaneous transaluminal angioplasty of the descending thoracic and abdominal aorta. Radiology 1993; 189: 173–9
20. 21. 22.
23. 24. 25.
26. 27. 28.
29. 30. 31. 32.
33.
34. 35.
Saddekni S, Sniderman KW, Hilton S et al. Percutaneous transluminal angioplasty for Takayasu’s arteritis. J Can Assoc Radiol 1982; 33: 205–7 Khalilullah M, Tyagi S, Lochan R et al. Percutaneous transluminal balloon angioplasty of the aorta in patients with aoritis. Circulation 1987; 76: 590–600 Kumar S, Mandalam KR, Rao VR et al. Percutaneous transluminal angioplasty in non specific aortoarteritis (Takayasu’s disease): Experience of 16 cases. Cardiovasc Intervent Radiol 1989; 12: 321–5 Tyagi S, Kaul UA, Nair M et al. Balloon angioplasty for renovascular hypertension in Takayasu’s arteritis. Am Heart J 1993; 125: 1386–93 Tyagi S, Jolly N, Khalilullah M. Multivessel angioplasty in Takayasu’s arteritis. Indian Heart J 1993; 45: 215–7 Sharma, Shrivastava S, Kothari SS et al. Influence of angiographic morphology on the acute and longer-term outcome of percutaneous transluminal angioplasty in patients with aortic stenosis due to nonspecific aortitis. Cardiovasc Intervent Radiol 1994; 17: 147–51 Tyagi S, Kaul UA, Satsangi DK et al. Percutaneous transluminal angioplasty for renovascular hypertension in children: Initial and long-term results. Pediatrics 1997; 99: 44–9 Sharma S, Gupta H, Saxena A et al. Results of renal angioplasty in nonspecific aortoarteritis (Takayasu disease). J Vasc Intervent Radiol 1998; 9: 429–35 Sharma S, Sharma S, Bahal VK et al. Stent treatment of obstructing dissection after percutaneous transluminal angioplasty of aortic stenosis caused by non specific aortitis. Cardiovasc Intervent Radiol 1997; 20: 377–9 Tyagi S, Verma PK, Kumar N et al. Stent angioplasty for relief of chronic mesenteric ischemia in Takayasu arteritis. Indian Heart J 1997; 49: 315–8 Gu ZM, GuiL, Wang JH et al. Role of aorto-angioplasty in hypertension caused by Takayasu’s arteritis. Chinese Med J 1991; 104: 363–8 Joseph G. Krishnaswami S, Barush DK et al. Transseptal approach to aortography and carotid artery stenting in pulseless disease. Cathet Cardiovasc Diagn 1997; 40: 416–20 Abraham KA, Rajagopal S. Balloon angioplasty and stenting of unprotected left main in aortoarteritis. In: Henry M, Amor M, ed. Tenth International Course Book of Peripheral Vascular Intervention. Paris: Europa Edition, 1999; 427–30 Joseph G, Kumar S. Angioplasty and stenting for supra-aortic vessels and descending thoracic aorta in inflammatory disease (aortoarteritis). In: Henry M, Amor M, ed. Tenth International Course Book of Peripheral Vascular Intervention. Paris: Europa Edition, 1999; 431–7 Dong Z, Li S, Lu X. Percutaneous transluminal angioplasty for renovascular hypertension in arteritis: Experience in China. Radiology 1987; 162: 477–79 Tyagi S, Arora R. Angioplasty and stenting of abdominal aorta, renal and iliac arteries in primary inflammatory aortoarteritis. In: Henry M, Amor M, ed. Tenth International Course Book of Peripheral Vascular Intervention. Paris: Europa Edition, 1999: 445–55
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39. 40.
Rath PC, Lakshmi G, Henry M. Percutaneous transluminal angioplasty using a cutting balloon for stenosis of the arch vessels in aortoarteritis. Indian Heart J 2004; 54: 54–7 Rajagopal S. Inflammatory arteritis in supra-aortic vessels: endovascular treatment. In Henry M, Ohki T, Polydorou A, Strigaris K, Kiskinis D, eds. Angioplasty and Stenting of the Carotid and Supra-aortic Trunks. London and New York: Martin Dunitz, 2004: 683–7
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Vascular involvement in Behçet’s disease TW Kwon
Introduction Behçet’s disease is a chronic recurrent inflammatory disorder usually affecting many organs. The disease derives its name from Hulusi Behçet,1 a Turkish dermatologist, who in 1936 described the symptomatic triad of oral and genital ulcers, and uveitis. The clinical manifestations include a variety of skin and mucosal lesions, uveitis that may result in blindness, a wide range of central nervous system abnormalities, major vessel disease, musculoskeletal problems, and gastrointestinal symptoms. Patients are usually 20–30 years old at the time of onset of the disease.2 Behçet’s disease has a worldwide distribution but has been shown to be prevalent in the Mediterranean countries, the Middle East, and Far East Asia. Turkey has the highest prevalence: 80–370 cases per 100,000 of population. The prevalence in Japan, Korea, China, Iran, and Saudi Arabia ranges from 13.5 to 20 cases per 100,000, whereas it is lower in Western countries: 0.64 per 100,000 in the UK and 0.12–0.33 per 100,000 in the US.3–6 The etiology is unknown. Behçet’s disease is associated with the histocompatibility type HLA-B51. This allele is an important contributor to the risk of Behçet’s disease in areas where the disease is prevalent but not in Western countries. The allele also affects the severity of disease, since it is more common among patients with posterior uveitis or progressive central nervous system disease than those with milder disease.4–9 Microbial infection has been implicated in the development of Behçet’s disease. However, none of these infectious agents have been proven to cause Behçet’s disease. In fact, the results of a series of studies led to the hypothesis that ubiquitous antigens, including heat shock protein of microorganisms, may trigger cross-reactive autoimmune responses in patients with Behçet’s disease.4,10 The spectrum of vascular disease is broad and unique in Behçet’s disease. It is one of the few types of vasculitis that can involve large vessels, both arteries and veins. The frequency of vascular involvement in Behçet’s disease is estimated to range from 2 to 46% and it is four to five times more common in men. 11–16 Vascular lesions seen in Behçet’s disease are composed of venous thrombosis, arterial thrombosis, and arterial aneurysm. Venous thrombosis is more common than other arterial lesions. Deep veins of the lower extremity are the most common sites of venous thrombosis, which constitute more than 60% of vascular lesions. 2,16,17 Inflammation of the aorta, pulmonary, and peripheral arteries is one of the most
serious complications of Behçet’s disease and is responsible for the majority of deaths.2,18 Its prevalence is about 1.5–3%, and is less common than venous disease.2,19 Urayama et al.20 found 22 cases with arterial involvement out of 868 cases of Behçet’s disease during their 40-year study period, and Hamza2 reported 2.2% of arterial involvement in his study. Aneurysm is reported to be more common than occlusion. Aneurysm formation is seen in almost all named arteries but the abdominal aorta is the most common site (Figure 86.1). Rupture is the most common complication of aneurysm and the most common cause of vascular-related death.2,13,21,22 Multiple aneurysms with Behçet’s disease are relatively common (Figure 86.2).23,24 Occlusive disease runs a relatively benign clinical course.21 Occlusive lesions occur in all types of arteries. However, the pulmonary artery is the most frequent location of arterial occlusion, followed in frequency by the subclavian, radial, and popliteal arteries.2 Diagnosis of Behçet’s disease is clinical. There is no universally accepted diagnostic test so the diagnosis of Behçet’s disease has relied on identification of several of its more typical clinical features.25 At present, the diagnosis is made on the basis of the criteria proposed by the International Study Group (ISG) for Behçet’s Disease in 1990 (Table 86.1). Basically, the criteria classify the manifestations of Behçet’s disease into major and minor criteria based not on their clinical severity but on their frequency, although that differs in different parts of the world. Vascular disease is one of the minor criteria for the diagnosis of Behçet’s disease in the ISG proposal and occurs late in the course of the disease, usually 5–10 years after the diagnosis.18,21 However, at onset it may present with manifestations of the vascular involvement instead of the classical triad, so the diagnosis must be made based on a variety of clinical pictures including the chronic flow of the disease.26–29 Schirmer et al.28 have suggested that large-vessel involvement should be added as a criterion because, in practice, many clinicians use these criteria for diagnostic purposes, and it would be valuable in the diagnosis of the atypical patient with early vessel involvement. In prevalent areas, when a patient is relatively young and shows an unusual location of the aneurysm or recurrent aneurysm, Behçet’s disease should be considered. The pathology and pathogenesis of vascular lesions in Behçet’s disease have been well documented. Vascular injuries, hyperfunction of neutrophils, and autoimmune responses are characteristics of Behçet’s disease.30 Inflammatory obliterative endarteritis of the vasa vasorum with immune deposition 743
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Table 86.1 Diagnostic criteria for Behçet’s disease proposed by the International Study Group for Behçet’s disease in 1990
A
RI
LI
Figure 86.1 Abdominal aortic aneurysm in Behçet’s disease. Saccular type of aneurysm and marked peri-aortic inflammation are shown (white arrows). (A: Abdominal aorta, IVC: Inferior vena cava, LI: left iliac artery, RI: right iliac artery).
causes destruction of the media and loss of elastic tissue resulting in the formation of a true aneurysm, or perforation of the vessel wall, triggering development of a false aneurysm or arterial dissection.31 Venous thrombosis may be involved by two mechanisms: vasculitis of the large veins and hypercoagulability. Panvasculitis, which is characteristic of Behçet’s disease, manifests as lymphocytic inflammatory infiltrates mainly involving the media and the adventitia at the acute phase and as a marked fibrotic reaction later on.32,33 Vessel occlusion associated with Behçet’s disease can also be attributed to intimal thickening and endothelial dysfunction caused by vasculitis. High plasma levels of von Willebrand factor, depression of prostacyclin production (PGI2) due to endothelial cell dysfunction,33,34 high endothelin 1 levels,35 low levels
A
A
Figure 86.2 Double aortic aneurysms in Behçet’s disease are shown (As). Lower one is ruptured and surrounding hematoma is seen (black circle).
Major symptoms
Minor symptoms
Recurrent genital ulcerations Aphthous ulceration or scarring Eye lesions Skin lesions Positive pathergy test
Gastrointestinal features Arthritis Family history Arthralgia Cerebral nervous system involvement Arterial occlusion or aneurysms Epididymitis Deep vein thrombosis Subcutaneous phlebitis
Basically, the criteria classify the manifestations of Behçet’s disease into major and minor criteria based on their frequency, although that differs in different parts of the world, and not on their clinical severity. At present, the diagnosis is made when recurrent oral ulceration (minor aphthous, major aphthous, or herpetiform ulceration observed by physician or patient, recurring at least three times in one 12-month period) plus two of the major symptoms exist.
of acquired protein S,36 or the presence of anticardiolipin antibodies37 has been reported to be related to the underlying thrombotic diathesis that might predispose to the development of occlusive changes in vessels in Behçet’s disease. The clinical course of Behçet’s disease is characterized by remissions and exacerbations that generally abate in intensity with the passage of time. There is still no definitive medical treatment, and there is no widely accepted way of assessing disease activity.38,39 In venous thrombosis, anticoagulants are used in combination with anti-inflammatory drugs. Corticosteroids can be given during flares of venous disease. First-line treatment with a combination of immunosuppressants, glucocorticoids, and anticoagulants seems superior to glucocorticoids plus anticoagulants in the treatment of superior vena cava syndrome, multiple extracranial or other large arterial occlusions.19,40,41 Caution is in order when using anticoagulants in patients with pulmonary artery aneurysms, given the risk of fatal hemoptysis.42 Because of a high rupture risk, aneurysms should be repaired in time. It has been reported that rupture is not correlated to the size of aneurysm in Behçet’s disease.43 Previously, open surgical repair was the only definitive treatment for vascular lesions, such as aneurysms in patients with Behçet disease,44,45 but the success rate of surgical management has not been high because a false aneurysm at the anastomotic site and/or graft occlusion often occurs after surgical repair. Of all the vascular lesions, aneurysm is the most complicated and challenging pathology for the vascular surgeon because of the technical difficulties and recurrent aneurysm. Since the first report of an abdominal aortic aneurysm due to Behçet’s disease, by Mishima46 in 1961, various authors have reported a high rate of recurrence of true or false aneurysms at the anastomotic site, aneurysm formation, and occlusions in other vessels.47,48
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Vascular involvement in Behçet’s disease Many attempts have been made to surgically manage these serious arterial lesions. Some authors have suggested performing a bypass with anastomoses on “intact” arteries, far away from the aneurysms, or performing an extra-anatomic bypass. 49,50 Others suggested simple aneurysmectomy or closure of the arterial defect by direct suture or patching. Arterial protection by prosthetic wrapping was also reported.51 Some authors insisted that the establishment of remission by the use of glucocorticoids before surgical intervention can decreases the incidence of post-operative anastomotic complications.40 Some authors supported a surgical approach with simple ligature of the artery to avoid complications of reconstructive surgery in peripheral arterial lesions.21 However, post-operative recurrence has still been noted above 30%. Recently, stent-graft treatment has been reported as one of the treatment modalities for an aneurysm to avoid a recurrent aneurysm at the anastomosis site which was commonly seen following surgical treatment (Figure 86.3).43,52,53 The main advantages of endovascular intervention are lower mortality rates (0.6–3.5%) and higher success rates.54 However, the experience with endovascular treatment in this specific subset of patients is usually limited, and it is not
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possible today to compare the results of these two modalities in Behçet patients. Furthermore, one of the most important aspects of Behçet’s disease is aneurysmal arteriopathy and the major problem of this complication is its tendency to develop recurrent false aneurysms at anastomotic and traumatic sites, such as angiographic punctures (Figure 86.4). 15,21,32,51,55,56 Another post-operative complication is graft occlusion.15,21 Systemic procoagulative tendency and intimal thickening caused by inflammation of native arteries may be an explanation for the high incidence of post-operative graft occlusion.57 Hosaka et al.57 reported that graft occlusion occurred in spite of anticoagulation or antiplatelet therapy so more intense preventive measures, including high-intensity anticoagulant therapy, might be necessary to prevent graft occlusion in patients with Behçet’s disease.
Summary Behçet’s disease is a chronic recurrent inflammatory disease usually affecting many organs. It is one of the few types of vasculitis that can involve large vessels, both arteries and veins.
(a)
(b)
(c)
(d)
Figure 86.3 Stent graft treatment in abdominal aortic aneurysm in Behçet’s disease: (a) saccular type of abdominal aortic aneurysm; (b) infrarenal aortic straight stent graft treatment; (c) complete exclusion of abdominal aortic aneurysm following stent-graft treatment at immediate postoperative follow-up CT scan; (d) disappearance of abdominal aortic aneurysm following stent-graft treatment at post-operative 2-year follow-up CT scan.
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RA
AA
(a)
(b)
Figure 86.4 Recurrent false aneurysms at anastomotic and traumatic sites: (a) anastomotic aneurysm (AA) following aortic graft interposition; (b) recurrent aneurysm (RA) following aortic stent graft treatment.
The spectrum of vascular disease is broad and unique in Behçet’s disease. The prognosis of arterial Behçet’s disease is poor, because aneurysm, of which rupture is the most common presentation, is the most common arterial lesion in patients with Behçet’s disease involving large arteries, and a recurrent aneurysm at the anastomosis site or remote artery is commonly seen. Furthermore, there is no definitive treatment modality proven to prevent recurrent aneurysms at the anastomosis site or remote artery. Endovascular interventions may be one of the treatment modalities but the result needs
long-term follow-up. Management, in the absence of knowledge of a cure of a condition of uncertain etiology, must consist of the control of symptoms and suppression of the inflammatory vasculitis. Immunosuppressant and anti-inflammatory medication should be conducted for suppression of the vasculitis.39 However, the role of immunosuppressant and anti-inflammatory medication for the prevention of the recurrent arterial lesion following intervention in Behçet’s disease also needs to be further evaluated.58
REFERENCES 1. 2. 3.
4. 5.
6. 7. 8.
Behçet H. "Über rezivierende, aphtöse, durch ein Virus verursachte Geschwiire am Mund, am Auge und an den Genitalien in [German]". Dermat Wochenschr 1937;105:1152–7 Hamza M. Large artery involvement in Behçet’s disease. J Rheumatol 1987;14(3):554–9 Kastner DL. Intermittent and periodic arthritic syndromes. In: Koopman WJ, ed. Arthritis and allied conditions: a textbook of rheumatology. 13th ed. Vol. 1. Baltimore: Williams & Wilkins, 1997;1279–306 Kaklamani VG, Variopoulos G, Kaklamanis PG. Behcet’s disease. Semin Arthritis Rheum 1998; 27:197–217 Nakae K, Masaki F, Hashimoto T, et al. Recent epidemiological features of Behcet’s disease in Japan. In: Wechsler B, Godeau P, eds. Behcet’s disease. Amsterdam: Excerpta Medica 1993; 145-51 Zouboulis CC, Kotter I, Djawari D, et al. Epidemiological features of Adamantiades-Behcet’s disease in Germany and in Europe. Yonsei Med J 1997; 38(6):411–22 Ohno S, Ohguchi M, Hirose S, et al. Close association of HLABw51 with Behcet’s disease. Arch Ophthalmol 1982;100(9): 1455–8 Inaba G. Clinical features of neuro-Behcet’s syndrome. In: Lehner T, Barnes CG, eds. Recent advances in Behcet’s disease. London: Royal Society of Medicine Services, 1986; 235–46
9. 10. 11.
12. 13. 14. 15. 16.
Meador R, Ehrlich G, and Von Feldt JM. Behçet’s disease immunopathologic and therapeutic aspects. Curr Rheumatol Rep 2002; 4(1): 47–54 Lehner T. The role of heat shock protein, microbial and autoimmune agents in the aetiology of Behcet’s disease. Int Rev Immunol 1997;14(1):21–32 Muftuoglu AU, Yurdakul S, Yazici H et al. Vascular involvement in Behçet’s disease – a review of 129 cases. In: Lehner T, Barnes CG, eds. Recent Advances in Behçet’s Disease. London: Royal Society of Medicine, 1986;103:225–60 Kuzu MA, Ozaslan C, Koksoy C, et al. Vascular involvement in Behçet’s disease: 8-year audit. World J Surg 1994;18(6): 948–53 Gurler A, Boyvat A, and Tursen U. Clinical manifestations of Behçet’s disease: an analysis of 2147 patients. Yonsei Med J 1997; 38(6): 423–7 Koc Y, Gullu I, Akpek G, et al. Vascular involvement in Behcet's disease. J Rheumatol 1992;19(3): 402–10 Le Thi Huong D, Wechsler B, Papo T, et al. Arterial lesions in Behcet's disease. A study in 25 patients. J Rheumatol 1995;22(11): 2103–13 Tohme A, Aoun N, El-Rassi B, et al. Vascular manifestations of Behcet’s disease Eighteen cases among 140 patients. Joint Bone Spine 2003;70(5): 384-9
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27. 28. 29. 30. 31. 32. 33. 34.
35. 36. 37.
Kabbaj N, Benjelloun G, Gueddari FZ, et al. Vascular involvement in Behcet’s disease. Based on 40 patients records. J Radiol 1993;74(12):649–56 Lie JT. Vascular involvement in Behçet’s disease: Arterial and venous and vessels all sizes. J Rheumatol 1992;19(3): 341–3 Sagdic K, Ozer ZG, Saba D, et al. Venous lesions in Behçet’s disease. Eur J Vasc Endovasc Surg 1996;11(4): 437–40 Urayama A, Sakuragi S, Sakai F et al. Angio- Behçet’s syndrome. In: Inaba G ed. International Symposium on Behçet’s disease. Tokyo: University of Tokyo Press. 1982:171–6 Tüzün Y, Besirly K, Sayin A, et al. Management of aneurysms in Behçet’s syndrome: an analysis of 24 patients. Surgery 1997; 121(2):150–6 Okita Y, Ando M, Minatoya K, et al. Multiple pseudoaneurysms of the aortic arch, right subclavian artery, and abdominal aorta in a patient with Behcet’s disease. J Vasc Surg 1998;28(4):723–6 Yamana K, Kosuga K, Kinoshita H, et al. Vasculo-Behçet's disease: immunological study of the formation of aneurysm. J Cardiovasc Surg 1988;29(6):751–5 Bartlett ST, McCarthy WI, Palmer AS, et al. Multiple aneurysms in Behçet's disease. Arch Surg 1988;123(8):1004–8 International Study Group for Behçet's disease. Criteria for diagnosis of Behçet's disease. Lancet 1990;335(8697):1078–80 Tunc R, Keyman E, Melikoglu M, et al. Target organ associations in Turkish patients with Behcet’s disease: a cross-sectional study by exploratory factor analysis. J Rheumatol 2002;29(11): 2393–6 Ates A, Tiryaki Aydintug O, Duzgun N, et al. Behcet’s disease presenting as deep venous thrombosis and priapism. Clin Exp Rheumatol 2004;22(1):107-9 Schirmer M, Calamia KT, and O’Duffy JD. Is there a place for large vessel disease in the diagnostic criteria of Behcet’s disease? J Rheumatol 1999;26(12): 2511-2 Silman A, Gul A. Is there a place for large vessel disease in the diagnostic criteria of Behcet’s disease? J Rheumatol 2000;27(8): 2050–1 Sakane T, Taneko M, Suzuki N, et al. Behcet’s disease. New Engl J Med 1999;341(17):1284–91 Matsumoto T, Vekusa T, and Fukuda Y. Vasculo-Behçet's disease: a pathologic study of eight cases. Hum Pathol 1991;22(1): 45–51 Ko G-Y, Byun JY, Choi BG, et al. The vascular manifestations of Behcet’s disease: angiographic and CT findings. Br J Radiol 2000; 73(876):1270–4 Hamza M. Maladie de Behcet. 4th ed. In: Kahn MF, editor. Maladies et syndromes systemiques. Paris: Flammarion MedecineSciences 2000; 883–924 Ozoran K, DuzgunN, Gurler A, et al. Plasma von Willebrand factor, tissue plasminogen activator, plasminogen activator inhibitor, and antithrombin III levels in Behcet’s disease. Scand J Rheumatol 1995;24(6):376–82 Ural AU. Increased plasma endothelin-1 levels in active Behcet’s disease. Clin Rheumatol 1997;16(1):59–61 Guermazi S, Hamza M, and Dellagi K. Protein S deficiency and antibodies to protein S in patients with Behcet’s disease. Thromb Res 1997;26:197–204 Tokay S, Direskeneli H, Yurdakul S, et al. Anticardiolipin antibodies in Behcet’s disease: a reassessment. Rheumatology (Oxford) 2001; 40(2):192–5
38. 39. 40. 41. 42. 43. 44. 45. 46. 47. 48. 49. 50. 51. 52. 53.
54. 55. 56. 57. 58.
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Hamuryudan V, Fresko I, Direskeneli H, et al. Evaluation of the Turkish translation of a disease activity form of Behçet's syndrome. Rheumatology (Oxford) 1999;38(8):734–6 Barnes CG and Yazici H. Behcet’s syndrome. Rheumatology (Oxford) 1999;38(12):1171–6 Kalco Y, Basaran M, Aydin U, et al. The surgical treatment of arterial aneurysms in Behcet’s disease: a report of 16 patients. J Vasc Surg 2005;42(4): 673–7 Ehrlich GE. Vasculitis in Behcet’s disease. Int Rev Immunol 1997;14(1): 81–8 Hamuryudan V, Yurdakul S, Moral F, et al. Pulmonary arterial aneurysms in Behcet’s syndrome: a report of 24 cases. Br J Rheumatol 1994;33(1): 48–51 Vasseur MA, Haulon S, Beregi JP, et al. Endovascular treatment of abdominal aneurysmal aortitis in Behcet’s disease. J Vasc Surg 1998;27(5): 974–6 Sener E, Bayazit M, Gol MK, et al. Surgical approach to aneurysms with Behçet's disease. Thorac Cardiovasc Surg 1992; 40(5): 297–9 Barlas S. Behçet's disease: an insight from a vascular surgeon’s point of view. Acta Chir Belg 1999;99(6): 274–81 Mishima Y, Ishikawa K, Kawase S. Behçet's syndrome with aneurysm (abstract). Jpn Circ J 1961;25:1211 Okada K, Eishi K, Takamoto S, et al. Surgical management of Behçet's aortitis: a report of eight patients. Ann Thorac Surg 1997; 64(1):116–9 Sasaki S, Yasuda K, Takigami K, et al. Surgical experiences with peripheral arterial aneurysms due to vasculo-Behçet's disease. J Cardiovasc Surg (Torino) 1998; 39(2):147–50 Chaillou P, Patra P, Noel SF, et al. Behçet's disease revealed by double peripheral arterial involvement. Ann Vasc Surg 1992;6(2):160–3 Sherif A, Stewart P, Mendes D. The repetitive vascular catastrophes of Behçet's disease: a case report with review of the literature. Ann Vasc Surg 1992;6(1): 85–9 Freyrie A, Paragona O, Cenacchi G, et al. True and false aneurysms in Behçet's disease: Case report with ultrastructural observations. J Vasc Surg 1993;17(4): 762–7 Park JH, Chung JW, Joh JH, et al. Aortic and Arterial Aneurysms in Behçet Disease: Management with Stent-Grafts: Initial experience. Radiology 2001;220(3):745–50 Bonnotte B, Krause D, Fanton AL, et al. False aneurysm of the internal carotid artery in Behçet’s disease: successful combined endovascular treatment with stent and coils (letter). Rheumatology (Oxford) 1999;38(6):576–7 Kasirajan K, Marek JM, and Langsfeld M. Behcet’s disease endovascular management of a ruptured peripheral arterial aneurysm. J Vasc Surg 2001;34(6):1127–9 Kingston M, Ratcliffe JR, Altree M, et al. Aneurysm after arterial puncture in Behcet's disease. Br Med J 1979;30:1766–7 Kwon TW, Kim DK, Yang SM, et al. Ruptured renal artery stump aneurysm in a renal autotransplanted Behçet’s disease patient. Yonsei Med J 2003;44(5): 943–5 Hosaka A, Miyata T, Shigematsu H, et al. Long-term outcome after surgical treatment of arterial lesions in Behcet disease. J Vasc Surg 2005;42(1):116–21 Kwon TW. Treatment results of aneurysms in Behcet’s disease(abstract). Proceedings of the 7th International Congress of the Asian Society for Vascular Surgery, Kuala Lumpur, 2006;34
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Potential of endovascular surgery in the treatment of patients with ischemic heart disease associated with other arterial pools’ pathology LB Bockeria, BG Alekyan, Yu I Buziashvili, EZ Golukhova, TG Niritina, NP Mironov, AV Ter-Akopyan, NV Zakarian, and AV Staferov
Introduction Atherosclerosis is a systemic disease involving different segments of the human arterial system. Physicians have long noted the high frequency rate of “associated” atherosclerotic lesions in patients with a dominating clinical picture of one pool’s lesion.1–3 With accounts of the severe clinical state of patients with multifocal atherosclerosis, as well as of a high percentage of complications developing directly after surgical treatment, endovascular interventions became the standard practice for this category of patients.4
Ischemic heart disease associated with internal carotid artery pathology Previously, stenting of the carotid arteries became a real alternative to carotid endarterectomy, particularly in patients with severe carotid arterial stenoses associated with concomitant diseases; that is, high-surgical-risk patients.5 With a high risk of stroke and acute myocardial infarction development after single-stage as well as after multi-stage operations in these severely ill patients, it is possible to perform endovascular interventions on coronary and carotid arteries. Material and methods This study comprised 60 patients who underwent internal carotid artery stenting. The first group comprised 35 patients who also underwent coronary stenting. The second group comprised 25 patients, who underwent aortocoronary bypass surgery 39 ± 22 days after internal carotid artery stenting. An asymptomatic course of cerebrovascular pathology was noted in 34 (57%) patients, while various symptoms of cerebrovascular insufficiency were noted in 26 (43%) patients. Transient ischemic attacks, as well as the symptoms of dyscirculatory encephalopathy, were noted in 19 (73%) patients.
Seven (27%) “symptomatic” patients had a history of ischemic stroke. After endovascular intervention on carotid arteries, 14 (56%) patients assigned to functional class IV and 11 (44%) patients assigned to functional class III of the CCS classification, underwent aortocoronary bypass surgery. Associated endovascular interventions on coronary arteries were performed in 11 (31%) patients assigned to functional class IV, in 16 (46%) patients assigned to functional class III, and in 8 (23%) patients with unstable angina. Left main coronary artery stenosis was revealed in 2 patients (3.3%). Three-vessel lesion was revealed in 32 (53.3%) patients, two-vessel lesion in 26 (43.3%) patients, and single-vessel lesion in 2 (3.3%) patients. One coronary artery was stented in 2 (6%) of 35 patients who underwent endovascular intervention on the coronary as well as on the carotid arteries. Two arteries in 19 (54%) and 3 coronary arteries were stented in 14 (40%) patients. In all, 82 arteries were stented. Among them the left anterior descending artery (LAD) was stented in 33 (40%) cases, the right coronary artery (RCA) in 28 (34%) and the arteries of the circumflex branch (CxB)/obtuse margin branch (OMB) system in 21 (26%) cases. In 8 (13%) patients left ventricular ejection fraction did not exceed 35%, 4 (7%) patients had rhythm disturbances and 9 (15%) had severe diabetes mellitus. Bilateral stenoses of the internal carotid artery were seen in 2 patients. In one patient ischemic heart disease and tight mitral stenosis were associated with atherosclerosis of the lower limb arteries and chronic obstructive lung disease. In another patient with a history of aortocoronary bypass surgery and endarterectomy from the right internal carotid artery, hemodynamically significant asymptomatic stenosis of the left internal carotid artery was associated with abdominal aortic aneurysm. This patient underwent stent-grafting of the abdominal aortic aneurysm and stenting of the left internal carotid artery at different stages of treatment (Figure 87.1).
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(c)
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Figure 87.1 Angiogram of a patient with multifocal atherosclerosis, ischemic heart disease, abdominal aortic aneurysm, and stenosis of the left internal carotid artery (ICA). As a first stage of treatment the operation of aortocoronary bypass grafting and endarterectomy from the right internal carotid artery were performed. The second stage consisted of stent-grafting of the abdominal aortic aneurysm: (a) before endovascular intervention; and (b) after stent-grafting of the aneurysm with the Excluder stent-graft (Gore-Tex). CT-angiography of the abdominal aorta: (c) before endovascular intervention; and (d) after stent-grafting of the aneurysm with “Excluder” stent-graft (Gore-Tex). The third stage, performed 9 months later, consisted of stenting of the left ICA stenosis.
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Echogenic homogenous plaque
(e)
(f)
Figure 87.1, cont’d (e) before intervention (echogenic homogenous plaque); and (f) after stenting of the left ICA (Precise stent). Complete stent deployment was confirmed by duplex scanning.
The problem of staged endovascular interventions aimed at the restoration of brain- and myocardium-supplying vessels was solved in relation to the severity of the clinical picture and the degree of atherosclerotic process. In patients with unstable angina and tight stenoses of the coronary artery we advocated myocardial revascularization as the first stage with subsequent interventions in internal carotid arteries. In patients with critical stenoses of the internal carotid artery, as well as in the presence of transient ischemic attacks, the first stage of treatment consisted of endovascular interventions aimed at the restoration of brain blood supply, which could also serve as a preparatory step for the second stage: aortocoronary bypass grafting. In 57 (95%) patients various brain-protective devices were used during the stenting of the internal carotid artery. In 46 cases we used the Angioguard (Cordis) device, in 3 the Percusurge (Medtronic), in 5 the Accunet (Guidant), in 2 the EPI (Boston Scientific), and in 1 case the Emboshield (Abbott) devices. In 3 cases the stenting of the internal carotid artery was performed before the introduction of brain-protecting devices into clinical practice. The following stents were used in the internal carotid artery: self-expanding stents (Smart and Precise (Cordis)), the Zilver (Cook) stent, as well as the balloon-expanding stent Palmaz (Cordis). Coronary arteries were stented with Bx Velocity (Cordis) and Tetra (Guidant) stents, and 23 (66%) patients received drug-eluting Cypher stents (Cordis). In three patients with over 90% stenosis of the internal carotid artery coronary balloons 3.0–3.5 mm were used for predilatation. Results The stenting of the internal carotid artery was technically successful in 98% of cases (59 patients). In one case, the brainprotecting device could not be passed through the subtotal stenosis of the left internal carotid artery. The mean degree of residual stenosis after stenting of the internal carotid arteries
decreased from 68.7 ± 7.2 to 8.3 ± 3.5%. Clinical symptoms of brain ischemia also regressed in 19 symptomatic patients. Coronary stenting was technically successful in 94% of cases. After coronary stenting positive dynamics was noted in most cases – the clinical picture of angina with functional class III persisted in 2 (6%) patients, functional class II in 5 (14%), and in 28 (80%) patients no clinical symptoms of angina were seen. Table 87.1 presents the rate of 30-day mortality, stroke, and/or myocardial infarction. One of the patients who underwent stenting of the internal carotid and the coronary arteries developed non-Q AMI 3 days after the intervention on the left internal carotid artery. Emergency PTCA and stenting of severe stenosis of the LAD were performed (Figure 87.2). Another patient from the same group had clinical signs of minor stroke after stenting of the left internal carotid artery. One patient with severe threevessel coronary disease, occlusion of the left internal carotid artery, and 80% stenosis of the right internal carotid artery died from acute heart failure with marked hypotension 5 hours after simultaneous stenting of the right carotid and three coronary arteries. Post-mortem examination revealed acute thrombosis of the LAD. In the group of patients undergoing stenting of the internal carotid artery combined with aortocoronary bypass surgery
Table 87.1 Results of different interventions in patients with IHD associated with internal carotid artery pathology (30 days)
30 days MI Minor stroke Mortality
Stenting of ICA + CA (n = 35) 1(2.8%) 1(2.8%) 1(2.8%)
Stenting of ICA + CABG (n = 25) 2 (8%) 1 (4%) 2 (8%)
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(d)
(b)
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(e)
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Figure 87.2 Angiogram of a patient with multifocal atherosclerosis, ischemic heart disease, exertional angina NYHA class IV (multivessel coronary disease), and stenosis of the left internal carotid artery (ICA). The first stage consisted of stenting of the left ICA: (a) stenosis of the left ICA; (b) after stenting with the Precise stent. Three days after ICA stenting the patient developed anterior non-Q AMI. Stenting of the LAD and RCA was performed: (c) before stenting of the LAD stenosis; (d) after stenting with the Cypher stent; (e) before recanalization and stenting of the RCA occlusion; and (f) after stenting with Cypher stents. (See Color plates.)
there were two cases of myocardial infarction after CABG and one minor stroke after stenting of the internal carotid artery. Two patients needed vascular operations in the site of puncture after stenting of the internal carotid artery (because of false aneurysm formation). One patient with three-vessel disease died while awaiting the second intervention (within 30 days after the stenting of the internal carotid artery). Another patient died after the operation of aortocoronary bypass surgery from non-cardiac complications (respiratory failure). Conclusion Some authors have presented the results of simultaneous hybrid operations (stenting of the internal carotid artery and aortocoronary bypass grafting), which consisted of the performance of stenting of the internal carotid artery just before the operation of aortocoronary bypass grafting.6,7 The advantages of this strategy in comparison with staged operations of endarterectomy and aortocoronary bypass grafting are the lowering of the risk of AMI development between
these two stages of revascularization. However, further large randomized trials are needed for fuller evaluation of this strategy.
Ischemic heart disease associated with vasorenal hypertension Uncontrolled hypertension or progressing of atherosclerotic stenoses of the renal arteries in patients with a stable course of ischemic heart disease can aggravate the symptoms of ischemia through the mechanism of oxygen consumption increase due to post-load increase. Revascularization of the renal artery in this group of patients can produce a positive effect and lead to the stabilization of myocardial ischemia symptoms.8,9 Materials and methods The study comprised 70 patients with significant (> 70%) stenoses of the renal arteries and drug-resistant hypertension. The data obtained during clinical and instrumental examination
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Potential of endovascular surgery in the treatment of patients with ischemic heart disease with the use of non-invasive methods enabled the determination of ischemic heart disease and the indications of selective coronary angiography in all patients. The mean age of patients was 63 ± 18 years, and mean LV ejection fraction 42 ± 18%. Hemodynamically significant stenoses of 3 coronary arteries were revealed in 24 (34%) patients, of 2 arteries in 28 (40%), and of 1 artery in 18 (26%) patients. Twenty-nine (41%) patients had angina of NYHA class IV, 23 (33%) exertional angina of NYHA class III, and 8 (11%) exertional angina of NYHA class II. Unstable angina was revealed in 10 (14%) patients. Bilateral stenoses of the renal arteries were revealed in 3 (6%) patients. The problem of staged endovascular interventions aimed at the restoration of kidneys and myocardium blood supply was decided in relation to the degree of atherosclerosis. In multiple and severe (over 75–80%) lesions of the coronary arteries associated with renal artery stenoses below 75%, we recommend performing myocardial revascularization first with subsequent interventions in the renal arteries. In patients with severe atherosclerotic changes in the renal arteries (over 80%),
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in comparison with coronary arterial stenoses, the first stage consisted of endovascular interventions aimed at the restoration of blood supply to the kidneys (Figure 87.3). The following stents were used for the stenting of the renal arteries: Perflex, Corinthian, Genesis (Cordis), Bridge (Medtronic), Radis (Sorin Biomedica). Coronary arteries were stented with the stents Bx Velocity (Cordis), Tetra (Guidant), and 46 (66%) patients received drug-eluting stents (Cypher, Cordis). Results In total, 146 arteries were stented. The stenting of the LAD was performed in 53 (36%) cases, of the RCA in 52 (36%), and of the arteries of the CxB.OMB system in 41 (28%) cases. Technical success immediately after intervention in the coronary arteries was noted in 98% of cases. After endovascular interventions the LV ejection fraction increased from 42 ± 18 to 48 ± 2.8%. Prior to endovascular surgery 19 (36%) patients were in NYHA class IV, 16 (30%) in NYHA class III, 8 (15%) in NYHA class II, and 10 (19%) patients
(a)
(b) Figure 87.3 Angiograms of a patient with two-vessel coronary disease associated with vasorenal hypertension and stenosis of the left renal artery. The first stage of treatment consisted of restoration of the blood flow in the left renal artery. (a) Critical ostial stenosis of the left renal artery, before the intervention. (b) After endovascular intervention and implantation of “Genesis” stent. Complete deployment of the stent was confirmed by intravascular ultrasound investigation. The second stage consisted in restoration of the coronary blood flow. (See Color plates.)
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(e)
(d)
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Figure 87.3, cont’d (c) Occlusion of the middle third of the RCA, before the intervention. (d) After RCA stenting (two Cypher stents were implanted: 3.0 × 23 mm and 2.75 × 23 mm). (e) Prolonged stenosis in the LAD, before the intervention. (f) Direct stenting of the LAD (Cypher stent, 3.0 × 33 mm). (See Color plates.)
had unstable angina. After stenting, 4 (8%) patients were in NYHA class III, 16 (30%) in NYHA class II, and 33 (62%) patients had no angina at all. In patients with combined lesions of the coronary and renal arteries, coronary endovascular interventions alone do not provide a marked clinical effect, comparable to the effect seen in patients with IHD without associated atherosclerotic lesions. It is thought that coronary intervention alone does not allow the complete recovery of patients with combined diseases. Even after successful interventions for the restoration of myocardial blood supply, the remaining hemodynamically significant stenoses of the renal arteries can lead to death or handicap in this category of patients. Endovascular methods aimed at ischemia treatment of the kidneys led to the decrease of arterial pressure in the majority of patients. This was accompanied by the improvement of patients’ general state, the disappearance of subjective symptoms reflecting the degree of hypertension syndrome, and an increase in physical activity of these patients. Angioplasty and stenting of the renal arteries were technically successful in 97.5% of cases. After endovascular interventions
in stenotic segments of the renal arteries the degree of stenosis decreased from 65.7 ± 18.4 to 7.8 ± 3.9%. We also noted a decrease in systolic (from 215 ± 24 to 137 ± 19 mmHg) and diastolic (from 142 ± 12 to 110 ± 9 mmHg) arterial pressure. Twenty-two (32%) patients had no hypertension, while improvement was noted in 38 (54%) patients. In 10 (14%) the state did not change. The number of drugs taken by the patients decreased from 2.9 prior to the procedure to 1.3 after endovascular interventions on renal arteries. In 58 patients with normal creatinine level renal function did not change. In 2 (3%) patients with increased plasma creatinine concentration, endovascular intervention on renal arteries resulted in this concentration decrease from 1.8 ± 0.45 to 1.4 ± 0.25 mg/dl. Long-term results (from 6 months to 3 years) were studied in 46 (66%) of 70 patients. Hypertension was absent in 17 (37%) patients, arterial pressure did not change in 24 (52%), and in 5 (11 %) patients arterial pressure returned to preprocedural level. No cases of renal function deterioration were seen. Control angiographic study was carried out in 19 (41%) patients. Coronary stents were permeable stents in all patients; renal in-stent restenosis occurred in 3 cases.
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Potential of endovascular surgery in the treatment of patients with ischemic heart disease The diameter of the stented renal artery in these patients was 5 mm, and renal arteries were stented because of ostial lesions. In 2 of 3 patients we used Corinthian stents (Cordis); in 1 patient, the Bridge stent (Medtronic). Balloon dilatation of the stenotic stents was performed in 2 patients. In one of them the second stent – Genisis (Cordis) – was implanted. Conclusion The restoration of blood supply to the kidneys is likely to prevent the development of chronic renal failure, heart failure with pulmonary edema, as well as of unstable angina. The decrease in arterial pressure (post-load) and preload leads to the decrease of oxygen consumption in the myocardium, which produces a positive effect in patients with pronounced coronary lesions.
Ischemic heart disease associated with lower limb ischemia Yearly mortality in patients with critical lower limbs ischemia approaches 25%, mainly due to myocardial infarction and ischemic stroke.10 At present the risk of chronic lower limb ischemia development increases in the presence of the following cardiovascular diseases: IHD, history of stroke, heart failure, and atrial flutter. Lower limb lesions often suggest the presence of multifocal atherosclerosis. Material and methods This study comprised 70 patients, who underwent endovascular interventions on the damaged segments. The main indications of the performance of minimally invasive interventions were severe ischemia of the lower limbs and pronounced myocardial ischemia, necessitating surgical treatment and making it impossible to perform a full-scale reconstructive vascular operation on the lower limb arteries. The age of patients ranged from 45 to 74 years (58.6 ± 6.2 years on average). The majority of patients (76%) had chronic IHD, 9 (13%) patients presented with different forms of acute coronary circulation disorders, 7 (10%) patients had post-infarction LV aneurysm. Three-vessel coronary disease was revealed in 39 (56%) patients, two-vessel disease in 26 (37%) and single-vessel disease in 5 (3.3%) patients with unstable angina. Angina of NYHA class IV was diagnosed in 19 (35%) of 54 patients with chronic IHD, exertional angina of NYHA class III in 21 (39%), and exertional angina of NYHA class II in 10 (26%) patients. Left ventricular ejection fraction was 44 ± 11.2% on average. A history of myocardial infarction was revealed in 18 (33%) patients with chronic IHD, 5 (9%) patients had various rhythm disturbances, and 16 (30%) had clinical signs of heart failure. Clinical signs of blood flow disturbances (intermittent claudication, pulse absence) in the aortoiliac segment were revealed in 52 (74%) patients, in the iliofemoral segment in 10 (14%), and in the femoropopliteal segment in 6 (9%) patients, while 2 (3%) patients with critical ischemia had both aortoiliac and femoropopliteal lesions confirmed by Doppler ultrasound. Bilateral lesion of aortoiliac segment was noted in 3 (6%) of 52 patients. Mean distance of intermittent claudication was 185.3 ± 120.0 m (range: 10–500 m).
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Isolated hemodynamically significant stenosis of the common iliac artery was revealed in 45 (86%) of 52 patients with lesion of the aortoiliac segment, and occlusion of the common iliac artery in 7 (14%) patients. Isolated hemodynamically significant stenosis of the external iliac artery was revealed in 4 (40%) of 10 patients with lesion of the iliofemoral segment, and occlusion of the external iliac artery in 6 (60%) patients. Stenosis of the left internal carotid artery was revealed in one patient with IHD, critical mitral stenosis, and bilateral occlusion of the aortoiliac segment. This patient underwent endovascular interventions on peripheral arteries and the left internal carotid artery at the first stage of treatment, while the second stage consisted of aortocoronary bypass grafting and mitral valve replacement (Figure 87.4). The stenting of the lower limb arteries was performed with self-expanding stent Smart (Cordis), as well as with the balloon-expandable stents Palmaz, Perflex, Corinthian (Cordis), and Jostent (Jomed). Coronary arteries were stented with the stents Crossflex, Bx Velocity (Cordis), Tetra (Guidant), S7 (Medtronic). Thirty-eight (54%) patients received drugeluting stents (Cypher, Cordis). It was impossible to perform exercise tests in these patients. Taking this fact into account, coronary angiography with angiography of peripheral arteries was performed in all patients. Results In total 174 coronary arteries were stented. LAD was stented in 65 (37%) cases, RCA in 61 (35%), and the arteries of the CxB.OMB system in 48 (28%) cases. After endovascular interventions in the coronary arteries, left ventricular ejection fraction increased on average from 39.3 ± 6.4 to 44.3 ± 4.8 %. Two patients (3%) were in NYHA class III, 18 (26%) in NYHA class II, and in 50 (71%) patients no angina was revealed. After endovascular interventions on the lower limb arteries the blood flow improved in all patients. According to the Doppler ultrasound data, the value of brachio-malleolar index rose from 0.48 to 0.92, and in the majority of patients collateral blood supply returned to the normal pathways. Long-term results were studied in 32 (46%) of 70 patients. Mean duration of the follow-up was 5.3 ± 1.6 years. Two patients died from progressive cardiovascular insufficiency, one patient from hemorrhagic stroke. After coronary stenting angina persisted in 3 (9%) patients, in 7 (22%) cases a significant improvement was noted, and 22 (69%) patients were completely free from angina. The performed exercise testing showed a high physical tolerance of patients. Two of them (6% were in NYHA class III, fewer than 7 (22%) in NYHA class II. Mean LV ejection fraction was 42.5 ± 6.1 %. Doppler ultrasound revealed normal blood supply in 24 (75%) of 32 patients, changes in normal blood supply in 2 (6%), and collateral blood supply in 6 (19%) patients. Control angiographic examination was performed in 11 (34%) of 32 patients on average 4.4 ± 1.2 years after the intervention. Coronary stents were permeable in 9 (82%) of 11 patients. In 2 (18%) patients we revealed hemodynamically significant restenosis of the ordinary metallic stents. These patients underwent repeated endovascular intervention with the implantation of Cypher stents. In-stent restenosis in the lower limb arteries was revealed in
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“Smart”
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(b)
“Smart”
(c)
(e)
(d)
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Figure 87.4 Angiogram of a patient with multifocal atherosclerosis, rheumatism, mitral valve stenosis, ischemic heart disease, occlusion of both iliofemoral segments, and stenosis of the left internal carotid artery (ICA) The first stage consisted of endovascular intervention on the lower limb arteries. (a) Occlusion of the right iliofemoral segment, before the intervention. (b) After recanalization, balloon dilatation and stenting (Smart stent). (c) Occlusion of the left iliofemoral segment, before the intervention. (d) After recanalization, balloon dilatation, and stenting (Smart stent). The second stage, performed in 2 days, consisted of stenting of asymptomatic stenosis of the left ICA. (e) Critical stenosis of the left ICA, before the intervention. (f) After Precise stent implantation. The third stage consisted of mitral valve replacement combined with aortocoronary bypass grafting. (See Color plates.)
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Conclusion The evaluation of the state of the myocardium and supplying coronary artery, as well as of the lower limb arteries in patients with pronounced lower limb ischemia allows us to determine not only the indications for intervention in coronary and peripheral arteries, but also the stage order of their performance.
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3. 4.
5.
Avtandilov G.G. Dynamics of Atherosclerotic Process in Humans. Moscow: Meditzina, 1979 Bourakovsky VI, Rabotnikov VS, Spiridonov AA et al. Surgical treatment of IHD, associated with atherosclerosis of the major arteries – one of the main problems of cardiovascular surgery. Kardiologia 1991; 31(7): 5–7 Ashor GW, Meyer BW et al. Coronary artery disease. Surgery in 100 pts. 65 years of age and older. Arch Surg 1973; 107: 30–3 Bockeria LB, Alekyan BG, Ter-Akopyan AV et al. Endovascular surgery in the treatment of patients with coronary artery disease associated with pathology of ICA. Grudnaya I serdechno- sosudistaya khirurgia (Thorac and Cardiovasc Surg). 2006; 6: 51–6 Yadav JS, Wholey MH, Kuntz RE et al. Protected carotid-artery stenting versus endoarterectomy in high-risk patients. N Engl J Med 2004; 351: 1493–501
6. 7. 8.
9. 10.
Alekyan BG, Yu I, Buziashvili SG et al. Successful stenting of stenotic internal carotid artery in a patient with IHD. Angiologia i sosudistaya khirurgia 1999; 3: 112–5 Chiariello L, Tomai F, Zeitani J, Versaci F. Simultaneous hybrid revascularization by carotid stenting and coronary artery bypass grafting. Ann Thorac Surg 2006; 81:1833–5 Bockeria LB, Alekyan BG, Spiridonov AA, et al. Endovascular surgery in multivascular atherosclerosis. Textbook of peripheral vascular interventions edited by R. Heuser and M. Henry. MD Martin Dunitz Taylor & Francis group. London 2004; 363–9 Valentine RJ, Clagett GP, Miller GL et al. The coronary risk of unsuspected renal artery stenosis. J Vasc Surg 1993 18: 433–40 Dormandy JA, Heeck L, Vig S. The fate of patients with critical leg ischemia, Semin Vasc Surg 1999; 12: 142–7
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SECTION XIV Treatments for restenosis
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Pathophysiology of restenosis E Kedhi, J-F Tanguay, and L Bilodeau
Definition Percutaneous transluminal angioplasty (PTA) in the last decade has become the basis of interventional vascular therapy. However, despite significant technique advancement, the reoccurrence of significant lumen area impairment after successful angioplasty, referred to as restenosis, remains the major limitation of vascular dilatation techniques. Reoccurrence of impaired lumen area is the result of arterial wall healing due to mechanical injury caused by the intervention. The underlying mechanism includes: acute elastic recoil, local thrombotic and inflammatory reactions leading to intimal hyperplasia and negative arterial remodeling.1 If a permanent stent is implanted during the angioplasty procedure, the in-stent restenosis is entirely due to intimal hyperplasia, because the scaffolding property of metallic stents eliminate elastic recoil and the negative remodeling process. Restenosis can be defined morphologically, by means of any imaging technique that can give an accurate estimation of lumen impairment, or clinically. Morphological evaluation of restenosis has been classically performed by means of quantitative computerized angiographic analysis (QCA). Although other imaging modalities such as intravascular ultrasound, duplex sonography, angio-computed tomography (CT) scanning and magnetic resonance imaging are being used for this purpose, as described elsewhere in this book, QCA remains the most commonly used technique in routine practice. Based on the measurements generated from the chosen imaging technique, derived data can be interpreted in binary or continuous outcomes. Binary restenosis is a definition based on the occurrence, or not, of an event. The most used binary restenosis definition based on angiographic data is the finding of a stenosis diameter of more than 50% at follow-up while a significant decrease in stenosis severity (less than 50%) was originally obtained immediately after angioplasty.2 The binary restenosis definition has different limitations. It does not give a true evaluation of neointimal proliferation (for example a stenosis diameter of 49% at follow-up with a baseline post-procedural stenosis diameter of 5% will not be considered as a restenotic lesion). Furthermore, it does not always correlate well with the physiological significance of stenosis and frequently does not accurately compare the exact vessel segment before and after balloon angioplasty. Restenosis definition expressed as continuous outcomes is based on the finding that after angioplasty intervention, restenosis occurs in all lesions following a nearly Gaussian distribution (i.e. restenosis can thus be viewed as the tail end of a Gaussian distribution, with some lesions crossing a more
or less arbitrary cut-off point, rather than as a separate disease entity that occurs in some lesions but not in others).3 By plotting minimal lumen diameter or stenosis diameter in a cumulative frequency curve, restenosis rates can be defined for every desired arbitrary chosen value. To give a better understanding of the mechanisms leading to restenosis and their timing, other variables have been developed. For example, acute gain is the difference between minimal lumen diameter before and after the procedure and represents the lumen gain immediately after the intervention. Late loss is the difference between lumen diameter immediately after the procedure with lumen diameter at follow-up. This variable represents the net effect of all different pathophysiologic mechanisms leading to restenosis. The ratio between late loss and acute gain is the loss index. This variable gives a better insight of the intervention’s net result at follow-up with regard to the initial lesion. Clinical restenosis refers to restenosis diagnosed due to the recurrence of a patient’s symptoms as a result of end-organ dysfunction; for example, recurrent angina (coronary), recurrent claudication (lower limb), or recurrent hypertension (renal artery). From these recurrent dysfunctions come the need for reintervention or, more precisely, the need for target lesion revascularization (TLR) or target vessel revascularization (TVR). TLR rates are classically lower than TVR rates, due to reintervention related to disease progression in the same vessel. Angiographically defined, restenosis rates are also commonly higher than TVRs and TLRs, due to some discrepancy between stenosis severity and the patient’s symptoms. Often in the literature, restenosis surrogates like primary or secondary patency rates are used to quantify a specific treatment success rate. Primary patency refers to stenosis severity under an arbitrary chosen value (often < 50%) at follow-up after one single intervention (i.e. without any intervention in the follow-up period). Secondary patency refers to stenosis severity under an arbitrary chosen value at follow-up (equal to the arbitrary value chosen for primary patency), regardless of reintervention/s required during the follow-up period, to maintain the lesion stenosis severity under that chosen value. Most restenosis occur within the first 6 months of intervention.4,5 The risk of restenosis is modulated by systemic factors, vessel and lesion morphology, and by vessel damage induced during angioplasty. Diabetes, through endothelial dysfunction, increase the secretion of growth factors and enhances platelet activity, and represent the most commonly associated risk factor.6–8 The other most powerful correlation of restenosis is the occurrence of restenosis at another treated site on the 763
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same vessel type.9 Lesion wise, plaque burden,10 obstruction length,10 and vessel diameter11 are all related to restenosis. In addition to vessel size, vessel type seems to play a major role in determining the risk for restenosis. Conductance vessels such as the aorta, carotids and iliac arteries are categorized as elastic arteries with their media composed mainly of fenestrated layers of elastin. Conversely, distributing vessels classified as muscular arteries such as the brachial, femoral, and coronary arteries are characterized by media composed mostly of smooth muscle cells (SMC), permitting active vessel diameter changes in response to end-organ need. An aggressive restenotic process is much more common in muscular arteries, raising the hypothesis that vessels containing proportionally more smooth muscle might respond more vigorously to arterial injury.12 In addition, elastic vessels stretch in response to balloon angioplasty, but muscular arteries tear, resulting in more severe local injury. Finally, the more severe the injury caused by angioplasty, the more aggressive the hyperplastic response will be.13 Restenosis after peripheral artery intervention represents a problem of different magnitude depending upon the target vessel type of location. Rates range from less than 5% in carotid arteries to as high as 53% in infrainguinal locations. These extreme differences are explained by numerous factors including: muscular versus elastic type of arteries (as discussed previously), target vessel diameter, plaque burden, and lesion morphology at presentation. Due to the major differences in restenosis, incidence, and modulating factors depending on the anatomic bed, the most important different anatomic vascular regions will be discussed separately.
Pathophysiologic mechanisms General concepts An integrated view of restenosis has been proposed by Welt and Rogers (Figure 88.1).14 In this model, balloon angioplasty or stent deployment cause severe trauma in the arterial wall due to de-endothelialisation, atherosclerotic plaque crush, and often dissection of tunica media and adventitia, leading to thrombus (platelets and fibrin) deposition in the injured sites. The adhesion molecules expressed on the surface of the activated platelets such as P-selectin serve as anchors for circulating lymphocytes. Once anchored to the thrombus layer, leucocytes will bind tightly with the help of leukocyte integrin family (i.e. Mac-1) adhesion molecules, to glycoprotein platelet (GP) receptors (i.e. directly to GP Ibα receptor or through cross-linking with fibrinogen to GP IIbIIIa receptor). Migration of leucocytes into the tissue is due to chemokines released by SMC and resident leukocytes. This phenomenon is followed by a cellular proliferation phase, also called granulation. Growth factors released from all the present cells (i.e. SMC, platelets, leucocytes) stimulate the proliferation and migration of SMC from media to neointima. The resultant neointima is composed of SMCs, extracellular matrix and macrophages recruited over several weeks. Following this phase, weeks to months after the intervention, the artery enters a phase of remodeling. This phase is pathologically characterized by fewer cellular elements, due to apoptosis of cellular elements, and greater extracellular matrix (ECM) protein degradation and resynthesis. The ECM is
composed of collagen and proteoglycans and constitutes the major component of mature restenotic plaque.15 Negative vessel remodeling (i.e. reduction in artery size) observed after balloon angioplasty is believed to occur as a result of ECM reorganization. There is a significant difference in the pathophysiology of restenosis between stenting and balloon angioplasty. Intravascular ultrasound human studies16 in restenosis after balloon angioplasty found that although negative remodeling (as measured by external elastic membrane area) and neointimal hyperplasia (as measured by plaque plus media cross-sectional area) contributed to restenosis, negative remodeling contributed substantially more. Angiographic analysis of the two first pivotal studies of coronary stents in humans (Stent Restenosis Study [STRESS]17 and Belgian Netherlands Stent Study [BENESTENT]18 revealed distinct qualitative and quantitative differences between balloon-injured and stented arteries. Stented arteries experienced a much larger initial lumen gain, which was presumably due to the rigid scaffolding provided by the stent which prevents acute elastic recoil. At follow-up, the luminal area was greater and binary restenosis was less in stented arteries than in balloon-dilated arteries. However, late loss (lumen immediately after follow-up minus lumen at follow-up) was greater in stented arteries. Tying these observations together, stents incur greater neointimal growth, with their net benefit being attributable to their larger initial lumen gain and prevention from remodeling. These results were confirmed by intravascular ultrasound (IVUS) studies, conducted by Hoffman et al.19 Preclinical studies have shown that although in both techniques restenosis is driven by inflammation, balloon angioplasty gives rise to a transient acute inflammation mediated mainly by neutrophils while stenting leads to a chronic inflammation mediated from macrophages,20,21 (Figure 88.2) mostly present in clusters around the stent struts. As described above, the neointimal hyperplasia and ECM accumulation are the result of the same vascular healing process. Thrombosis and inflammation are at the basis of this process therefore they will be discussed more in detail in the following paragraphs. The role of thrombosis in restenosis In an animal model of angioplasty, platelet deposition was noted to occur immediately after injury. Platelets were found to relate directly to intimal proliferation after arterial injury, and severe thrombocytopenia inhibited intimal thickening, an effect that correlated with the degree of thrombocytopenia.22 After arterial injury, platelets rapidly adhere to the site of injury by several adhesion receptors: thromboxane A2 is generated, changes in the glycoprotein IIb/IIIa complex occur, which then binds to fibrinogen, subsequently leading to platelet aggregation and activation.23 Activated platelets release, among other factors, platelet-derived growth factor (PDGF), a potential SMC mitogen.24 Platelet-derived growth factor is the most important growth factor released by activated platelets. The association between PDGF and vascular SMC proliferation and migration has been demonstrated in animal experiments.25,26 Other platelet-released factors like transforming growth factor-beta (TGF β), serotonin, and thromboxane A2 all play a role in SMC proliferation27,28
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Pathophysiology of restenosis as demonstrated in animal studies. TGF β is also proven to stimulate the ECM production.26 P-selectin, a glycoprotein stored in the alpha-granules of platelets, is expressed on the platelet surface after platelet activation. It is implicated in platelet–leukocyte interactions, and decreased neointimal formation has been demonstrated in P-selectin-deficient mice.29 Histamine released from activated platelets at the site of vascular injury has been postulated to induce intimal hyperplasia through H1 receptors.30 Interleukin-1 derived from platelets increases production of interleukin-6 and interleukin-8, which are important mediators of inflammation at the vascular injury site.12,31 Platelets, when activated, can enhance thrombin generation by five to six fold.32 Thrombin, a powerful mitogen, contributes
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to SMC proliferation by inducing platelet release of PDGF.33 Thrombin may also exert a direct mitogenic stimulation on vascular SMCs.34 During organization of thrombus, thrombin becomes bound to the extracellular matrix and remains in its active form,35 being released gradually to exert a prolonged effect on SMC proliferation. These effects could be of significance, as increased thrombin generation has been demonstrated after PTCA in humans.36 Despite the multifactorial contribution of platelets in neointimal plaque formation, thrombosis wanes before intimal thickening peaks and antithrombotic therapy fails to eliminate restenosis, leading to the hypothesis that inflammation rather than thrombosis plays the major role in neointimal hyperplasia.37
(d) Leukocyte Infiltration
(a) Diseased Artery Pre-Stent
SMC Proliferation/Migration
Atherosclerotic Plaque with Resident Macros Media MaC-1 (CD11b/CD18)
Endothelium
Fibrinogen
GPIIb/IIIa
SMCs
GPIb1
Growth Factors (FGF,PDGF,IGF,TGF-β,VEGF)
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(b) Immediate Post-Stent
Endothelial Denudation, Platelet/Fibrinogen Deposition
(e) Neointimal Growth
Continued SMC Proliferation and Macro Recruitment
Neointima
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(c) Leukocyte Recruitment
More ECM Rich Over Time
Cytokine Release
PSGL-1
Repaired Endothelium P-Selectin
Macros
Cytokines Neutros (MCP-1,IL-6,IL-8)
Figure 88.1 (a) Mature atherosclerotic plaque before intervention; (b) immediate result of stent placement with endothelial denudation and platelet/fibrinogen deposition; (c, d) leucocyte recruitment, infiltration and SMC proliferation and migration in the days after injury; (e) neointimal thickening in the weeks after injury, with continued SMC proliferation and monocyte recruitment; (f) long-term (weeks to months) change from a predominantly cellular to a less cellular and more ECM-rich plaque. Taken from: Welt FG, Rogers C. Inflammation and restenosis in the stent era. Arterioscler Thromb Vasc Biol 2002; 22: 1769–76 (See Color plates.)
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The role of inflammation in the development of restenosis A large body of evidence from clinical or preclinical studies suggest that intimal inflammation is a determinant of in-stent neointimal growth. In animal models, inflammatory cells are recruited as a precursor of intimal thickening.38,39 In stented rabbit iliac arteries, monocyte adhesion correlated with neointimal size.40 A subsequent study showed peak monocyte adherence to the lumen surface 3 days after stenting, which correlated with intimal cellular proliferation.41 In porcine coronary stents, lymphohystiocytic cell infiltration around stent struts was associated with increased intimal thickness and percentage lumen area stenosis.42 Inflammatory cells associated with coronary stent placement in humans have been also described.43 Neutrophils surrounding stent struts, typically observed early after stent placement, are absent beyond 30 days after deployment. In contrast, chronic inflammatory cells (macrophages and lymphocytes) are seen both early (3–7 days) and late (≥ 6 months) after stenting.42 The same authors found a strong correlation between the extent of medial damage, inflammation, and neointimal thickness.44 Moreover, systemic markers of inflammation appear to be predictive of restenosis after balloon angioplasty. A transient rise of C-reactive protein compared to the baseline is observed after stenting of stable angina patients, and a return to baseline levels occurs after 48–72 hours.45 Other studies have shown that balloon dilatation or stenting are associated with an upregulation of neutrophil CD11b that is positively correlated with clinical restenosis and late lumen loss.46–48 Furthermore, multiple animal studies demonstrated that treatments that inhibit inflammatory cell adhesion molecules reduced intimal growth (Figure 88.2). For example, in rabbit iliac artery stents, M1/70, a monoclonal antibody to the adhesion molecule Mac-1 reduced leukocyte recruitment more than two-fold and reduced intimal area.49 P-selectin knockout mice treated with carotid ligation had a 76% reduction in neointima/media area and reduced vessel wall leukocytes.50 A monoclonal antibody against intercellular adhesion molecule-1 reduced the intima/media ratio by ≈50% in the rat carotid balloon injury model.51 Regarding the mechanisms of leukocyte contribution in neointima formation, it appears that multiple mechanisms are involved; direct bulk effect due to leukocyte accumulation within the intima,52 production of reactive oxygen intermediates,52 by production of growth and chemotactic factors,53 and by production of enzymes capable of degrading the extracellular constituents and thereby facilitating cell migration.54,55 In view of these preclinical and clinical evidences of the key role of inflammation in restenosis, different clinical studies using anti-inflammatory therapies are being pursued. Some of them will be discussed in the next chapter. Finally the neointimal plaque is the result of cellular proliferation and ECM accumulation.
Cellular proliferation As described above, post-intervention thrombosis and inflammation reactions are responsible for the release of chemotactic and mitogenic factors.56,57 These growth factors
elicit a cascade of intracellular signal pathways and overexpression of genes critical to proliferation and migration of medial SMCs. SMC proliferation begins in the media in the first 24 hours following angioplasty. Evidence from animal studies, using cellular proliferation markers, suggests peak proliferation rates of up to 10–20% of total medial cells 5–7 days after injury.58–60 Although different mitogens released from platelets, leucocytes and fibroblasts have been proven in vitro to stimulate SMC proliferation, the basic fibroblast growth factor (bFGF) released from dying SMCs appears to be the predominant mitogenic factor of medial SMC proliferation. However, even though treatment with anti-bFGF reduced SMC proliferation by more than 80%, it did not prevent intimal thickening.61 In days 4–7 after the intervention a migration of the SMCs from the media through the elastic lamina into the neointima takes place. If the media SMC proliferation is not a prerequisite for neiointimal thickening it appears that this migration of medial SMCs into the neointima is absolutely required for neointimal hyperplasia. Several molecules such as angiotensin II, bFGF, TGF β and the platelet derived growth factor-BB (PDGF-BB) may act as SMC chemotactic factors.62 Modulation of PDGF-BB had an important impact in SMC migration but not in SMC proliferation. Once migrated to the neointima the SMCs undergo a process of replication. The peak of this replication process is reached weeks after the intervention. This process is crucial for the development of neointimal hyperplasia. Extracellular matrix ECM is the major component of mature restenotic plaque. Although previous restenosis models have referred to this ECM accumulation as a late event in restenosis, recent animal and human studies have shown that ECM production and deposition parallels SMC proliferation. The ECM consists of varying concentrations of proteoglycans (versican, biglycan, and decorin), hyaluronan, and collagen (types I and III). The ECM modulates important events within the developing neointima including: cell proliferation, migration, growth factor expression, and remodeling.63 Proteoglycans and hyaluronan are synthesized by SMCs and participate in regulation of vascular permeability, lipid metabolism, and thrombosis.64 In humans, analysis of coronary and peripheral atherectomy specimens from restenosic lesions, obtained 5 days to 17 months after angioplasty, showed strong hyaluronan staining around stellate SMCs.65 Hyaluronan staining was strongest where collagen staining was weakest and vice versa. Studies of coronary in-stent restenosis atherectomy specimens suggest that over time, the myxomatous composition of the neointima (proteoglycans and hyaluronan) decreases with an increase in collagen content.66 These changes in ECM components give rise to ECM volume contraction, which is correlated to negative remodeling after balloon angioplasty and late neointimal thinning after stenting. Several studies have documented neointimal regression in long-term follow-up after catheter-based interventions. In humans, coronary arteries where Palmaz–Schatz stents were implanted showed a small but significant increase in angiographic minimal lumen diameter at 3 years versus 6 months.67 Angiographic imaging follow-up studies in
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Pathophysiology of restenosis patients with coronary artery stents demonstrated a significant 10% increase in minimal lumen diameter, corresponding to a 22% reduction in stenosis diameter at 12 months.68 Over the same time interval, intravascular ultrasound showed a 13% increase in lumen volume and a 28% reduction in neointimal volume.69 Thinning of the in-stent neointima (increased transparency) 3 years after stenting has been visualized by coronary angioscopy.69 Post-mortem pathological neointimal regression studies have revealed that beyond 18 months, the stent neointima becomes less cellular (potentially via SMC apoptosis) and richer in type I collagen.70 Endothelial dysfunction In native arteries, the endothelial cells (ECs) serve as a natural permeability barrier between blood-borne elements and the media, produce molecules involved in vascular tone modulation (NO, PGI2, PGE2, PAF), and release SMC growth inhibitory factors, which are important in the prevention of neointimal hyperplasia.71,72 The migration of the SMCs into the intima is likely to contribute to the failure of re-endothelialization. This may be due to the fact that the SMCs migrate into the intima before ECs. Since the SMCs are releasing mediators that inhibit ECS growth, absence or incomplete re-endothelialization may result.73,74 Different studies have shown that stimulating the re-endothelialization process of injured arteries reduces neointimal hyperplasia and promotes the injured arteries’ vasomotor function recovery. In light of these findings, different therapeutic strategies using vascular endothelial growth factor (VEGF), intracoronary gene transfer of VEGF, estradiol and other NO donors, endothelial nitric oxide synthase (eNOS) gene transfection and transplantation of endothelial progenitor cells (EPCs) are being tried. Some of these techniques have given promising results in the preclinical phase and are now being tested in human trials. Some of these strategies will be discussed in detail in the next chapter.
Restenosis incidence based on anatomic bed Carotid arteries Carotid artery angioplasty with stenting has emerged as an alternative to carotid surgery. PTA and stenting in these conductive vessel types result in a high rate of procedure success, low peri-procedural complication rate and low restenosis rate. Indeed, restenosis rates ranging from 5–8% have been reported.75 Risk factors related to restenosis after carotid angioplasty are: female gender, advancing age, and the number of stents implanted. Restenotic lesions after carotid endarterectomy in particular are at higher risk of in-stent restenosis.76 Renal arteries Previous studies have shown high restenosis rates after balloon angioplasty of the atherosclerotic induced renal artery stenosis. Since stent use, the restenosis rate is significantly lower (range: 15–25%). In the GREAT trial, where sirolimus-eluting stents (SES) were compared to bare stainless-steel balloon-expandable stents in the treatment of renal arteries,77 restenosis rate in the
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bare metal stent arm was 14.3 versus 6.7% in the drugeluting stent group. Cigarette smoking and a vessel diameter < 4 mm,78 have been demonstrated to be related to higher rates of restenosis. Of interest, differently from other vascular sites, there is a trend for restenosis progression even after the first 6 months after angioplasty.78 Subclavian arteries Subclavian arteries are conductive type arteries and show low rates of restenosis after balloon angioplasty with provisional stenting. Restenosis rates have been reported to vary between 5 and 7%.79,80 Illiac arteries The restenosis rate after angioplasty (with or without stenting) in this conductance anatomical bed is as low as expected. One-year patency rate is higher after balloon angioplasty for iliac stenosis than for iliac occlusions; respectively, 78% (67–92%) and 68% (59–94%).81 The Dutch Iliac Stent Trial failed to show any significant difference between PTA and stent treated groups.82 However, recent trials have shown that stent use gives low rates of restenosis (8% at 9 months for the Palmaz multicenter registry, 12% at 6 months in the Wallstent registry, and 6% at 12 months in the self-expanding nitinol stent CRISP trial). Whether stenting is superior to PTA in the treatment of iliac artery disease remains a matter for debate, although results of these new stent trials have lowered threshold towards stent usage in all but focal (TASC type A) lesions, where PTA results are quite favorable.
Stent
Balloon
4 days
7 days
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Figure 88.2 Immunohistochemical identification of macrophages within primate iliac arteries injured with either stents or balloon injury alone. Note that there is a steady accumulation of macrophages within stented segments with clustering of macrophages surrounding the stent struts, whereas there is virtually no accumulation within the balloon-injured segments. Horvath C, Welt FG, Nedelman M et al. Circ Res 2002; 90: 488–94. (See Color plates.)
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Infrainguinal vessels (superficial femoral, popliteal, and tibial arteries) Until recently, the infrainguinal vessels represent the highest restenotic lesion location with high recurrence rates. Occlusion recanalizations result in higher restenosis rates than stenotic lesions.81 The indication (claudication vs. critical limb ischemia) is also an important factor of restenosis in this location.82 Three-year follow-up patency rates range from 61% to 30% respectively for claudicants with stenosis
versus patients with critical limb ischemia and occlusions.83 Recent trials using self-expanding nitinol stents have shown significantly better outcomes in terms of long restenosis rates at follow-up (22% at 1 year,84 21.9% at 2 years.85 Until now, SES trials in the treatment of femoropopliteal lesions have failed to show any superiority versus self-expanding nitinol stents.84 Meanwhile, studies with paclitaxel-eluting stents are still ongoing. New therapy options and their clinical results will be discussed in detail in the next chapter.
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Dangas G, Fuster V. Management of restenosis after coronary intervention. Am Heart J 1996; 132: 428–36 Serruys PW, Foley DP, Kirkeeide RL, King SB. Restenosis revisited: Insights provided by quantitative coronary angiography (Editorial). Am Heart J 1993; 126: 1243–67 Rensing BJ, Hermans WM, Deckers JW et al. Lumen narrowing after transcutaneous coronary balloon angioplasty follows a near Gaussian distribution: A quantitative angiographies study in 1445 successfully dilated lesions. J Am Coll Cardiol 1992; 19: 939–45 Nobuyoshi M, Kimura T, Nosaka H et al. Serial angiographic follow-up of 229 patients. J Am Cardiol 1988; 12: 616–23 Serruys PW, Luijten HE, Beatt KJ et al. Incidence of restenosis after successful angioplasty: A time-related phenomenon. Circulation 1988; 77: 361–71 Weintraub WS, Kosinski AS, Brown CL, King SB III. Can restenosis after coronary angioplasty be predicted from clinical variables? J Am Coll Cardiol 1993; 21: 6–14 Rensing BJ, Hermans WR, Deckers JW et al. Which angiographic variables best describes functional status 6 months after successful single vessel coronary balloon angioplasty? J Am Coll Cardiol 1993; 21: 317–24 Lambert M, Bonan R, Coté G et al: Multiple coronary angioplasty: A model to discriminate systemic and procedural factors related to restenosis. J Am Coll Cardiol 1988; 12: 310–14 Weintraub WS, Brown CL, Liberman HA et al. Effect of restenosis at one previously dilated coronary site on the probability of restenosis at another previously dilated coronary site. J Am Cardiol 1993; 72: 1107–13 Hirshfeld JWJ, Wchwartz JS, Jugo R et al. Restenosis after coronary angioplasty: A multivariate statistical model to relate lesion and procedure variables to restenosis. J Am Cardiol 1991; 18: 647–56 Weintraub WS, Douglas JS, Ghazzal Z et al. Evaluation and prediction of clinical restenosis (Abstract). Circulation 1996; 94: 1–90 Schartz RS. In: Topol EJ, ed. Animal model of human coronary restenosis. Textbook of Interventional Cardiology. Philadephia: WB Saunders, 2002: 358–78 Schwartz R, Huber K, Murphy J et al. Restenosis and the proportional noeintimal response to coronary artery injury: Results in a porcine model. J Am Coll Cardiol 1992; 19: 267–74 Welt FG, Rogers C. Inflammation and restenosis in the stent era. Arterioscler Thromb Vasc Biol 2002; 22: 1769–76 Schwartz RS, Huber KC, Murphy JG et al. Restenosis and proportional neointimal response to coronary artery injury: results in a porcine model. J Am Coll Cardiol 1992; 19: 267–74 Mintz GS, Popma JJ, Pichard AD et al. Arterial remodeling after coronary angioplasty: a serial intravascular ultrasound study. Circulation 1996; 94: 35–43 Fischman DL, Leon MB, Baim DS et al. A randomized comparison of coronary artery-stent placement and balloon angioplasty in the treatment of coronary artery disease. N Engl J Med 1994; 331: 496–501 Serruys PW, de Jaegere P, Kiemeneij F et al. A comparison of balloon-expandable-stent implantation with balloon angioplasty in patients with coronary artery disease. N Engl J Med 1994; 331: 489–95 Hoffmann R, Mintz GS, Dussaillant GR et al. Patterns and mechanisms of in-stent restenosis: a serial intravascular ultrasound study. Circulation 1996; 94: 1247–54 Paolini JF, Kjelsberg MA, Edelman ER, Rogers CDK. Sustained expression of chemokines monocyte, chemoattractant protein-1 and interleukin-8 after stent- but not balloon-induced arterial injury. J Am Coll Cardiol 2000; 35: 15 (abstract) Horvath C, Welt FG, Nedelman M, Rao P et al. Targeting CCR2 or CD18 inhibits experimental in-stent restenosis in primates: inhibitory potential depends on type of injury and leukocytes targeted. Circ Res 2002; 90: 488–94
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Moore S, Friedman RJ, Singhal DP et al. Inhibition of injury induced thromboatherosclerotic lesions by anti-platelet serum in rabbits. Thromb Haemost 1975; 35: 70–81 Fox JEB. Platelet biology and retenosis. Presented at the Restenosis Summit VIII, Cleveland Clinic Heart Center, May 1996: 234 Casscells W. Smooth muscle cell growth factors. Prog Growth Factor Res 1991; 3: 177–206 Uchida K, Sasahara M, Morigami N et al. Expression of platelet derived growth factor B-chain in neointimal smooth muscle cells of balloon injured rabbit femoral arteries. Atherosclerosis 1996; 124: 9–23 Bornfeldt KE, Raines EW, Nakano T et al. Insulin-like growth factor-1 and platelet derived growth factor-BB induce direct migration of human arterial smooth muscle cells via signalling pathways that are distinct from those of proliferation. J Clin Invest 1994; 93: 1266–74 Nabel EG, Shum L, Pompili VJ et al. Direct transfer of transforming growth factor beta 1 gene into arteries stimulates fibrocellular hyperplasia. Proc Natl Acad Sci USA 1993; 90: 10759–63 Pakala R, Willerson JT, Benedict CR. Effect of serotonin, thromboxane A2, and specific receptor antagonists on vascular smooth muscle cell proliferation. Circulation 1997; 96: 2280–6 Kumar A, Hoover JL, Simmons CA et al. Remodeling and neointimal formation in the carotid artery of normal and P-selectin-deficient mice. Circulation 1997; 96: 4333–42 Miyazawa N, Watanabe S, Matsuda A et al. Role of histamine H1 and H2 receptor antagonists in the prevention of intimal thickening. Eur J Pharmacol 1998; 362: 53–9 Loppnow H, Bil R, Hirt S et al. Platelet-derived interleukin-1 induces cytokine production, but not proliferation of human vascular smooth muscle cells. Blood 1998; 91: 134–41 Walsh PN, Schmaier AH. Platelet-coagulant protein interactions. In: Colman RW, Hirsh J, Marder VJ, Salzman EW, eds. Hemostasis and Thrombosis: Basic Principles and Clinical Practice, 3rd ed. Philadelphia: J.B. Lippincott, 1994: 629–51 Maruyama I, Shigeta K. Regulation of the endothelial function by thrombomodulin and/or thrombin receptor. Rinsho Ketsueki 1994; 35: 234–7 McNamara CA, Sarembock IJ, Gimple LW et al. Thrombin stimulates proliferation of cultured rat aortic smooth muscle cell by a proteolytically activated receptor. J Clin Invest 1993; 91: 94–8 Wilner GD, Danitz MP, Mudd MS et al. Selective immobilization of alpha-thrombin by surface-bound fibrin. J Lab Clin Med 1981; 97: 403–11 Marmur JD, Merlini PA, Sharma SK et al. Thrombin generation in human coronary arteries after percutaneous transluminal balloon angioplasty. J Am Coll Cardiol 1994; 24: 1484–91 Libby P, Schwartz D, Brogi E, Tanaka H, Clinton SK. A cascade model for restenosis: a special case of atherosclerosis progression. Circulation 1992; 86: III-47–52 Tanaka H, Sukhova GK, Swanson SJ et al. Sustained activation of vascular cells and leukocytes in the rabbit aorta after balloon injury. Circulation 1993; 88: 1788–803 Rogers C, Welt FG, Karnovsky MJ et al. Monocyte recruitment and neointimal hyperplasia in rabbits: coupled inhibitory effects of heparin. Arterioscler Thromb Vasc Biol 1996; 16: 1312–8 Rogers C, Edelman ER. Endovascular stent design dictates experimental restenosis and thrombosis. Circulation 1995; 91: 2995–3001 Rogers C, Welt FGP, Karnovsky MJ et al. Monocyte recruitment and neointimal hyperplasia in rabbits: coupled inhibitory effects of heparin. Arterioscler Thromb Vasc Biol 1996; 16: 1312–8 Kornowski R, Hong MK, Tio FO et al. In-stent restenosis: contributions of inflammatory responses and arterial injury to neointimal hyperplasia. J Am Coll Cardiol 1998; 31: 224–30
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Farb A, Sangiorgi G, Carter AJ et al. Pathology of acute and chronic coronary stenting in humans. Circulation 1999; 99: 44–52 Farb A, Weber DK, Kolodgie FD, Burke AP, Virmani R. Morphological predictors of restenosis after coronary stenting in humans. Circulation 2002; 105: 2974–80 Gaspardone A, Crea F, Versaci F et al. Predictive value of C-reactive protein after successful coronary artery stenting in patients with stable angina. Am J Cardiol 1998; 82: 515–8 Inoue T, Sakai Y, Morooka S et al. Expression of polymorphonuclear leukocyte adhesion molecules and its clinical significance in patients treated with percutaneous transluminal coronary angioplasty. J Am Coll Cardiol 1996; 28: 1127–33 Mickelson JK, Lakkis NM, Villarreal-Levy G, Hughes BJ, Smith CW. Leukocyte activation with platelet adhesion after coronary angioplasty: a mechanism for recurrent disease? J Am Coll Cardiol 1996; 28: 345–53 Neumann FJ, Ott I, Gawaz M, Puchner G, Schomig A. Neutrophil and platelet activation at balloon-injured coronary artery plaque in patients undergoing angioplasty. J Am Coll Cardiol 1996; 27: 819–24 Rogers C, Edelman ER, Simon DI. A mAb to the 2-leukocyte integrin Mac-1 (CD11b/CD18) reduces intimal thickening after angioplasty or stent implantation in rabbits. Proc Natl Acad Sci USA 1998; 95: 10134–9 Kumar A, Hoover JL, Simmons CA et al. Remodeling and neointimal formation in the carotid artery of normal and P-selectin-deficient mice. Circulation 1997; 96: 4333–42 Yasukawa H, Imaizumi T, Matsuoka H et al. Inhibition of intimal hyperplasia after balloon injury by antibodies to intercellular adhesion molecule-1 and lymphocyte function-associated antigen-1. Circulation 1997; 95: 1515–22 Chen Z, Keaney JF Jr, Schulz E et al. Decreased neointimal formation in Nox2- deficient mice reveals a direct role for NADPH oxidase in the response to arterial injury. Proc Natl Acad Sci USA 2004; 101: 13014–9 Assoian RK, Fleurdelys BE, Stevenson HC et al. Expression and secretion of type beta transforming growth factor by activated human macrophages. Proc Natl Acad Sci USA 1987; 84: 6020–4 Garbisa S, Ballin M, Daga-Gordini D et al. Transient expression of type IV collagenolytic metalloproteinase produced by human mononuclear phagocytes. J Biol Chem 1986; 261: 2369–75 Sukhova GK, Shi G-P, Simon DI, Chapman HA, Libby P. Expression of the elastinolytic cathepsins S and K in human atheroma and regulation of their production in smooth muscle cells. J Clin Invest 1998; 102: 576–83 Ross R, Glomset JA. The pathogenesis of atherosclerosis. N Engl J Med 1976; 296: 369–77 Groves HM, Kilough-Rathbone RL, Richardson M et al. Platelet interaction with damaged rabbit aorta. Lab Invest 1978; 40; 194–9 Rogers C, Edelman ER, Simon DI. A mAb to the beta2-leukocyte integrin Mac-1 (CD11b/CD18) reduces intimal thickening after angioplasty or stent implantation in rabbits. Proc Natl Acad Sci USA 1998; 95: 10134–9 Simon DI, Chen Z, Seifert P et al. Decreased neointimal formation in Mac-1(-/-) mice reveals a role for inflammation in vascular repair after angioplasty. J Clin Invest 2000; 105: 293–300 Boehm M, Olive M, True AL et al. Bone marrow–derived immune cells regulate vascular disease through a p27(Kip1)-dependent mechanism. J Clin Invest 2004; 114: 419–26 Schwartz SM, deBlois D, O’Brian ERM. The intima soil for the atheroslerosis and restenosis. Circ Res 1995; 77: 445–65 Linder V, Reidy MA. Proliferation of smooth muscle cells after injury is inhibited by an other antibody against basic fibroblast growth factor. Proc Natl Acad Sci USA 1991; 88: 3739–43 Hay ED. Cell Biology of Extracellular Matrix. New York: Plenum Press, 1991
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Wight TN. Cell biology of arterial proteoglycans. Arteriosclerosis 1989; 9: 1–20 Riessen R, Wight TN, Pastore C et al. Distribution of hyaluronan during extracellular matrix remodeling in human restenotic arteries and balloon injured rat carotid arteries. Circulation 1996; 93: 1141–7 Chung IM, Gold HK, Schwartz SM et al. Enhanced extracellular matrix accumulation in restenosis of coronary arteries after stent deployment. J Am Coll Cardiol 2002; 40: 2072–81 Kimura T, Yokoi H, Nakagawa Y et al. Three-year follow-up after implantation of metallic coronary-artery stents. N Engl J Med 1996; 334: 561–6 Kuroda N, Kobayashi Y, Nameki M et al. Intimal hyperplasia regression from 6 to 12 months after stenting. Am J Cardiol 2002; 89: 869–72 Asakura M, Ueda Y, Nanto S et al. Remodeling of in-stent neointima, which became thinner and transparent over 3 years: serial angiographic and angioscopic follow-up. Circulation 1998; 97: 2003–6 Farb A, Kolodgie FD, Hwang JY et al. Extracellular matrix changes in stented human coronary arteries. Circulation 2004; 110; 940–7 Thorin E. Merkin D. Bertrand OF et al. Influence of post-angioplasty π-irradiation on endothelial function in porcine coronary arteries. Circulation 2000; 101; 1430–1 Asahara T, Chen D, Tsurumi Y et al. Accelerated restitution of endothelial integrity and endothelium-dependent function after phVEGF165 gene transfer. Circulation 1996: 94: 3291–302 Casscells W, Growth factor therapies for vascular injury and ischemia. Circulation 1995; 91: 2699–702 Cascells W. Migration of smooth muscle and endothelial cell: Critical events in restenosis. Circulation 1992; 86: 723–9 Khan MA, Liu MW, Chio FL et al. Predictors of restenosis after successful carotid artery stenting. Am J Cardiol 2003; 92: 895–7 Setacci C, Pula G, Baldi I et al. Determinants of in-stent restenosis after carotid angioplasty; a case-control study. J Endovasc Ther 2003; 10: 1031–8 Sapoval M, Zähringer M, Pattynama P et al. Low-profile stent system for treatment of atherosclerotic renal artery stenosis: The Great trial. J Vasc Interv Radiol 2005; 16: 1195–202 Shammas NW, Kapalis MJ, Dippel EJ et al. Clinical and angiographic predictors of restenosis following renal artery stenting. J Invas Cardiol 2004; 16: 10–13 McNamara TO, Greasler LE, Fisher JR et al. Initial and longterm results of treatment of brachiocephalic arterial stenosis and occlusions with balloon angioplasty, thrombolysis, stents. J Invas Cardiol 1997: 9; 372–83 Henry M, Amor M, Henry I et al. Percutaneous transluminal angioplasty of the subclavian arteries. J Endovasc Surg 1999: 6; 33–41 Transatlantic Inter-Societal consensus. Management of peripheral arterial disease. J Vasc Surg 2000; 31: S1–S296 Tottero E, van der Graaf Y, Bosch JL et al. Randomised comparison of primary stent placement versus primary angioplasty followed by selective stent placement in patients with iliac-artery occlusive disease. Dutch Iliac Stent Trial Study Group. Lancet 1998; 351: 1153–9 Murandin GSR, Bosch JL, Hunink MGM. Balloon dilatation and stent implantation for treatment of femoropopliteal arterial disease: meta-analysis. Radiology 2001; 221: 137–45 Mewissen MW Self-expanding nitinol stents in the femoropoliteal segment: technique and mid term results. Tech Vasc Interv Radiol 2004: 7: 2–5 Duda SH, Bosiers M, Lammer J et al. Drug-eluting and bare Nitinol stents for the treatment of atherosclerotic lesions in the superficial femoral artery: long-term result from the SIROCCO trial. J Endovasc Ther 2006; 13(6): 701–10
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Interventional therapy: new approaches E Kedhi and L Bilodeau
Peripheral artery restenosis, as mentioned in the previous chapter, characterizes certain vessel types, sizes, and locations. Muscular distributive vessels such as the superficial femoral arteries (SFA) represent the classical nidus for restenosis after angioplasty and as such, they have been considered optimal for investigation of innovative preventive measures or new therapeutic strategies. They also share some structural and pathological similarities with extensively studied coronary arteries. As a consequence, some concepts applied in coronary angioplasty can, to a certain extent, show favorable results in SFAs. Among these, avoidance of intervention on a small caliber vessel with extensive plaque burden and with existing collateralization offers a good example of lesion selection in order to optimize results and prevent complications. In addition, procedure wise, operators will aim at obtaining the largest lumen after the procedure or the lowest residual stenosis (< 30%), knowing the delicate balance between the severity of the produced injury and the required acute gain in luminal area. In contrast with the coronary arteries, where stenting has consistently shown an antirestenotic effect,1–3 this therapeutic modality until recently had failed in reducing restenosis rates in SFAs.4–7 Indeed, the first results from studies using the Wallstent (Boston Scientific, Natick, MD) and Palmaz stent (Cordis, Miami, FL) showed low patency rates at 12 months follow-up (range: 22–61%).8 For this reason the TACS recommendations published in 2000 did not recommend femoropopliteal stenting as a primary approach to the interventional treatment of intermittent claudication but only as a salvage treatment for acute complications of PTA failures. Further technological improvement in endovascular endoprostheses led to the development of self-expanding nitinol stents. These new stents, due to their design, exert a continuous radial force on the vessel wall. Furthermore, the elastic proprieties of nitinol confer to these stents much higher flexibility than their stainless-steel predecessors, allowing stenting of longer arterial segments and presenting stent fractures at predetermined flexion points. Different studies of primary SFA stenting using self-expanding nitinol stents have shown significantly lower intermediate and long-term binary restenosis rates in comparison to PTA or stainless steel stents.9–11 Mewissen reported a restenosis rate of 22% at 12 months12 while Duda et al. reported a restenosis rate of 21.9 % at 24 months follow-up.13 Furthermore, due the flexibility of these stents, longer and more complex lesions could be treated with good results.12 Under the evidence of the drastic reduction of restenosis rate induced from the use of drug-eluting stents (DES) in the coronary system,14–18 different investigations using DES in 770
peripheral arteries were started. The two drugs used until now in the peripheral system are sirolimus and paciltaxel. Sirolimus (rapamycine), is a macrocyclic lactone derived from Streptomyces hygroscopicus with potent immunosuppressive and cytostatic properties. The cytostatic effects of sirolimus are due to its binding to the mammalian target of rapamycin (mTOR), leading to mTOR activation inhibition. Although the consequences of mTOR activation inhibition are not completely known, this process leads to DNA replication inhibition and, as a result, the arrest of the cell cycle in the late G1 phase.19,20 Apart from smooth muscle cell (SMC) proliferation inhibition, rapamycin also has an inhibitory effect on SMC migration.21,22 Furthermore, sirolimus exerts an antiinflammatory effect, which was paralleled with neointimal hyperplasia inhibition in animal models.23 Rapamycin has also been shown to inhibit total protein and collagen synthesis involved in extracellular matrix (ECM) formation.24 Due to these properties sirolimus is an excellent antirestenotic agent and different trials of sirolimus-eluting stents have already proven its efficiency in the coronary system.25, 15–18 Paclitaxel was isolated from the bark of the Western yew tree in 1971.26 It acts by binding specifically to the tubulin subunit of microtubules, antagonizing the disassembly of this key cytoskeletal protein. As a result, bundles of microtubules and other aberrant structures, derived from microtubules, accumulate in the mitotic phase of the cell cycle, leading to the arrest of mitosis in G2/M phase. It has been shown that paclitaxel, due to its effect on microtubule function, also inhibits the SMC migration,27,28 conferring to this molecule another important antirestenotic property, which in combination with its antiproliferative effects make this molecule a very valid antirestenotic agent. Two prospective, randomized trials, SIROCCO I and II29,30 compared the sirolimus-eluting self-expanding nitinol Smart stent (SES) (Cordis, Miami, FL) with the uncoated Smart stent (Cordis, Miami, FL). Both groups showed to be effective treatments in revascularizing the diseased SFA. Angiographic binary restenosis in the SIROCCO I trial at 6 months was 0% for the sirolimus-eluting group and 23.5% in the uncoated stent group, (p > 0.05). Twenty-four-month follow-up showed maintained low restenosis rates for both treatments in a majority of patients. However, according to Duplex ultrasound data, restenosis rate was 22.9% in the sirolimus group and 21.1% in the uncoated stent group, with no significant further difference in terms of target vessel revascularization (TLR) and mortality between the two groups. This lack of difference in the two treatments groups is due to a low restenosis
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Interventional therapy: new approaches rate in the uncoated stent group, in a degree that has never been observed before. After these deceiving results obtained from the SIROCCO trials, different companies reduced or stopped their research projects with SES in the SFA. The only ongoing trial with drug-eluting stents is the Zilver Ptx trial. This randomized trial started in March 2005 and will include 480 patients in multiple centers in the US. The trial will compare the paclitaxel-eluting Zilver 5 (Cook, Bloomington, IN) stent with PTA alone in lesions up to 7 cm in length. In a second phase, this study will compare the same treatment strategies for lesions up to 14 cm. The follow-up period will be 12 months. Although nitinol self-expanding stents have set a major step ahead in the treatment of the SFA, stent fracture, due to lower limb flexion movements, appears to remain a limitation of this device. The SIROCCO trials showed that selfexpanding nitinol stent fracture occurred more frequently than previously believed. In these trials, stent fracture was observed at 18.2% at 6 months and in 24% after 24 months follow-up. Surprisingly in these studies, no correlation was found between the stent fracture rate and restenosis rate. Another recently published study from Scheinert et al. showed even higher rates of stent fracture after systematic x-ray follow-up of stented SFAs.31 Stent fractures were observed in 37.2% of the cases. Both studies showed that stent fracture occurs more often after long-segment SFA stenting than short segment stenting. In contrast with the SIROCCO findings, the Scheinert study showed that stent fracture was associated with restenosis in two-thirds of the cases. Because of these contradictory data, further studies need to address the occurrence and the clinical relevance of this phenomenon. The Edwards Life Stent NT (Edwards Life Science, Irvine, CA) has been proposed for the treatment of femoropopliteal lesions. Due to its special design, this stent is expected to better respond to multiple vectorial forces transmitted to the artery during leg movements or musculature contractions, with lower fracture rate. The efficiency of this device is being examined in the RESILENT trial, an ongoing multicenter randomized trial that compares the Life Stent NT with standard PTA in SFA lesions. Until now, percutaneous treatment of arteries below the knee has been reserved for patients who were unsuitable candidates for bypass surgery, therefore data regarding stenting of arteries below the knee are very limited. Feiring et al.32 reported a register of 82 patients in which primary belowthe-knee stenting yielded comparable results to tibial bypass intervention in restoring the straight inline arterial flow in patients with critical limb ischemia or lifestyle limiting claudication. Recently, similar registers from different centers33 regarding the use of DES in these vascular segments looks promising but before this practice becomes widely accepted, randomized prospective studies are required. As a conclusion, the use of self-expanding nitinol stents has significantly changed the patency rates after treatment of femoropopliteal lesions compared to stainless steel stents. Due to this device, even more complex lesions, such as TASC type C and D lesions, can now be treated endovascularly with a high rate of procedural success and higher long-term patency rates. Drug-eluting stents, in contrast with the coronary artery
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experience, have failed until now to show any superiority versus non-coated stents in restenosis reduction in the peripheral system. Another stent concept to reduce restenosis has been the use of covered stents. Recently the Viabahn, an expanded polytetrafluoroethylene (ePTFE) lining nitinol stent (W.L. Gore and Associates, Flagstaff, AZ), has received indication from the Food and Drug Administration (FDA) for the treatment of atherosclerotic disease of the SFAs. Clinical data in support of this device is limited. In a randomized study from Saxon et al.,34 comparing the Viabahn covered-stent with PTA for the treatment of SFA lesions less then 13 cm long, two-year patency rates were 87 and 25% for the covered-stent and PTA groups respectively (p = 0.002). Due to the very promising results of this study and other small registries, VIBRANT, a large, multicenter, randomized, post-market trial, comparing the Viabahn stent with bare nitinol stents is ongoing. In order to improve patency rates, other variations of angioplasty such as brachytherapy, cryoplasty, excimer laser, atherectomy, and other techniques have been introduced in attempt to minimize restenosis rates. Some of the above mentioned techniques and the related clinical experiences will be discussed in detail in the following sections.
Brachytherapy Radiation, delivered during brachytherapy, results in DNA chain breaks leading to cell death during cell division. In peripheral interventions, brachytherapy was reported efficient both for restenosis prevention and treatment in SFAs, renal artery stenosis and arteriovenous dialysis shunts in several small registries.35–37 The first well-documented randomized trial of brachytherapy for prevention of restenosis in de novo SFA lesions was the Vienna-2 study.38 In this trial, 113 patients with de novo or recurrent femoropopliteal lesions were randomized to PTA plus brachytherapy or PTA alone. The cumulative patency rate at 12 months follow-up was higher in the PTA plus brachytherapy group (63.6%) than in the PTA alone group (35.5%). The 3-year follow-up of this study showed some superiority in the brachytherapy group but 5-year follow-up results showed that brachytherapy did not result in lower restenosis rates compared to PTA alone.39 This “catch-up” phenomenon has been attributed to a delayed restenotic process after brachytherapy. Due to the initial positive results of brachytherapy in combination with PTA shown from the Vienna 2 study, two other randomized trials, the Vienna V trial40 and the PARIS trial41 were started to evaluate the role of brachytherapy in the reduction of restenosis, respectively after stenting and after PTA of femoropopliteal lesions. In contrast with the Vienna 2 trial, in the Vienna V trial, brachytherapy in combination with femoropopliteal stenting in high-risk patients did not improve 6-month outcomes because of the high incidence of thrombotic occlusions. The Paris trial was the largest (203 patients) multicenter, randomized, double-blind control study that evaluated brachytherapy after PTA for SFA stenosis in the US. The patients were followed for 12 months with clinical visits at 3,
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6, and 12 months and follow-up angiography was performed at 12 months. The follow-up results showed no significant differences between the two treatment groups. The restenosis rate was similar in both groups; that is, 28.6% in the brachytherapy group and 27.5% in the placebo arm. In addition, there was no further significant difference in the minimal lumen diameter, late loss, or in the number of thrombotic total occlusions between the two groups. In another study from Diehm et al., in which 147 patients with femoropopliteal lesions were treated with PTA plus brachytherapy versus PTA alone, the 5-year follow-up failed to show long-term benefits in the brachytherapy group.42 The most interesting brachytherapy result from the Vienna group consisted of the finding of significant restenosis reduction after femoropopliteal angioplasty of recurrent but not de novo lesions43 when using gamma radiation. This is at the moment the only evidence defending indication for brachytherapy. Furthermore, the use of brachytherapy implies multiple logistic problems, such as instrument and staff safety issues and multidisciplinary cooperation. In addition, the required device calibration before treatment often leads to longer procedural times. Based on the limited benefits as well as regulatory and safety issues, this therapy is being abandoned in most peripheral intervention laboratories. In the last few years, reports of external beam radiation (EBR) in prevention of restenosis after PTA44 or stenting45 for peripheral arterial disease has generated a lot of interest. As opposed to brachytherapy where radiation delivery occurs during the procedure, EBR can be performed the day after on an ambulatory basis, facilitating the logistic and safety of such intervention. Furthermore, EBR dosimetry appears to be more precise and less dependant upon characteristics.
Cryoplasty Cryoplasty is a new dilatation technique which combines classical PTA with cooling of the arterial wall. The device used is a microprocessor-controlled coaxial dual balloon (PolarCath, Boston Scientific). The cooling is achieved by inflating the balloon with nitrous oxide rather than contrast/saline mixture. The liquid evaporation rapidly cools the outer surface of the balloon from 37∞C to –10∞C. The temperature difference is transmitted to the adjacent vessel wall where it causes freezing of the intracellular fluid. This acute phase change triggers apoptosis of SMCs.46 The resulting non-inflammatory cell death leads to reduced neointimal hyperplasia. Furthermore, freezing-induced alterations in collagen and elastin fibers may temporally reduce the elastic recoil.47,48 The first clinical data for cryoplasty come from Fava et al. in which the procedural success was 93% for a group of 15 patients with femoropopliteal lesions. The 6-month followup showed 0% binary restenosis and a 14.4-month follow-up showed a primary patency rate of 83.3%.49 A larger multicenter prospective registry (PVD Chill IDE) evaluated the cryoplasty effect in 102 patients with femoropopliteal lesions of < 10 cm. The 9-month follow-up of this study showed a clinical patency rate of 82% and a primary patency rate of 70%. Furthermore, this register showed a low rate (7%) of significant dissection (≥ C type), compared with traditional PTA (45%).50 The patency rate of cryoplasty in this study was
comparable with the results of 2-year follow-up of the SIROCCO I trial, where restenosis was observed in 22%. Another indication of this technique is the in-stent restenosis. Cryoplasty alone or in association either with laser or excisional atherectomy in a small group of 18 patients treated for in-stent restenosis resulted in 94% procedural success and a 10-month clinical patency rate of 78%.51 Recently Das et al. presented the 6-month data of the Below-The-Knee Chill trial, an ongoing, prospective, multicenter trial where cryoplasty is used for chronic limb ischemia percutaneous revascularization. The preliminary results of this trial showed a high procedural success rate (97%) and a surprising 93% freedom from amputation rate at 6 months. Although cryoplasty results are very promising in the femoropoliteal as well as the tibioperoneal arteries, the final results of this study and further larger randomized studies need to be performed before this technique can become widely used.
Excimer laser angioplasty Excimer laser-assisted angioplasty (ELA) has recently re-emerged as a technique in the treatment of peripheral arterial disease. Although the technique has been known and used since the 1980s, significant technology improvements and better understanding of laser/tissue interactions have generated new interest in this technique. Actual excimer lasers are pulse-wave devices operating at ultraviolet wavelength (308 nm). Laser energy has photomechanical, photochemical, and photothermal absorption effects in biological tissues, which result in degradation of arterial plaque, thrombus, and to a lesser degree calcium, into tiny particles.52 Intravascular ultrasound (IVUS) studies in coronary arteries have shown that lumen gain after ELA is mostly due to tissue ablation and to a lesser extent, vessel expansion.53 Based on animal studies, transient vessel expansion is believed, at least partially, to be due to the generation of shock waves and vapor microbubbles during ELA use. Due to these properties, excimer laser technology is being presented as a valuable tool especially for the treatment of lesions with large plaque volume, long lesions with severe stenosis, or occlusions that are difficult or impossible to treat with standard PTA equipment. The first trials54–57 using ELA in SFA occlusions showed a high procedural success rate. Secondary patency rate was 86.3% at 36 months follow-up after ELA for short SFA lesions (1–10 cm) and 43% at 4-year follow-up after ELA for long SFA occlusions (range: 16–38 cm). Although additional interventions were required in the majority of patients to maintain these patency rates, these results were encouraging, especially in those patients who were not good candidates for bypass surgery. Despite the positive results of the above mentioned trials the only randomized trial that directly compared ELA to PTA, the PELA (Peripheral Excimer Laser Angioplasty) trial58 showed no significant difference between the two groups regarding technical success, primary patency, the need for reintervention at 1 year, and limb functional outcomes. Laser-Assisted Angioplasty for Critical Limb Ischemia (LACI), is another multicenter prospective trial which examined the efficiency of ELA in patients that were poor candidates for surgical revascularization.59 This trial enrolled 145 patients
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Interventional therapy: new approaches with 155 limbs in 14 centers between the US and Germany. Most of the patients in this group had TASC type C and D lesions. Sixty percent of lesions were located in the popliteal and infrapopliteal locations. The laser treatment delivery had a 99% success rate when a guidewire could cross, and the flow was re-established in 89% of cases. The 6-month follow-up showed a limb salvage rate of 93% and only 9 patients required an amputation. Limb salvage rates of 93% are among the highest reported for endovascular therapy in complex infrainguinal disease showing once again the efficiency of this technique in this group of patients. In-stent restenosis is another niche indication for ELA. Results from coronary studies60 have shown that laser catheters have the ability to safely navigate through the stent body without damaging it. These results can be important especially in the setting of SFA in-stent restenosis of nitinol self-expanding stents where fractures are frequently observed, making these stents even more prone to PTA balloon-induced damage. As a conclusion, EL debulking facilitated angioplasty is emerging as a convenient and easy to use technique, especially for long occlusive lesions in patients with critical limb ischemia. Further studies are necessary to evaluate the long-term effects of excimer laser debulking in the setting of in-stent restenosis.
Directional atherectomy Another debulking angioplasty variant is the directional atherectomy. This technique is proposing the use of the SilverHawk® Plaque Excision catheter (FoxHollow Technologies, Redwood City, CA). The advantage of the SilverHawk® device compared to earlier atherectomy devices is that all vessel barotrauma has been eliminated because the catheter does not use a balloon opposed to directional cutting window into the plaque. The procedural results of this device are being collected in the TALON multicenter registry. The only prospective registry for the use of SilverHawk® atherectomy device in femoropopliteal artery lesions comes from Zeller et al.61 Long-term clinical results of this study using duplex ultrasound evaluation of restenosis at follow-up showed that the use of directional atherectomy was better for de novo lesions than for restenotic lesions. The de novo lesion primary patency rates at 1 year and 18 months after the procedure were comparable with that of stenting using bare or drug-eluting nitinol stents in the SIROCCO trial. Directional atherectomy can be performed as a stand-alone procedure or in combination with low-pressure balloon dilatation in the majority of cases and stenting was required only in 6% of patients. Although these results appear promising, longer follow-up data of randomized trials are missing. However, considering the still unresolved issue of stent fractures after SFA treatment, this technique becomes interesting because it can achieve similar high procedural acute and mid-term outcomes while avoiding barotrauma and stenting in the majority of cases.
Coated balloons A new treatment option in the coronary and peripheral system consists of using coated balloons. The treatment
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rationale resides in the fact that this treatment offers local drug release without the need for stent implantation, reducing the restenosis with a dual mechanism: the drug-coating antirestenotic effect and minimization of vessel wall injury with balloon angioplasty alone without stenting. The preliminary results of the ongoing randomized THUNDER trial62 in which PTA performed with a coated balloon catheter was compared to standard PTA in femoropopliteal lesions, were presented recently in the 2006 TCT meeting. The balloon catheter used in this study was the PACCOCATH ISR (Bavaria Medizin Technologie, Oberpfaffenhofen, Germany). In this device, the drug used is paclitaxel, bound directly to the outer balloon surface. A single balloon inflation, at a pressure of 6 atmospheres for 60 seconds, resulted in deposition in the vessel wall of 20% of the total dose on the balloon surface.63 The 6-month followup of this study showed a significantly lower lumen loss in the coated than in the uncoated balloon group. The binary restenosis and TLR were also lower in the coated balloon group. The preliminary results of this study are in line with the results of the use of the same coated-balloon catheter in preclinical64–67 and coronary in-stent restenosis68 trails. Although these first results are very exciting in both coronary and peripheral lesions, it is still too early to draw any definitive conclusions. As a conclusion, new stent devices have significantly reduced the restenosis rates after the treatment of highly restenotic peripheral anatomic regions. In contrast to the coronary system, sirolimus-eluting stents have not been proven superior to nitinol self-expanding stents in the treatment of SFAs. An ongoing trial will evaluate the role of paclitaxel eluting-stent in the same setting. Stent fracture appears to occur frequently after treatment of SFAs with self-expanding stents but the clinical relevance of this phenomenon remains unclear. Cryoplasty appears promising, especially for the treatment of critical limb ischemia and below-the-knee lesions. Brachytherapy remains a useful treatment option only in the setting of restenotic lesions but external beam radiation has been recently proposed as an efficient treatment alternative. Debulking techniques either with excimer laser or atherectomy device are also useful tools in treatment of large plaque volume and long occlusive lesions but their antirestenotic benefit remains unproven. Covered stent devices have been recently FDA approved for use in SFAs despite a lack of clear evidence of antirestenotic effect. Finally drug-eluting balloon angioplasty is emerging as a new and elegant treatment modality for primary restenosis prevention in the peripheral vascular system. Long-term efficacy and safety, especially thrombosis related, remains unknown. Thanks to a better understanding of restenosis mechanisms and to the development of new technologies and devices, significant progress in the treatment of restenosis has been achieved. Nowadays, endovascular treatment can be applied successfully, in terms of peri-procedural results and long-term patency, even in complex lesions located in very restenotic anatomical regions that until now have been treated surgically. The ongoing trials will give further insight regarding the restenosis phenomenon and treatment modalities lining-up the way for better treatment results in the near future.
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Serruys PW, de Jagere P, Kiemeneis F et al. A comparison of balloon expandable stent mplantation with balloon angioplasty in patients with coronary artery disease. N Engl J Med 1994; 331: 495–501 Fishman DL, Leon MB, Baim DS et al. A randomised comparison of coronary artery stent pacement and balloon angioplasty in the treatment of the coronary artery disease. N Engl J Med 1994; 331: 496–501 Serruws PW, Van Hout B, Bonnier H et al. Randomised comparison of implantation of heparin coated stents with balloon angioplasty in selected patients with coronary artery disease (Benestent-II). Lancet 1998: 352: 673–81 Cejna M, Thurner SA, Illiasch H et al. PTA vs Palmatz stent placement in femoropopliteal artery obstructions: a multicenter prospective randomised study. J Vasc Intervn Radiol 2001; 12: 23–31 Grimm J, Muller-Hulsbeck S, Jahne T et al. Randomised study to compare PTA alone versus PTA with Palmatz stent placement for femoropopliteal lesions. J Vasc Intervn Radiol 2001; 12: 953–42 Muradin GS, Bosch JL, Stijen Tet al. Balloon dilation and stent implantation for the treatment of femoropopliteal arterial disease: meta-analysis. Radiology 2001; 221: 137–45 Vroegindewiej D, Vos LD, Tielbeck AV et al. Balloon angioplasty combined with primary stenting versus balloon angioplasty alone in femoropopliteal obstructions: a comparative randomized study. Cardiovasc Intervent Radiol 1997: 20: 420–5 Transantlantic Intersociety Consensus Group. Management of peripheral arterial disease (PAD). Transantlantic Inter-society Consensus (TASC). Eur J Vasc Endovasc Surg 2000; 19 (suppl. A): Si–Sxxviii, S1–S250 Sabeti S, Mlekusch W, Amighi J et al. Primary patency of longsegment self-expanding nitinol stents in the femoropopliteal arteries. J Endovasc Ther 2005; 12: 6–12 Lugmayr HF, Holzer H, Kastner M et al. Treatment of complex arteriosclerotic lesions with nitinol stents in the superficial femoral and popliteal arteries: a midterm follow-up. Radiology 2002; 222: 37–43 Sabeti S, Schillinger M, Amighi J et al. Patency of femoropopliteal arteries treated with nitinol versus stainless steel self-expanding stents: propensity score-adjusted analysis. Radiology 2004; 232: 516–21 Mewissen M. Self-expanding nitinol stents in the femoropopliteal segment: technique and mid term results. Tech Vasc Interv Radiol 2000; 7: 2–5 Duda SH, Bosiers M, Lammer J et al. Drug-eluting and bare Nitinol stents for the treatment of atherosclerotic lesions in the superficial fe; oral artery: long-term result from the SIROCCO trial. J Endovasc Ther 2006; 13(6): 701– Grube E, Silber S Hauptmann KE et al. Taxus I: six and twelve month results from a randomised, double blind trial on a w release paclitaxel eluting stent for de novo coronary lesions. Circulation 2003; 559–64 Moses J, Leon M, Popma J et al. Sirolimus-eluting stents versus standard stents in patients with stenosis in a native coronary artery. N Engl J Med 2003; 349: 1315–23 Gallo R, Padurean A, Jayaraman T et al. Inhibition of intimal thickening after balloon angioplasty in porcine coronary arteries by targeting regulators of the cell cycle. Circulation 1999; 99: 2164–70 Klugherz B, Llanos G, Lieuallen W et al. Twenty-eight-day efficacy and phamacokinetics of the sirolimus-eluting stent. Coron Artery Dis 2002; 13: 183–8 Gregory CR, Huang X, Pratt RE et al. Treatment with rapamycin and mycophenolic acid reduces arterial intimal thickening produced by mechanical injury and allows endothelial replacement. Transplantation 1995; 59: 655–61 Marx SO, Jayaraman T, Go LO et al. Rapamycin-FKBP inhibits cell cycle regulators of proliferation in vascular smooth muscle cells. Circ Res. 1995; 76: 412–7 Braun-Dullaeus RC, Ziegler A, Bohle RM et al. Quantification of the cell-cycle inhibitors p27(Kip1) and p21(Cip1) in human atherectomy specimens: primary stenosis versus restenosis. J Lab Clin Med 2003; 141: 179–89 Sun J, Marx SO, Chen HJ et al. Role for p27(Kip1) in vascular smooth muscle cell migration. Circulation 2001; 103: 2967–72 Poon M, Marx SO, Gallo R et al. Rapamycin inhibits vascular smooth muscle cell migration. J Clin Invest 1996; 98: 2277–83 Suzuki T, Kopia G, Hayashi S et al. Stent-based delivery of sirolimus reduces neointimal formation in a porcine coronary model. Circulation 2001; 104: 1188–93
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Goueffic Y, Potter-Perigo S, Chan CK et al. Sirolimus blocks the accumulation of hyaluronan (HA) by arterial smooth muscle cells and reduces monocyte adhesion to the ECM. Atherosclerosis 2006; Dec 13: Epub ahead of print Morice M, Serruys P, Sousa J et al. A randomized comparison of a sirolimus-eluting stent with a standard stent for coronary revascularization. N Engl J Med 2002; 346: 1773–80 Wani MC, Taylor HL, Wall ME et al. Plant antitumor agents. VI. The isolation and structure of Taxol, a novel antileukemic and antitumor agent from Taxus brevifolia. J Am Chem Soc 1971; 93: 2325–7 Sollott SJ, Cheng L, Pauly RR et al. Taxol inhibits neointimal smooth muscle cell accumulation after angioplasty in the rat. J Clin Invest 1995; 95: 1869–76 Zhou X, Li J, Kucik DF. The microtubule cytoskeleton participates in control of beta 2 integrin avidity. J Biol Chem 2001; 276: 44762–9 Duda SH, Bosiers M, Lammer J et al. Drug-eluting and bare Nitinol stents for the treatment of atherosclerotic lesions in the superficial fe; oral artery: long-term result from the SIROCCO trial. J Endovasc Ther 2006; 13(6): 701–10 Duda SH, Bosiers M, Lammer J et al. Sirolimus-eluting versus bare nitinol stent for obstructive superficial femoral artery disease: the SIROCCO II trial. J Vasc Interv Radiol 2005; 16(3): 331–8 Sheinert D, Scheinert S, Sax J et al. Prevalence and clinical impact of stent fractures after femoropopliteal stenting. J Am Coll Cardiol 45: 312–5 Feiring Aj, Wesolowski AA, Lade S. Primary stent supported angioplasty for the treatment of below-knee critical ischemia and severe claudication: Early and one year outcomes. J Am Coll Cardiol 2004; 44: 2307–14 Tepe G. Drug-eluting stents for infrainguinal occlusive disease: Progress and challenges. Semin Vasc Surg 2006; 19: 102–8 Saxon RR, Coffman JM, Gooding JM et al. Long-term results of ePTFE stent-graft versus angioplasty in the femoropopliteal artery: single center experience from a prospective randomised trial. J Vasc Interv Radiol 2003: 14: 303–11 Bottcher HD, Schopohl B, Liermann D et al. Endovascular irradiation: a new method to avoid recurrent stenosis after stent implantation in peripheral arteries – technique and primary results. Int J Radiat Oncol Biol Phys 1994; 29: 183–6 Waksman R, Laird JR, Jurkovitz CT et al. Intravascular radiation therapy after balloon angioplasty of narrowed femoropopliteal arteries to prevent restenosis: results of the feasibility clinical trial. J Vasc Interv Radiol 2001; 12: 915–21 Wolfram RM, Pokrajac B, Ahmadi R et al. Endovascular brachytherapy for prophylaxis against restenosis after long-segment femoropopliteal placement of stents: initial results. Radiology 2001; 200: 724–9 Minar E, Pocrajac B, Maca T et al. Endovascular brachytherapy for prophylaxis of restenosis after femoropopliteal angioplasty: results of a prospective, randomised study. Circulation 2000; 102: 2694–9 Wolfram RM, Budinsky AC, Pocrajac B et al. Endovascular brachytherapy for prophylaxis of restenosis after femoropopliteal angioplasty: five-year follow-up prospective randomised study. Roswitha M, Wolfram RM, Budinsky AC et al. Vascular brachytherapy: with 192 Ir after femoropopliteal stent implantation in high-risk patients: 12-month follow-up results from the Vienna-5 Trial. Radiology 2005; 236: 343–51 Waksman R, Laird JR, Jurkowitz CT et al. Intravascular radiation therapy after balloon angioplasty of narrowed femoropopliteal arteries to prevent restenosis: results of the PARIS feasibility clinical trial. J Vasc Interv Radiol. 2001; 12: 915–21 Diehm N, Silvestro A, Do DD et al. Endovascular brachytherapy after femoropopliteal balloon angioplasty fails to show robust clinical benefit over time. J Endovac Ther 2005; 12 (6): 7233–30 Wolfram RM, Budinsky AC, Pocrajac B et al. Endovascular brachytherapy: restenosis in de novo versus recurrent lesions of femoropopliteal artery– the Vienna experience. Radiology 2005; 236(1): 338–42 Therasse E, Donath D, Lespérance J et al. External beam radiation to prevent restenosis after superficial femoral artery balloon angioplasty. Circulation 2005; 111: 3310–5 Zabakis P, Karadamakis DM, Siablis D et al. Exteranl beam radiation reduces the rate of restenosis in patients with femoral stenting: results of a randomised study. Radiother Oncol 2005; 74(1): 1–2 Grassl ED, Bischof JC. In-vitro model systems for evaluation of smooth muscle cell response to cryoplasty. Cryobiology 2005; 50: 162–73
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Soloff BL, Nagle WA,Moss AJ et al. Apoptosis induced by cold shock in vitro is dependent in cell growth phase. Biochem Biophys Res Comm 1987; 145: 876–83 Gage A, Fazekas G, Riley E et al. Freezing injury to large blood vessels in dogs. Surgery 1967; 61: 748–54 Fava M, Layola S Polydoou A et al. Cryoplasty for femoropopliteal arterial disease: late angiographic results of initial human experience. J Vasc Intervent Radiol 2004; 15: 1239–43 Laird J, Jaff MR, Biamino G et al. Cryoplasty for the treatment of femoropopliteal arterial disease: results of a prospective, multicenter registry. J Vasc Interv Radiol 2005; 16: 10067–73 Joye JD. An overview of cryoplasty. Endovasc Today; 3(9): 54–6 Topaz O. Plaque removal and thrombus dissolution with pulsed-wave lasers photoacoustic energy: biotissue interactions and their clinical manifestations. Cardiology 1996; 87: 384–91 Mintz GS, Kovach JA, Javier SP et al. Mechanisms of lumen enlargement after excimer laser coronary angioplasty. Circulation 1995; 92: 3408–14 Scheinert D, Laird JD, Schroeder M et al. Excimer laser-assisted recanalisation of long, chronic superficial femoral artery occlusions. Scheinert D, Schroeder M, Ludwig J et al. Stent supported recanalisation of chronic iliac artery occlusions. Am J Med 2001; 110: 708–15 Steinkamp Hj, Wissgot C, Rademaker J et al. Short (1–10 cm) superficial femoral artery occlusions: results of treatment with excimer laser angioplasty. Cardiovac Intervent Radiol 2002; 25(5): 388–96 Wissgot C, Scheinert D, Rademaker J et al. Treatment of superficial femoral artery occlusions with excimer laser angioplasty: long-term results after 48 months Laird JR, Peripheral excimer laser angioplasty (PELA) trial results. Presented at late breaking clinical trials. Transcatheter Cardiovascular Therapeutics (TCT) Annual Meeting, Washington DC, September 24–28, 2002.
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Laird JR, Zeller T, Gray Bh et al. Limb salvage following laser-assisted angioplasty for critical limb ischemia: results of the LACI multicenter trial. J Endovasc Ther 2006; 13(1): 1–11 Koster R, Hamm CW, Seabra-Gomes R et al. Laser angioplasty of restenosed stents: results of a multicenter surveillance trial. The Laser Angioplasty of Restenosed Stents (LARS) Investigators. J Am Coll Cardiol 1999; 34(1): 25–32 Zeller T, Rastan A, Sixt S et al; Long-term results after directional atherectomy of femoropopliteal lesions. J Am Coll Cardiol 2006; 48(8) 1573–8 Tepe G, Zeller T, Albrecht T, Speck U. Local taxan with short time exposure for reduction of restenosis in distal arteries. THUNDER TRIAL 6-month data. Oral Presentation at the Transcatheter Cardiovascular Therapeutics (TCT) Annual Meeting, Washington DC, 2006. Scheller B, Speck U, Abramjuk C et al. Paclitaxel balloon coating, a novel method for prevention and therapy of restenosis. Circulation 2004; 110: 810–4 Axel DI, Kunert W, Goggelmann C et al. Paclitaxel inhibits arterial smooth muscle cell proliferation and migration in vitro and in vivo using local drug delivery. Circulation 1997; 96: 636–45 Scheller B, Speck U, Romeike B et al. Contrast media as carriers for local drug delivery: successful inhibition of neointimal proliferation in the porcine coronary stent model. Eur Heart 2003; 24: 1462–7 Scheller B, Speck U, Schmitt A et al. Addition of paclitaxel to contrast media prevents restenosis after coronary stent implantation. J Am Coll Cardiol 2003; 42: 1415–20 Seck U, Scheller B, Abramjuk C et al. Neointima inhibition: comparison of effectiveness of non-stent based local drug delivery and a drug eluting stent in porcine coronary arteries. Radiology 2006; 240: 411–8 Scheller B, Hehrlein C, Bocksch W et al. Treatment of coronary in-stent restenosis with a paclitaxel-coated balloon catheter. N Engl J Med 2006; 355: 2113–24
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Update on peripheral vascular brachytherapy R Waksman
Introduction
Understanding gamma radiation
With the growing popularity of peripheral vascular medicine, identifying a reliable treatment to the plaguing recurrence of restenosis will increase and augment the benefits of vascular intervention. Investigators have shown that the endovascular delivery of radiation therapy is one such treatment. Combating restenosis in the peripheral vascular system is contingent upon understanding the processes, mechanisms, and potential targets affected by using brachytherapy. The successful outcome of clinical trials in the coronary arteries facilitated recognition of vascular brachytherapy to become the standard of care for the treatment of in-stent restenosis (ISR). Expansion of the indications to de novo lesions identified the potential but also the limitations of the technology (late thrombosis and edge effect). Simultaneously investigators embarked on a series of studies utilizing vascular brachytherapy as adjunct therapy for intervention in peripheral arteries. As patients in the baby boomer generation near their 60s, the full impact of peripheral and coronary atherosclerosis in the US is apparent. Whereas coronary vascular procedures increase at a rate of 8% per year, there is greater growth in the frequency of peripheral procedures, estimated at 19% per year. Despite new advances such as drug-eluting stents, atherectomy devices, thrombectomy, and endoluminal grafts, the restenosis rate after peripheral artery intervention continues to compromise the overall success of these procedures. Restenosis is still considered the ‘Achilles heel’ of percutaneous endovascular intervention.1–8 Among the approaches for restenosis prevention and treatment in the peripheral arterial system (PAS), only vascular brachytherapy (VBT) is reported to be safe and effective in this select group of patients. This article reviews the status of VBT, the available systems and dosimetry for use, and provides a summary of the latest reports from the clinical trials utilizing VBT to prevent or treat restenosis in the PAS.
Gamma rays are photons that originate from the center of the nucleus, as opposed to x-rays, which originate from the orbital outside of the nucleus. Gamma rays have deeply penetrating energies between 20 keV and 20 MeV, which require an excess of shielding, as compared to beta and x-ray emitters. The only gamma ray isotope currently in use is Ir-192. Other isotopes which emit both gamma and x-rays are iodine-125 (I-125) and palladium-103 (Pd-103), which have lower energies and require higher activities to deliver the prescribed dose in an acceptable dwell time (< 20 minutes). The latter isotopes are either not available in such activities or too expensive for this application. The dosimetry of Ir-192 is well understood and due to lesser fall-off in dose compared with beta emitters, the dose gradient at the area of interest is acceptable. Ir-192 is available in activities of up to 10 Ci, but due to the high penetration, the average shielding of a catheterization laboratory will not be able to handle more than 500-mCi source in activity. This limitation is associated with dwell times > 12 minutes for doses > 15 Gy when prescribed at 2 mm radial distance from the source.
Radiation systems for the peripheral vascular system The vessel size of the PAS favored the use of gamma radiation due to the penetration characteristics of the emitter. The majority of investigational work performed in the PAS used Ir-192 in doses of 14–18 Gy prescribed at 2 mm from the source center. 776
Understanding beta radiation Beta rays are high-energy electrons emitted by nuclei and contain too many or too few neutrons. These negatively charged particles have a wide variety of energies including transition energy, particularly between parent-daughter cells, and have a wide variety of half-lives, from several minutes (Cu-62) to 30 years (Sr/Y-90). Beta emitters rapidly lose their energy to the surrounding tissue and their range is within 1 cm of tissue. Therefore, they are associated with a higher gradient to the near wall. The use of beta sources for vascular application is attractive from both the radiation exposure and safety points of view.
External radiation External beam radiation is a viable option for the treatment of peripheral vessels because it allows a homogenous dose distribution with the possibility of fractionation. External radiation is currently used in a few centers for the treatment of ISR of the superficial femoral artery (SFA). Preliminary reports are encouraging, although caution should be applied
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to this strategy because of the potential for radiation injury to the nerve, vein, and the skin. Preliminary attempts with external radiation for the treatment of arteriovenous dialysis grafts failed to reduce the restenosis rate. This unsuccessful attempt was attributed to the conservative use of low doses and thrombosis of these grafts. Using stereotactic techniques to localize the radiation to the target area may improve the results of this approach. In their study, Therasse et al. tested the theory that external beam radiation would be more practical to administer than VBT after percutaneous transluminal angioplasty (PTA) in reducing restenosis. After femoropopliteal PTA without stent placement, 99 patients were randomly assigned to 0 Gy (placebo; n = 24), 7 Gy (n = 24), 10.5 Gy (n = 26), or 14 Gy (n = 25) of external beam radiation of the PTA site (with a 3-cm margin at both extremities) in one session 24 hours after PTA. Restenosis > 50% was present in 50%, 65%, 48%, and 25% of patients, for the 0-, 7-, 10.5-, and 14-Gy groups, respectively (p = 0.072). At 18 months, repeated revascularizations were required in 25% of patients in the 0 Gy group versus 12% of patients in the 14-Gy group (p = 0.24). It was found that a single session of external beam radiation of 14 Gy of the femoropopliteal angioplasty site significantly reduced restenosis at 1 year.9
Catheter-based gamma systems The most common catheter-based system used for SFA application is the MicroSelectron HDR system (NucletronOdelft, Delft, The Netherlands), which uses a computerized, high-dose rate afterloader system that delivers a 3-mm stepping, 10 Ci activity of Ir-192 into a closed-lumen radiation catheter (Figure 90.1) The Peripheral Brachytherapy Centering Catheter (Paris; Guidant Corporation, Indianapolis, IN) is a 7-French, double-lumen catheter with multiple centering balloons near its distal tip that enable the catheter to be in the center of the lumen of large peripheral vessels during inflation. The Paris catheter is no longer available. The only closed-end lumen catheter available is that used for oncology applications.
Catheter-based beta systems The only catheter-based beta system available is the BetaCath system, with a source train of up to 60 mm, which can be pulled back to allow coverage of long lesions. (Figure 90.2) The main limitation of the system is the penetration of the beta emitter, which is weakened significantly beyond 5 mm. This system can be used for below-the-knee applications or for other small vessels, including in-stent renal stenosis. It is recommended to perform the radiation prior to the intervention to ensure better centering and a higher dose to the treated proliferating tissue. Other innovative catheter-based radiation system developments have been halted because of the declining interest in the VBT field or slow recruitment into clinical trials. Included among these halted developments was the Radiance balloon system, (Radiance Medical Systems, Irvine, CA) which was
Figure 90.1 afterloader.
MicroSelectron high dose rate automatic
particularly attractive for peripheral applications because it is associated with apposition of a solid beta P-32 source attached to the inner balloon surface into the surface of the vessel wall. Another approach was the use of low x-ray energy delivered intraluminally via a catheter. The emitter was 5 mm in length and 1.25–2.0 mm in diameter and could be administered distally to the lesion and pulled back to cover the entire lesion length. The Corona system, a modification of the BetaCath system, was used to accommodate beta systems with the Sr/Y-90 emitter in the peripheral system. In this system, the balloon was filled with CO2, allowing centering and preventing dose attenuation. A clinical study in SFA for ISR lesions entitled MOBILE was terminated because of poor enrolment. The Corona system was also used in the BRAVO study for patients with AV dialysis grafts.
Clinical trials Liermann and Schopohl were the first to perform VBT for the treatment of ISR in the peripheral arteries. Known as the Frankfurt Experience, this pilot study was conducted in 30 patients with ISR in their SFAs.10–13 Patients underwent atherectomy and PTA followed by endovascular radiation using the MicroSelectron HDR afterloader and a non-centering catheter with Ir-192 (Please see Table 90.1 for a list of SFA Radiation Trials). No adverse effects from the radiation treatment were reported at up to 7-year follow-up. The 5-year
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Transfer device using hydraulic delivery of the radiation source train
Figure 90.2
Novoste’s Beta-Cath system.
patency rate of the target vessel was 82%, with only 11% stenosis within the treated segment reported. Late total occlusion developed in 7% of the treated vessels after 37 months.
The Vienna experience A series of studies was conducted at the University of Vienna. The majority were randomized studies targeting the SFA with or without stents using the MicroSelectron HDR afterloader with or without a centering catheter utilizing different doses. Vienna I was a pilot study with an indication of radiation safety after PTA that showed only 60% patentcy at 1 year.14 The Vienna II trial had 113 patients with de novo or recurrent femoropopliteal lesions who were randomized to PTA plus
Table 90.1
brachytherapy (n = 57) or PTA alone (n = 56). The primary end point of cumulative patency rate at 12 months’ follow-up was higher in the PTA plus brachytherapy group (63.6%) compared to the PTA group (35.3%). The patients from this study were followed-up to 36 months and demonstrated durability of the results15 (Figure 90.3). In Vienna III, a centering catheter that was used for the same patient population with a dose of 18 Gy showed a restenosis rate of 23.4% in the irradiated group compared to 53.3% in the placebo arm.16 Vienna IV was a pilot study examining radiation with stenting of the SFA; and Vienna V was a randomized study for similar indications. Both Vienna IV and V demonstrated an increase rate of subacute and late thrombosis when stents were combined with radiation, with up to 16.7% in the radiation group versus 4.3% in the control stenting without radiation. Once thrombosis was controlled, the radiation group had less restenosis.17
SFA radiation trials
Study
# Pts.
Randomized
Center Cath.
Frankfurt Vienna 1 Vienna 2 Vienna 3 Vienna 4 Vienna 5 PARIS pilot PARIS randomized Swiss 4 arm study
40 10 113 134 33 98 40 300 346
— — Yes Yes No Yes No Yes Yes
— No No Yes Yes Yes Yes Yes Yes
*Excluding thrombosis cases.
Dose (Gy) 12 12 12 18 14 14 14 14 12
@ mm
r r r r r r r
+ + + + + + +
3 3 0 2 2 2 2 2 2
Patency control % — — — 46 — 45 — 80 58
Patency VBT % 82 60 72 77 79 88* 88 76 83
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Patterns of Restenosis
Restenosis Free Survival Curves 100
PTA+BT
90
Placebo
PTA
80 70 60 50 40 30 20
P=0.005
10
Radiation
0 0 3 6 9 12 15 18 21 24 27 30 33 36 months
Figure 90.3
Results from Vienna II.
To summarize, the Vienna trials demonstrated efficacy of gamma radiation in reduction of restenosis following PTA to the SFA. However, these studies also demonstrated late catch-up of restenosis and late thrombosis in arteries that underwent stenting and radiation therapy.
The PARIS trials The Paris Radiation Investigational Study (PARIS) is the first FDA-approved, multicenter, randomized, double-blind, controlled study involving 300 patients following PTA to SFA stenosis using a gamma radiation Ir-192 source. Utilizing the MicroSelectron HDR afterloader, a treatment dose of 14 Gy was delivered via a centered segmented end-lumen balloon catheter. The primary objectives of this study were to determine angiographic evidence of patency and a reduction of > 30% of the restenosis rate of the treated lesion at 6 months. A secondary end point aimed to determine the clinical patency at 6 and 12 months by treadmill exercise and by the ankle–brachial index (ABI). In the feasibility phase of PARIS, 40 patients with claudication were enroled. The mean lesion length was 9.9 ± 3.0 cm with a mean reference vessel diameter of 5.4 ± 0.5 mm. The 6-month angiographic follow-up was completed on 30 patients; 13.3% of them had evidence of clinical restenosis.18 Because of poor enrolment, only 203 patients with claudication and femoropopliteal disease were enroled in the study. After successful PTA, a segmented centering balloon catheter was positioned to cover the PTA site. The patients were transported to the radiation oncology suite and randomized to receive either radiation therapy using the MicroSelectron HDR afterloader with Ir-192 at a dose of 14 Gy at 2 mm into the vessel wall (105 patients), or treatment
with a sham control in 98 patients. Patients were followed for 12 months, with clinic visits at 1, 6, and 12 months and follow-up angiography at 12 months. The restenosis rate at follow-up was similar in both groups (28.6% brachytherapy vs. 27.5% placebo) There was no significant difference in minimal lumen diameter, late loss, or the number of total occlusions. Exercise ABI, resting ABI, and maximum walking time were not different between treatment groups. For patients older than 65 years, maximum walking times at 6 and 12 months were better in the brachytherapy group. In the subgroups of patients with diabetes, male patients, or patients receiving clopidogrel or who have a proximal/medial lesion, maximum walking time in the brachytherapy group was better than in the placebo at 6 months but not different at 12 months. More studies to support the effectiveness of gamma radiation for ISR were recently published by Krueger et al.19 In this study, 30 patients who underwent PTA for de novo femoropopliteal stenoses were randomly assigned to undergo 14 Gy centered endovascular irradiation (irradiation group, n = 15) or no irradiation (control group, n = 15). Intra-arterial angiography was performed 6, 12, and 24 months after treatment; and duplex ultrasonography was performed the day before and after PTA and at 1, 3, 6, 9, 12, 18, and 24 months later. Baseline characteristics did not differ significantly between the two groups. Mean absolute individual changes in degree of stenosis, compared with the degrees of stenosis shortly after PTA in the irradiation group versus in the control group were 10.6% ± 22.3 versus 39.6% ± 24.6 (p < 0.001) at 6 months, 2.0% ± 34.2 versus 40.6% ± 32.6 (p = 0.002) at 12 months, and 7.4% ± 43.2 versus 37.7% ± 34.5 (p = 0.043) at 24 months. The rates of target lesion restenosis at 6 months (p = 0.006) and 12 months (p = 0.042) were significantly lower in the irradiation group. The authors concluded that endovascular radiation was effective for
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patients who were treated with angioplasty for de novo femoropopliteal lesions.
Restenostic lesions and VBT The effectiveness of VBT for restenotic SFA lesions was examined in another randomized study reported by Zehnder et al. In this study, gamma radiation was used at a dose of 12 Gy. The primary endpoint was > 50% restenosis at 12 months assessed by duplex Doppler. The recurrence rate in the radiation arm was 23% versus 42% in the PTA alone group.20 This study demonstrated that VBT can be effective in restenotic lesions.
Brachytherapy and probucol In another randomized, four-arm study for patients with PTA lesions, patients were randomized to VBT, VBT and probucol, probucol alone, or placebo. The recurrence rate in the radiation arm alone was 17%, VBT and probucol was 20%, probucol alone was 27%, and the placebo group was 42%. This study confirms prior observations regarding the effectiveness of VBT for the treatment of SFA lesions without additional benefit of probucol when compared to PTA alone.21
AV Dialysis studies An initial study at Emory University in 1994 to treat patients who had failed PTA of arteriovenous dialysis grafts using the MicroSelectron HDR afterloader reported 40% patency rate at 44 weeks;22 however, the long-term results of this study were similar to stand-alone PTA without radiation. Similar disappointing results were reported by Parikh et al. from a pilot study utilizing external radiation doses of 12 Gy and 18 Gy for AV dialysis shunts in 10 patients.23 At 6 months, target lesion revascularization was 40%, but at 18 months all grafts failed and required intervention. Cohen et al. randomized 31 patients to PTA or stent placement alone followed by external radiation of 14 Gy in two 7-Gy fractions and reported restenosis rates of 45 versus 67% in the irradiated and control groups, respectively, at 6 months.24 New studies are currently underway using lowdose external radiation to reduce restenosis of vascular access for AV grafts in hemodialysis patients, as are other studies using a centering device to deliver an accurate homogenous dose of radiation after PTA. The Beta Radiation following balloon angioplasty for improving life span of recurrent failed ArterioVenous fistulae (BRAVO) study was a pilot study utilizing the Corona system with an Sr/Y90 beta emitter. In the study of 10 patients with an average of 3.9 previous angioplasties to their AV graft, there was 60% primary patency and cumulative patency of 80% at 12-month mean follow-up.25
several studies aimed to look into the efficacy of gamma brachytherapy for the treatment of ISR in renal arteries. Kuchulakanti et al.26 studied 11 patients who presented with renal ISR documented by selective renal angiography and who were assigned to treatment with γ -BT using Ir-192, followed by balloon angioplasty, laser, or restenting (Figure 90.4). The patients were followed clinically at 1, 3, 6, and 9 months, and duplex ultrasound was conducted at 9 months. Procedural success was 100% and free of complications. Clinical follow-up was available in all patients and duplex ultrasound in 10 patients. No significant changes in blood urea nitrogen, serum creatinine, creatinine clearance, or the number of antihypertensive medications were observed at follow-up. One patient (9.1%) required target lesion revascularization at 9 months. It was found that gamma brachytherapy as adjunct therapy for the treatment of renal artery ISR appears safe and feasible. However, the clinical benefit of this therapy has to be proven in a large randomized clinical trial. Smaller renal arteries with ISR can utilize the BetaCath system that is currently used for ISR in coronary arteries; however the dose should be adjusted to the vessel size.
Limitations to brachytherapy Although clinical trials using VBT for both coronary and peripheral applications have demonstrated positive results in reducing restenosis rates, these trials have also identified 2 major complications related to the technology – late thrombosis, especially in the presence of stents, and edge stenosis. Late thrombosis is probably due to the delay in healing associated with radiation. It has been demonstrated that late thrombosis can be remedied through the prolonged administration of antiplatelet therapy after intervention. The main explanation for the occurrence of the edge effect is a combination of low doses at the edges of the radiation source and an injury created by the device for intervention that is not covered by the radiation source. It has been shown that wider margins of radiation treatment to the intervening segment significantly reduce the edge effect.
Vascular brachytherapy for in-stent restenosis of renal arteries The incidence of ISR after renal artery stenting is 12–21%, yet there is no standard treatment method for this problem. Vascular brachytherapy is not approved for this indication but
Figure 90.4 Active Ir-192 source across the in-stent restenosis lesion at the ostium of left renal artery.
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Update on peripheral vascular brachytherapy With the growing popularity of peripheral vascular medicine, identifying a reliable treatment for the plaguing recurrence of restenosis will increase and augment the benefits of vascular intervention. Investigators have shown that the endovascular delivery of radiation therapy is one such treatment. Combating restenosis in the peripheral vascular system is contingent upon understanding the processes, mechanisms, and potential targets affected by brachytherapy use. The successful outcome of clinical trials in the coronary
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arteries facilitated the recognition of VBT as being the standard of care for the treatment of in-stent restenosis. Expansion of the indications to de novo lesions identified the potential, but also the limitations, of the technology. Simultaneously, investigators embarked on a series of studies utilizing VBT as adjunct therapy for intervention in peripheral arteries. The outcome of these trials will determine the future role of vascular brachytherapy as a tool for prevention of restenosis in the peripheral vascular system.
REFERENCES 1. 2.
3. 4. 5. 6.
7. 8.
9. 10.
11.
12. 13.
Murray RR Jr, Hewews RC, White RI Jr et al. Long-segment femoro-popliteal stenoses: is angioplasty a boon or a bust? Radiology 1987; 162: 473–6 Vroegindeweij D, Kemper FJ, Teilbeek AV et al. Recurrence of stenosis following balloon angioplasty and Simpson atherectomy of the femoropopliteal segment. A randomized comparative. 1 year follow-up study using color flow duplex. Eur J Vasc Surg 1992; 6: 164–71 Rees CR, Palmaz JC, Becker GJ et al. Palmaz stent in atherosclerotic stenosis involving the ostia of the renal arteries: Preliminary report of a multicenter study. Radiology 1991; 181: 507–14 Hunink MFM, Magruder CD, Meyerovitz MF et al. Risks and benefits for femoropopliteal percutaneous balloon angioplasty. J Vasc Surg 1993; 17: 183–94 White GF, Liew SC, Waugh RC et al. Early outcome of intermediate follow-up of vascular stents in the femoral and popliteal arteries without long term anticoagulation. J Vasc Surg 1995; 21: 279–81 Dolmath BL, Gray RJ, Horton KM et al. Treatment of anastomotic bypass graft stenosis with directional atherectomy: short term and intermediate-term results. J Vasc International Radiology 1995; 6: 105–13 Johnston KW. Femoral and popliteal arteries: Reanalysis of results of angioplasty. Radiology 1987; 162: 473–6 Haude M, Erbel R, Issa H et al. Quantitative analysis of elastic recoil after balloon angioplasty and after intracoronary implantation of balloon-expandable Palmaz–Schatz stents. J Am Coll Cardiol 1993; 21: 2634 Therasse E, Donath D, Lesperance J et al. External beam radiation to prevent restenosis after superficial femoral artery balloon angioplasty. Circulation 2005; 111: 3310–5 Liermann DD, Bottcher HD, Kollath J et al. Prophylactic endovascular radiotherapy to prevent intimal hyperplasia after stent implantation in femoropopliteal arteries. Cardiovasc Intervent Radiol 1994; 17: 12–6 Bottcher HD, Schopohl B, Liermann D et al. Endovascular irradiation – a new method to avoid recurrent stenosis after stent implantation in peripheral arteries: technique and preliminary results. Int J Rad Oncol Biol Phys 1994; 29: 183–6 Liermann D, Kirchner J, Schopohl B et al. Brachytherapy with iridium-192 HDR to prevent restenosis in peripheral arteries: an update. Herz 1998; 23: 394–400 Sidawy AN, Weiswasse JM, Waksman R. Peripheral vascular brachytherapy. J Vasc Surg 2002; 35: 1041–7
14. 15.
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Minar E, Pokrajac B, Ahmadi R et al. Brachytherapy for prophylaxis of restenosis after long-segment femoropopliteal angioplasty: pilot study. Radiology 1998; 208: 173–9 Minar E, Pokrajac B, Maca T et al. Endovascular brachytherapy for prophylaxis of restenosis after femoropopliteal angioplasty: results of a prospective randomized study. Circulation 2000; 102: 2694–9 Pokrajac B, Schmid R, Poetter R et al. Endovascular brachytherapy prevents restenosis after femoropopliteal angioplasty: results of the Vienna-3 multicenter study. Int J Radiat Oncol Biol Phys 2003; 57(suppl): S250 Wolfram RM, Pokrajac B, Ahmadi R et al. Endovascular brachytherapy for prophylaxis against restenosis after long-segment femoropopliteal placement of stents: initial results. Radiology 2001; 220: 724–9 Waksman R, Laird JR, Jurkovitz CT et al. Intravascular radiation therapy after balloon angioplasty of narrowed femoropopliteal arteries to prevent restenosis: results of the PARIS feasibility clinical trial. J Vasc Interv Radiol 2001; 12: 915–21 Krueger K, Zaehringer M, Bendel M et al. De novo femoropopliteal stenoses: endovascular gamma irradiation following angioplasty – angiographic and clinical follow-up in a prospective randomized controlled trial. Radiology 2004; 231: 546–54 Zehnder T, von Briel C, Baumgartner I et al. Endovascular brachytherapy after percutaneous transluminal angioplasty of recurrent femoropopliteal obstructions. J Endovasc Ther 2003; 2: 304–11 Gallino A, Do DD, Alerci M et al. Effects of probucol versus aspirin and versus brachytherapy on restenosis after femoropopliteal angioplasty: the PAB randomized multicenter trial. J Endovasc Ther 2004; 11: 595–604 Waksman R, Crocker IA, Kikeri D et al. Long term results of endovascular radiation therapy for prevention of restenosis in the peripheral vascular system. Circulation 1996; 94(8)I–300: 1745 Parikh S, Nori D, Rogers D et al. External beam radiation therapy to prevent postangioplasty dialysis access restenosis: a feasibility study. Cardiovasc Radiat Med 1999; 1: 36–41 Cohen GS, Freeman H, Ringold MA. External beam irradiation as an adjunctive treatment in failing dialysis shunts. JVIR 2000; 11: 1364 Bonan R. BRAVO. Presented at Cardiovascular Revascularization Therapies 2004 Waksman R, Kuchulakanti PK, Laird JR et al. Gamma brachytherapy for the treatment of in-stent restenosis of renal arteries. Vasc Dis Man 2006; 3(1):178–83
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Gene-based and angiogenesis therapy in cardiovascular diseases R Baffour, S Fuchs, and R Kornowski
What is gene therapy? A gene (within each cell’s DNA) is an inheritable (able to be passed on from one generation to the next generation) material found in every cell. Genes are necessary for each cell to “know” how to grow and develop. In a way, genes may be thought of as “cellular recipes.” Since organs are made up of many cells, it is necessary for the cells to grow and develop normally for the organ to function in a healthy manner. Gene therapy involves the introduction of normal or modified genes into cells of a specific, predetermined organ. The purpose of this introduction is to correct or alter cellular functions such that the disorder will become corrected or be prevented. There has been much interest in using gene therapy to treat inheritable diseases, long-term health disorders, and cancer. Many clinical studies are underway worldwide in the treatment of inflammatory diseases, inheritable enzyme deficiency diseases, cancer, and so on. Cardiovascular diseases have become a new aim for gene therapy research. Cardiovascular gene therapy is being evaluated for angiogenesis (the procedure of causing new blood vessel growth) in ischemic territories, the prevention of restenosis after angioplasty, and the treatment of atherosclerosis, hereditary forms of hypercholesterolemia, and congestive heart failure. In vivo gene therapy (gene therapy performed within the cell of a living being either human or animal) usually relies on a vector to introduce the gene into the cell. Vectors are special biological complexes that are able to pass through the cellular membrane (outside barrier of each cell). A vector may be thought of as “a vehicle with correct identification to cross a biological barrier” that permits the genetic material (DNA) to get inside the cell. Vectors currently in use include plasmids (“naked” DNA fragments) with or without liposome complexes, adeno-associated viruses, adenoviruses, and retroviruses. These viruses are replication deficient. In adenoviral methods of delivery, the virus infects the cells bordering the point of injection. It does this with a very high degree of efficiency. The growth factor’s DNA then travels from the cytoplasm of the cell to the nucleus, where it is made into an active protein. The active protein is then secreted from the cell and travels throughout the heart to stimulate blood vessel growth where it is most needed and acts on nearby endothelial cells. With plasmids, a therapeutic gene (“naked” DNA) is injected into the target tissue and is taken up by the target cells. The newly introduced DNA segment can serve as a template for RNA to form new/deficient therapeutic proteins, 782
although new DNA segments do not integrate into the native cellular DNA. Table 91.1 specifies various vectors in investigational usage for gene therapy. Figure 91.1 shows schematics for gene therapy using adenoviral vector or plasmid (“naked” DNA segment), and Figure 91.2 shows the pathology of heart tissue after gene transfer.
Angiogenic growth factors Angiogenic growth factors are very powerful elements that cause blood vessels cells to grow. Endothelial cells are necessary to the structure of blood vessels. Growth factors or angiogenic genes have been demonstrated to show new blood vessel growth in animal studies and in the heart and leg of humans in phase I clinical trials.1–21 There are several varieties of growth factors. Growth factors cause sprouting of new endothelial cells from existing blood vessels. These new blood vessels are then directed to grow towards the areas of maximal ischemia. The new blood vessels are then able to supply blood from a healthy area of the heart or peripheral limb into the unhealthy areas of the muscle. This identification of angiogenic growth factor “prototypes,” such as vascular endothelial growth factor (VEGF),22–26 basic fibroblast growth factor (bFGF, or FGF2) and acidic FGF (aFGF, or FGF1), occurred in the late 1970s and early 1980s.27–31 The practical application of these agents in cardiovascular ischemic syndromes had to await the development of technologies that allowed the angiogenic proteins to be produced in sufficient quantities, and subsequently the development of DNA technology and gene delivery techniques so that gene therapy studies became possible. Once these biotechnology breakthroughs were achieved, studies exploring the potential of various angiogenesis strategies to develop clinically relevant therapeutic approaches to both myocardial and leg ischemia have been conducted, so that over the past halfdecade the field has moved forward with great momentum. Using gene therapy constructs presents a potential advantage over “simple” administration of angiogenic protein, since gene therapy can be considered a biological form of a sustained delivery system. A protein, injected once intramuscularly, would be unlikely to persist in the tissue long enough to exert an important biological effect. Once transfected, the target cell expresses gene product for days, weeks, or longer, depending on the specific tissue transfected and on the specific vector used.
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Characteristics of various vectors Transfection efficacy
Host response
Target cells
DNA integration
DNA capacity
Plasmid DNA Retrovirus Adenovirus
Low Low High
Cycling Cycling All
No Yes No
Adeno-associated virus Oligonucleotide
Unclear
Against gene product Against gene product Against gene product and viral proteins Against gene product
Unclear
High
Low
Cycling> quiescent All
Not limited Limited to viral size Limited by deletion size in virus Limited to viral size
No
NA
NA, not applicable.
Proof of the concept that gene therapy can improve collateral function in the heart was demonstrated by Giordano et al.32 They found in a porcine model of myocardial ischemia (ameroid occlusion of the circumflex coronary artery) that a single-dose intracoronary administration of an adenoviral vector carrying the FGF5 transgene into the non-occluded coronary results in more than 90% “first-pass” myocardial uptake, causing increased myocardial flow and function. Hammond and colleagues have since demonstrated that FGF4 produces similar effects in restoring myocardial flow and function. Other investigators have also performed studies
DNA genome
employing the rabbit hindlimb model of ischemia and have reported that injection into the femoral artery of the VEGF165 transgene carried in a plasmid vector improves collateral flow.33 As stated above, a protein, injected once intramuscularly, would be unlikely to persist in the tissue long enough to exert an important biological effect. Although multiple injections of protein might well improve collateral flow,34 such a strategy has practical limitations. Therefore, once it was demonstrated that an adenoviral vector carrying a reporter transgene efficiently expresses its gene product after intramyocardial
Therapeutic gene
Nuclear pore
Non-viral vector
(a)
DNA plasmid
Lipid (b) Figure 91.1 Representation of gene transfer using adenoviral vector or plasmid (“naked” DNA segment). (a) Adenoviral vector with the attached therapeutic gene infects cell through specific receptors. In the cytoplasm of the cell, the virus delivers the therapeutic gene to the nucleus through the nuclear pore where the gene is expressed. (b) Liposome delivers plasmid DNA through receptormediated endocytosis or fusion with cell membrane. Plasmid DNA is then released in the cytoplasm and transported to the nucleus, where the therapeutic gene is expressed.
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(b)
(c)
Figure 91.2 Gross (a) and microscopic (b) pathology of heart tissue (cross-section) injected with the adenovirus vector containing the β-galactosidase reporter transgene and subsequently stained with X-gal solution. Note the areas of positive staining. Histopathology shows myocytes transfected by adenovirus-β-galactosidase gene with typical nuclear as well as cytoplasmic staining (original magnification × 40). (c) A representative injection site relative to fluorescent microsphere location shown under ultraviolet light. This shows successful gene delivery identified by co-injection of fluorescent beads and either β-galactosidase marker or VEGF-121 isoform gene.
injection,35 this approach to gene delivery was explored as an approach for gene therapy. Proof of the concept that intramyocardial injection could enhance collateral flow and improve impaired myocardial function was demonstrated in a porcine model of myocardial ischemia. This was achieved by the transepicardial injection of an adenoviral vector carrying the VEGF121 transgene performed following thoracotomy.36 The feasibility of catheter-based transendocardial delivery of angiogenic genes has recently been shown,37,38 demonstrating that the direct injection of angiogenesis factors into the myocardium can be accomplished without the need for open chest thoracotomy.
Patient candidates for angiogenic gene therapy Growth factors, given either as genes or peptides, have been demonstrated to induce new blood vessel growth in animal studies and in the heart and leg of humans in phase I clinical trials (testing safety and effectiveness).32,33,35–37,39–45 By increasing the bloodflow with the growth of new blood vessels, they may cause the chest pain and other ischemic manifestations to decrease or even disappear. Research trials in cardiology include patients with severe anginal symptoms (symptoms of chest pain with very little exertion or at rest) who have been turned down for bypass surgery and angioplasty. Similarly, patients with advanced peripheral vascular disease who were poor candidates for conventional surgical revascularization and endovascular interventional therapy have undergone gene therapy research trials.18,19 Almost all angiogenic gene therapy studies have involved attempts to enhance angiogenesis and collateral development in ischemic tissue beds. However, a recent report suggests that transfer of an angiogenic (VEGF) gene may also be effective in treating ischemic peripheral diabetic neuropathy in an experimental model of this disease.46
Routes of administration for gene delivery Various delivery routes, including transcatheter, intraoperative intramyocardial injection, intrapericardial and catheter-based transendocardial, have been used to locally transfer angiogenic growth factors or genes in coronary studies.35,37,38,47,48 Delivery routes used in peripheral vascular disease studies are transcatheter and direct injection into skeletal muscle.18,19 Which of these approaches for both coronary and peripheral vascular disease are most safe and effective remains to be determined. Theoretically, it would seem that local gene delivery via direct intramuscular injection might be more effective than other routes, since genes can be targeted to specific ischemic areas of the myocardium or peripheral muscle.
Clinical experiences Several clinical trials in both coronary and peripheral vascular disease studies have been reported (Table 91.2). In essence, nearly all of these studies were phase I trials, which demonstrated the safety and feasibility of growth factor or gene therapy. For example, in a preliminary study VEGF165 protein was administered by the intracoronary route to establish the correct dose and infusion rates. In this study, three treatment groups of patients, including a placebo-controlled group, were assessed at baseline and 60 days later. The assessments included exercise treadmill time, retinal photographs and angina class determination. However, a subsequent randomized double-blind phase II study (VIVA trial) using intracoronary followed by three intravenous doses of VEGF165 protein showed no beneficial effect as assessed by treadmill exercise performance, the primary endpoint.17 Indeed, there were similar performance improvements in treated and untreated patients. Similar disappointing results have been reported
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Gene-based and angiogenesis therapy in cardiovascular diseases Table 91.2 Clinical trials: gene therapy in coronary vascular disease (CVD) and peripheral vascular disease (PVD) Reference
Treatment Disease Results
Rosengart VEGF et al. (1999)15
CVD
Losordo et al. VEGF (1998)16
CVD
Isner et al. (1996)18
VEGF
PVD
Baumgartner VEGF et al. (1998)19
PVD
Isner et al. (1998)20
PVD
VEGF
Collateral development + Myocardial function + Left ventricular ischemic zone – Collateral development + Intra-arterial bloodflow + Angiogenesis + Development of spider angiomas Ankle–brachial index + Collateral development + Distal bloodflow + Development of transient lower limb edema Non-healing ulcer healed Distal limb perfusion + Limb bloodflow + Collateral development + Development of transient ankle and calf edema +
+, stimulation; –, reduction.
recently following intracoronary administration of basic FGF protein in a blinded randomized phase II trial.49 Other investigators have reported enhanced angiogenesis and growth of collaterals after intramuscular injection of the plasmid encoding VEGF165 in patients with critical limb ischemia.18,19 However, these two studies had no controlled groups for comparison. In one of these studies, VEGF plasmid was transferred to the distal popliteal artery of a patient with an ischemic limb. At 4 and 12 weeks after gene transfer, follow-up assessments were performed. Angiography revealed collateral development, and intra-arterial Doppler bloodflow showed improvement.18 Ongoing clinical trials include two pioneering randomized controlled phase I studies using the electromagnetic catheterbased transendocardial injection technique (Biosense, Johnson and Johnson, NJ) of either VEGF-II plasmid or adenovirus containing the VEGF121 transgene. These studies are designed to test the feasibility and safety aspects of such catheter-based approaches for transendocardial angiogenic gene delivery. The studies include appropriate “control” patients who are blinded to the actual treatment. In addition, preliminary efficacy endpoints may reveal the potential efficacy of such pro-angiogenic intervention among patients by including subjective and objective efficacy measures of myocardial ischemia. In a recent study, similar to the discussed ongoing trials, Vale and colleagues used left ventricular (LV) electromechanical mapping (EMM) to assess infarcted, ischemic, and normal myocardium before and after gene transfer.50 They treated patients with chronic myocardial ischemia, not amenable to current therapeutic interventions, with direct myocardial injection of VEGF plasmid through a small incision in the left lateral chest. Sixty days after gene transfer, there was significant improvement in the areas of
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myocardial ischemia as assessed by LV EMM, suggesting increased perfusion of the ischemic myocardium as a result of gene therapy.50 The results of a phase II clinical trial of recombinant fibroblast growth factor-2 (FGF-2) protein in peripheral artery disease were recently presented.51 The pre-specified efficacy analysis of change in peak walking time (PWT) at day 90 showed a positive trend in patients receiving a single bolus of FGF-2 compared to control patients or patients receiving a double bolus FGF-2 dose (34.1 vs. 20.1 vs. 14.1 increase vs. baseline, p = 0.07). Intra-coronary administration of Ad FGF-4 showed promising results in patients with coronary disease who elected to undergo this mode of experimental treatment instead of coronary angioplasty or bypass surgery.52 At 12 weeks following treatment, more patients receiving IC gene transfer had significant improvement in exercise treadmill time compared to placebo treated patients (45 vs. 21.1). These recent trials have confirmed safety, feasibility, and also suggested positive trends for either protein-based (peripheral artery disease) or gene-based (coronary disease) pro-angiogenesis interventions.
Potential hazards with gene therapy It is conceivable that angiogenic agents that cause beneficial effects in chronic ischemic disease may cause unnecessary side-effects as well. For that reason, it is pertinent that the risk/benefit ratio should be taken into consideration before any therapeutic angiogenesis is instituted. Obviously, only a low risk ratio should be acceptable. Administration of angiogenic agents as treatment modality for chronic disease may be inappropriate in the presence of proliferative retinopathy, since these agents may enhance angiogenesis in this disease. Other areas of concern are undesired angiogenesis in normal tissues, and kidney damage. The angiogenic effects of growth factors appear to be restricted to injured or ischemic tissue, where there is upregulation of angiogenic receptor genes.53.54 This may not necessarily apply to a normal organ, which has been exposed to high doses of angiogenic agents for an extended time. Agents such as VEGF may cause increased vascular permeability that may lead to multiple organ edema.53 Other potential undesired effects include growth of tumors and atherogenic plaque formation as demonstrated in some experimental studies.56–60 It is reported that a patient with critical limb ischemia developed spider angiomas after phVEGF165 gene transfer.18 To our knowledge, there are no other clinical reports that suggest that angiogenic agents give rise to the growth of new tumor. Some angiogenic agents such as VEGF and bFGF proteins can cause hypotension following endovascular administration.61–63 Similar responses are reported particularly in patients who receive rapid administration of high doses of bFGF.14,21
Prevention of atherosclerosis, restenosis and congestive heart failure Atherosclerosis is a complex disease linked with multiple genes and risk factors such as family history, hypercholesterolemia, hypertension, smoking, diabetes mellitus, and others.
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To date, it appears that only a few distinct causes of this disease are amenable to gene therapy. Animal and clinical studies have shown that gene replacement therapy can prevent genetic disorders, such as low-density lipoprotein (LDL) receptor deficiency, which cause premature atherosclerosis.64–66 In these studies, few patients with homozygous familial hypercholesterolemia were successfully treated with liver-directed LDL receptor gene transfer. Another potential approach to prevent atherosclerosis is the use of genes which produce proteins that either impede this disease or stabilize susceptible lesions.67 Gene therapy to prevent neointimal formation following coronary angioplasty and stenting may be a viable option to current therapeutic interventions, most of which have been unsuccessful in decreasing the numbers of restenoses.68 Because there are several mechanisms involved in restenosis, such as smooth muscle cell proliferation, thrombosis, platelet activation, and remodeling, transfer of multiple genes may be required to completely prevent restenosis.68 Some studies have demonstrated decreased neointimal formation by transfer of different genes to the media of vessels after injury. For example, the transfer of human tissue inhibitor of the metalloproteinase 1 gene can prevent smooth muscle cell migration and neointimal formation in an in vitro human saphenous vein model.69 Another theoretical approach may be the use of anti-restenotic gene-containing growth factor inhibitors that may decrease blood vessel supply to the neointima tissue. Animal studies suggest that overexpression or downregulation of some myocardial genes may be an effective treatment for congestive heart failure, and this potentially may be applicable to similar disease in humans. Transfer of β2 adrenergic
receptor genes has been shown to enhance heart function in transgenic mice with heart failure.70 Similarly, transfer of a gene whose product inhibits the activity of β-adrenergic receptor kinase, an enzyme that desensitizes and controls β-adrenergic receptors, has been shown to prevent heart failure in a rabbit model of cardiomyopathy.71
Conclusion Substantial knowledge has been acquired over recent years about the use of gene therapy as a treatment modality for cardiovascular diseases. However, much still needs to be learned before such treatment becomes successful in patients. In the past, efficient and safe deliveries of genes to the right targets were the major limitations of gene therapy. Better vectors and delivery systems have been developed over recent years with improved transfection efficiency and delivery to the target tissue, either the ischemic myocardium or peripheral limb. Preliminary clinical results are encouraging with regard to the feasibility and safety of gene therapy approaches applied to the cardiovascular system. Because of the complex nature of cardiovascular diseases, which involve multiple genes, the use of a single gene to treat a disease may not give the best possible result. Perhaps one should consider the idea of using multiple genes in combination, sequentially or in concert, to achieve a more effective intervention. We should also be aware of serious complications and potential side-effects of gene therapy. Thus, cautiously controlled clinical trials must be completed to determine whether the risk/benefit ratio is sufficiently low such that the accompanying risks of gene therapy are overshadowed by the benefits achieved.
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Banai S, Jaklitsch MT, Shou M et al. Angiogenic-induced enhancement of collateral blood flow to ischemic myocardium by vascular endothelial growth factor in dogs. Circulation 1994; 89: 2183–9 Takeshita S, Zheng LP, Brogi E et al. Therapeutic angiogenesis: a single intraarterial bolus of vascular endothelial growth factor augments revascularization in a rabbit ischemic hind limb model. J Clin Invest 1994; 93: 662–70 Pearlman JD, Hibberd MG, Chaung ML et al. Magnetic resonance mapping demonstrates benefits of VEGF-induced myocardial angiogenesis. Nat Med 1995; 1: 1085–9 Harada K, Friedman M, Lopez JJ et al. Vascular endothelial growth factor administration in chronic myocardial ischemia. Am J Physiol 1996; 270: H1791–802 Yanagisawa-Miwa A, Uchida Y, Nakamura F et al. Salvage of infarcted myocardium by angiogenic action of basic fibroblast growth factor. Science 1992; 257: 1401–3 Battler A, Scheinowitz M, Bor A et al. Intracoronary injection of basic fibroblast growth factor enhances angiogenesis in infarcted swine myocardium. J Am Coll Cardiol 1993; 22: 2001–6 Harada K, Grossman W, Friedman M et al. Basic fibroblast growth factor improves myocardial function in chronically ischemic porcine heart. J Clin Invest 1994; 94: 623–30 Uchida Y, Yanagisawa-Miwa A, Ikuta M et al. Angiogenic therapy of acute myocardial infarction (AMI) by intrapericardial injection of basic fibroblast growth factor (bFGF) and heparin sulfate (HS): an experimental study. Circulation 1994; 90(suppl I): I–296 (abstr) Unger EF, Banai S, Shou M et al. Basic fibroblast growth factor enhances myocardial collateral flow in a canine model. Am J Physiol 1994; 35: H1588–95 Lazarous DF, Scheinowitz M, Shou MN et al. Effects of chronic systemic administration of basic fibroblast growth factor on collateral development in the canine heart. Circulation 1995; 91: 145–53
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Schumacher B, Pecher P, von Specht BU, Stegmann T. Induction of neoangiogenesis in ischemic myocardium by human growth factors: first clinical results of a new treatment of coronary heart disease. Circulation 1998; 97: 645–50 Sellke FW, Laham RJ, Edelman ER et al. Therapeutic angiogenesis with basic fibroblast growth factor: technique and early results. Ann Thorac Surg 1998; 65: 1540–4 Laham RJ, Sellke FW, Edelman ER et al. Local perivascular delivery of basic fibroblast growth factor in patients undergoing coronary bypass surgery: results of a phase I randomized, double-blind, placebo-controlled trial. Circulation 1999; 100: 1865–71 Unger EF, Goncalves L, Epstein SE et al. Effects of a single intracoronary injection of basic fibroblast growth factor in stable angina pectoris. Am J Cardiol 2000; 85: 1414–19 Rosengart TK, Lee LY, Patel SR et al. Angiogenesis gene therapy: phase I assessment of direct intramyocardial administration of an adenovirus vector expressing VEGF121 cDNA to individuals with clinically significant severe coronary artery disease. Circulation 1999; 100: 468–74 Losordo DW, Vale PR, Symes JF et al. Gene therapy for myocardial angiogenesis: initial clinical results with direct myocardial injection of phVEGF165 as sole therapy for myocardial ischemia. Circulation 1998; 98: 2800–4 Henry TD, Annex BH, Azrin MA et al. Double blind, placebo controlled trial of recombinant human vascular endothelial growth factor – the VIVA trial. J Am Coll Cardiol 1999; 33(suppl A): 384A (abstr) Isner JM, Pieczek A, Schainfeld R et al. Clinical evidence of angiogenesis after arterial gene transfer of phVEGF165 in patient with ischaemic limb. Lancet 1996; 348: 370–4 Baumgartner I, Pieczek A, Manor O et al. Constitutive expression of ph VEGF165 after intramuscular gene transfer promotes
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collateral vessel development in patients with critical limb ischemia. Circulation 1998; 97: 1114–23 Isner JM, Baumgartner I, Rauh G et al. Treatment of thromboangiitis obliterans (Buerger’s disease) by intramuscular gene transfer of vascular endothelial growth factor: preliminary clinical results. J Vasc Surg 1998; 28: 964–73 Lazarous DF, Unger EF, Epstein SE et al. Basic fibroblast growth factor in patients with intermittent claudication: results of a phase I trial. JACC (in press) Dvorak HF, Orenstein NS, Carvalho AC et al. Induction of a fibrin-gel investment: an early event in line 10 hepatocarcinoma growth medicated by tumor-secreted products. J Immunol 1979; 122: 166–74 Senger Dr, Galli SJ, Dvorak AM et al. Tumor cells secrete a vascular permeability factor that promotes accumulation of ascites fluid. Science 1983; 219: 983–5 Senger DR, Perruzzi CA, Feder J, Dvorak HF. A highly conserved vascular permeability factor secreted by a variety of human and rodent tumor cell lines. Cancer Res 1986; 46: 5629–32 Senger DR, Connolly D, Perruzzi CA et al. Purification of a vascular permeability factor (VPF) from tumor cell conditioned medium. Fed Proc 1987; 46: 2102 Connolly DT, Olander JV, Heuvelman D et al. Human vascular permeability factor. Isolation from U937 cells. J Biol Chem 1989; 264: 20017–24 Esch F, Baird A, Ling N et al. Primary structure of bovine pituitary basic fibroblast growth factor (FGF) and comparison with the amino-terminal sequence or bovine brain acidic FGF. Proc Natl Acad Sci USA 1985; 82: 6507–11 Gambarini AG, Armelin HA. Pituitary fibroblast growth factors. Partial purification and characterization. Braz J Med Biol Res 1981; 14: 19–27 Logan A, Berry M, Thomas GH et al. Identification and partial purification of fibroblast growth factor from the brains of developing rats and leucodystrophic mutant mice. Neuroscience 1985; 15: 1239–46 Baird A, Esch F, Gospodarowicz D, Guillemin R. Retina- and eyederived endothelial cell growth factors: partial molecular characterization and identity with acidic and basic fibroblast growth factors. Biochemistry 1985; 24: 7855–60 Baird A, Esch F, Bohlen P et al. Isolation and partial characterization of an endothelial cell growth factor from the bovine kidney homology with basic fibroblast growth factor. Regul Pept 1985; 12: 201–13 Giordano FJ, Ping P, Mckirnan D et al. Intracoronary gene transfer of fibroblast growth factor-5 increases blood flow and contractile function in an ischemic region of the heart. Nature Med 1996; 2: 534–9 Witzenbichler B, Asahara T, Murohara T et al. Vascular endothelial growth factor-C (VEGF-C/VEGF-2) promotes angiogenesis in the setting of tissue ischemia. Am J Pathol 1998; 153: 381–94 Baffour R, Berman J, Garb JL et al. Enhanced angiogenesis and growth of collaterals by in vivo administration of recombinant basic fibroblast growth factor in a rabbit model of acute lower limb ischemia: dose–response effect of basic fibroblast growth factor. J Vasc Surg 1992; 16: 181–91 Guzman RJ, Lemarchand P, Crystal RG et al. Efficient gene transfer into myocardium by direct injection of adenovirus vectors. Circ Res 1993; 73: 1202–7 Mack CA, Patel SR, Schwartz EA et al. Biologic bypass with the use of adenovirus-mediated gene transfer of the complementary deoxyribonucleic acid for VEGF-12, improves myocardial perfusion and function in the ischemic porcine heart. J Thorac Cardiovasc Surg 1998; 115: 168–77 Vale PR, Losordo DW, Tkebuchava T et al. Catheter-based myocardial gene transfer utilizing nonfluoroscopic electromechanical left ventricular mapping. J Am Coll Cardiol 1999; 34: 246–54 Kornowski R, Leon MB, Fuchs S et al. Electromagnetic guidance for catheter-based transendocardial injection: a platform for intramyocardial angiogenesis therapy. Results in normal and ischemic porcine models. J Am Coll Cardiol 2000; 35: 1031–9 Lazarous DF, Shou M, Stiber JA et al. Pharmacodynamics of basic fibroblast growth factor: route of administration determines myocardial and systemic distribution. Cardiovasc Res 1997; 36: 78–85 Lopez JJ, Laham RJ, Stamler A et al. VEGF administration in chronic myocardial ischemia in pigs. Cardiovasc Res 1998; 40: 272–81 Roth D, Maruoka Y, Rogers J et al. Development of coronary collateral circulation in left circumflex Ameriod-occluded swine myocardium. Am J Physiol 1987; 253: (5 Pt 2): H 1279–88
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Hariawala MD, Horowitz JR, Esakof D et al. VEGF improves myocardial blood flow but produces EDRF-mediated hypotension in porcine hearts. J Surg Res 1996; 63: 77–82 Bauters C, Asahara T, Zheng LP et al. Site-specific therapeutic angiogenesis after systemic administration of vascular endothelial growth factor. J Vasc Surg 1995; 21: 314–24 Asahara T, Bauters C, Zheng LP et al. Synergistic effect of vascular endothelial growth factor and basic fibroblast growth factor on angiogenesis in vivo. Circulation 1995; 92(suppl): II365–71 Laham RJ, Rezaee M, Garcia L et al. Tissue and myocardial distribution of intracoronary, intravenous, intrapericardial, and intramyocardial 125I-labeled basic fibroblast growth factor (bFGF) favor intramyocardial delivery. JACC 2000; 35: 10A Schratzberger P, Schratzberger G, Silver M et al. Favorable effect of VEGF gene transfer on ischemic peripheral neuropathy. Nature Med 2000; 6: 405–13 Landau C, Jacobs AK, Haudenschild CC. Intrapericardial basic fibroblast growth factor induces myocardial angiogenesis in a rabbit model of chronic ischemia. Am Heart J 1995; 129: 924–31 Laham RJ, Hung D, Simons M. Therapeutic myocardial angiogenesis using percutaneous intrapericardial drug delivery. Clin Cardiol 1999; 22(suppl. 1): 16–9 Chronos N et al. Vale PR, Losordo DW, Milliken CE et al. Left ventricular electromechanical mapping to assess efficacy of ph VEGF165 gene transfer for therapeutic angiogenesis in chronic myocardial ischemia. Circulation 2000; 102: 965–74 Lederman RJ. American College of Cardiology Meeting, April 2001 Grines C et al. American College of Cardiology Meeting, April 2001 Schaper W, Gorge G, Winkler B, Schaper J. The collateral circulation of the heart. Prog Cardiovasc Dis 1988; 31: 57–77 Lee PL, Johnson DE, Cousens LS et al. Purification and complementary DNA cloning of a receptor for basic fibroblast growth factor. Science 1989; 245: 57–60 Thurston G, Rudge JS, Ioffe E et al. Angiopoietin-1 protects the adult vasculature against plasma leakage. Nature Med 2000; 6: 160–3 Flugelman MY, Virmani R, Correa R et al. Smooth muscle cell abundance and fibroblast growth factors in coronary lesions of patients with nonfatal unstable angina. A clue to the mechanism of transformation from the stable to the unstable clinical state. Circulation 1993; 88: 2493–500 Schwarz ER, Speakman MT, Patterson M et al. Evaluation of the effects of intramyocardial injection of DNA expressing vascular endothelial growth factor (VEGF) in a myocardial infarction model in the rat – angiogenesis and angioma formation. J Am Coll Cardiol 2000; 35: 1323–30 Nabel EG, Yang ZY, Plautz G et al. Recombinant fibroblast growth factor-1 promotes intimal hyperplasia and angiogenesis in arteries in vivo. Nature 1993; 362: 844–6 Edelman ER, Nugent MA, Smith LT, Karnovsky MJ. Basic fibroblast growth factor enhances the coupling of intimal hyperplasia and proliferation of vasa vasorum in injured rat arteries. J Clin Invest 1992; 89: 465–73 Lazarous DF, Shou M, Scheinowitz M et al. Comparative effects of basic fibroblast growth factor and vascular endothelial growth factor on coronary collateral development and the arterial response to injury. Circulation 1996; 94: 1074–82 Horowitz JR, Rivard A, van der Zee R et al. Vascular endothelial growth factor/vascular permeability factor produces nitric oxide-dependent hypotension. Evidence for a maintenance role in quiescent adult endothelium. Arterioscler Thromb Vasc Biol 1997; 17: 2793–800 Ku DD, Zaleski JK, Liu S, Brock TA. Vascular endothelial growth factor induces EDRF-dependent relaxation in coronary arteries. Am J Physiol 1993; 265: H586–92 Wu HM, Yuan Y, McCarthy M, Granger HJ. Acidic and basic FGFs dilate arterioles of skeletal muscle through a NO-dependent mechanism. Am J Physiol 1996; 271: H10897–93 Kozarsky KF, McKinly DR, Austin LL et al. In vivo correction of low density lipoprotein receptor deficiency in the Watanabe heritable hyperlipidaemic rabbit with recombinant adenoviruses. J Biol Chem 1994; 29: 13695–703 Pakkanen T, Laitinen M, Hippelainen M et al. Enhanced plasma cholesterol lowering effect of retrovirus-mediated LDL receptor gene transfer to WHHL rabbit liver after improved surgical technique and stimulation of hepatocyte proliferation by combined partial liver resection and thymidine kinase–ganciclovir treatment. Gen Ther 1999; 6: 34–41 Grossman M, Rader DJ, Muller DW et al. A pilot study of ex vivo gene therapy for homozygous familial hypercholesterolaemia. Nature Med 1995; 1: 1148–54
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Shah AS, Lilly RE, Kypson AP et al. Intracoronary adenovirusmediated delivery and overexpression of the beta (2)-adrenergic receptor in the heart: prospects for molecular ventricular assistance. Circulation 2000; 101: 408–14 White DC, Hata JA, Shah AS et al. Preservation of myocardial beta-adrenergic receptor signaling delays the development of heart failure after myocardial infarction. Proc Natl Acad Sci USA 2000; 97: 5428–33
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SECTION XV PTA/stenting complications
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Complications of peripheral interventions DT Cragen and RR Heuser
Introduction Every facet of medical practice is permeated by the concept of risk–benefit ratio with the understanding that there are unintended consequences to every action (and even inaction) that we take. A patient may be instructed to exercise more because he/she has significant risk factors for coronary disease, yet studies have shown that he/she is much more likely to die during exercise than during the rest of the day because the associated catecholamine surge and increased cardiac output can destabilize plaques, increase myocardial oxygen demand, and lead to acute myocardial infarction. However, regular exercise has clearly been shown to be one of the best prescriptions for preventing coronary disease. Furthermore, aspirin is one of the most effective and versatile drugs available and prevents mortal events in patients with coronary artery disease, cerebrovascular disease, and peripheral arterial disease; yet it carries with it a finite risk of life-threatening gastrointestinal bleeds and anaphylactic reactions. It therefore follows that every percutaneous and surgical procedure also has associated risks and complications. Simply placing a needle into the vascular space at the beginning of every procedure has associated risks of bleeding, hematomas, pseudoaneurysm formation, infection, and nerve damage, just to name a few. Proceeding to diagnostic angiography has its attendant risks and complications and interventional procedures have yet more associated complications. Preventing complications is the first essential step to effectively managing complications. Complications can be prevented through thorough physician training and preparation, staff education, preprocedural planning, appropriate patient selection, use of appropriate therapies, and recognizing the limits of the operator and the equipment. Even under optimal conditions, complications will still occur in an imperfect world. The operator therefore needs to appreciate the risks of each complication and understand the management of each such that the effects can be minimized. The patient also needs to be informed of and understand the relevant risks of complications such that he/she can make an informed decision to proceed with the procedure or to consider other alternatives. What is a complication? Each study and each operator may have their own unique preconceptions as to what constitutes a complication. In one study, for example, a hematoma may be significant if it reaches a diameter of 7 cm, but another study may not consider a hematoma significant until it reaches 10 cm. Restenosis may not be evident in study A if angiographic
follow-up is performed at 3 months post-intervention in one study, yet study B with a similar patient population would show a higher rate of restenosis simply because follow-up angiography was performed at 12 months. This makes it difficult to compare procedure complication rates between studies. Despite these limitations, this chapter will review the published literature relevant to complications of peripheral interventions. An attempt at an exhaustive review of every serious complication of every unique intervention will not be made; rather, this chapter will focus on the complications common to peripheral interventions performed throughout the body. Becker et al. completed a significant meta-analysis of percutaneous transluminal angioplasty (PTA) procedures in 1989 and compiled the published complications of 4,662 PTAs including peripheral and renal procedures (brachiocephalic procedures were excluded).1 This report from the prestent era described an overall procedural risk of major or minor complications of less than 10.1%. This figure includes the risk of the following major complications: death, 0.23%; arteriovenous fistula, 0.09%; thrombus or embolism, 4.8%; and arterial rupture/perforation, 0.26%. Minor complications included a 3.7% risk of hematoma or pseudoaneurysm and a < 0.88% risk of transient acute tubular necrosis. The mortality rate in this study was 0.2%. In an AHA Task Force report by Pentecost et al. of 3,784 procedures, similar complication rates were observed.2 Access site complications were most common at a rate of 4.0% including a 3.4% rate of bleeding/hematoma, 0.5% of pseudoaneurysm formation, and 0.1% rate of arteriovenous fistula. Complications at the angioplasty site occurred at a 3.5% rate including 3.2% thrombus formation and 0.3% rupture/perforation rate. Distal vessel complications included a 2.3% embolization rate and 0.4% dissection rate. Systemic complications included a 0.2% incidence of renal failure, a 0.2% incidence of fatal myocardial infarction, and a 0.55% rate of stroke. Limb loss occurred in 0.2% of patients and overall mortality was reported to be 0.2%. Two percent of patients required surgical repair after their intervention. A prospective single-center study of complications of lower-extremity PTA in 410 procedures in 295 patients also demonstrated similar complication rates.3 Access site complications were the most frequent with a 5.4% incidence of hematoma, 1.2% rate of pseudoaneurysm formation, 0.5% risk of arteriovenous fistula, and 0.5% rate of retroperitoneal hematoma. Angioplasty site complications occurred with a 1.5% incidence of distal embolization, 0.7% rate of 791
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angioplasty site thrombosis, and a 0.7% rate of both site thrombosis and embolization. These complications summated to a 10.5% complication rate that is quite comparable to the rates seen in the two prior reviews. Complication rates depend on multiple patient factors (co-morbidities, age, smoking history, disease burden) but also procedural factors, including the site treated, the vascular access used, choice of equipment including sheath sizes, and the type of lesion treated. Matsi and Manninen showed that treatment of occluded vessels carried a significantly higher complication rate (18%), than the 7% rate seen in patients treated for stenoses, a difference that was statistically significant (p = 0.002).3 Treatment of popliteal and infrapopliteal vessels also carries a much higher complication rate (19%) than treatment of iliofemoral disease (5%) in a review of 453 angioplasties by Gardiner et al.4
Vascular access site As described above, multiple studies of peripheral intervention confirm that the most common site of complication from a peripheral intervention is at the initial vascular access site. The importance of obtaining access safely, efficiently, and with minimal trauma should not be trivialized, as the success of the remainder of the procedure is dependent on it. The choice of which access site (or sites) to use is critical to the procedure and should be carefully determined as an essential part of preprocedural planning. The site chosen should depend on the site to be treated, the type of treatment planned, the sheath size needed to deliver the planned endovascular tools, the operator’s comfort and experience, and foreknowledge of the patient’s vascular anatomy obtained through careful history and physical examination and possibly from prior vascular studies. Potential complications associated with vascular access include local bleeding, hematoma (both local and retroperitoneal), vessel thrombosis, pseudoaneurysm formation, and creation of an arteriovenous fistula. Many of these complications are caused by improper access technique and can be prevented. Poor puncture technique can include puncturing the vessel too proximal or too distal or using multiple punctures to cannulate the vessel. Post-procedural care can also significantly impact the rate of complications, particularly inadequate or misplaced manual compression of the puncture site and removal of the sheath inappropriately early while the anticoagulant effect is still quite pronounced. Access site Choice of the access site is based upon a variety of factors described above and should predominantly be chosen based on the site most likely to lead to procedural success. In some cases, patient factors such as severe back pain may favor a radial or brachial approach in order to minimize post-procedural bed rest. Consideration of the complication rates of each access site may be warranted if more than one site is reasonable and appropriate. The randomized access study for coronary intervention randomized 900 patients with approximately 300 patients each getting coronary intervention via the radial, brachial, and femoral access approaches.5 Procedural success was nearly
identical in all three groups. Major access site complications were absent in the radial group but occurred in 2.0% of the transfemoral group and 2.3% of the transbrachial group. The transradial approach was associated with a 3% risk of asymptomatic loss of the radial pulse at 1-month follow-up after the procedure. Local bleeding and hematoma Uncontrolled bleeding and/or hematoma formation at the site of vascular access is one of the most frequent complications associated with peripheral percutaneous intervention.1–3 Many anatomic, procedural, hematological, and human factors account for this high risk (Table 92.1).6 Bleeding may either be free-flowing or accumulate subcutaneously into a hematoma. Hematomas generally resolve spontaneously over weeks as the blood constituents are degraded and reabsorbed. Large hematomas, however, can lead to nerve impingement and injury and, in the case of the femoral nerve, lead to quadriceps weakness that can take weeks or months to resolve. Continuing expansion of the hematoma or free-flowing blood may required prolonged compression of the vascular puncture site. While external devices have been developed to facilitate compression of the femoral access site, studies have not shown a clear benefit to these devices over manual compression; in fact, manual compression appears to be the safest and most reliable technique in achieving hemostasis of the femoral artery.7 Care should be taken with external compression devices to not occlude distal flow for more than several minutes or limb-threatening ischemia and thrombosis can occur. Free-flowing blood at the access site suggests a vessel laceration which may occur from “bayoneting” the sheath into the artery rather than smoothly twisting the sheath, or rarely Table 92.1 Factors predisposing to vascular access site bleeding complications7 Anatomic factors Elderly patient Obese patient Female patient Calcified vessels Procedural factors Through-and-through puncture High puncture (above inguinal ligament) Low puncture (profunda or superficial femoral artery) Multiple punctures Large sheath size Prolonged procedure time Long indwelling sheath time Hemodynamic factors Severe hypertension Hematological factors Platelet antagonists (aspirin, clopidogrel, glycoprotein IIb/IIIa antagonists) Antithrombotic agents (warfarin, heparinoids) Thrombolytic agents Underlying coagulopathy or thrombocytopenia Human factors Inexperience Inability to gain “control” of site upon sheath removal Inadequate duration of compression to achieve hemostasis
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Complications of peripheral interventions by direct incision by the scalpel used to nick the skin. Minor lacerations may improve if a larger diameter sheath is placed in the vessel, but larger lacerations usually require prolonged compression and rarely surgical correction. The risk of retroperitoneal bleed increases if the femoral access site is above the inguinal ligament and if the access needle punctures both the anterior and posterior walls of the artery. Retroperitoneal bleed after femoral access should be suspected with unexplained hypotension, ipsilateral flank pain, and/or new femoral neuropathy.8 Hematomas, especially in the thigh and peritoneum, can be insidious and associated with significant blood loss – often much more than is apparent on surface examination. Patients with femoral sticks can quickly and easily bleed 1–2 liters or more and become hypotensive and even go into shock. Prompt recognition and management of blood loss is critical. Isotonic fluid resuscitation and blood products should be administered urgently and consideration should be given to reversing anticoagulant therapy. Only after the patient has been properly resuscitated with fluids and/or blood should consideration be given to imaging studies (i.e. ultrasound of the groin or computed tomography of the abdomen) that could delay appropriate therapy. Pseudoaneurysm A pseudoaneurysm is a hematoma that is encapsulated by adjacent soft tissue or by the adventitial layer of the artery yet is still in communication with the artery. It most commonly occurs at the site of femoral access and is associated with puncture sites below the common femoral artery, abnormal hemostasis, and inadequate compression (Table 92.2).6 It occurs in 0.5–1.2% of peripheral vascular procedures in large published reports.2,3 Symptoms include tenderness, swelling, and bruising near the groin access site. Physical exam will often reveal exquisite tenderness and an associated pulsatile mass. There is frequently an audible bruit overlying the site. Whenever a large hematoma is present and particularly if the pain appears out-of-proportion to the exam, a pseudoaneurysm should be considered. Diagnosis can be confirmed by Doppler ultrasonography, which should reveal a high-velocity jet across a defect in the arterial wall into an adjacent fluid collection. The goal in management is to thrombose the contents of the pseudoaneurysm pouch and abolish the communication with the artery. Many small pseudoaneurysms will spontaneously close with time and observation alone may be sufficient. In one study of 16 pseudoaneurysms, 56% closed spontaneously with observation alone.9 When indicated, pseudoaneurysms
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may respond well to compression of the neck of the pseudoaneurysm. Compression of the neck of the pseudoaneurysm is usually performed with direct pressure of an ultrasound probe, which is used to guide the compression and document cessation of flow into the pseudoaneurysm during compression. Many patients require significant analgesia and occasionally sedation for these procedures, which can last up to 60 minutes and have success rates of 63–88%.10 More recently, ultrasound-guided thrombin injection has been proposed and widely utilized to close the pseudoaneurysm sac. Bovine thrombin is slowly injected into the sac either through endovascular catheters or through direct percutaneous needle access and thrombosis is observed by ultrasound, generally within seconds. Success rates in multiple studies are reported at 93–100%.10 One randomized study of thrombin injection versus ultrasound-guided compression in 30 patients with iatrogenic pseudoaneurysms reported 100% closure of the sac in patients treated with thrombin and only 40% closure with ultrasound-guided compression at 48 hours.11 There are still well-recognized features of pseudoaneurysms that require urgent surgical repair: rapidly expanding sac, infected pseudoaneurysm, distal ischemia or neuropathy due to local compression, failure of percutaneous technique, and local soft tissue or skin ischemia due to pressure.10 However, with the reported success of the compression and thrombin techniques above, the vast majority of pseudoaneurysms can now be managed percutaneously with less morbidity to the patient. Arteriovenous fistula Simultaneous puncture of the artery and vein can lead to an arteriovenous fistula (Figure 92.1), which is not usually immediately evident, but may take several days to develop.
Table 92.2 Factors associated with increased risk of pseudoaneurysm formation7 ●
● ● ● ● ● ●
Low vascular access in the superficial femoral or profunda artery Severe peripheral vascular disease Large sheaths Prolonged sheath time Prolonged anticoagulation Impaired platelet function and low platelet count Premature ambulation
Figure 92.1 Angiographic appearance of an arteriovenous fistula with simultaneous filling of the right superficial femoral artery (left) and vein (right).
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Less commonly, a hematoma from a bleeding artery may decompress into the adjacent vein to form a fistula. Risk factors that increase the risk of AV fistula formation include: ● ●
●
●
multiple punctures to obtain vascular access; low puncture below the common femoral artery with transection of the adjacent venous branch; high puncture (common femoral artery and adjacent lateral femoral circumflex vein); impaired clotting.6
Clinically, the patient may present with distal limb swelling and tenderness due to venous congestion and an audible to-and-fro continuous bruit over the puncture site. The incidence of AV fistulas in large studies is 0.1–0.5%. Conservative management is usually indicated for small to moderate arteriovenous fistulas as most will close spontaneously. Large-volume fistulas or fistulas causing prominent symptoms may be closed either surgically or, as has been recently described, percutaneously with the use of covered stents.12 Access site infections Groin infections are exceedingly rare after percutaneous procedures. In two large studies involving a total of 6,672 patients undergoing catheterization procedures, only 8 infectious complications were observed, an incidence of only 0.12%.13,14 The usual skin flora of gram-positive bacteria, especially coagulase-negative Staphylococcus species, cause most access site infections and can lead to an endarteritis. The presence of a hematoma, the use of vascular closure devices, and the presence of foreign bodies within the artery are all risk factors for the development of infection. Erythema, induration, and fluctuance can all be presenting signs of a cellulitis and/or underlying abscess. Ultrasonic evaluation may help in identifying an abscess cavity. Cellulitis should be managed with antibiotics only, but surgical drainage may also be required for a significant abscess cavity. Dissection Dissection of the access site generally occurs due to needle or wire trauma (Figure 92.2). Increased wire and catheter manipulation at the access site increases the risk of developing a dissection. The incidence is reported at < 0.4% but is likely higher given that small dissections may go unnoticed and generally have a benign course. Most dissections pose no significant risk to the patient or the affected limb. This is in part because most femoral, brachial, and radial accesses are obtained retrogradely and prompt recognition of the dissection and removal of the equipment will usually allow the dissection to be “tacked down” by the antegrade flow. Dissections that are flow limiting or associated with thrombus should be surgically or percutaneously repaired. Thromboembolism With the current aggressive use of anticoagulants, bleeding complications far exceed thrombotic complications in modern clinical practice. Thrombosis can occur at the access site in < 1% of patients after intervention. Vascular size is the most
Figure 92.2 Angiographic appearance of a non-flow limiting arterial wall dissection of the left iliac artery caused by a guidewire.
significant predictor of thrombosis, hence radial and brachial access has a higher rate of thrombosis than femoral.15 Diffuse peripheral vascular disease can predispose to thrombosis, particularly when the sheath is nearly occlusive in the access vessel. Arterial occlusion is associated with severe limb pain, numbness, cyanosis, absence of palpable distal pulses, pallor, and a cool extremity. When thrombotic occlusion is suspected, the patient should be immediately heparinized and percutaneous or surgical embolectomy is warranted on an emergency basis. Percutaneous embolectomy can be performed via a separate access site and aspiration catheters or rheolytic thrombectomy can be employed to reduce the clot burden. Angioplasty and/or stenting can then be performed as warranted and if a significant clot burden persists, intraarterial thrombolytic therapy may be considered. Vascular closure devices Vascular closure devices are being used with increasing frequency after peripheral interventions despite any data suggesting an improved safety profile with these devices. The most widely used devices currently fall into four classes: percutaneous suture closure, percutaneous clip or staple closure, collagen-mediated plugging of the access tract, and external compression devices. Randomized studies, retrospective reviews, and meta-analyses of closure devices have not shown any significant difference in complication rates including pseudoaneurysm formation, bleeding, hematoma, or the need for urgent vascular surgery (Figure 92.3).16–18 These devices have been shown to reduce time to ambulation and length of hospital stay. Furthermore, they have been widely accepted by patients for comfort reasons and have found widespread acceptance in current practice.
Angioplasty site Complications at the angioplasty site comprise most of the remaining complications. Large studies suggest that the
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(b)
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Figure 92.3 Femoral arterial thrombosis following deployment of a Duett closure device. (a) Patent right common femoral artery prior to deployment of the Duett device. (b) acute arterial thrombosis in the right common femoral artery. (c) Recanalization of the right common femoral artery after thrombectomy therapy with the AngioJet system.
incidence of angioplasty site complications is 2.9–3.5% and includes thrombus formation, vessel perforation, and vessel dissection.2,3 Embolization can also occur to the distal vessel and in the AHA Task Force Review occurred in up to 2.3% of patients. As stents have become more commonplace, the treatment of angioplasty site complications has improved dramatically and likely leads to an underreporting of easily managed dissections and perforations. Perforation/dissection Perforation of the artery at the angioplasty site occurs in about 0.3% of procedures (Figure 92.4).1,2 Perforation may be caused by aggressive over dilation of a lesion, balloon rupture (especially small pin-hole leaks with a high-pressure jet), and
(a)
(b)
endovascular instruments such as atherectomy devices. Many perforations will respond to simple balloon tamponade at the site of perforation and a covered stent successfully treats the vast majority of the remaining perforations. Surgery is rarely indicated due to the success of endovascular repair. Dissection, on the other hand, occurs in the vast majority of lesions treated with PTA and is an expected result of dilating a stenotic lesion. Most dissections are inconsequential, especially in the era of routine stent placement. Flow-limiting dissections were rare in the prestent era and are now generally managed aggressively with stent implantation (Figure 92.5). Loss of guidewire access after a significant dissection occurs can be serious, as reaccessing the true lumen becomes quite difficult and the end-organ may become quite ischemic during attempts to do such. Rarely, surgery may still be required.
(c)
Figure 92.4 Renal artery dissection during angioplasty and stent placement. (a) Severe ostial stenosis of the left renal artery. (b) Angiogram following stent placement in the left renal artery. (c) Angiogram revealing dissection at the left renal artery.
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(a)
(b)
(c)
(d)
(e)
Figure 92.5 Superficial femoral artery perforation. (a) Total occlusion of the left superficial femoral artery. (b) Balloon angioplasty of the left superficial femoral artery. (c) Serial stent placements to a long segment of the left superficial femoral artery. (d) Post-stent balloon angioplasty. (e) Angiogram revealing perforation after post-stent balloon angioplasty.
Abrupt closure/thrombosis Abrupt closure or acute thrombosis at the treated site occurred in 2–4% of lesions treated in the prestent era and generally included all closures that occurred immediately or within the first 24 hours.1,19 Complex lesions, tandem lesions, and multivessel disease were predictive of closure periprocedurally. Angiographic correlates with acute closure included long lesions, dissection, use of oversized balloons relative to the reference segment, residual stenosis > 50%, and intraluminal thrombus. Aspirin and appropriate anticoagulation have both been shown to be protective against angioplasty site thrombosis. In the absence of glycoprotein receptor antagonists, the activated clotting time should be maintained at least > 250 seconds. Most commonly, thrombosis occurs with recognized or occult dissection. When it arises, stenting is generally very effective at treating the thrombosis. Occasionally, additional anticoagulant and even intra-arterial thrombolytics can be infused to resolve the thrombosis. Acute/subacute stent thrombosis Stents are placed after angioplasty to decrease elastic recoil, tack down dissections that can lead to thrombosis, and treat other complications as described above. Paradoxically, although stents are used to treat thrombotic complications of angioplasty, the introduction of a metal foreign body in the vasculature can itself be a nidus for thrombus formation. Peripheral stent thrombosis is less common than coronary stent thrombosis owing to the larger diameter lesions and higher flow rates through most vessels being treated. However, as peripheral techniques improve and more small vessels (i.e. infrapopliteal) interventions are performed, stent thrombosis rates will likely increase. Stent thrombosis can be prevented with the use of high-pressure inflations and dual anti-platelet therapy including aspirin and a thienopyridine, usually clopidogrel. Currently, if not contraindicated, aspirin therapy is recommended indefinitely for patients with peripheral arterial disease and clopidogrel for a minimum of 1 month after bare metal stent placement. Drug-eluting stents, while currently being placed in the
periphery on an off-label basis, may have an increased risk of stent thrombosis associated with delayed endothelialization, but this area remains under-studied. Emergency treatment of stent thrombosis may be required if the patient develops symptoms of limb ischemia. Heparin infusion and consideration for intra-arterial thrombolytics are indicated. Repeat angioplasty at the site of thrombosis may also be employed to re-establish distal flow.
Systemic Systemic complications can occur related to the anticoagulants, iodinated contrast, and radiation employed during peripheral intervention procedures. These complications can be life threatening or lead to increased morbidity and prolonged hospital stays, but they are, for the most part, preventable. Contrast-related complications Contrast media complications are generally divided into two types: anaphylactic and toxic. Anaphylactic reactions include urticaria, angioedema, bronchospasm, and can progress to circulatory shock. Prompt recognition is required and the anaphylactic patient will generally respond to aggressive hydration and intravenous epinephrine in an emergent situation. Patients with a history of anaphylactic reactions to iodinated contrast and/or shellfish, should understand the slightly increased risks of peripheral interventions. Generally, this risk can be minimized and nearly eliminated by pretreatment of the patient with oral corticosteroids for 12–24 hours preprocedurally. We generally administer intravenous antihistamines at the time of the procedure to blunt any histaminergic response. In urgent or emergency situations, intravenous corticosteroids at the time of the procedure have also been effective in avoiding anaphylaxis. Contrast nephropathy is the most common serious toxic effect of contrast media, but other toxic effects include a hot flushing sensation, nausea, vascular congestion, metallic taste, and arrhythmias. Risk factors for contrast-induced nephropathy (CIN) are summarized in Table 92.36 and the incidence
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Complications of peripheral interventions Table 92.3
Risk factors for contrast nephropathy20
Patient related Chronic kidney disease Diabetes mellitus Urgent procedure Intra-aortic balloon pump Congestive heart failure Age Hypertension Low Hematocrit Hypotension Left ventricular ejection fraction < 40% Not Patient Related Contrast properties High osmolar contrast Ionic contrast Contrast viscosity Contrast volume
observed in peripheral interventional trials is 0.2–0.88%. Most studies define CIN as an increase in serum creatinine level by 25% or an absolute increase of 0.5 mg/dl within 2–7 days after exposure, which may seem like mild changes but do in fact have profound prognostic implications.20 Despite the worsened prognosis associated with CIN, contrast nephropathy is generally reversible after reaching a nadir at 5–7 days, function generally returns to normal by 14 days.20 Patients should be routinely screened before the interventional procedure for significant risk factors for developing CIN. Modifiable risk factors should be treated and patients with multiple risk factors should be counseled about the increased risks and, when appropriate, a change in treatment modalities. Multiple conflicting studies exist about the optimal medical regimen to reduce the incidence of CIN, but a recent exhaustive review of published reports of CIN prophylaxis suggests that high-risk patients be administered n-acetylcysteine or ascorbic acid at high doses peri-procedurally (20).20 There is also evidence to support hydration with either normal saline at 1ml/kg/hour for 6–12 hours before and after the procedure or sodium bicarbonate 154 mEq/l in 5% dextrose and water at a rate of 3 ml/kg/hour for 1 hour before the procedure and for up to 6 hours after the procedure. Use of contrast media should be minimized and iso-osmolar or low-osmolar contrast is preferred. Cholesterol embolization Cholesterol embolization is a rare but catastrophic complication of interventional procedures. While not exclusively caused by diagnostic and interventional catheter manipulations, 76–79% of all cases are iatrogenic in origin.21 In some series, 50% of all cases are secondary to angioplasty procedures and the majority of the remainder are related to anti-coagulation.21 Risk factors for cholesterol embolization include male gender, tobacco use, and underlying atherosclerosis. The mechanism involves unroofing an atheroma and allowing cholesterol crystals into the blood circulation. The atheroma can be traumatized by wires, catheters, or even by dissolution of an overlying fibrin cap. The source is generally
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felt to be atheromas of the thoracic aorta, but in at least one study, two-thirds of patients had an abdominal aortic aneurysm.22 The cholesterol emboli distribute in the circulation and lodge in distal capillaries proportional to the blood flow. It is no surprise then that the kidneys, which receive approximately 20% of the cardiac output, are significantly affected. Clinically, patients have progressive renal failure, gut ischemia, and cutaneous necrosis. It is classically associated with livedo reticularis, a characteristic rash. Diagnosis is suspected in patients with livedo reticularis rash, kidney failure, and evidence of skin or organ necrosis – especially if seen within days of a catheterization procedure. Unfortunately, symptoms can be delayed by weeks, especially when caused by anticoagulants, and diagnosis can be missed or at least delayed. Biopsy of an affected area of the skin can confirm the presence of cholesterol crystals and secure the diagnosis. Treatment is still widely debated, but hydration, blood pressure control, and dialysis should all be considered. Despite treatment, mortality in these patients is reported as high as 81%.23,24 Radiation injuries Use of appropriate shielding, minimizing fluoroscopic and cineangiographic acquisition times, and proper positioning of the x-ray tube should always be employed to minimize radiation to the patient and operators. While radiation leads to small, finite increases in lifetime risk of malignancies, the patient exposure from a typical peripheral intervention is minimal and cannot be measured except on a population basis. Radiation skin injury is a more immediate concern seen in patients, particularly in long cases where imaging was performed with the x-ray tube in the same position throughout the case. Signs of acute radiation exposure at doses in the interventional laboratory take weeks to months to become apparent and are dose dependent. Generally erythema occurs with 6 Gy of exposure, hyperpigmentation and desquamation with 10–15 Gy, and ulceration at an exposure of 18–20 Gy.25 Other changes such as dermal atrophy, telangiectasias, ulceration, and fibrosis are seen as early as 10 weeks, but may sometimes develop years later.25
Conclusion Most complications related to peripheral intervention occur at the arterial puncture site, but treatment site and systemic complications can also occur. The best way to manage complications is to prevent them from occurring by careful planning, appropriate patient selection, operator and staff education and experience, and the correct use of appropriate sheaths and endovascular tools. Despite optimal preparation and technique, complications will still occur at the access site, treatment site, and systemically. Prompt recognition of a complication when it occurs and an understanding of the underlying pathophysiology are critical to minimizing the impact of a complication on the patient. Advancements in endovascular techniques have allowed most complications to be treated percutaneously and significantly obviate the need for surgical intervention with its attendant morbidity.
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REFERENCES 1. 2. 3. 4. 5.
6. 7. 8. 9. 10. 11. 12. 13.
Becker G, Katzen B, Dake M. Noncoronary angioplasty. Radiology 1989; 170: 921–40 Pentecost MJ, Crique MH, Dorros G et al. Guidelines for peripheral percutaneous transluminal angioplasty of the abdominal aorta and lower extremity vessels. Circulation 1994; 89: 511–31 Matsi PJ, Manninen HI. Complications of lower limb percutaneous angioplasty: a prospective analysis of 410 procedures on 295 consecutive patients. Cardiovasc Intervent Radiol 1999; 21: 361–6 Gardiner GA, Meyerovitz MF, Stokes KR et al. Complications of transluminal angioplasty. 1986; 159: 201–8 Kiemeneij F, Laarman GJ, Odekerken D et al. A randomized comparison of percutaneous transluminal coronary angioplasty by the radial, brachial, and femoral approaches: The Access Study. J Am Coll Cardiol 1997; 29: 1269–75 Kamineni R, Kelly L, Heuser RR. Complications of peripheral interventions. In: Heuser RR, Biamino G, eds. Peripheral Vascular Stenting, second edition. London: Taylor & Francis, 2005: 187–98 Benson LM, Wunderly D, Perry B et al. Determining best practice: Comparison of three methods of femoral sheath removal after cardiac interventional procedures. Heart Lung 2005; 34: 115–21 Kent KC, Moscucci M, Mansour KA et al. Retroperitoneal hematoma after cardiac catheterization: prevalence, risk factors, and optimal management. J Vasc Surg 1994; 20: 905–10 Kent KC, McArdle CR, Kennedy B et al. A prospective study of the clinical outcome of femoral pseudoaneurysms and arteriovenous fistulas induced by arterial puncture. J Vasc Surg 1993; 17: 125–31 Morgan R, Belli A. Current treatment methods for postcatheterization pseudoaneurysms. J Vasc Interv Radiol 2003; 14: 697–710 Lonn L, Olmarker A, Geterud K et al. Treatment of femoral pseudoaneurysms. Percutaneous US-guided thrombin injection versus US-guided compression. Acta Radiologica 2002; 43(4): 396–400 Samal AK, White CJ. Percutaneous management of access site complications. Cathet Cardiovasc Interv 2002; 57: 12–23 Cleveland KO, Gelfand MS. Invasive staphylococcal infections complications percutaneous transluminal angioplasty: three cases and review. Clin Infect Dis 1995; 21: 93–6
14. 15.
16. 17. 18.
19. 20. 21. 22. 23. 24. 25.
Smith TP, Cruz CP, Moursi MM et al. Infectious complications resulting from use of hemostatic puncture closure devices. Am J Surg 2001; 182: 658–62 Johnson LW, Lozner EC, Johnson S et al. Coronary arteriography 1984–1987: A report of the registry of the Society for Cardiac Angiography and Interventions. Cathet Cardiovasc Diagn 1989; 17: 5–10 Silver S. Hemostasis success rates and local complications with collagen after femoral access for cardiac catheterization: analysis of 6007 published patients. Am Heart J 1998; 135: 152–6 Meyerson SL, Feldman T, Desai TR et al. Angiographic access site complications in the era of arterial closure devices. Vasc Endovascular Surg 2002; 36: 137–44 Kim MC, Kini AS, Lee PC et al. Does the use of vascular closure devices decrease vascular complications in the current era of percutaneous coronary I intervention? Am J Cardiol 2002; 90(suppl. 6A): 169H (abstract) Gardiner GA, Meyerovitz MF, Stokes KR et al. Complications of transluminal angioplasty. Radiology 1986; 159: 201–8 Pannu N, Wiebe N, Tonelli M. Prophylaxis strategies for contrastinduced nephropathy. J Am Med Assoc 2006; 295: 2765–79 Scolari F, Tardanico R, Zani R et al. Cholesterol crystal embolism: a recognizable cause of renal disease. Am J Kidney Dis 2000; 36: 1089–109 Belenfant X, Meyrier A, Jacquot C. Supportive treatment improves survival in multivisceral cholesterol crystal embolism. Am J Kidney Dis 1999; 33: 840–50 Fine MJ, Kapoor WN, Falanga V. Cholesterol crystal embolization: a review of 221 cases in the English literature. Angiology 1987; 38: 769–84 Kim F, Wong M, Chan SK et al. Acute renal failure after streptokinase therapy in a patient with acute myocardial infarction. Am J Kidney Dis 1995; 26: 508–10 Archambeau JO, Pezner R, Wasserman T. Pathophysiology of irradiated skin and breast. Int J Radiat Oncol Biol Phys 1995; 31: 1171–85
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Contrast-induced nephropathy G Marenzi and AL Bartorelli
Introduction Contrast-mediated imaging studies and interventions are a relevant part of modern medical practice. An increasing number of patients, estimated at 30 million annually in the US, receive contrast agents during diagnostic or interventional procedures.1 One of the most important complications of contrast agents is kidney toxicity, and contrast-induced nephropathy (CIN) is one of the leading causes of renal impairment, and the third leading cause of hospital-acquired renal failure.
Definition Contrast-induced nephropathy is usually defined as an acute decline in renal function, characterized by an absolute rise of at least 0.5 mg/dl (44 µmol/l) in serum creatinine, or by a relative increase of at least 25% over the baseline value, occurring 48–72 hours after the systemic administration of contrast medium, and in the absence of other causes (atheromatous emboli, hypotension or nephrotoxins).2
Epidemiology Whereas the overall incidence of CIN in the general population is estimated to be lower than 3%, its rate is much higher in several patient subsets, reaching values as high as 20–30% in high-risk patient groups such as patients with chronic renal impairment, diabetes mellitus, congestive heart failure, acute myocardial infarction and older age. It is even higher (up to 50%) in those with severe renal insufficiency (stage 4 nephropathy).3 Notably, multiple risk factors are often simultaneously present in the same patient, with additive influence on the rate of this serious complication.4,5
Pathogenesis The exact mechanism of CIN has not completely been elucidated. However, it is suggested that it is caused by a combination of direct toxic effects on tubular epithelial cells and renal ischemia.6 Direct toxic effects on the proximal convoluted tubular cells and in the inner cortex of the kidneys, which cause epithelial cell vacuolization, interstitial inflammation and cellular necrosis, have been demonstrated to follow exposure to a variety of iodinated contrast agents.
Studies in animals have suggested that oxidant-mediated injury, due to enhanced production of oxygen-free radicals and lipid peroxidation of biological membranes, might be implicated. Apoptosis, as a result of cellular injury, has also been involved. Regional hypoxia of the kidney is another potential cause of CIN. Indeed, the deeper portion of the outer medulla of the kidney is particularly vulnerable, since this area is maintained at the verge of hypoxia, with pO2 levels often as low as 20 mmHg. In addition to the low oxygen tension, the relatively high oxygen requirements, due to salt reabsorption, account for this vulnerability. Two possible mechanisms by which medullary hypoxia and ischemia might occur in response to contrast agent exposure have been proposed. Firstly, contrast agents may cause renal vasoconstriction, and both increased activity of several intrarenal mediators (adenosin, vasopressin, angiotensin II, dopamine-1, and endothelin), and decreased activity of renal vasodilators (nitric oxide and prostaglandins) have been implicated as causative factors. Secondly, by causing erythrocyte aggregation, contrast media may decrease renal blood flow indirectly, resulting in impaired oxygen delivery. Iso-osmolar dimeric contrast media, probably as a consequence of their high viscosity, have been reported to cause more red blood cell aggregation, cessation of flow in the renal microcirculation, and greater reduction of renal blood flow than lowosmolality monomeric contrast media.7 Other experimental studies have suggested that iso-osmolar dimeric contrast media may worsen medullary hypoxemia more than lowosmolar contrast agents.8 A diminished transit time of the higher viscosity dimeric contrast agent in the tubule might lead to a decrease of both glomerular filtration rate and renal blood flow by compression of peri-tubular vessels. Moreover, the reduced tubular transit time of the non-ionic dimers may result in a longer time for solute transport and increased oxygen utilization. Experimental studies on the role of osmolality, per se, in the pathogenesis of CIN have provided conflicting data. Although clinical trials indicate a lower incidence of CIN when using low-osmolality, as compared to highosmolality contrast media, the advantages of iso-osmolality agents are still uncertain. In summary, several pathophysiological mechanisms can contribute to kidney function impairment. The nephrotoxic effects of iodinated contrast media may occur primarily through direct cytotoxicity and regional ischemia of the medullary portions of the kidney. Factors other than osmolality (i.e. viscosity, hydrophilicity) may contribute substantially to their toxic effect. 799
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Risk factors
The MDRD equation for estimation of glomerular filtration rate (eGFR) from serum creatinine is as follows:
Identification of patients at increased risk for the develop ment of CIN is of major importance. The risk of developing clinically significant acute renal failure (ARF) greatly depends on the presence of several risk factors. Indeed, the risk of CIN is related to a variety of patient characteristics, clinical settings, and other modifiable factors (Table 93.1). Pre-existing renal disease is the most crucial risk factor in the development of CIN. The higher the baseline creatinine value, the greater the risk of CIN. However, baseline creatinine is not reliable enough for identification of patients at risk. This is because the creatinine value varies with age, gender, and muscle mass. To evaluate renal function reliably, assessment of creatinine clearance, based on the Cockgroft–Gault formula,9 or the “modification of diet in renal disease” equation (MDRD),10 should be performed. The Cockgroft–Gault formula for estimation of creatinine clearance (CrCl) from serum creatinine is as follows:
CrCl (ml/min) =
(140 − age in years) × body weight in kg 72 × serum creatinine in mg/dl
The resulting value must be multiplied by 0.85 for women.
Table 93.1 nephropathy
Risk
factors
for
contrast-induced
Patient-related Chronic kidney disease (stage III or greater) Diabetes mellitus (type I or type 2) Volume depletion Older age Congestive heart failure (or left ventricular ejection fraction < 40%) Hypertension Anemia and blood loss Hypoalbuminemia (< 35 g/l) Nephrotoxic drug use (NSAIDs, cyclosporine, amynoglicosides) Diuretics ACE inhibitors Hypotension or pre-procedural hemodynamic instability Urgent procedure (acute myocardial infarction) Intra-aortic balloon pump use Renal transplant Not Patient Related Contrast properties High osmolar contrast Ionic contrast Contrast viscosity Contrast volume Intra-arterial administration NSAIDs = nonsteroidal anti-inflammatory drugs; ACE= angiotensinconverting enzyme.
eGFR (ml/min/1.73 m2) = [186.3 × (serum creatinine–1.154) × (age–0.203)] Calculated values are multiplied by 0.742 for women and by 1.21 for African Americans. Several studies have shown that an estimated glomerular filtration rate of 60 ml/min/1.73 m2 is a reliable cut-off point for identifying patients at high risk for the development of CIN. Therefore, calculation of creatinine clearance for risk assessment is highly recommended before exposure to contrast media. Diabetes mellitus represents another important risk factor. Patients with diabetes mellitus and renal impairment have a substantially higher risk of CIN than patients with renal impairment alone. Other risk factors include older age, congestive heart failure, reduced effective arterial volume – as seen in patients with dehydration – nephrosis, cirrhosis, type and volume of contrast agents, pre-existing anemia and procedure-related blood loss, concurrent use of potentially nephrotoxic drugs (e.g. diuretics, aminoglycosides), as well as drugs impairing the renovascular autoregulation (e.g. nonsteroidal anti-inflammatory drugs, angiotensin converting enzyme inhibitors).4,5 An increased risk of ARF is usually observed in those clinical settings in which additional factors affecting renal function are present. Patients who undergo primary percutaneous coronary intervention in the acute phase of myocardial infarction are at higher risk for CIN, because of hemodynamic instability, use of large volumes of contrast media, and the fact that starting renal prophylactic measures prior to the procedure is difficult, if not impossible.11 Multivariate prediction scoring schemes have been developed for patients undergoing both elective or primary percutaneous coronary interventions, and indicate that patients with multiple risk factors may have a very high, if not certain, probability of CIN.5,11 Peripheral vascular interventions, which offer a non-surgical solution to several vascular pathologies previously treated with open surgical procedures, represent an overlooked cause of CIN. Indeed, percutaneous interventions make treatment available to higher risk patients, whose peripheral vascular disease is an indication of more severe and diffuse atherosclerosis. Moreover, it is not unusual that multiple lesions, located in different peripheral vessels, are treated simultaneously in the same patient, sometimes in combination with intervention of coronary lesions. Thus, high contrast volume may be required – a factor that has been demonstrated to have a direct relationship with CIN risk.12 Finally, because most of these patients suffer from generalized atherosclerotic vascular disease, they are also at increased risk of developing ARF secondary to atheroembolic disease.13 Recently, the impact of endovascular aortic aneurysm repair (EVAR) on post-operative renal function has come under close scrutiny. Of particular concern is the demonstration by several investigators of progressive renal dysfunction over time after EVAR.14–17 Although patients receiving EVAR are spared the ischemic insult of aortic cross-clamping, and have less peri-operative hemorrhage,18,19 the potential nephrotoxicity of large-volume contrast administration must be considered. In our experience, patients undergoing EVAR receive a higher contrast volume than those treated with other
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peripheral vascular interventions (Table 93.2). Our data are in agreement with those of a recent study that enrolled 97 patients undergoing endovascular repair of thoracic aneurysms who received an average contrast volume of 307 ± 188 ml.20 Of note, post-procedural ARF (increase > 25% and/or > 0.5 mg/dl in preprocedure serum creatinine) occurred in 34% of patients, who showed a significantly lower survival at 1 year (65 vs. 90%). High contrast volume in EVAR is the result of the multiple angiographies, often needed for correct endograft positioning, and for assessing, particularly in complex anatomy patients, the results of type I endoleak treatment at the proximal or distal fixation sites after stent-graft implantation. In addition to contrast volume, other factors may be responsible for progressive renal dysfunction after this type of endovascular intervention. Firstly, the only independent risk factor that has been linked with the development of post-operative renal failure after infrarenal EVAR is preoperative renal insufficiency.21 In addition, manipulation of the endograft and the maneuvers involved in repositioning it within the aneurysm, together with balloon inflation at the proximal fixation site, may result in thromboembolism of the renal artery and renal infarction. The type of endograft used for proximal fixation in abdominal aorta aneurysms must be added to the list of factors that may have an influence on renal function. Indeed, suprarenal fixation of aortic stent-grafts, for the purpose of preventing migration and achieving complete hemostatic seal, is still creating concerns with regard to long-term effects. Interference with renal artery flow, cross-sectional narrowing of the renal ostium, renal infarction, and biological response of the aorta may be the result of continued injury from the suprarenal stent, and may play a role in renal function deterioration over time.22,23 Finally, the repeated administration of contrast media during peri-procedural evaluation and follow-up surveillance with CT angiography represents an additional risk for progressive renal dysfunction.17,21
creatinine level begins to rise within 24 hours after administration of contrast medium in 80% of patients in whom CIN develops, typically peaking on the second or third day. Usually, serum creatinine returns to the baseline level within 7–10 days. Although the clinical relevance of CIN may not be immediately evident, given the subclinical course and the high frequency of recovery of renal function, some degree of residual renal impairment has been reported in as many as 30% of those affected, and up to 7% of them may require temporary dialysis or progress to end-stage renal failure.24 Serious clinical consequences, including death, may occur in patients developing CIN. Patients with CIN were observed to have a multitude of non-cardiac in-hospital complications, including hematoma formation, pseudoaneurysms, stroke, coma, adult respiratory distress syndrome, pulmonary embolism, and gastrointestinal hemorrhage.12 Patients who develop CIN after percutaneous coronary intervention have a 15-fold higher rate of major adverse cardiac events during hospitalization than patients without CIN. They also have a six-fold increase in myocardial infarction and an 11-fold increase in coronary vessel reocclusion.25 Although few patients with CIN require dialysis (< 1%), these patients have a more complicated clinical outcome than patients who do not require dialysis, including a significantly higher rate of non-Q-wave myocardial infarction (46 vs. 15%), pulmonary edema (65 vs. 3%), and gastrointestinal bleeding (16 vs. 1%). Moreover, they have a 15-fold longer stay in the intensive care unit and a 5-fold longer in-hospital stay.26 In-hospital and long-term mortality are significantly increased by CIN, likely as a result of the associated morbidity. Several studies have reported an increased death rate for patients developing CIN, ranging from between 5 and 10% for in-hospital mortality, to between 25 and 30% for 1-year mortality. Mortality rates reach 27 and 54%, respectively, for patients who have developed CIN and required dialysis after the procedure.3–5,11,24–26
Clinical presentation and outcome
Prevention
The clinical course of CIN is usually benign, and spontaneous recovery of renal function ensues within 1–2 weeks. The serum
Because the occurrence of CIN can be predicted in most cases, preventive strategies represent the only effective therapeutic approach. All patients receiving contrast should be evaluated for their risk of CIN. The patient’s history, as well as knowledge of renal function, can be used to identify “high risk” for CIN individuals. As serum creatinine is now generally accepted to be an insensitive indicator of renal function,27 renal function should be estimated by either the Cockcroft– Gault formula or the MDRD equation. An estimated glomerular filtration rate below 60 ml/minute should be considered as a “high risk” condition for CIN.28 Several strategies have been devised to afford patients some level of protection against CIN (Table 93.3). A common approach is to ensure adequate volume expansion with fluids beginning before and continuing until sometime after the administration of contrast medium. A number of studies have evaluated the role of pharmacologic adjunct therapies designed to inhibit vasoconstriction and oxidative stress. However, with the exception of volume expansion and antioxidant agents, few of these adjunctive therapies have shown any clear and consistent benefit.
Table 93.2 Contrast volume in elective peripheral vascular interventions performed at the Centro Cardiologico Monzino from 2001 to 2006* Procedure Carotid artery PTA Renal artery PTA Subclavian artery PTA Femoral artery PTA Iliac artery PTA EVAR
n 239 163 23 90 99 71
Mean ± SD (ml) 189 261 285 324 351 446
± ± ± ± ± ±
170 366 126 179 431 185
*32% of the index procedures were associated with other peripheral or coronary interventions. EVAR: Endovascular aortic repair. PTA: percutaneous transluminal angioplasty.
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Table 93.3 Prophylactic strategies evaluated for contrast-induced nephropathy risk reduction • Positive results (potentially beneficial) Hydration Theophylline/aminophylline N-acetylcisteine Ascorbic acid Statins Prostaglandin E1 Hemofiltration Low- and iso-osmolar contrast media • Neutral results (no consistent effect) Fenoldopam Dopamine Calcium channel blockers Amlodipine Felodipine Nifedipine Nitrendipine Atrial natriuretic peptide L-Arginine • Negative results (potentially detrimental) Furosemide Mannitol Endothelin receptor antagonist Hemodialysis
General measures Drugs that adversely affect renal function should be withheld prior to and immediately following contrast exposure. In general, drugs that produce volume depletion or renal vasoconstriction should be reviewed for their risks and benefits prior to contrast exposure. When withdrawal of these drugs is not associated with increasing risk to the patients, it should be undertaken for at least 48 hours following contrast exposure in “high-risk” patients, or until renal function is restored to baseline levels. When possible, repeated contrast exposure should be delayed for 72 hours, and the smallest possible amount of non-ionic, low-osmolality, or iso-osmolality contrast medium should be used in patients with risk factors.28 Fluid administration Hydration remains the cornerstone for the prevention of CIN. Hydration results in plasma volume expansion with concomitant suppression of the renin–angiotensin–aldosterone system, downregulation of the tubuloglomerular feedback, dilution of the contrast media (and thus prevention of renal cortical vasoconstriction), and avoidance of tubular obstruction.29 Simple volume expansion with intravenous administration of half-isotonic (0.45%) or isotonic (0.9%) saline, prior and after the administration of contrast medium, has been considered the standard for care in patients undergoing radio-contrast procedures. However, many aspects regarding the type of fluid administered, the optimal doses, and timing remain undefined. By comparing patients treated with hydration plus mannitol, and hydration plus furosemide, Solomon et al.30 demonstrated that intravenous infusion of 0.45% saline (1 ml/kg/hour), starting 4–6 hours before contrast medium administration, and continued for 24 hours afterwards,
reduced the risk of CIN in patients with mild renal insufficiency undergoing cardiac angiography. More recent evidence suggests that hydration with isotonic saline is superior to half-isotonic saline.31 The advantage of isotonic hydration is certainly demonstrated in patients with normal renal function and with a low-risk of CIN, but these results on the superiority of isotonic versus half-isotonic hydration cannot be transferred conclusively to patients with moderate and severe chronic renal failure. Recently, Merten et al.32 demonstrated that hydration with sodium bicarbonate (154 mEq/l of sodium bicarbonate in dextrose and water at a rate of 3 ml/kg/hour for 1 hour before contrast media exposure, followed by 1 ml/kg/hour during and for 6 hours after the procedure) is more effective than hydration with sodium chloride for prophylaxis of CIN. These authors postulated that the effects of bicarbonate on urine pH may reduce oxygen free-radical formation, thereby reducing contrast-induced injury. Although a clearly emerging concept is that volume expansion is critical in the prevention of CIN, the prognostic impact of hydration has never been evaluated, and we have no information on the possible advantage of this strategy on CIN-associated cardiovascular complications and mortality rate in high-risk populations. Unfortunately, we also lack data from controlled clinical trials that define the most effective hydration period, infusion rate, or hydration volume. Additional studies are also required to investigate the role of hydration in patients with congestive heart failure and renal insufficiency, a population that has always been poorly represented in previous studies, and in which vigorous hydration before percutaneous cardiovascular interventions is difficult logistically and poorly tolerated. For these patients, many studies have reported a hydration rate reduction to 0.5 ml/kg/hour. However, the efficacy of this “prudential” hydration regimen in the prevention of CIN has never been demonstrated. Vasodilators Due to the potential role of hemodynamic effects induced by contrast agents, numerous vasodilators drugs have been tested for the prevention of acute reduction in renal function. The possible role of endothelin-induced renal vasoconstriction has led to the evaluation of a non-selective endothelin receptor antagonist in a multicenter, double-blind randomized trial of high-risk patients undergoing coronary angiography.33 Compared with those randomized to placebo, a significantly higher percentage of patients who received active therapy developed CIN (56 vs. 29%; p = 0.002). However, this study evaluated a mixed endothelin A and B receptor antagonist, and this disappointing result may tentatively be explained by endothelin B receptor inhibition which favors vasoconstriction. To date, it is not known whether selective endothelin A blockade may be beneficial in preventing CIN. Atrial natriuretic peptide has been considered as prophylaxis in high-risk patients, since its administration has been associated with beneficial effects in animal models of CIN. However, no benefit was observed with the intravenous administration of this agent in a large multicenter, prospective, double-blind, placebo-controlled randomized trial.34 Calcium channel blockers, such as verapamil, diltiazem, and amlodipine have been found to attenuate the renal vasoconstrictor response to radio-contrast media, and to inhibit CIN in rats. A randomized placebo-controlled study of
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Contrast-induced nephropathy 35 patients with renal insufficiency has shown that oral nitrendipine (20 mg/day for 3 days) is effective for preventing the decrease in glomerular filtration rate.35 In contrast, other studies with nitrendipine, felodipine, and amlodipine did not confirm the beneficial effects of calcium antagonists for prevention of CIN.36–38 However, it must be emphasized that only dihydropyridine calcium channel blockers have been clinically tested so far. These agents have a more potent peripheral vasodilating effect than verapamil or diltiazem. Therefore, a possible protective renal effect from calcium channel inhibition may be offset by the hypotension effect caused by these drugs and the consequent reduction of renal perfusion pressure. Currently, the use of calcium channel blockers to prevent CIN is not recommended. However, their discontinuation at the time of contrast exposure is not required in patients taking these drugs for other indications. Prostaglandin E1 (PGE) has vasodilatory effects and may be promising as a prophylactic agent against CIN. However, further studies are needed to confirm the effectiveness of this agent. Contrast media stimulates the intrarenal secretion of adenosine, which binds to the renal adenosine receptor and acts as a potent vasoconstrictor, primarily in the efferent arterioles, reducing renal blood flow. As this vasoconstrictive response can be blunted with theophylline in experimental animals, multiple investigators have evaluated the adenosine antagonists (aminophylline and theophylline) as a potential means of reducing the risk of CIN in human subjects. However, these studies have been limited by a small sample size, variation in timing and dosage of drug administration, and varying definitions of CIN. A recent meta-analysis suggests that theophylline may be helpful,39 and further studies are needed to definitively determine its efficacy, safety, and utility. Although theoretically justified, studies testing the effectiveness of low (< 2 µg/kg/minute) doses of dopamine have shown negative or neutral results. The failure of dopamine may be due to hypovolemia and tachyarrhythmia induced by the associated diuretic and pro-arrhythmogenic effects, both leading to decreased cardiac output and reduced effective circulating arterial volume. In contrast to dopamine, fenoldopam is a selective dopamine-1 receptor agonist with systemic and renal arteriolar vasodilatory properties that does not stimulate dopamine-2 or adrenergic receptors, even when administered in higher doses. Fenoldopam significantly increases renal blood flow and decreases renal vascular resistance, without altering glomerular filtration rate. Following preliminary studies indicating a benefit of fenoldopam in reducing CIN, more recent prospective, randomized trials did not show any positive effect.40 Based on the aggregate results of these studies, fenoldopam has no proven indication as a prophylactic measure. Diuretics Furosemide inhibits sodium-potassium-chloride co-transport in the thick ascending limb of the loop of Henle. This segment of the nephron is at greatest risk of ischemic injury attributable to the combination of high metabolic demand and low oxygen delivery. It has been postulated that inhibition of active ion transport in this nephron segment would reduce oxygen utilization and decrease the risk of nephrotoxicity resulting from contrast-stimulated vasoconstriction. In the study
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by Solomon et al.30 there were no beneficial effects of the osmotic diuretic mannitol when added to saline hydration, and there was an exacerbation of contrast-induced renal dysfunction with the administration of the loop diuretic furosemide, used together with saline hydration. Indeed, mannitol increases the intrarenal secretion of adenosine, a potent renal vasocostrictor, resulting in a reduction of renal blood flow. Furosemide-induced diuresis may result in hypovolemia, and this may actually increase the risk of CIN. Antioxidants In recent years, many clinical studies have been conducted with the use of antioxidant compounds in an attempt to prevent CIN. N-acetylcysteine (NAC) has direct vasodylating effects on kidneys vessels, contributing to improved renal hemodynamics. Moreover, it may attenuate endothelial dysfunction, and more notably it is able to scavenge oxygen-free radicals, thus preventing direct oxidative tissue damage occurring in patients receiving contrast. Tepel et al.41 first reported that NAC (600 mg orally twice daily) plus hydration before and after contrast administration offers good protection against CIN in patients with renal insufficiency undergoing computed tomography with a constant dose (75 ml) of contrast (2 vs. 21%; p = 0.01). This finding was supported by some, but not all, subsequent clinical trials. Recently published meta-analyses of several prospective randomized trials recorded an overall significant relative risk reduction in chronic renal failure patients receiving NAC.42,43 However, as the characteristics of these trials are greatly heterogeneous, the benefit of oral NAC among all individuals with renal insufficiency cannot be confirmed with certainty.44 However, recent studies utilizing a greater dose of NAC seem to support the hypothesis of a dose-dependent protective effect of NAC (Figure 93.1).45–47 Additional evidence of the antioxidant strategy effectiveness comes from the recent observation that ascorbic acid may prevent CIN.48 Renal replacement therapies The potential protective effects and therapeutic advantage of a non-pharmacological approach, based on the use of renal replacement therapies (RRTs), such as hemodialysis, hemodiafiltration and hemofiltration, has been a matter of intense investigative interest in recent years. Contrast media are mainly excreted by glomerular filtration. When renal function is normal, the half-life of contrast agents is approximately 2 hours, but it can be prolonged to over 30 hours in patients with severe renal insufficiency, in proportion to the extent of renal impairment.49 Effective contrast removal by the artificial membranes used with RRTs, through a process similar to spontaneous glomerular filtration, has been demonstrated in renal failure patients.50 On the basis of studies demonstrating its effectiveness in contrast media removal, hemodialysis has been proposed for the prevention of CIN after radiographic procedures. However, despite confirmation of an effective extracorporeal plasma clearance achieved by hemodialysis, no clear benefit, or even potential harm, was demonstrated over hydration when this treatment was performed immediately after administration of contrast media.51–54 The discrepancy between the effective removal of contrast media by hemodialysis,
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Primary PCI (Marenzi et al.47)
25
25 20 Incidence of CIN (%)
Incidence of CIN (%)
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15 11% 10
3.5%
5
0
NAC standard dose
15
15%
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8%
5 0
NAC high dose
NAC standard dose
NAC high dose
Figure 93.1 Dose-dependent protective effect of n-acetylcysteine (NAC) against contrast-induced nephropathy (CIN). PCI: percutaneous coronary intervention.
and the lack of a preventive effect against CIN may be the result of hemodialysis-related nephrotoxicity, caused by activation of inflammatory reactions, coagulation processes, and release of vasoactive substances that may induce acute hypotension. Furthermore, hemodynamic instability due to the osmotic shift of fluid from the intravascular to the interstitial and intracellular compartments, and to the dialysisassociated ultrafiltration, is frequently observed during hemodialysis. Hypovolemia can induce renal hypoperfusion, vasoconstriction, and ischemic injury. Thus, the hemodynamic consequences of hemodialysis may offset the positive effect derived from the removal of contrast agent from the circulation. A third possible reason may be the rapid onset of renal injury, after the administration of contrast media, which may occur before starting hemodialysis. Indeed, renal hypoperfusion has been noted within 20 minutes after the injection
of contrast suggesting that the renal injury may occur at its first renal hemodynamic passage.55 In contrast, most of the studies started hemodialysis after a relatively long time, even hours, following the initial injection of the agent. Thus, one of the explanations for the lack of clinical benefit could also be the long delay between exposure to and elimination of the contrast agents. It is noteworthy, however, that two studies in which hemodialysis and hemodiafiltration – a dialysis procedure that is hemodynamically better tolerated than hemodialysis – were started immediately before the contrast agent administration, and then continued for some hours after, did not demonstrate any appreciable protection against CIN.56,57 In contrast to these results, a study from our institute provided evidence that hemofiltration, a simpler form of RRT (Figure 93.2), offers protection against CIN in high-risk patients.3
Replacement fluid Venous line
Filter
Ultrafiltrate
Peristaltic pump
Arterial line
Figure 93.2
Graphic representation of the extracorporeal circuit used in hemofiltration.
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Contrast-induced nephropathy One-hundred-and-fourteen consecutive patients with advanced renal insufficiency undergoing PCI were randomly assigned to either hemofiltration or isotonic saline hydration. Treatment (fluid replacement rate set at 1,000 ml/hour without weight loss) was initiated 4–6 hours before radio-contrast administration, stopped for the duration of the angiographic procedure, and resumed and continued for 18–24 hours after the procedure. CIN occurred in only 5% of patients in the hemofiltration group, and in 50% of patients in the control group (p < 0.001). No patient in the hemofiltration group required emergency hemodialysis, whereas 18% of patients in the control group needed hemodialysis. The in-hospital and 1-year mortality rates were significantly reduced in patients treated with hemofiltration when compared to the control group (Figure 93.3). The mechanisms involved in the prophylactic effect of hemofiltration remain unclear. Positive effects may derive from its ability to remove contrast agent from the circulation, thereby reducing kidney exposure to its nephrotoxic effects. However, this hypothesis is questioned by the results of a recent randomized clinical study, in which two different hemofiltration protocols for the prevention of CIN in patients with severe renal insufficiency (creatinine clearance < 30 ml/minute), scheduled for elective cardiovascular procedures, were compared.58 One group was treated with hemofiltration for 18–24 hours after the procedure (post-hemofiltration group), while another group underwent hemofiltration for 6 hours before, and for 18–24 hours after contrast administration (pre/ post-hemofiltration group). Twenty-six percent of patients in the post-hemofiltration group experienced CIN, as compared with only 3% of the pre/post-hemofiltration group (p = 0.0013). The latter group experienced a lower in-hospital clinical complication rate and mortality (0 vs. 10%).
This study confirmed that hemofiltration is particularly effective in preventing CIN and the associated poor outcome in high-risk patients. It also demonstrated that a preprocedural session is necessarily required in order to obtain the full clinical benefit of this treatment. In conclusion, the interest of using RRT for the prevention of CIN in high-risk patients has not vanished, but has only progressively moved from a post-procedural to a preprocedural application (Figure 93.4), and focused on the possibility of obtaining a safe and hemodynamically tolerated highvolume hydration rather than a mechanical removal of contrast agent. Hemofiltration represents an important advance in CIN prevention, because it is the first strategy to effectively attenuate the risk of CIN, allowing us to extend the range of patients with advanced renal insufficiency that can undergo invasive cardiovascular procedures safely. Further investigation, however, is needed to confirm the positive clinical impact of such an approach in order to better elucidate the mechanisms through which hemofiltration exerts its positive effects, and to identify patients and clinical settings in which the greatest benefit can be obtained.
Conclusion and future directions There is an increasing awareness that CIN represents an important clinical problem with serious sequelae, particularly in high-risk patients undergoing percutaneous cardiovascular interventions. The pathogenetic mechanisms of CIN are multifactorial and not well characterized. The increasing number of diagnostic and therapeutic procedures that require the use of contrast media makes the prevention of CIN an important goal. However, the optimal CIN prophylactic strategy remains
In-Hospital
1-Year (cumulative) 40
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p = 0.01
p= 0.02
14%
Mortality (%)
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30% 30
10
20
5
10
10%
2% 0
0 n=1 Hemofiltration
Figure 93.3
n=8 Controls
805
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n=9
Hemofiltration
Controls
In-hospital and 1-year mortality rate in chronic renal failure patients treated with hemofiltration and in controls.
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Contrast media Exposure time
Hemodiafiltration Hemofiltration
Moon51 Lehnert52 Sterner53 Vogt54 Frank56 Gabutti57 Marenzi3 Marenzi58 −6
−5
−4
−3
−2
−1
+1
+2
+3
+4
+5
+6 +24 hours
Figure 93.4 Time of beginning and duration of different renal replacement therapies in relation to contrast media exposure as reported by studies evaluating the prophylactic effect of these preventive measures.
uncertain. The current best approaches for the prevention of CIN include: accurate risk assessment of the patient, adequate hydration, avoidance of concomitant use of nephrotoxic medications, and use of the lowest possible volume of low-osmolar contrast agents. Prophylactic strategies, including use of bicarbonate solution and administration of NAC at doses commensurate to the contrast volume required, have shown favorable results, and may be recommended for CIN prevention.
Under special circumstances, when a diagnostic and therapeutic procedure requiring contrast media is needed in very-high-risk patients, the use of hemofiltration has been shown to improve short- and long-term outcomes. Future studies are warranted to better define the specific role of each of these approaches, with particular emphasis toward hard clinical end-points, optimally customized prophylactic protocols, and their most costeffective combined application.
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Maitino AJ, Levin DC, Parker L et al. Nationwide trends in rates of utilization of noninvasive diagnostic imaging among the Medicare population between 1993 and 1999. Radiology 2003; 227(1): 113–7 Barrett BJ, Parfrey PS. Preventing nephropathy induced by contrast medium. N Engl J Med 2006; 354(4): 379–86 Marenzi G, Marana I, Lauri G et al. The prevention of radiocontrast-agent-induced nephropathy by hemofiltration. N Engl J Med 2003; 349(14): 1331–8 McCullough PA, Wolyn R, Rocher LL et al. Acute renal failure after coronary intervention: incidence, risk factors and relationship to mortality. Am J Med 1997; 103(5): 368–75 Mehran R, Aymong ED, Nikolsky E et al. A simple risk score for prediction of contrast-induced nephropathy after percutaneous coronary intervention. J Am Coll Cardiol 2004; 44(7); 1393–9 Persson PB, Tepel M. Contrast medium-induced nephropathy: the pathophysiology. Kidney Int 2006; 69 (suppl. 100): S8–10 Schrader R. Contrast material-induced renal failure: an overview. J Intervent Cardiol 2005; 18(6): 417–23 Liss P, Nygren A, Erikson U et al. Injection of low and iso-osmolar contrast medium decreases oxygen tension in the renal medulla. Kidney Int 1998; 53(3): 698–702 Cockcroft DW, Gault MH. Prediction of creatinine clearance from serum creatinine. Nephron 1976; 16(1): 31–41
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Levey AS, Bosch JP, Lewis JB et al. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study Group. Ann Intern Med 1999; 130(6): 461–70 Marenzi G, Lauri G, Assanelli E et al. Contrast-induced nephropathy in patients undergoing primary angioplasty for acute myocardial infarction. J Am Coll Cardiol 2004; 44(9): 1780–5 Rihal CS, Textor SC, Grill DE et al. Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation 2002; 105(19): 2259–64 Rudnick MR, Berns JS, Cohen RM et al. Nephrotoxic risks of renal angiography: contrast-media associated nephrotoxicity and atheroembolism – a critical review. Am J Kidney Dis 1994; 24(9): 713–27 Alsac JM, Zarins CK, Heikkinen MA et al. The impact of aortic endografts on renal function. J Vasc Surg 2005; 41(6): 926–30 Parmer SS, Carpenter JP. Endovascular aneurysm repair with suprarenal vs. infrarenal fixation: a study of renal effects. J Vasc Surg 2006; 43(1): 19–25 Greenberg RK, Chuter TA, Lawrence-Brown M et al. L. Analysis of renal function after aneurysm repair with a device using suprarenal fixation (Zenith AAA Endovascular Graft) in contrast to open surgical repair. J Vasc Surg 2004; 39(6): 1219–28
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Surowiec SM, Davies MG, Fegley AJ et al. Relationship of proximal fixation to postoperative renal dysfunction in patients with normal serum creatinine concentration. J Vasc Surg 2004; 39(4): 804–10 Adriansen ME, Bosch JL, Halpern EF et al. Elective endovascular versus open surgical repair of abdominal aortic aneurysms: systemic review of short-term results. Radiology 2002; 224(3): 739–47 Zeebregts CJ, Geelkerken RH, van der Palen J et al. Outcome of abdominal aneurysm repair in the era of endovascular treatment. Br J Surg 2004; 91(5): 563–8 Eggebrecht H, Breuckmann F, Martini S et al. Frequency and outcomes of acute renal failure following thoracic aortic stent-graft placement. Am J Cardiol 2006; 98(4): 458–63 Parmer SS, Fairman RM, Karmacharya J et al. A comparison of renal function between open and endovascular aneurysm repair in patients with baseline chronic renal insufficiency. J Vasc Surg 2006; 44(4): 706–11 Blocker D, Krauss M, Mansmann U et al. Incidence of renal infarction after endovascular AAA repair: relationship to infrarenal versus suprarenal fixation. J Endovasc Ther 2003; 10(6): 1054–60 Sun Z, Stevenson G. Transrenal fixation of aortic stent-grafts: short- to midterm effects on renal function. A systematic Review. Radiology 2006; 240(1): 65–72 Gruber L. Clinical features and prognostic implications of contrastinduced nephropathy. In: Bartorelli AL, Marenzi G, eds. Contrastinduced Nephropathy. London: Taylor & Francis, 2006: 35–45 Bartholomew BA, Harjai KJ, Dukkipati S et al. Impact of nephropathy after percutaneous coronary intervention and a method for risk stratification. Am J Cardiol 2004; 93(12): 1515–9 Gruber L, Mehran R, Dangas G et al. Acute renal failure requiring dialysis after percutaneous coronary interventions. Catheter Cardiovasc Interv 2001; 52(4): 409–16 National Kidney Foundation (NKF) Kidney Disease Outcome Quality Initiative (K/DOQI) Advisory Board. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis 2002; 39(suppl. 2): S17–31 Solomon R, Deray G, on behalf of The Consensus Panel for CIN. How to prevent contrast-induced nephropathy and manage risk patients: practical recommendations. Kidney Int 2006; 69 (suppl. 100): S51–53 Erley CM. Does hydration prevent radiocontrast-induced acute renal failure? Nephrol Dial Transplant 1999; 14(5): 1064–6 Solomon R, Werner C, Mann D et al. Effects of saline, mannitol, and furosemide on acute changes in renal function induced by radiocontrast agents. N Engl J Med 1994; 331(21): 403–11 Mueller C, Buerkle G, Buettner HJ et al. Prevention of contrast media-associated nephropathy: randomized comparison of 2 hydration regimens in 1620 patients undergoing coronary angioplasty. Arch Intern Med 2002; 162(3): 329–36 Merten GJ, Burgess WP, Gray LV et al. Prevention of contrastinduced nephropathy with sodium bicarbonate. A randomized controlled trial. J Am Med Assoc 2004; 291(19): 2328–34 Wang, A, Holcslaw, T, Bashore, TM et al. Exacerbation of radiocontrast nephrotoxicity by endothelin receptor antagonism. Kidney Int 2000; 57(9): 1675–80 Kurnik, BR, Allgren, RL, Genter, FC et al. Prospective study of atrial natriuretic peptide for the prevention of radiocontrast-induced nephropathy. Am J Kidney Dis 1998; 31(9): 674–80 Neumayer HH, Junge W, Kufner A et al. Prevention of radiocontrast-media-induced nephrotoxicity by the calcium channel blocker nitrendipine: a prospective, randomized clinical trial. Nephrol Dial Transplant 1989; 4(12): 1030–6 Carraro M, Mancini W, Artero M et al. Dose effect of nitrendipine on urinary enzymes and microproteins following non-ionic radiocontrast administration. Nephrol Dial Transplant 1996; 11(3): 444–8 Spangberg-Viklund B, Berglund J, Nikonoff T et al. Does prophylactic treatment with felodipine, a calcium antagonist, prevent
38. 39. 40. 41. 42. 43.
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low-osmolar contrast-induced renal dysfunction in hydrated diabetic and nondiabetic patients with normal or moderately reduced renal function? Scand J Urol Nephrol 1996; 30(1): 63–8 Arici M, Usalan C, Altun B et al. Radiocontrast-induced nephrotoxicity and urinary alpha-glutathione S-transferase levels: effect of amlodipine administration. Int J Urol Nephrol 2003; 35(2): 255–61 Ix JH, McCulloch CE, Chertow GM. Theophylline for the prevention of radiocontrast nephropathy: meta-analysis. Nephrol Dial Transplant 2004; 2004; 19(11): 2747–53 Stone GW, McCullough PA, Tumlin JA et al. Fenoldopam mesylate for the prevention of contrast-induced nephropathy. A randomized controlled trial. J Am Med Assoc 2003; 290(17): 2284–91 Tepel M, van Del Giet M, Schwarzfeld NR et al. Prevention of radiographic-contrast-agent-induced reductions in renal function by acetylcysteine. N Engl J Med 2000; 343(3): 180–4 Birck R, Krzossok S, Markowetz F et al. Acetylcysteine for prevention of contrast nephropathy. Lancet 2003; 362(9389): 598–603 Alonso A, Lau J, Jaber BL et al. Prevention of radiocontrast nephropathy with N-acetylcysteine in patients with chronic kidney disease: a meta-analysis of randomized, controlled trials. Am J Kidney Dis 2004; 43(1): 1–9 Kshirgsagar AV, Poole C, Mottl A et al. N-acetylcysteine for the prevention of radiocontrast induced nephropathy: a meta-analysis of prospective controlled trials. J Am Soc Nephrol 2004; 15(3): 761–9 Baker CSR, Wragg A, Kumar S et al. A rapid protocol for the prevention of contrast-induced renal dysfunction: the RAPPID study. J Am Coll Cardiol 2003; 41(12): 2114–8 Briguori C, Colombo A, Violante A et al. Standard vs double dose of N-acetylcysteine to prevent contrast agent associated nephrotoxicity. Eur Heart J 2004; 25(3): 206–11 Marenzi G, Assanelli E, Marana I et al. N-acetylcysteine and contrast-induced nephropathy in primary angioplasty. N Engl J Med 2006; 354(26): 2773–82 Spargias K, Alexopoulos E, Kyrzopoulos S et al. Ascorbic acid prevents contrast-mediated nephropathy in patients with renal dysfunction undergoing coronary angiography or intervention. Circulation 2004; 110(18): 2837–42 Morcos SK, Thomsen HS, Webb JAW et al. Dialysis and contrast media. Eur Radiol 2002; 12(12): 3026–30 Schindler R, Stahl C, Venz S et al. Removal of contrast media by different extracorporeal treatments. Nephrol Dial Transplant 2001; 16(7): 1471–4 Moon SS, Back SE, Kurkus J et al. Hemodialysis for elimination of the nonionic contrast medium iohexol after angiography in patients with impaired renal function. Nephron 1995; 70(4): 430–7 Lehnert T, Keller E, Gondolf K et al. Effect of hemodialysis after contrast medium administration in patients with renal insufficiency. Nephrol Dial Transplant 1998; 13(2): 358–62 Sterner G, Frennby B, Kurkus J et al. Does post-angiographic hemodialysis reduce the risk of contrast medium nephropathy? Scand J Urol Nephrol 2000; 34(5): 323–6 Vogt B, Ferrari P, Schonholzer C et al. Prophylactic hemodialysis after radiocontrast media in patients with renal insufficiency is potentially harmful. Am J Med 2001; 111(9): 692–8 Russo D, Minutolo R, Cianciaruso B, et al. Early effects of contrast media on renal hemodynamics and tubular function in chronic renal failure. Am J Soc Nephrol 1995; 6(5): 1451–8 Frank H, Werner D, Lorusso V et al. Simultaneous hemodialysis during coronary angiography fails to prevent radiocontrastinduced nephropathy in chronic renal failure. Clinical Nephrology 2003; 60(3): 176–82 Gabutti L, Marone C, Monti M et al. Does continuous venovenous hemodiafiltration concomitant with radiological procedures provide a significant and safe removal of the iodinated contrast ioversol? Blood Purif 2003; 21(2): 152–7 Marenzi G, Lauri G, Campodonico J et al. Comparison of two hemofiltration protocols for prevention of contrast-induced nephropathy in high-risk patients. Am J Med 2006; 119(2): 155–62
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SECTION XVI Pharmacological treatments and risk factor management
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Pharmacological treatment in peripheral arterial disease GI Pandele and C Dima-Cozma
Introduction Peripheral arterial disease (PAD) is a type of localized systemic atherosclerosis/atherothrombotic disease affecting about 12% of the adult population in the US, and is connected with primary causes of mortality like myocardial infarction and stroke. In a study evaluating coronary artery disease in peripheral vascular patients, more than 90% of patients had significant coronary artery disease, as revealed by coronary angioplasty.1 The strong association between PAD and coronary disease explains why about 80% of the mortality in PAD patients is due to cardiovascular events. Early diagnosis of peripheral arterial disease (PAD) is assessed by measuring the resting and post-exercise systolic blood pressure in the ankle and the arm with a Doppler ultrasonic probe. The measurement is made in the dorsalis pedis, posterior tibial, and brachial arteries after the patient rests supine for 10 to 15 minutes. An abnormal ankle–brachial index (ABI), an index of severity of underlying PAD, is defined as < 0.90 at rest. In the recent PARTNERS study (PAD Awareness, Risk and Treatment: New Resources for Survival – The USA PARTNERS Study Screening), patients with an increased risk for PAD by this technique, more than 800 patients from a cohort of 6979 patients aged ≥ 70 years or aged 50–69 years, with a history of cigarette smoking or diabetes, were newly diagnosed with PAD. Thus, the primary concern is to treat atherosclerosis as a systemic disease by aggressive modification of risk factors: smoking cessation, treatment of hypertension, diabetes, and atherogenic dyslipidemia, associated with antiplatelet therapy for all patients with PAD. For symptomatic patients with intermittent claudication many therapies were or are under investigation and new prospective randomized trials will evaluate the new treatments.2,3
Risk factor modification in PAD The systemic nature of PAD imposes as the first goal in treating these patients to modify risk factor profile. Unfortunately, few data are available about the risk factor modification in PAD in comparison with a large amount of data derived from clinical trials on coronary or cerebrovascular disease. The most significant risk factors for developing PAD are cigarette smoking and diabetes; other risk factors involved including atherogenic dyslipidemia, hypertension, hyperhomocysteinemia, and low levels of estrogen.
Smoking cessation Cigarette smoking is a major modifiable risk factor for cardiovascular disease, affecting the coronary, cerebrovascular, and peripheral arterial territories, associated with approximately 20% of deaths in the US. Cigarette smoking is considered the single most important risk factor for PAD, the risk being 16-fold higher for claudication in patients with PAD over 45 years who smoke. The 5-year mortality rate among PAD smokers is > 60%.4 There is a relationship between cigarette smoking and other risk factors such as higher levels of serum cholesterol, platelet aggregation, prothrombotic state, and coronary vasomotor reactivity.5–8 Based on the large sample size of the Third National Health and Nutrition Examination Survey (NHANES III) a relationship between cigarette smoking status and a novel risk factor for cardiovascular disease suggests that inflammation and hyperhomocysteinemia are also potential mechanisms by which smoking promotes atherosclerotic disease.9 Cigarette smoking increases the risk of atherosclerosis and survival rates are better in non-smokers than in those who have smoked or continue to smoke. Smoking cessation is considered the most important advice because of the beneficial effects on the progression of arterial disease. A meta-analysis published by Girolami et al. concluded that smoking cessation was able to improve maximal treadmill walking distance.10 Smoking cessation reduces the progression of disease, demonstrated by lower rates of amputation and rest ischemia, and is also associated with a lower risk of myocardial infarction and stroke. The best evidence in efficacy for smoking cessation are counseling and pharmacotherapy, both methods combined giving the highest rates of smoking cessation.11 The physician three minutes counseling results in a doubling of cessation rates compared with no intervention and increase the smoking cessation by approximately 30%.12 The products now available and approved by the FDA for smoking cessation are five nicotine replacement products (lozenge, gum, transdermal patch, vapor inhaler, and a nasal spray) and Zyban (a sustained-release bupropion). All of these products proved to be effective because they suppress the necessity of smoking and the symptoms of nicotine withdrawal.13 Other drugs as northriptyline or clonidine, used in Europe because have been found to help smoking cessation, are not approved by the FDA. A good result in smoking cessation was obtained when the physician gave the patient images of atherosclerosis in carotid and femoral arteries.14 After the success of replacement therapy associating nicotine with and 811
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without antidepressive drugs, bupropion, a new drug, administered in a controlled, double-blind, randomized trial, showed a sustained abstinence rate at 1 year.15 Treatment of dyslipidemia A modified lipid profile with elevated low-density lipoproteins (LDL) and low levels of high-density lipoproteins (HDL) is an important risk factor for the development and progression of atherosclerosis in PAD. After modest results of diet and exercise on lipid profile, the majority of patients need to be treated with lipid lowering drugs. One of the largest and best-controlled study that provided evidence of the benefit of simvastatin treatment in PAD is the Heart Protection Study. The study was conducted in 20,536 high-risk individuals, who were followed for 5 years, and provided an evidence of slowing evolution of PAD.16 The effect of cholesterol lowering therapy on the risk of onset or worsening of intermittent claudication was also reported in the 4S Study.17 In addition to the effect of lowering serum cholesterol concentration, the HMG-CoA reductase inhibitor class (statins) improve endothelial function and serum P-selectin concentrations. New data emerging from recent studies provide evidence that treatment with statins in patients with PAD improved walking ability, independent of its effects on serum lipid levels.18,19 In a study published by Mondillo et al., high-dose short-term therapy with simvastatin, 40 mg daily, clearly improved walking performance, ankle–brachial pressure indexes, and symptoms of claudication in hypercholesterolemic patients with peripheral vascular disease. The improvement in the resting ankle–brachial index in the simvastatin-treated patients was relatively small in comparison with the increase in walking performance, suggesting that the effect of statins is not correlated with the reduction in size of peripheral atherosclerotic plaques but could be a result of functional effects like plaque stabilization and a potential improvement in endothelial function.19 In experimental studies, statin treatment was able to improve collateral vessel formation in mice who overexpressed lipoprotein (a), or Lp(a), by stimulating the human hepatocyte growth factor gene.20 This particular effect of statin in improvement of vascular function is relatively specific, because fibric acid derivatives like bezafibrate that improve lipid profile had no impact on mortality in patients with PAD.21 The effects of lipid-lowering therapy on atherosclerosis in PAD was estimated in several trials. In the Saint Thomas Trial, patients with PAD (25 men) were treated with a modified diet, cholestyramin, nicotinic acid, or clofibrate. A follow-up of 1 month revealed promising results in femoral atherosclerosis progression.22 In another trial, 188 men with evidence of atherosclerosis in coronary and peripheral arteries were treated randomly with cholestipol plus niacin or placebo. Cholestipol plus niacin therapy was associated with stabilization or regression of femoral atherosclerosis.23 In the Probucol Quantitative Regression Swedish Trial, 303 patients treated with a modified diet and cholestyramine and subsequently randomly with probucol or placebo for three years, no improvement in femoral atherosclerosis or ABI values were observed, in contrast with improvements in serum LDL and HDL cholesterol levels.24 In both trials lipidlowering therapy was not associated with improvement in
total mortality. In the Scandinavian Simvastatin Survival Study, the reduction in cholesterol level was associated with a 38% reduction in the risk of worsening symptoms of intermittent claudication.25 In a study published by Kroan et al., 42 patients were randomly treated with simvastatin plus apheresis, or simvastatin alone, for a period of 2 years. In the group receiving combined therapy there was a 19% reduction in serum Lp(a) as compared with a 15% increase in the group treated by simvastatin alone (p < 0.001). New stenoses in femoral and tibial artery territories, detected with duplex ultrasonographic imaging, had increased from 6 to 13 in the simvastatin-treated group, in comparison with a decrease from 9 to patients in the simvastatin plus apheresis-treated group (p = 0.002). These results sustain the idea that high serum concentrations of Lp(a) are important in femoral and tibial atherosclerosis progression.26 In 833 patients with previous myocardial infarction and elevated cholesterol, ileal bypass surgery to lower serum lipid levels showed that lowering cholesterol for 10 years was associated with a slow-down of peripheral atherosclerosis progression, with a 44% reduction in abnormal ABI, and a 30% reduction in clinical manifestations of PAD in comparison with the control group.27 As a conclusion of these studies, lipid-lowering therapy benefits patients with PAD. The current recommendations of target values for LDL cholesterol are less than 100 mg/dl or 2.6 mmol/l and for serum tryglicerides less than 150 mg/dl or 1.7 mmol/l. The treatment should be started with statins and niacin should be added for increasing HDL cholesterol concentrations and lowering serum triglyceride concentrations, without alterations in glucose metabolism.28 It may be expected that lowering cholesterol would reduce the risk of myocardial infarction and total mortality in patients with PAD. A 10% reduction of cholesterol will produce a 15% reduction in death rate from coronary heart disease and 11% reduction in the overall risk of death. Treatment of diabetes mellitus There is some controversy as to whether diabetes mellitus is really a modifiable risk factor for cardiovascular disease, because intense control of blood glucose is able to prevent microvascular, but not macrovascular, complications. There are two well-known studies on the influence of treatment of diabetes mellitus on cardiovascular complications. The Diabetes Control and Complication Trial compared intensive and conventional insulin therapy in 1441 patients with type 1 diabetes mellitus. Intensive treatment had no effect on the risk of PAD, although there was a bad trend towards the reduction in cardiovascular events.29 The second trial conducted in type 2 diabetes mellitus, the UK Prospective Diabetes Study (UKPDS) also compared intensive drug therapy using sulfonylureas or insulin with dietary therapy. As in the previous study, intensive drug therapy had no effect on the risk of death or amputation due to PAD, though the study revealed a trend toward a reduction in myocardial infarction. This approach sustained the idea that intensive blood glucose control in type 1 and type 2 diabetes mellitus had no favorable effect on PAD. The goal of treatment for patients with diabetes and PAD is to maintain Hb A1c levels under 7.0 %.30,31
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Pharmacological treatment in peripheral arterial disease Treatment of other metabolic risk factors Hyperhomocysteinemia is recognized as an independent risk factor for PAD and cardiovascular death because accelerating atherosclerosis by the complex intervention in LDL cholesterol generates reactive oxygen species, which leads to endothelial dysfunction and proliferation of vascular smooth-muscle cells.32 The causes of hyperhomocysteinemia can be treated by supplementing the diet with vitamin B12 or folate, both of which reduce serum homocysteine concentration, although there is no clinical evidence of beneficial influence in patients with PAD.33 A very interesting hypothesis considered as an important factor for atherothrombosis is the relationship between hyperhomocysteinemia and increased levels of asymmetric dimethylarginine (ADMA), detected in a variety of cardiovascular risk states associated with increased incidence of PAD-like hyperhomocysteinemia,34 hypercholesterolemia,35 diabetes mellitus,36 and hypertension.37 Dimethylamine hydrolases (DDAH), the enzymes that metabolize ADMA, are able to promote angiogenic processes in cells and in culture,38 while ADMA inhibits angiogenesis in animal models.39 The associations between cardiac risk factors and ADMA levels and the role of ADMA in producing endothelial dysfunction support the link between ADMA and cardiovascular disease, but many of the studies are rather small, because of the difficulty of measuring ADMA. The most obvious treatment objective for reversing the effects of increased ADMA is arginine administration, because arginine is able to displace ADMA and restore NOS activity.40 In patients with peripheral vascular disease, treatment with arginine increased the walking distance.41 A therapeutic alternative would be to increase DDAH expression or activity by thiazolidinediones and metformin, estrogens or retinoic acid.42,43 The rise in coronary artery disease and atherosclerosis after menopause is explained by the protective action of estrogen and the hormonal differences between the sexes may be due by the influence of estrogens. Some studies have showed a reduced risk after estrogen replacement therapy. In the prospective Heart and Estrogen/Progestin Replacement Study (HERS), 2,763 postmenopausal women with coronary heart disease, randomized to estrogen or placebo and having the primary outcome (the occurrence of non-fatal myocardial infarction or death from coronary heart disease) and as secondary outcomes (coronary revascularization, unstable angina, congestive heart failure, resuscitated cardiac arrest, stroke or transient ischemic attack and PAD complicated by obstruction, dissection or rupture, other than for the coronary arteries and all cause mortality) concluded no significant differences between placebo and estrogen replacement therapy for the primary and secondary cardiovascular outcomes. Furthermore, cardiovascular events increased slightly in the group receiving hormone replacement therapy during the first year of supplement therapy and the risk of venous thromboembolism in particular also increased, particularly in the early stages of therapy.44
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(JNC VII) established that the risk of cardiovascular disease, which begins at 115/75 mmHg, doubles with each increment of 20/10 mmHg. PAD is equivalent in risk to ischemic heart disease and any class of antihypertensive drugs can be used in most patients with PAD, with the condition of other risk factors aggressively managed in combination with aspirin use.45 The angiotensin-converting inhibitor ramipril significantly reduced myocardial infarction, stroke, and death in patients at high risk for cardiovascular events. Of 9,297 patients, 4,051 had PAD and the results seem to be independent of blood pressure reduction of only 3 mmHg. Furthermore, an important reduction of blood pressure by 21 mmHg, as was obtained by treatment with atenolol and nifedipine, was associated with worsening claudication symptoms. The hypertension should be treated until the goal of JNC VII is accomplished (130/80 mmHg), because the HOPE study stated that treatment with ACE inhibitors in persons with normal arterial pressure values is able to prevent myocardial infarction, stroke, and death in patients with peripheral vascular disease.46 The HOT study revealed the importance of including patients with PAD in trials of the secondary prevention of cardiovascular disease and concluded that angiotensin-converting enzyme inhibitors may reduce the risk of ischemic events in these patients.47 In the ALLHAT study (The Antihypertensive and Lipid Lowering to Prevent Heart Attack Trial)48 a total of 33,357 patients, aged 55 years or older, with hypertension and at least one other coronary heart disease risk factor, were investigated in a randomized, double-blind, active, controlled clinical trial and followed for 4–8 years. Participants were randomly assigned to receive chlorthalidone (12.5–25 mg/day, n = 15,255), amlodipine (2.5–10 mg/day, n = 9,048) or lisinopril (10–40 mg/day, n = 9054). The primary outcomes were combined fatal coronary heart disease or non-fatal myocardial infarction, analyzed by intent to treat. Secondary outcomes were all-cause mortality, stroke, combined coronary heart disease and combined cardiovascular disease, treated stroke, angina without hospitalization, heart failure, and PAD. There were no significant differences between amlodipine and chlorthalidone for primary and secondary outcomes of allcause mortality, combined coronary heart disease, stroke and PAD. For PAD the risk reduction was 0.82 for amlodipine versus chlorthalidone and 1.04 lisinopril versus chlorthalidone. The ALLHAT Study attempted to detect clinically meaningful differences in cardiovascular disease outcomes, indicated that thiazide-type diuretics should be considered first for pharmacologic therapy of hypertensive patients and are able to reduce the relative risk for PAD in the similar proportion like for calcium blockers and angiotensin-converting enzyme inhibitors. Among the subpopulation of patients with PAD (4,051) participating in the Heart Outcomes Prevention Evaluation Study, ramipril therapy produced more than a 20% reduction in the risk of cardiovascular death relative to placebo.49
Antiplatelet drug therapy Treatment of hypertension Hypertension is a major risk factor for PAD. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure
Antiplatelet drug therapy is able to reduce the risk of ischemic events. The meta-analysis conducted by the Antiplatelet Trialist Collaboration on 102,459 patients, evaluated the outcomes for acute or prior myocardial infarction, ischemic
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stroke, or other vascular disease including PAD. It concluded that antiplatelet drug therapy reduced the risk of fatal or nonfatal cardiac events from 11.9% in the control group to 9.5% in the treated group. The subgroup of 3,295 patients with claudication was allocated to treatment with aspirin and, after 27 months of follow-up, there was a reduction of the risk for myocardial infarction, stroke or death from vascular causes of 18%.50 The doses recommended by the American College of Chest Physicians were between 75 and 325 mg per day for patients with PAD, although the FDA experts formally considered there to be insufficient evidence to approve the use of aspirin in patients with PAD.51 In the Physicians Health Study, a primary prevention trial, aspirin was able to improve peripheral circulation and to reduce the need for peripheral arterial surgery.52 Aspirin therapy significantly improved peripheral circulation. In patients with PAD, submitted to peripheral angioplasty, vascular graft pathway in saphenous vein or prosthetic graft and followed for about 19 months showed a 43% reduction in the rate of vascular graft occlusion.53 Aspirin was administered alone or in combination with dipyridamole, sulfinpyrazone or ticlopidine. Low doses (75–325 mg per day) or high doses (600–1500 mg per day) of aspirin administered alone or in combination, had the same efficiency. Thienopyridines Ticlopidine inhibits platelet activation by blocking adenosine diphosphate receptors on the platelet surface. In comparison with placebo, ticlopidine was more efficient in reducing the risk of fatal and non-fatal myocardial infarction or stroke, and diminishing the severity of intermittent claudication and the need for interventional procedures.54,55 However, treatment with ticlopidine is associated with a substantial risk of thrombocytopenia and neutropenia in 2.3%, and is even thrombotic to thrombocytopenic purpura.56,57 Clopidogrel belongs to the same group of thienopyridine drugs but its hematologic side-effects are fewer and its benefits in the therapy of patients with PAD has the support of data derived from the Clopidogrel Versus Aspirin in Patients at risk of Ischemic Events (CAPRIE) trial. The aim of the trial was to compare the efficacy of clopidogrel (75 mg per day) with aspirin (325 mg per day), on a cohort of more than 19,000 patients with recent myocardial infarction, recent ischemic stroke, or PAD. The patients with PAD were selected on the presence of intermittent claudication, with an ABI of 0.85 or less, or a history of claudication with previous bypass surgery, angioplasty, or amputation. All patients were symptomatic and treatment with clopidogrel was associated with an 8.7% reduction of fatal or non-fatal ischemic stroke, fatal or non-fatal myocardial infarction, or death from other vascular causes. These results convinced the FDA to approve clopidogrel in the secondary prevention of atherosclerotic disease. Clopidogrel and aspirin were well tolerated, though there was an estimated risk of four cases per million patients of thrombotic thrombocytopenic purpura. The primary endpoint in the 6,452 patients treated reached at annual rate of 4.9% for aspirin and 3.7% for clopidogrel, with an adjusted risk reduction of 23.8%. There are other studies evaluating the efficacy of clopidogrel in the treatment of PAD, like CAMPER, on patients with PAD in post-angioplasty, on 2,000 patients followed for 30 months; CASPAR with 1,500 patients in
post-bypass followed for 2 years; and CHARISMA, conducted in 15,200 patients with cerebral, coronary, and PAD at high risk.58,59 Dual thromboxane A2 blockers Thromboxane A2 (Tx A2) is formed in excess in patients with peripheral arterial disease, especially in diabetes, and exerts deleterious effects in arterial endothelium.60,61 There are drugs that selectively inhibit thromboxane synthase and thromboxane A2 receptor antagonists. Tx A2 blockers act partially by inhibition of thromboxane biosynthesis or action, but mainly by increased local formation of prostaglandins Pg I2, derived from the metabolism of prostaglandin endoperoxides Pg H2, the precursor of Tx A2. A trial demonstrating a significant reduction of overall mortality by a dual Tx A2 blocker (picotamide), in comparison with aspirin, in diabetic patients with PAD who were high-risk for ischemic events took place in 2004. There was 2.5% absolute risk reduction and 45% relative risk reduction, with 40 patients treated for 2 years to prevent one death.62 In the study of Balsano et al., 2,304 patients with peripheral arterial disease were treated with picotamide or placebo for 18 months and obtained a reduction of 19% (non-significant) in fatal and non-fatal events in the treated group in comparison with placebo group.63 Because of systemic atherosclerosis associated with PAD, the prevention of ischemic events must be realized with aspirin, which is considered the primary antiplatelet drug owing to its efficiency in preventing thrombotic complications and in conserving vascular graft patency. There is also sufficient evidence for picotamide and clopidogrel to be used for the prevention of ischemic events in patients with PAD and these may be even more effective than aspirin.31,64 Although aspirin is the most widely used and cheapest antiplatelet drug, approximately 10–18% of the population appear to be unable to take it because of gastrointestinal discomfort or risk of gastrointestinal hemorrhage. Clopidogrel and picotamide are presently much more expensive and their use is selectively limited to those patients who cannot tolerate aspirin.65 The efficacy and safety of clopidogrel was analyzed in three clinical trials. In the CAPRIE (Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events) trial, clopidogrel was compared with aspirin in a broad spectrum of patients with atherothrombosis, in which a significant reduction in rehospitalization for ischemic events was noted (unstable angina, transient ischemic attack, and peripheral limb ischemia) as well as added bleeding events secondary to therapy with clopidogrel and aspirin. Rehospitalization for ischemia or bleeding was reduced from 13.68 to 12.57%, which meant a relative risk reduction of 1.1%. The number of patients to treat after 1 year was 91.66 The assumed estimated risk for vascular disease, ischemic stroke, and myocardial infarction, and the need for hospitalization because of ischemia or bleeding in patients who received ASA was 22.3% while for patients receiving clopidogrel only 15.9%. In the subset of patients with CABG under treatment with clopidogrel, the relative risk reduction of ischemic events was 28.9%, the highest in the CAPRIE study. The PAD subgroup in the CAPRIE trial, including nearly 6,500 patients, was more important than any other prospective study, because they demonstrated the therapeutic superiority
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Pharmacological treatment in peripheral arterial disease of clopidogrel in comparison with aspirin in the treatment of PAD.58 The guidelines recommend the use of 75 mg clopidogrel daily in the treatment of PAD. The real problem is that clopidogrel is much more expensive that aspirin.67 A new trial, CHARISMA (Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Management and Avoidance Trial), will help further define the effectiveness and cost-efficiency of association clopidogrel– aspirin versus monotherapy in the secondary prevention of cerebral, coronary, and PAD and in primary prevention with high atherothrombotic risk.68
Drug therapy for claudication In a critical analysis of a 75 published clinical trials on the treatment of intermittent claudication by Cameron et al., it was evident that 75% of these trials utilized a small sample size, without placebo group or blinded randomization, and had inappropriate endpoints.69 After more recent elaborated consensus guidelines for conducting clinical trials in patients with PAD, an evaluation of old and new drugs was required in light of the new objective criteria.70,71 The drugs approved by FDA for medical treatment of intermittent claudication are pentoxifylline, a hemorheologic agent, and cilostazol, a phosphodiesterase III inhibitor. Vasodilator drugs Vasodilator drugs like papaverine were the first drugs studied for the treatment of intermittent claudication, but the majority of studies failed to find any evidence of clinical efficacy of these drugs.72 The pathophysiologic explanation for the failure of vasodilator therapy is that during exercise, the resistance vessels dilate distal to a stenosis in response to ischemia and vasodilators have no influence on them. The decreased resistance in responsive vessels creates a relative steal phenomenon, contributing to the diminishing blood flow and perfusion pressure of the ischemic leg. Furthermore, in contrast to their effects on myocardial oxygen consumption in coronary disease, vasodilators are unable to modify the skeletal muscle oxygen demand. Nowadays, scientific evidence does not support the treatment of intermittent claudication with vasodilators.31 Pentoxifylline Pentoxifylline is a methylxanthine derivative with hemorrheological properties, causing a decrease in blood viscosity, an increase in numbers of erythrocytes and white blood cells, a lowering of plasma fibrinogen and pro-inflammatory cytokines such as IL-12, TNFα, IFNγ, and antiplatelet effects. It also control the spontaneous cytotoxicity of peripheral blood monocytes through the inhibition of perforin-mediated cell membrane damage.73–76 Monocytes are the only white blood cell type significantly and independently associated with PAD.77 Pentoxifylline, in one of the first randomized trials, increased maximal treadmill walking distance by 12% in comparison with placebo, without statistical significance.78 In a recent trial published by De Sanctis et al., pentoxifylline was significantly superior to placebo in rising walking distance, both after 6 and 12 months of therapy.79 A meta-analysis of
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pentoxifylline treatment studies in peripheral arterial occlusive disease found a net increase of 44 m in maximal treadmill distance.80 In conclusion, pentoxifylline appears to have a limited effect on walking and these data are insufficient to support its widespread use.80–83 Cilostazol Cilostazol was introduced for the therapy of intermittent claudication following approval by the FDA in 1999. The drug inhibits phosphodiesterase type 3, which produces an increasing concentration of cAMP in the cell. Cilostazol produces vasodilatation, activates lipoproteinlipase, inhibits platelet aggregation and neoformation of thrombus on atherosclerotic plaques, and impairs smooth muscle proliferation.84–86 In four placebo-controlled trials of cilostazol, on 1,534 patients with intermittent claudication, 100 mg twice daily of this drug improved the pain-free and maximal treadmill walking distance in comparison with placebo.87,88 At a daily dose of 200 mg (100 mg twice daily), cilostazol was superior to both placebo and pentoxiffyline, increasing ABI, improving absolute claudication index and rising serum HDL-cholesterol levels by 40–50% in comparison with placebo, and improving the quality of life, as measured by the medical outcomes scale (SF-36). Headaches, dizziness, palpitation and transient diarrhea are important side-effects of cilostazol.89,90 In patients with heart failure it should be administered with caution because of a high incidence of ischemic events (myocardial infarction, stroke), in patients with PAD. With these limitations, cilostazol should be a very efficient drug for a large proportion of PAD patients. The main limitation today comes from the risk of death with this class of drugs: cardiovascular death in 0.6% of cilostazol-treated patients in comparison with 0.5% in the placebo group, and myocardial infarction in 1.5% in the cilostazol-treated group in comparison with 1.1% in placebo-treated patients. This explains the warning about treatment with cilostazol in patients with PAD associated with heart failure and because other phosphodiesterase III inhibitors have been shown to reduce survival.31,91,92 Calcium channel blockers given in association with cilostazol can raise the serum level of the drug. The daily dose is limited to 500 mg orally twice per day. Naftidrofuryl Naftidrofuryl is an antagonist of the 5-hydroxytriptamine receptor, available in Europe but not in the US. In five placebo-controlled trials, naftidrofuryl improved pain-free treadmill walking distance, without influence on maximal walking distance.93–95 Treatment with naftidrofuryl was associated with fewer cardiovascular events than placebo.96 Another serotonin antagonist, ketanserin, did not improve the claudication distance in a multicenter trial.97 Levocarnitine and proprionyl levocarnitine The metabolic abnormalities that develop in the skeletal muscle of the lower extremities are associated with increased accumulation of intermediates of oxidative metabolism like acylcarnitines. Claudication is the result of alteration in skeletal muscle metabolism by reduced blood flow.98–100
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Muscular metabolism and exercise performance of the ischemic muscle may be improved by levocarnitine, 2 g twice daily, and propionyl levocarnitine, the latter being more effective in improving maximal treadmill walking distance.101 In two multicenter randomized trials, propionil levocarnitine administered in 730 patients improved claudication, walking distance in comparison to placebo, and quality of life.102,103 Prostaglandins In both intermittent claudication and critical leg ischemia, treatment with prostaglandins has been reported to improve clinical pattern. Intravenous administration of prostaglandin E1 (Pg E1) or its precursor improved claudication distance in patients with intermittent claudication.104 In initial trials, prostaglandins were evaluated in critical leg ischemia and the endpoints watched were relief of ischemia, pain, healing of ischemic ulcers, and reduction in the rate of amputation.105,106 One of the first open trials tested prostaglandin E1 versus a mixture of energy-rich phosphates for walking exercise in 45 selected patients. The maximal walking distance increased from 139 to 180 m, under energy-rich phosphates from 95 to 200 m, and under prostaglandin E1 from 70 to 400 m.107 In another prospective double-blind study, prostaglandin E1 was administered intra-arterially and energy rich phosphates were studied comparatively. Pain-free walking distance increased significantly in both groups (60 to 225 m by prostaglandin E1 and 70 to 175 m by energy rich phosphates), as did maximal walking distance measured on a treadmill (from 90 to 300 m in prostaglandin E1-treated patients and from 107 to 280 m in patients treated with energy-rich phosphates).108 Administered intravenously, prostaglandin E1 was also effective in increasing the walking distance, but not in the same range as after intra-arterial application.109 Critical limb ischemia Treatment with intra-arterial prostaglandin E1 avoided major limb amputation in patients with critical limb ischemia (3 amputations in 31 patients treated with prostaglandin E1 versus an amputation of 26 patients treated with adenosine triphosphate) and the long-term efficacy was significantly better for the group treated with prostaglandin: 1/18 amputation versus 4/16 in patients treated with adenosine triphosphate.110,111 Intravenous administration of prostaglandin E1 in patients with critical limb ischemia was apprended with favorable results. In 202 patients (25% with thrombangeitis obliterans in stages III and IV, in whom bypass surgery or transluminal angioplasty was not possible or successful), treatment with prostaglandin E1, 40 µg twice daily, for a period of 27 days, determined that the rest pain disappeared in 28% or was markedly impaired in 40%, healed completely in 20% and partially in 39% and amputation was necessary in 20%. After a period of 22 months in 91 patients, 12% had a relapse.112 In comparison with naftidrofuryl, in the treatment of claudication, and with pentoxyphylline for critical limb ischemia, prostaglandin E1 was significantly better.113,114 The spectrum of beneficial effects of therapy with prostaglandin E1 extends from PAD to Raynaud’s phenomenon.115–118 The benefits with prostanoids in PAD are explained by complex pharmaceutical properties such as vasodilatatory potency, which has also been demonstrated in collateral vessels.119,120 They have also
antiaggregation action. Iloprost is ten-fold more effective than prostacyclin, which is ten-fold more effective than prostaglandin E1.121 Prostaglandin E1 inhibits deposition of platelets on the atherosclerotic plaque, an action synergistic with endogenous generated EDRF.122 In ischemic leg, prostaglandin E1 may reduce switching from lipid oxidation to glucose oxidation. Impairment of the lactate/pyruvate quotient is caused by iloprost and prostaglandin E1.123,124 Prostanoids improved macro and microcirculation in ischemic leg. Intra-arterial and intravenous treatment with iloprost increased blood flow in the femoral artery, and increased skin microcirculation, as was demonstrated by transcutaneous measurement laser Doppler fluximetry and capillary microscopy.125 Because prostaglandin E1 is rapidly transformed by pulmonary metabolism, in proportion by more than 90%, intermittent intra-arterial administration is the preferred method, in doses of 5 µg/60 minutes and is possible that metabolites such as H2-prostaglandin E1 are also vasoactive. By percutaneous application the dose is 60 µg/120 cm2.126,127 In conclusion, prostanoids has been proved to be effective in many clinical trials in critical limb ischemia of PAD. Recently, an orally active prostaglandin I2 analog was proved to be more effective than placebo in patients with intermittent claudication128 but at higher doses it had substantial side-effects such as headache, flushing, and gastrointestinal intolerance.129 Sulodexide Sulodexide, a drug with high affinity for antithrombin III and heparin cofactor II, is a highly purified glycosaminoglycan associating fast (morning) heparin fraction 7,000 dalton 80% and dermatan sulphate fraction 25,000 dalton 20%. The drug is rapidly absorbed by the gastrointestinal tract. Its metabolic effects include the release of lipoproteinlipase, increasing the catabolism rate of chylomicrons and very low lipoproteins, and increasing the hepatic catabolism of cholesterol-rich lipoproteins. Besides these effects on lipid profile, sulodexide also blocks platelet activation and adhesion by inhibition factor X, activates tissue-plasminogen activator (tPA) by inhibition of plasminogen activating inhibitor (PAI-1), and has an auto-proliferative effect on smooth muscle cells.130 In a meta-analysis, Guddi et al. analyzed the results of 19 clinical trials, performed by different Italian research groups during a 15-year period, including 849 diabetic and nondiabetic PAD patients, showed that sulodexid is effective in treating and preventing PAD. Administered intramusculary for a period of 10–20 days and then orally for an average 70 days, sulodexide significantly increased the claudication distance evaluated as pain-free walking distance (PFWD) on a treadmill measured in meters, with a difference of 36% between groups in favor of sulodexide. The results of meta-analyses sustain the idea that sulodexide is suitable for long-term therapy and it could be a drug of choice for PAD patients, particularly if they are diabetic, and/or elderly.131 In a very recent multicentric, randomized, double-blind study, Locheri et al. showed in 286 patients with intermittent claudication stage II Leriche Fontaine, treated with sulodexide for 20 days intramusculary and then 6 months orally, that PFWD increased from 200 to 340 m, at statistical significance difference to placebo (p < 0.001). The metabolic and
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Pharmacological treatment in peripheral arterial disease hematological effects like the decrease in fibrinogen, triglycerides, inhibition of PAI-1 with concomitant increase of tPA, and the inhibition of the activation of factor X are of major clinical interest. In the absence of other effective non-surgical therapies, sulodexide is recommended in patients with PAD, particularly if they are diabetic, elderly, or have thrombosis.132–134 Experimental or investigational agents for PAD include macrolide antibiotics for the treatment of chlamydia infection, hyperbaric oxygen and angiogenic growth factors (perhaps the most promising therapeutic solution).135
Thrombolytic and antiplatelet drugs in the treatment of arterial thrombosis and graft occlusions In addition to the current techniques to dissolve clots that focus on the fibrin and thrombin components, but have no effect on the platelet function, a new class that blocks the final common pathway of platelet aggregation, the glycoprotein IIb/IIIa platelet receptor antagonist, has been developed. Because the experience with these drugs in peripheral vascular thrombolysis is still modest, the drugs utilized in coronary thrombolysis as tissue-type plasminogen activator (rtPA), alteplase or recombinant activator (rPA) reteplase has been extrapolated from experiences in the coronary literature. Combination therapy using both thrombolytic and antiplatelet drugs in the peripheral vascular system was used to accelerate lysis and potentially to improve long-term patient outcome.136–138 In an article published by Tepe and colleagues on the use of combination therapy (abciximab and urokinase) for patients with PAD, there are favorable outcomes and short lysis time. In another study, Tepe et al. reported their experience with urokinase combined simultaneously with abciximab, either by constant infusion or pulse therapy, in 14 patients with peripheral arterial occlusion. Heparin doses were associated to maintain the activation of thromboplastin time at 50–70 seconds. There was a primary success rate of 100%, with the treatment time between 50 minutes to 8 hours (a mean of 2 hours).139,140 In a randomized trial of 84 patients in which the two equal groups received aspirin versus abciximab and intra-arterial therapy with rtPA, the group receiving abciximab has a shorter duration of clot lysis (75 vs. 110 minutes, p < 0.001), a reduced rate of rehospitalization, reintervention, amputation, and significantly long-term outcome improvement at 3 months.141 Eptifibatide (180 µg/kg bolus, followed by 2 µg/kg infusion combined with a reduced dose of 1 mg/hour rtPA, continued for 12 hours) provided complete lysis with no distal embolization, in a case initially resistant to rtPA.142 The low dose of rPA (0.25 units/hour) combined with the usual doses of abciximab in 26 patients and for a mean treatment time of 8 hours, were accompanied by 92% success rate, with no significant bleeding complications.143 In a randomized study, Duda and colleagues enrolled 20 patients to receive urokinase, aspirin, and heparin versus combination therapy with urokinase, abciximab, and heparin for another group of 50 patients. The amputation-free survival rates at 90 days follow-up were 96% for the combination therapy versus 80% for the placebo group (p = 0.04).
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Survival without open surgery or major amputation at 90 days was 92% for the combination therapy group versus 75% for the placebo group, without major bleeding complications for the combination group. This study supports the use of IIb/IIIa inhibitors because of the efficient thrombolysis and the ability of these agents to protect the distal vascular circulation by prevention of platelet embolization into the distal circulation and the improved outcomes a long time after intervention.144 Combination therapy with local catheter-delivered fibrinolytics rPA or rtPA and the systemic GPIIb/IIIa antagonist abciximab, associated with heparin, will attack the clot at its multiple components: the plasminogen activator against fibrin, heparin against thrombin, and the IIb/IIIa antagonists against platelets. The combination of drugs will make thrombolysis safer and faster, permitting accelerated reperfusion, preventing reocclusion and reducing fibrinolytic risk.144,145
Exercise rehabilitation therapy Exercise rehabilitation therapy is one of the most effective medical therapies because it is able to improve symptoms of claudication, being associated with an average 179% increase in initial claudication distance and 122% increase in maximal walking distance on the treadmill and improvements in community-based walking ability functional status, physical functioning, and quality of life.146 In the last half century, walking exercise has been recommended for non-pharmacological treatment of claudication, and a number of studies demonstrated improvement in treadmill walking distance by 96% and pain free walking time of 134%. Another study, using guided treadmill walking, demonstrated improvements in peak exercise performance and peak oxygen consumption. A vigorous exercise training program, followed for a long time, in motivated patients, may be as beneficial as angioplasty, even more so. 147–149 In a recent meta-analysis from the Cochrane Collaboration that considered only randomized controlled trials, it was shown that exercise programs of rehabilitation were associated with significant improvements in walking time, in comparison with angioplasty and antiplatelet therapy.150 The benefit of exercise induced in patients with PAD is not explained by an increased collateral blood flow but by other potential mechanisms, such as improvement in endothelial vasodilator function, improved blood viscosity and enhanced oxygen availability, and diminished blood viscosity and inflammation response. The intermediary metabolism of skeletal muscle is improved, as is shown by increased oxygen extraction in the legs and the lower levels of acylcarnitine in muscles.151–153 Regular exercise also increased central arterial compliance and this may be another mechanism by which it lowers the risk of cardiovascular disease, especially in aging persons.154
Conclusion PAD is a chronic vascular disease caused by atherosclerosis in lower limb arteries, and is associated with a considerable risk of fatal ischemic heart disease and ischemic stroke, as compared with general population. Because of the general trend in population aging and the extent of metabolic diseases
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like obesity, type 2 diabetes mellitus, and dyslipidemia, a predicted growth of PAD is awaited over the next few decades. Only one-half of elderly patients with documented PAD are symptomatic and this explain why an important proportion of patients with PAD are discovered with critical ischemia. Elderly patients with PAD are at increased risk for all-cause mortality, cardiovascular mortality, and mortality from coronary arterial disease. A lot of cohort studies have found a positive association between type 2 diabetes mellitus and PAD. In a recent follow-up study on 48,607 men in the US, the results indicated that duration of type 2 diabetes is associated strongly with the risk of developing PAD.155 In persons with PAD, the main risk factor should be avoided or healed, such as cessation of cigarette smoking, control of hypertension, diabetes and dyslipidemia. A lot of drugs are indicated for achieving these goals: statins, angiotensin converting enzyme inhibitors, oral antidiabetics and insulin, beta-blockers, antiplatelet agents, aspirin, and clopidogrel. The latter two have to be extended to all persons with PAD. In critical leg ischemia, cilostazol (unless cardiac failure is not present), prostanoids, and sulodexide may improve the condition by reducing the composite endpoints of death, major amputation and recovery from leg ischemia and life quality. Exercise rehabilitation programs enhance biomechanical performance with greater improvement in maximal walking distance, and the greatest benefit will be obtained when
sessions are at least 30 minutes in duration and take place at least three times per week, for more than 6 months. As the number of elderly persons increases, the incidence of atherosclerotic disease will rise, as will the number of reconstructive procedures to be performed, because older patients are more likely to be referred with rest pain and ulceration than for claudication.156 Furthermore, the actual data suggest that age should not be seen as a contraindication to reconstructive surgery and an aggressive approach to revascularization will result in an improved limb salvage rate, reduced mortality, and total cost. PAD represents a highly prevalent manifestation of atherosclerosis associated with an important risk of illness and death and a marked limitation in ambulatory capacity and quality of life. Patients with lower limb arterial atherosclerosis should be considered candidates for secondary prevention strategies, just like patients with coronary artery disease. Antiplatelet drugs are more effective than angiotensin-converting enzyme inhibitors in reducing the risk of fatal and non-fatal ischemic events, and aspirin or clopidogrel should be considered in all patients with PAD.157 The indications of angioplasty and bypass surgery are incapacitating claudication, limb-threatening ischemia, rest pain, non-healing ulcers, infection or gangrene, and vasculogenic impotence. Percutaneous angioplasty is recommended for localized stenosis less than 10 cm in length. Compared to percutaneous transluminal angioplasty alone, associated stenting improves 3-year patency by 26%.158,159
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Sinzinger H, Fitschra P, O’Grady J et al. Synergistic effect of prostaglandin E1 and isosorbide dinitrate in peripheral vascular disease. Lancet 1990; 1: 627 Stiegler H, Rett K, Wirkemanger M et al. Metabolic effects of prostaglandin E1 on human skeletal muscle. Vasa 1988; 17: 5–11 Rexroth W, Amendt K, Rommelle K et al. Effecte von prostaglandin E1 auf hämodynamik met extremitätenstoffwechsel bei gsunden und patienten mit arterieller verschlu β krankheit stadium III and IV. Vasa 1985; 14: 220–8 Creutzig A, Caspary L. Prostanoids in therapy of peripheral arterial occlusive disease. Therapie 1991; 46: 241–5 Simmet T, Peskav BA. Prostaglandin E1 and arterial occlusive disease: pharmacological considerations. Eur J Clin Invest 1988; 18: 549–55 Heidrich H, Rauft J, Peters A et al. Intravenöse prostanosin therapie bei peripher arteriellen durchblutangsstresingen in Fontaine stadium III and IV. In: Heidrich H, Böhme H, Rogath W, eds. Prostaglandin E1 – Wirkungen und Therapeutische Wirksamkeit. Heidelberg: Springer, 1988: 111–9 Mohler ER, Hiatt WR, Olin JW et al. Treatment of intermittent claudication with beraprost sodium, an orally active prostaglandin I2 analogue. A double blind, randomised, controlled trial. J Am Coll Cardiol 2003; 41: 1679–86 Lievre M, Morand S, Besse B et al. A dose-effect study of beraprost sodium in intermittent claudication. J Cardiovasc Pharmacol 1996; 27: 788–93 Mauro M, Ferraro G, Palmieri G. Profibrinolytic and antithrombotic effects of sulodexide oral administration: a double blind cross-over placebo-controlled study. Curr Ther Res 1992; 51: 345–50 Guddi A, Galetti C, Illumminati B et al. Metaanalysis of some results of clinical trials on sulodexide therapy in peripheral occlusive arterial disease. J Int Med Res 1996; 24: 389–406 Dormandy JA, Murray GD. The fate of the claudication: a prospective study of 1969 claudicants. Eur J Vasc Surg 1991; 5: 131–3 Banerjek AK, Pearson J, Gilliand EL et al. A six year prospective study of fibrinogen and other risk factors associated with mortality in stable claudicants. Thromb Haemost 2002; 68: 261–3 German Society for Angiology. Guidelines for therapeutic studies in Fontaine’s stages II–IV peripheral arterial occlusive disease. Vasa 1995; 25: 114–89 Ouriel K. Peripheral arterial disease. Lancet 2001; 358: 1257–64 Moliterno DJ, Topol EJ. Conjunctive use of glycoprotein IIb/IIIa antagonists and thrombolytic therapy for acute myocardial infarction. Thromb Haemost 1997; 78: 214–9 Cannon CP. Overcoming thrombolytic assistance: rationale and initial clinical experience combining thrombolytic therapy and glycoprotein IIb/IIIa receptor inhibition for acute myocardial infarction. J Am Coll Cardiol 1999; 34: 1395–402 Coller BS. Blockade of platelet GP IIb/IIIa receptors as an antithrombotic strategy. Circulation 1995; 92: 2373–80 Tepe G, Duda SH, Evley CM et al. The adjuvant use of the monoclonal antibody C7E3 Fab in peripheral arterial thrombolysis. Circulation 1997; 166: 524–7 Tepe G, Schott H, Evley CM et al. Platelet glycoprotein IIb/IIIa receptor antagonist used in conjunction with thrombolysis for peripheral arterial thrombosis. Am J Roentgenol 1999; 172: 1343–6
141.
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149. 150. 151. 152. 153. 154. 155. 156. 157. 158. 159.
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Selweiser J, Kirch W, Koch R et al. Short and long term results of abciximab versus aspirin in conjunction with thrombolysis for patients with peripheral occlusive arterial disease and arterial thrombosis. Angiology 2003; 57: 913–23 Gray WA. Successful resolution of a peripheral arterial resistant thrombus in a patient with combined eptifibatide and thrombolytic therapy. J Invasive Cardiol 2000; 12: 19D–20D McMara TO. Combination of Reo Pro and Retavase in thrombolysis of peripheral arterial occlusion: preliminary results. J Vasc Intervent Radiol 2001; 12: 123 Duda SM, Banz K, Ouriel K et al. Cost–effectiveness analysis of treatment of subacute peripheral artery occlusions with thrombolysis with and without adjunction abciximab. J Vasc Intervent Radiol 2001; 21: S70 Shlavsky H, Goldberg R. Combination therapy in peripheral vascular disease: the rationale of using both thrombolytic and antiplatelet drugs. J Am Coll Surg 2002; (suppl. 1): 103–13 Dormandy JA, Rutherford RB. Management of peripheral arterial disease (PAD). Transatlantic Inter-Society Consensus (TASC). J Vasc Surg 2000; 31 (suppl.1): S1–296 Lundren F, Dahllof A, Involholm K et al. Intermittent claudication – surgical reconstruction or physical training? A prospective randomised trial of treatment efficiency. Ann Surg 1989; 209: 346–55 Gray TS, McMillan PJ, Fletcher EWL et al. Is percutaneous transluminal angioplasty better than exercise for claudication? Preliminary results from a prospective randomised trial. Eur J Vasc Surg 1990; 4: 135–140 Hiatt WR, Regensteiner JG, Hargaten ME et al. Benefit of exercise conditioning for patients with peripheral arterial disease. Circulation 1990; 81: 602–9 Leng GL, Towler B, Ernest E. Exercise for intermittent claudication. Cochrane Database. Syst Rev 2000; 2 Stewart KJ, Hiatt WR, Regensteiner JG et al. Exercise training for claudication. N Engl J Med 2002; 347: 1941–51 Zettergunst S. The effect of active training on the nutritive blood flow exercising ischemic legs. Scand J Clin Lab Invest 1970; 25: 101–11 Hiatt WR, Regensteiner JG, Wolfoll EE et al. Effect of exercise training on skeletal muscle histology and metabolism in peripheral arterial disease. J Appl Physiol 1996; 81: 780–8 Tanaka H, Dinneno AE, Monahan DK et al. Aging, habitual exercise and dynamic arterial compliance. Circulation 2000; 102: 1270–5 Abdelaim KW, Merhent TA, Rium BE et al. Effect of type 2 diabetes and its duration on the risk of peripheral arterial disease among men. Am J Med 2004; 116: 236–40 Michaels JA, Gallaud RB. Case mix and outcome of patients referred to the vascular service or a district general hospital. Ann Roy Coll Surg Engl 1993; 75: 358–61 Hiatt RW. Medical treatment of peripheral arterial disease and claudication. N Engl J Med 2001; 344(21): 1608–21 Weitz JI, Byrne J, Clagett GI et al. Diagnostic and treatment of chronic arterial insufficiency of the lower extremities: a critical review. Circulation 1996; 94: 3026–49 Palmaz JL, Garcia OT, Schatz RA et al. Placement of balloon expandable intraluminal stents in iliac arteries. First 171 procedures. Radiology 1990; 174: 969
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Risk factors in peripheral arterial disease GI Pandele and C Dima-Cozma
The prevalence of peripheral arterial disease (PAD) in Europe and North America was recently evaluated at about 16% for the adult population 55 years and older (amounting to 27 million people from which 10.5 million are symptomatic and 16.5 million asymptomatic). When a specific-risk population is screened, the detection rate varies between 20 and 30%. Because PAD represents a distinct atherothrombotic syndrome with high risk of events occurring in cardiovascular and cerebrovascular territory, there is an increasing interest in accurate methods for its diagnosis and treatment. The US PARTNERS study assessed the rate of physician and patient awareness of PAD diagnosis and evaluated the influence of antiplatelet agents on risk factor profile.1 Based exclusively on the classic history of claudication alone, the physicians can detect PAD in only 10–15% of cases.2 If we consider bedside pulse examination alone, valuable on this technique for diagnosis remains only 50% of PAD3. We have to take into account that appreciated by the presence of intermittent claudication PAD is only symptomatic and depends on varying levels of sensitivity.4,5 Other diagnostic tools currently used to detect PAD such as peripheral pulse measurement do not provide a high degree of accuracy because of high false positive and high false negative results. As a result of recent epidemiological studies, the risk factors for PAD are conventionally divided into major risk factors such as age, male gender, history of cardiovascular diseases (prior myocardial infarction, heart failure, history of stroke or transient ischemic attack, TIA), diabetes, dyslipidemia, hypertension, hyperhomocysteinemia, hyperfibrinogenemia, cigarette smoking; and minor risk factors such as high-fat diet, excessive alcohol consumption, being of non-Caucasian race, hypercoagulable states, C-reactive protein, asymmetric dimethylarginine (ADMA).6,7
Age Incidence of PAD increases in parallel with age at a rate of 1.5–2-fold for every 10 years increase in age.8,9 In studies undertaken in the US, Europe and the Middle East, the prevalence of PAD varied from 4.6% (in the Jerusalem Lipid Research Clinic Prevalence study) to 19.1% (in the Rotterdam study). In the San Diego study, PAD was detected in less than 3% of those younger than 60 and rose to 20% in those over 75 years.10 In the Whitehall study, which included 18,388 males living in London, aged 40–64 years, claudication was estimated 822
to be present in about 1%. The prevalence and incidence of claudication increased with age.11 In a study published by Criqui et al., claudication was estimated at 1.6–4.5% for a population older than 40 years.12 In the US, approximately 8–10 million individuals have PAD.
Male gender In the San Diego study, PAD was 27% more prevalent in men than in women.10 In the Framingham study, in a community of 5,209 subjects aged 35–85 years, the 2-year incidence of claudication was 7.1% for men and 3.6% for women. In the US PARTNERS program with patients recruited from 320 primary care patients, the prevalence of PAD in those older than 70 years and/or older than 50 years with co-morbidities, smoking and concomitant diabetes was 29%.1
History of cardiovascular disease In patients with critical limb ischemia annual mortality is almost 25% and is due to myocardial infarction and ischemic stroke.13 The major cardiovascular diseases are now known to raise the risk of PAD: ischemic heart disease, prior stroke, cardiac failure, atrial fibrillation, and occlusive PAD is often a sign of widespread cardiovascular disease. The observation could have genetic implications, because premature atherosclerosis is frequently seen in family groups.
Cigarette smoking The relationship between smoking and PAD was first identified by Erb in 1911, who reported a three-fold rise in risk of PAD in smokers.14 There is a direct relationship between the number of cigarettes smoked and the increase in risk for PAD.15 Furthermore, cessation of smoking is followed by a rapid decrease in the risk for PAD.16 The US Department of Health and Human Services established that smoking is the most important documented cause of disease ever investigated in the history of medicine.17 In different observational studies the risk of PAD varied from two-fold to five-fold in smokers.18,19 Critical limb ischemia and the need for amputation is more frequent in patients who continue to smoke than in those who gave it up.20 In the CAPRIE study,21 90% of patients
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Risk factors in peripheral arterial disease with PAD were current or former smokers and in the Whitehall study 84% of patients were current smokers or ex-smokers.22 Smoking represents the main risk factor for development of PAD, according to the risk of coronary artery disease in smokers.23,24 Furthermore, 90% of patients with aortoiliac disease and 91% of those with femoropopliteal disease were current or former cigarette smokers. In the longitudinal Framingham study, conducted on 5209 men and women, showed that smoking is strongly correlated with the development of intermittent claudication.25 Cigarette smoke is toxic and contains around 4000 chemicals of which nicotine and carbon monoxide are the most significant. Because of the greater affinity of carbon monoxide for hemoglobin over that of oxygen, smoking results in alterations to oxygen transport with vasoconstriction and injury to the vascular wall by the combined action of nicotine and carbon monoxide, with increased thrombophylia that raises the risk of thrombosis over the atheromatous plaques. An important phenomenon associated with smoking is the alteration of platelet function in smokers, by increased aggregability, even after smoking a single cigarette.26 The influence of smoking on plasma lipoproteins is complex: LDL from smokers is more atherogenic because it is prone to easier oxidation, and HDL plasma level is lower than in non-smokers.27 The relationship between cigarette smoking and elevated levels of fibrinogen and homocysteine was examined in the NHANES III survey, a study conducted between 1988 and 1994. A strong positive independent and dose-response relationship between cigarette smoking and elevated levels of C-reactive protein, fibrinogen, and homocysteine was identified. These results sustain the idea that the significant mechanisms by which cigarette smoking promotes atherosclerotic disease include inflammation and hyperhomocysteinemia.28
Glucose intolerance and diabetes mellitus In the Framingham study, glucose intolerance appears to be a more important risk factor for PAD than for coronary artery disease or stroke.23 Diabetes mellitus is the most important risk factor for large vessel atherosclerotic occlusive disease and PAD is severe and often extensive, with involvement of the proximal lower limb (femoral and popliteal) arteries (as in non-diabetics) but with predominant distal disease affecting tibial and peroneal arteries.1,6,18,24,29 In comparison with non-diabetic patients, diabetics have a two- to four-fold increase in risk of developing intermittent claudication.30 The relationship between diabetes and atherosclerosis is still not completely understood, because development of atherosclerosis may coexist with impaired glucose tolerance and impaired fasting glucose. Maintaining good glycemic control is independent of PAD progression and abnormal levels of blood glucose or hemoglobin A1c (Hb A1c) have not been strongly correlated with the severity of PAD.31 In diabetes mellitus, PAD is often a clinical problem because of interactions between microvascular disease including coexistent neuropathy and macrovascular disease.32 PAD in diabetics is more closely correlated with the duration of the disease, the degree of hyperglycemia, and the presence of microvascular disease than in
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atherosclerosis affecting the coronary and cerebral arteries.33–35 Peripheral arteriopathy below the knee was related to the duration of disease, the degree of hyperglycemia and microvascular disease, while disease above the knee correlated better with cigarette smoking, hypercholesterolemia, and hypertension, the well-known risk factors for large vessel atherosclerosis. Over 6% of the US population have diabetes mellitus and the incidence is rising. The Framingham study demonstrated that diabetes is a powerful risk factor for atherosclerotic coronary and peripheral arterial disease, independent of other atherogenic risk factors, with a relative risk two-fold for men and three-fold for women.36 The risk of stroke is 2.5- fold higher in patients with diabetes, which is strongly associated with atherosclerosis of the extracranial internal carotid artery.37,38 Though recognized as a significant risk factor for PAD, diabetes is sometimes undiagnosed until the patient presents with symptoms in the leg or often patient leg ischemia, which is associated with impaired fasting glucose, impaired glucose tolerance, post-prandial high glucose levels or abnormal Hb A1c levels. Insulin resistance and hyperinsulinemia are conditions known to be associated with all glucose intolerance categories but are also an independent powerful predictor of cardiovascular risk. Hyperinsulinemia is now recognized as part of metabolic syndrome, characterized by a cluster of clinical and biochemical disturbances such as visceral obesity, hypertriglyceridemia, elevated apolipoprotein B concentrations, low HDL-cholesterol, and a procoagulant state.39
Dyslipidemia The abnormal metabolism of plasma lipid may generate numerous forms of dyslipidemia, from hypercholesterolemia to hypoalphalipoproteinemia, and can be caused by genetic, dietary, or secondary disease factors. Many major epidemiological studies have shown a significant correlation between elevated serum cholesterol or elevated LDL levels or decreased HDL levels and the risk of atherosclerosis. Vascular beds belonging to heart, brain, and lower limbs are influenced by vascular risk factors such as high total cholesterol and low density lipoprotein cholesterol, and coexistence of high LDL cholesterol with other risk factors substantially increases the risk of atherosclerosis.22,40 High total cholesterol, LDLcholesterol, triglycerides, and lipoprotein (a) are independent risk factors for peripheral arterial obstructive disease.1,6,41 A 10 mg/dl increase in total cholesterol concentration amplifies the risk of PAD by approximately 10%. Opposite effects showed high levels of HDL cholesterol and apolipoprotein A1 (Apo A1).39 The increased lipoprotein (a) serum levels represent a newly recognized independent risk factor for atherosclerosis in coronary and peripheral arteries. In PAD, lipoprotein (a) levels above normal are 30 mg/dl.42
Homocysteine Elevation in homocysteine levels is strongly associated with the premature development of atherosclerosis in carotid, coronary, and peripheral arteries and increases the risk for
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approximately two fold. Hyperhomocysteinemia is defined by high levels of fasting, non-fasting or post-methionine loading (PML) of total homocysteine (tHcy): tHcy levels ≥ 12 to ≤ 100 µmol/l fasting or non-fasting or ≥ 50 to ≤ 140 µmol/ l 6 hours PML.43. Homocysteine is a sulfur-containing amino acid at a level of about 5–15 µmol/l in healthy persons. Hyperhomocysteinemia is a risk factor for PAD in men and in young women.44–46 The mechanisms associated with hyperhomocysteinemia in accelerating atherosclerosis are thrombophilia, endothelial dysfunction, proliferation of vascular smooth muscle cells, lipid peroxidation and oxidation of LDL-cholesterol. In young women in whom PAD develops at an early age, there exists a strong prevalence of conventional cardiovascular risk factors and associated hyperhomocysteinemia by a strong synergic effect.47,48 The two-fold increased risk in young women with PAD and hyperhomocysteinemia is equivalent to the relative risk with traditional risk factors of hypertension, hypercholesterolemia and obesity and is surpassed only by smoking and diabetes mellitus.49 Hyperhomocysteinemia, an inherited autosomal recessive disease, is characterized by abnormalities in methionine metabolism because of a deficiency in cystathione β-synthase, methionine synthase and 5-10-methylenetetrahydrofolic acid reductase. Beside the genetic causes, hyperhomocysteinemia may have an acquired cause that includes vitamin B12 and folic acid deficiencies and is associated with diseases like psoriasis, renal failure, and acute lymphocytic leukemia. The vascular diseases determined by hyperhomocysteinemia is both atherosclerotic and thromboembolic affecting many arterial sizes and territories.50 Kang and collaborators, in a meta-analysis published in 1992, found the incidence of hyperhomocysteinemia was more significant in subjects with PAD (41.8%) than in coronary patients (11.9%) and the direct relationship between the number of vascular territories interested by atherosclerosis and the levels of hyperhomocysteinemia.50 Two more recent studies, the Scottish Heart Health study and US Nurses Health study found a strong relationship between tHcy levels, cardiovascular death, and symptomatic peripheral vascular disease.51,52
Hypertension Hypertension, a well-recognized risk factor for atherosclerotic disease, especially for brain and coronary artery, is considered to increase the risk in patients with PAD by approximately two to three times.1,8,53 As an independent risk factor, hypertension is considered to be less important than others like smoking and dyslipidemia.54 Systolic hypertension seems to have a greater effect on proximal PAD and the risk increased proportionally with the severity of hypertension.6
Fibrinogen and increased blood viscosity Recognized only recently as a cardiovascular risk factor, elevated fibrinogen concentrations are associated with approximately two-fold to four-fold increased risk of myocardial infarction and stroke.55 Single blood fibrinogen levels associated with increased blood viscosity appears to be an independent
risk factor for PAD.56,57 Greater fibrinogen levels correspond to increased blood viscosity and more severe claudication.58 Elevated blood viscosity contributes to the development of atherosclerosis by increasing platelet adhesion to the subendothelium, by increasing protein infiltration into the arterial wall and by modifying vascular shear forces.59 These atherogenic components are more evident in men. Fibrinogen synthesized in the liver has a crucial role in blood coagulation because it affects hemostasis, blood rheology, platelet aggregation, and endothelial function.55 As the precise role of fibrinogen in atherogenesis is not yet completely understood it may be more of a marker instead of being actually responsible for cardiovascular risk itself. The importance of fibrinogen as a risk factor is greatest for stroke and least for PAD in men and greatest for coronary heart disease in women.60 Factor VIII/von Willebrand factor Like fibrinogen, both factor VIII and the von Willebrand factor (vWF) are acute phase proteins and coagulation factors that participate in clot formation and platelet adhesion. The two proteins circulate as a complex, the stability of factor VIII being determined by vWF, which is produced by endothelial cells.61 Both factor VIII and vWF were predictive for atherothrombotic ischemic events in patients with vascular disease.62 Deficiency in the fibrinolytic system Inhibition of the fibrinolytic system can occur at the level of plasminogen activator’s inhibitor (PAI) or at the level of plasmin, especially by a2-antiplasmin. In the last 20 years many studies emphasized the role of PAI-1 as an important cardiovascular risk factor in addition to fibrinogen, factor VII and vWF in peripheral vascular disease. Elevated levels of PAI-1 were identified in the intima and media of different segments of peripheral atherosclerotic arteries.63 Decreased fibrinolysis and propensity to thrombus extension are conditioned by increased plasma PAI-1 activity.64 In subjects with a decreased ankle–brachial index (ABI), higher PAI-1 levels suggest a strong link of association with peripheral arterial stenosis.65 The same group showed that high values of fibrinogen levels, even in-between the normal ranges, increase the risk for peripheral vascular disease independently of coexistence of cardiovascular and cerebrovascular disease history. Elevated PAI-1 activity in survivors of myocardial infarction was correlated with peripheral vascular disease and triglyceride levels.66 The vWF antigen level varied according to the associated endothelial dysfunction or in normal limits.67 The Progetto Lombardo AtheroThrombosis study reported a relationship between factor VIII activity and ankle/arm systolic blood pressure.62 The main haemostatic risk factors in peripheral arterial disease are given in Table 95.1. The actual data about intervention of haemostatic risk factor in peripheral vascular disease highlights the importance of fibrinogen and PAI-1 activity in pathogenesis and the functional significance of progressive peripheral vascular disease.
Other risk factors Diet and the level of alcohol consumption are minor risk factors. In the Physician’s Health study, it was emphasized that moderate
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Table 95.1 The main haemostatic risk factors in peripheral arterial disease (modified from Philip SC et al., Am Heart J 1997; 134: 980) PAD Fibrinogen (mg/dl) PAI-1 (units/ml) vWF (%) Factor VIIc (%)
Controls
335 (280–360) 14.6 (12.1–26.8) 167 (112–192) 92 (82–103)
alcohol consumption is associated with a slightly decreased risk of PAD. Diets with increased consumptions of fiber and decreased consumptions of meat are protective.68 Increased excretion of urinary albumin are an independent prediction for PAD.69, 70 As a marker of systemic inflammation, elevated levels of C-reactive protein predict future risk of developing symptomatic PAD. C-reactive protein may have procoagulant effects by enhancing expression of tissue factor.71 The severity of claudication symptoms is correlated with NO synthesis and influence of ADMA levels72. Osteopontin is a little-studied risk factor. Osteopontin is an extracellular matrix glycoprotein, isolated first in mineralized bone matrix (where it is produced by osteoblasts), but is also
270 8 182 90
(240–305) (4.4–14.9) (156–262) (80–103)
p value 0.0001 0.04 0.009 NS
synthesized by cardiac fibroblasts, myocytes, smooth muscle cells, leucocytes, macrophages and other epithelial cells. Osteopontin is reported to be involved in the process of aldosterone–angiotensin II-induced fibrosis in heart failure. In a cardiovascular context, osteopontin seems abundant at sites of calcification in human atherosclerotic plaques or intima calcification (mediocalcosis Monckeberg). In conclusion, an accurate appreciation of the risk factors is still unavailable and the safest clinical, widely applicable objective method to assess peripheral vascular obstructive disease remains, indirectly, ankle–brachial index (ABI). The ABI appears to be the most effective accurate and practical method along with symptoms for the detection of PAD.
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63. 64.
65. 66. 67. 68. 69. 70. 71. 72.
A’Brook R, Tavendale R, Tunstall-Pedoe H. Homocysteine and coronary risk in the general population: analysis from the Scottish Heart Health Study and Scottish MONICA Surveys. Eur Heart J 1998; 19(suppl. 8): Abstract Ridker PM, Buring JE, Manson JE et al. A prospective study of total plasma homocysteine and the risk of future cardiovascular events among apparently healthy women. Circulation 1998; 98 Suppl I: 810, Abstract Sutton KL, Wolfram SKI, Kuller LH. Carotid and lower extremity arterial disease in elderly adults with isolated systolic hypertension. Stroke 1987; 18: 817–22 Jurgens JL, Barker MW, Hines EA. Atherosclerosis: a review of 520 cases with special reference to pathogenic and prognostic factors. Circulation 1960; 21: 188–95 Ernst E, Resch KL. Fibrinogen as a cardiovascular risk factor. A metaanalysis and review of the literature. Ann Intern Med 1993; 118: 956–63 Dormandy JA, Hoave E, Khattas AH et al. Prognostic significance of rheological and biochemical findings in patients with intermittent claudication. Br Med J 1973; 4: 581–3 Lee AJ, Lowe GDO, Woodward M et al. Fibrinogen in relation to personal history of prevalent hypertension, diabetes, stroke, intermittent claudication, coronary heart disease and family history. The Swedish Heart Health Study. Br Heart J 1993; 69: 338–42 Lowe GDO, Fowkes FGH, Dawes I et al. Blood viscosity, fibrinogen and activation of coagulation and leukocytes in peripheral arterial disease and the normal population in the Edinburgh Artery Study. Circulation 1993; 87: 1915–20 Lee AJ, Mowbray PI, Lowe GDO et al. Blood viscosity and elevated carotid intima–media thickness in men and women. The Edinburgh Artery Study. Circulation 1998; 97: 1467–73 Kannel WB. Influence of fibrinogen on cardiovascular disease. Drugs 1997; 54: 32–40 Conlan MG, Folsom AR, Finch A et al. Association of factor VIII and von Willebrand factor with age, race, sex and risk factors for atherosclerosis, The Atherosclerosis Risk in Communities (ARIC) Study. Thromb Haemost 1993; 70: 380–5 Castellano M, Boschetti C, Cofrancesco E et al. and the PLAT Study Group. The PLAT Study: hemostatic function in relation to atherosclerotic ischemic events in vascular disease patients. Arterioscler Thromb 1992; 12: 1063–70 Schneiderman J, Sawdey MS, Keetan MR et al. Increased type I plasminogen activator inhibitor gene expression in atherosclerotic human arteries. Proc Nath Acad Sci USA 1992; 89: 6998–7002 Levi M, Biemond BJ, Van Zonneveld AJ et al. Inhibition of plasminogen activated inhibitor 1 activity results in promotion of endogenous thrombolysis and inhibition of thrombus extension in models of experimental thrombosis. Circulation 1992; 85: 305–12 Philipp CS, Cisar AL, Kim CH et al. Association of hemostatic factors with peripheral vascular disease. Am Heart J 1997; 134: 978–84 Gray RP, Mohamed Ali V, Patterson D et al. Determinants of plasminogen activator inhibitor-1 activity in survivors of myocardial infarction. Thromb Haemost 1995; 73, 261–7 Philipp CS, Smith FB, Lowe GDO et al. Smoking, haemostatic factors and lipids peroxides in a population case control study of peripheral arterial disease. Atherosclerosis 1993;102: 155–162 Donnan PT, Thomson M, Fowkes FGR et al. Diet as a risk factor for peripheral arterial disease in the general population: The Edinburgh Artery Study. Am J Clin Nutr 1993; 57: 917–21 Yudkin JS, Forrest RD, Jackson CA. Microalbuminuria as predictor of vascular disease in non-diabetic subjects: Islington Diabetes Survey. Lancet 1988; 2: 530–3 Davidson D. In: Preventive Cardiology. Williams & Wilkins: 29–57 Ridker PM, Cushman M, Stampfer MJ et al. Plasma concentration of C-reactive protein and risk of developing peripheral vascular disease. Circulation 1998; 97: 425–8 Boger RH, Bode-Boger SM, Thiele W et al. Biochemical evidence for impaired nitric oxide synthesis in patients with peripheral arterial occlusive disease. Circulation 1997; 95: 2068–74
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SECTION XVII Venous disease
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The anatomy, epidemiology, and pathophysiology of venous disease JI Greenberg, N Angle, and J Bergan
Introduction Leaps in our understanding of the epidemiology and pathogenesis of venous disease have recently been realized. The rigorous study of venous disease in the clinic, the vascular laboratory, and the research laboratory has allowed rejection of unfounded dogma in favor of an entirely new understanding of venous disease at the molecular level. Nevertheless, fundamental knowledge of physiology and anatomy of the deep and superficial veins of the lower extremities is required before discussion of venous diseases and their interventions. Unfortunately anatomic descriptions of veins, as taught in medical school, have little clinical relevance; but anatomy as seen through the eyes of generations of practicing surgeons has great practical utility.1
have lost valvular function and have bidirectional flow which is both proximal and distal. Unlike deep veins that accompany and are named after their matching arteries, superficial veins do not have accompanying arteries; they are instead organized in a series of subcutaneous
Anatomy Veins of the lower extremities can be divided into three systems: superficial, deep and perforating. An illustration of the most common veins rendered varicose is shown in Figure 96.1. Superficial veins are located between the muscular fascia and the skin. Deep veins are enclosed by deep fascia and lie within muscles. Perforating veins penetrate anatomic layers and have been referred to incorrectly as communicating veins. A special compartment exists for the great saphenous vein (GSV, new terminology).2–5 Similarly, a compartment exists for the small saphenous vein. These compartments are bounded superiorly by the superficial fascia and inferiorly by the deep fascia. On ultrasound examination, each appears as the so-named saphenous “eye.” Because of its deep position in the subcutaneous tissue, the real GSV is rarely obvious in a thigh with normal amounts of fat. Dilated, protuberant, and tortuous veins usually visible on the medial aspect of the thigh and leg are frequently considered to be varicose GSVs. The computed tomogram in Figure 96.2 demonstrates what is most common; that in most cases, the visible varicose veins of the medial thigh and leg are saphenous vein tributaries. A vein’s most characteristic features are its valves. These were first described anatomically in the sixteenth century and described in terms of their physiology a century later by William Harvey.6 Valves direct blood flow to the heart from both the superficial and deep veins and are found even in the most minute telangiectasias in the skin. Telangiectasias, spider veins, thread veins, varicose veins, and varicose reticular veins
Figure 96.1 This drawing illustrates the overall patterns of veins relevant to surgical intervention. 1: External pudendal; 2: superficial epigastric vein; 3: anterolateral tributary vein; 4: medial thigh varicosities; 5: medial posterior tributary vein; 6: extension of anterolateral tributary; 7: vein of Giacomini in the region of Dodd perforating veins; 8: Boyd perforating veins; 9: the 24-cm perforating vein and its connection to 10: posterior arch vein; 11: great saphenous vein; 12: dorsal arch vein; 13: paratibial perforator. (From Blanchemaison P, Greney P: Atlas of Anatomy of the Superficial Veins of the Lower Limbs. Paris: Servier, 1998).
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Figure 96.2 (a) Transverse macroscopic section from a cadaveric thigh. Note the thickness of the saphenous fascia (arrows); (b) computed tomography scan from medial thigh showing the saphenous fascia (black arrows) and the superficial course of the collateral saphenous veins (white arrows).
channels that drain into two major superficial veins, the great saphenous vein and the small saphenous vein. These enter and empty into deep veins at the saphenofemoral junction and the saphenopopliteal junction. The latter connection has great variability.
Physiology The venous system serves as a reservoir and transport system for circulating blood. It is estimated that 60–75% of the blood in the body is found in the veins. It is the smallest veins that function as the reservoir for much of the body’s blood volume. About 80% of the total is contained in veins that are less than 200 µm in diameter. The splanchnic venous circulation and the cutaneous veins are richly supplied by the sympathetic nervous system fibers, as are veins in skeletal muscle, and are responsive to catecholamines. Arterial pressures are generated by muscular contractions of the heart but pressures in the venous system are largely determined by gravity. With the body in the horizontal position, pressures in the veins of the lower extremity are similar to the pressures in the abdomen, chest, and extended arm. However, in an upright position dramatic changes in venous pressure occur. The only point at which the pressure remains constant is a stable point just below the diaphragm. All pressures distal to this point are increased due to the weight of the
blood column from the right atrium. In the upright position, largely because of reflux through the valveless vena cava and iliac veins, approximately 500 ml of blood accumulates in the lower extremities. Some of this becomes tissue fluid which diffuses into the tissues, is collected by the lymphatic system, and eventually returns to the venous system. Venous valves play an important role in transporting blood from the lower extremities to the heart. Upward movement is contingent on valve closure, and in order for valve closure to occur, there must be a reversal of the normal transvalvular pressure gradient. Back pressure resulting in flow exceeding 30 cm/second leads to valve closure.7 Direct observation of human venous valves via specialized ultrasound techniques has revealed that venous flow is not normally in a steady state but is irregularly pulsatile.8 Venous valves undergo opening and closing cycles. Even when fully opened, the cross-sectional area between the leaflets is 35% smaller than that of the vein distal to the valve. Flow through the valve separates into a proximally directed jet and distal flow into the sinus pocket proximal to the valve cusp. The vortical flow prevents stasis and ensures that all surfaces of the valve are exposed to shear stress. Valve closure develops when the vortical flow pressure exceeds the proximally directed jet flow. Intuitively, the role of venous valves during muscular exercise is to promote antegrade flow from superficial veins to deep veins while preventing retrograde motion in the opposite direction. Normally functioning perforating vein valves protect the skin and subcutaneous tissues from the effects of muscular contraction pressure, possibly exceeding 100– 130 mmHg, which may cause pooling of fluid in the superficial circulation.7 In particular, volume and pressure changes in veins within the calf occur with muscular activity. In the resting position, with the foot flat on the floor, there is no muscleinstigated flow. However, in the heel strike position, the venous plexus under the heel and plantar surface of the foot (Bejar’s plexus) is emptied proximally.9 Properly functioning valves ensure that blood flows from the foot and ankle into the deep veins of the calf. Then, calf contraction transports this blood into the deep veins of the thigh, and henceforth, blood flow proceeds to the pelvic veins, vena cava, and ultimately to the heart all due to the influence of lower extremity muscular contraction. The role of venous valves in an individual quietly standing is not well understood. Pressures in the superficial and deep veins should theoretically be the same during quiet standing, but as Arnoldi has found, the pressure in the deep veins is 1 mm higher, which would tend to keep the valves in the perforating veins closed.10
Epidemiology It has been estimated that venous ulcers cause the loss of approximately 2 million working days and incur treatment costs of approximately $3 billion per year in the US.11 Overall, chronic venous disease has been estimated to account for 1–3% of the total health care budgets in countries with developed health care systems. To corroborate this fact, and to further extend our understanding of the epidemiology of venous disease, Criqui et al. undertook a large population based study in 2003. The study involved a cross-sectional analysis of
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The anatomy, epidemiology, and pathophysiology of venous disease a population that included the then current and previous employees of the University of California, San Diego (UCSD).12 The study is one of only two studies to explore the functional epidemiology of lower extremity venous disease using present day diagnostic techniques. The UCSD study included 2,211 subjects. The average age was 59 with 65% women and 35% men; the ethnic distribution was population appropriate and was a particular focus of the study. The extent of venous disease seen in this population is illustrated in Table 96.1. The prevalence of visible and functional (ultrasonographic) venous disease was 81 and 27.9% respectively; emphasizing the extent of venous disease as the most common disorder treated by vascular interventionalists. Men’s legs were more than three times as likely as those of women to be visibly normal (33.6 vs. 11.0%), whereas women had substantially more telangiectasias and varicose veins. The prevalence of trophic changes was higher in men. With age, there was little change in telangiectasias but a linear increase in varicose veins and a marked increase in trophic changes. Compared with non-Hispanic Whites, minority groups in general had a lower prevalence of both visible and functional disease. An exception was for varicose veins and superficial functional disease in Hispanics, who had a slightly higher prevalence of these conditions than non-Hispanic Whites. Of note, 21.0% of all legs with varicose veins and 25.9% of all legs with trophic changes were functionally normal. More legs with trophic changes evidenced superficial functional disease alone (52.2%) than deep functional disease (22.0%). Of the legs with deep functional disease, 48.0% also evidenced superficial functional disease. The only other study to undertake the functional epidemiology of lower extremity venous disease was the Edinburgh Vein Study.13 The overall incidence of functional venous disease was higher in Scotland than in San Diego with a number of similar demographic features. A prominent feature of both
studies is the discordance between visible and functional disease, particularly in deep versus superficial veins. Moreover, edema and thrombotic events were clearly linked to the presence of visible and functional venous disease, but also occurred in their absence.
Pathophysiology Primary venous insufficiency Explanations of venous pathophysiology as published in reviews, texts, and monographs are currently out of date. Rather than repeat old dogma, we offer the modern theory of venous disease based on new and rigorous science. A dysfunctional venous system is caused by injury to vein walls and venous valves. This is known because such damage is readily demonstrable on plain light microscopy.14 Factors that enter into such injury include heredity, obesity, female gender, pregnancy, and a standing occupation in women (Table 96.2). Vein wall injury allows the vein to elongate and dilate. An increase in vein diameter is one cause of valve dysfunction and reflux. The effect of persistent valvular reflux is a chronic increase in distal venous pressure. This venous pressure increases as one proceeds from the inguinal ligament past the knee to the ankle. The prolonged venous hypertension initiates a cascade of pathologic events (Figure 96.3). These manifest themselves clinically as lower extremity edema, pain, itching, skin discoloration, and ulceration.14 The earliest signs of venous insufficiency are often varicose veins in the epidermis and dermis, called telangiectasias. Slightly deeper are flat, blue-green veins of the reticular (network) system. These may become varicose as well. And finally, deeper yet are the varicose veins themselves. All of these abnormal veins and venules have one thing in common. They are elongated, tortuous and have dysfunctional venous valves.
Table 96.1 Visible and functional chronic venous disease in 4,422 legs of 2,211 study participants, San Diego, CA, 1994–199812
Visible disease
Normal Spider veins Varicose veins Trophic changes Total*
Normal
Superficial disease*
Deep disease*
Total
No.
%**
No.
%
No.
%
No.
%
978 2321 164 53
22.1 52.5 3.7 1.2
5 20 526 107
0.1 0.5 11.9 2.4
36 75 92 45
0.8 1.7 2.1 1.0
1019 2416 782 205
3516
79.5
658
14.9
248
5.6§
4422 100.0
23.0 54.6 17.7¶ 4.6‡
*Adapted from Criqui et al. Am J Epidemiol 2003; 158: 448–456. †Based
on ultrasonographic findings.
**Percentages do not total 100 because of rounding. ¶Of
the 782 legs with varicose veins, 697 (89.1%) also had spider veins. the 205 legs showing trophic changes, 188 (91.7%) also had spider veins and 141 (68.8%) also varicose veins. §Of the 248 legs showing deep functional disease, 119 (48.0%) also had superficial functional disease. ‡Of
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Table 96.2
Risk factors for chronic venous disease
Risk factors for chronic venous disease Genetic factors Female sex (progesterone) Pregnancy Age Greater height Prolonged standing Obesity
Manifestations of telangiectasias, reticular varicosities and varicose veins are grouped together under the term primary venous insufficiency (Figure 96.4). Chronic venous insufficiency Skin changes of hyperpigmentation, scarring from previous ulceration, and active ulcerations are grouped together under the term chronic venous insufficiency (CVI). Numerous theories have been postulated regarding the cause of chronic venous insufficiency and the cause of venous ulceration.15 All of the theories proposed in the last century have been disproven. An example is the theory of venous stasis first proposed in a manuscript by John Homans at Harvard in 1917.16 It was a treatise on diagnosis and management of patients
with chronic venous insufficiency and in it Dr. Homans coined the term “post-phlebitic syndrome” to describe the skin changes of CVI. He stated: “Overstretching of the vein walls and destruction of the valves... interferes with the nutrition of the skin... therefore, skin which is bathed under pressure with stagnant venous blood will form permanent open sores or ulcers.” This statement, like many others that describe venous conditions and their treatments, is steeped in dogma and is short of observational fact. The term “stasis ulcer” honors that misconception, as do the terms “venous stasis disease” and “stasis dermatitis.” Alfred Blalock, who later initiated and was best known for cardiac surgery, disproved the theory by studying oxygen content from varicose veins and normal veins.17 He pointed out that the oxygen content of the femoral vein in patients with severe chronic venous insufficiency was greater than the oxygen content of the contralateral non-affected limb. Because oxygen content was higher, some investigators felt that arteriovenous fistulae caused venous stasis and varicose veins. That theory, though disproved, has some basis in fact since the entire thermal regulatory apparatus in limbs depends on the opening and closing of arterial venous shunts. These shunts are important as they explain some accidents that happen during sclerotherapy when sclerosant entering a vein is shunted into the arterial system and distributed in its normal territory.18 Microsphere investigations have failed to show any shunting and the theory of arteriovenous communications has died despite the fact that
Valvular distortion, leakage
Venous dilation
Capillary hypertension Altered shear stress
Venous hypertension
Edema
Chronic reflux
Valve, Veinwall damage
Figure 96.3
The many paths to inflammation and the genesis of lower extremity venous insufficiency.
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Figure 96.4 Telangiectasias, reticular varicosities, and varicose veins (From Campbell B. Understanding Varicose Veins. Family Doctor Publications, 2000).
these shunts actually exist and do open under the influence of venous hypertension.19 Hypoxia and its role in chronic venous insufficiency was investigated throughout the last 25 years of the twentieth century. English investigators thought that a fibrin cuff, observed histologically, blocked transport of oxygen and was responsible for skin changes of CVI at the ankles and distally.7 This theory has since been abandoned. There are two elements that interact to cause all of the manifestations of lower extremity venous insufficiency. These are failure of the vein valves and vein walls, and skin changes at the ankles; both of which are related to venous hypertension and the inflammatory cascade.
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Our work suggests that venous hypertension causes a shear stress-dependent leukocyte–endothelial interaction, which has all of the manifestations of chronic inflammation.14 This includes leukocyte rolling, firm adhesion, and subsequent migration (diapedesis) through the endothelial barrier into the parenchyma of valves and vein walls.20 There, macrophages elaborate matrix metalloproteinases (MMPs), which destroy elastin and possibly collagen as well. Vein walls become stretched and elongated. Vein valves become perforated and even scarred to the point of total destruction. These changes are seen both macroscopically and angioscopically.21 Similar changes have been produced in the experimental animal by constructing arteriovenous fistulae. This produces a localized venous hypertension which causes the venous valve changes seen pathologically in man. The second manifestation of chronic venous insufficiency, also an inflammatory cascade, is seen in the skin. Skin biopsies have shown that liposclerotic eczematous skin demonstrates macrophage infiltration.22 Activation of leukocytes promotes the expression of CD11b, an important cell surface integrin for capillary adhesion. Leukocyte diapedesis into the extracellular space is facilitated by the induction of endothelial intercellular adhesion molecule-1 (ICAM-1) with their subsequent transgression into post-capillary venules. This has come to be known as the “leukocyte trapping hypothesis” and is verified by a number of ultrastructural studes.23 Accompanying this leukocyte influx and trapping is the disorderly activation of dermal fibroblasts through TGF-β1 deposition.24,25 The result is dermal fibrosis. Clearly, chronic venous insufficiency of the skin and its subcutaneous tissues is a disease of chronic inflammation, dependent upon venous hypertension. The primary injury is extravasation of macromolecules and red blood cells into the dermal interstitium. The hyperpigmentation of skin in lipodermatosclerosis may not be just a byproduct of capillary hyperpermeability. The extravasation of red cells leads to elevated levels of ferritin and ferric iron in affected skin.26 This leads to further oxidative stress and the development of a microenvironment that exacerbates tissue damage and delays healing. Thus the causes of the disparate pathologic processes which eventuate in varicose veins and the skin changes of chronic venous insufficiency are beginning to be explained by the triggering effect of shear stress which initiates the inflammatory cascade, which in turn lies at the bottom of primary venous insufficiency and the effects of severe chronic venous insufficiency.
REFERENCES 1.
2. 3. 4. 5.
Mózes, G, Carmichael, SW, Gloviczki, P. Development and anatomy of the venous system. In: Gloviczki P and Yao JST, eds. Handbook of Venous Disorders, second edition. London: Arnold, 2003 Caggiati A, Ricci S. The long saphenous vein compartment. Phlebology 1997; 12: 107–16 Caggiati A, Bergan JJ. The saphenous vein: derivation of its name and its relevant anatomy. J Vasc Surg 2002; 35: 172–5 Caggiati A, Bergan JJ, Gloviczki P et al. Nomenclature of the veins of the lower limbs: an international interdisciplinary consensus statement. J Vasc Surg 2002; 36: 416–22 Caggiati A. Fascial relationships of the short saphenous vein. J Vasc Surg 2001; 34: 241–6
6. 7. 8. 9. 10.
Harvey W. An anatomical description concerning the movement of the heart and blood in living creatures [Whitteridge G, trans.]. Oxford: Blackwell Scientific Publications, 1976 Coleridge Smith PD. The microcirculation in venous hypertension. Vasc Med 1997; 2: 203–13 Van Cleef JF, Hugentobler JP, Desvaux P, Griton P, Cloarec M. Étude endos copique des reflux valvulaires saphéniens. J Mal Vasc 1992; 17 (suppl. B): 113–6 Weijers RE, Kessels AG, Kemerink GJ. The dampening properties of the heel region of the foot during simulated heelstrike. J Biomech. 2005; 38(12): 2423–30 Arnoldi CC. The function of the venous pump in chronic venous insufficiency: A phlebographic study. J Cardiovasc (Torino) 1961; 2: 116–27
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Textbook of peripheral vascular interventions Van den Oever R, Hepp B, Debbaut B, Simon I. Socio-economic impact of chronic venous insufficiency: an underestimated public health problem. Int Angiol 1998; 17: 161–7 Criqui MH, Jamosmos M, Fronek A. Am J Epidemiol 2003; 158: 448–56 Evans CJ, Allan PL, Lee AJ et al. Prevalence of venous reflux in the general population on duplex scanning: the Edinburgh Vein Study. J Vasc Surg 1998; 28: 767–76 Schmid-Schönbein, GW, Takase, S, Bergan, JJ. New advances in the understanding of the pathophysiology of chronic venous insufficiency. Angiology 2001; 52 (suppl. 1): S27–34 Browse NL, Burnand KG. The cause of venous ulceration. Lancet 1982; 1998(ii): 243–45 Homans J. The etiology and treatment of varicose ulcer of the leg. Surg Gynecol Obstet 1917; 24: 300–11 Blalock A. Oxygen content of blood in patients with varicose veins. Arch Surg 1929; 19: 898–904 Bergan JJ, Weiss RA, Goldman MP. Extensive tissue necrosis following high-concentration sclerotherapy for varicose veins. Dermatol Surg 2000; 26: 535–42 Ahren K, Janson PO, Selstam G. Search for arterio-venous shunts in the rabbit ovary in situ using perfusion of microspheres. J Reprod Fertil 1974; 41(1): 133–42
20. 21.
22. 23. 24.
25.
26.
Takase S, Lerond L, Bergan JJ, Schmid-Schönbein GW. The inflammatory reaction during venous hypertension in the rat. Microcirculation 2000; 7: 41–52 Hoshino S, Satokawa H, Ono T, Igari T. Surgical treatment for varicose veins of the legs using intraoperative angioscopy. In: Raymond-Martimbeau P, Prescott R, Zummo M, eds. Phlebologie 92. Paris: John Libbey Eurotext, 1992; 1083–5 Coleridge Smith PD. Microcirculation disorders in venous leg ulcer. Microcirculation in CVI 2001: 1–10 Bergan JJ. Medicographia 2006; 28(2): 101–8 Pappas PJ, You R, Rameshwar P et al. Dermal tissue fibrosis in patients with chronic venous insufficiency is associated with increased transforming growth factor- β1 gene expression and protein production. J Vasc Surg 1999; 30: 1129–45 Sansilvestri-Morel P, Rupin A, Jaisson S et al. Synthesis of collagen is dysregulated in cultured fibroblasts derived from skin of subjects with varicose veins as it is in venous smooth muscle cells. Circulation 2002; 106: 479–83 Ackerman Z, Seidenbaum M, Loewenthal E, Rubinow A. Overload of iron in the skin of patients with varicose ulcers: possible contributing role of iron accumulation in progression of the disease. Arch Dermatol 1988; 124: 1376–8
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Diagnostic evaluation of venous disease B Abai and N Labropoulos
Introduction The central and peripheral veins are prone to disease processes. This is especially true for the veins of the lower extremity which have the disadvantage of gravity. The processes that can lead to pathology are obstruction and reflux or a combination of the two. The veins in the lower extremities are divided into deep and superficial systems. The superficial venous system includes the great saphenous vein (GSV), the small saphenous vein (SSV), their accessory veins, and other less common non-saphenous veins. The deep veins are the common femoral, femoral, deep femoral, popliteal, anterior tibial, posterior tibial, peroneal, soleus, and gastrocnemius veins. A series of perforating veins pierce through the deep fascia and connect the superficial and deep systems. History and physical examination have been unreliable in evaluation and diagnosis of venous pathology. Only 12–31% of patients who are referred to the vascular laboratory for suspected deep vein thrombosis (DVT) have a positive study.1–3 In addition, up to 50% of patients who have acute DVT may lack any signs or symptoms.4,5 Phlebography, plethysmography, and radioisotope scanning have been replaced by duplex ultrasound (DU) scanning. Plethysmography is still used for evaluating the amount of reflux and the efficiency of the calf muscle pump. Phlebography, although invasive, still plays a minor diagnostic role but is still routinely used during endovenous treatment of the main deep veins.
Deep venous thrombosis DVT is a common and potentially fatal disease process. The incidence of this disease is not clear but it is estimated that 1 in 1000 adults suffer from it.6,7 In the acute setting DVT can lead to venous thromboembolism (VTE). The consequences of VTE range from pulmonary hypertension, symptomatic pulmonary embolism (PE), and fatal PE. The incidence of PE in patients with DVT is > 50% in patients with proximal DVT.8 In addition, there are long-term consequences to VTE. Patients can develop post-thrombotic syndrome (PTS) as a consequence of proximal obstruction and damage to the veins of the affected extremity. The incidence of PTS in patients with DVT is around 25% at 5 years.9 The three classically described contributing factors to deep vein thrombosis are stasis, endothelial injury, and hypercoagulability. These processes usually in combination lead to DVT.
The risk factors for developing DVT are increasing age, obesity, surgery, trauma, sepsis, hospital or nursing home admission, malignancy, extremity paresis, central venous catheter or transvenous pacemaker, prior superficial vein thrombosis, varicose veins, pregnancy, oral contraceptives, and hormone replacement therapy.10,11 Knowledge of these risk factors will enable screening for DVT and help determine the underlying causes that may have lead to DVT in a patient. Duplex ultrasound is the test of choice for diagnosis of DVT. Four categories of patients are generally examined at the vascular laboratory using duplex ultrasound (DU) for venous thrombosis. These are patients with signs and symptoms of pulmonary embolism, patients with extremity pain and/or swelling, patients at increased risk of developing DVT, and patients with superficial thrombophlebitis who might be at risk for progression of clot to the deep system. Ultrasound evaluation can readily determine the presence of thrombosis in the vein. The sensitivity and specificity of DU evaluation are 97 and 94% for evaluation of DVT, respectively.12
Duplex ultrasound technique for evaluation of DVT Using B-mode, the anatomy of the venous system is evaluated. The vein wall and lumen are visualized in real-time. This is followed by color-flow scanning which allows for real-time evaluation of flow within the vein. The use of correct frequency in a transducer is a trade-off of resolution, which is better with higher frequencies, and depth of examination which can be better achieved with a lower frequency. The frequencies that allow evaluation of the deep veins are 4–7 MHz in the normal patient. In obese patients, a 2–3 MHz transducer is required to evaluate the veins that are deeper. This lower frequency is also useful in evaluation of the veins in the pelvis and abdomen. The examiner should make sure that the three phases of venous examination are addressed. Initially, the examiner should check for thrombus visualization. Next the examiner will evaluate the compressibility of the vein. Fresh thrombi that might be missed with initial visualization will prevent the opposing vein walls touching. In order to ensure adequate compression has been applied, the wall of the adjacent artery should be partially deformed by the amount of pressure. Finally, the flow evaluation is performed using color Doppler. The venous flow is evaluated by augmentation using 835
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compression distal to the site of imaging. The patient is placed on the examination table. The table is positioned in reverse Trendelenburg and the room is kept at a warm temperature to allow for optimal venous imaging. The knee is held in a slightly bent position with external hip rotation to avoid venous compression. The examination starts below the inguinal ligament with the common femoral vein and saphenofemoral junction. The vein is first viewed transversely followed by compression. Then the probe is turned to evaluate the vein in the longitudinal view. Color is used to ensure flow through the lumen of the vein as well as augmentation. Then the probe is moved down the thigh along the course of the vein at 3–5 cm intervals and the whole process is repeated. The femoral vein is examined all the way down to the adductor canal. Next the popliteal vein is assessed. It is important to note that the popliteal vein can be in duplicate or in rare instances triplicate and all these should be evaluated for the presence of DVT. The entire vein is examined from its origin to the tibial veins. The popliteal fossa is also examined for Baker’s cysts or hematoma as these may cause symptoms similar to DVT. Next the veins of the calf are examined. This part of the examination may not be necessary if a thrombus has been detected in a proximal deep vein. The examination starts at the ankle where initially the posterior tibial and peroneal veins are visualized. The probe is placed above the ankle level. The posterior tibial veins are located behind the tibia and the peroneal veins are medial to the fibula. Alternatively, the peroneal vein can be examined from the posterolateral aspect of the calf if the medial approach is not adequate. These veins are then followed from the ankle all the way up to the popliteal vein. The anterior tibial veins are visualized from an anteriolateral position deep to the anterior tibialis muscle, but these veins are not routinely imaged as the prevalence of thrombosis is very low. The soleal and gastrocnemius veins are also examined as they commonly develop thrombosis. Finally, GSV and SSV are visualized and examined in a similar fashion. In select patients it may be necessary to examine the inferior vena cava and the iliac veins for thrombosis. This will be indicated in patients with symptoms that might lead the clinician to suspect thrombosis of the proximal veins. Asymmetry in the signal and flow augmentation in the common femoral veins may also lead the examiner to assess these veins. The vein is normally a thin-walled structure with low flow. On initial inspection of the neurovascular bundle, the artery will have thicker walls but is usually smaller in size. The interior of the vein should be dark on ultrasound as the density of blood is low. Next, using the ultrasound probe the vein is compressed. In a normal study with a moderate amount of pressure, one is able to appose the walls of the vein. Using color Doppler, the flow in a normal vein should encompass the entire lumen and should fluctuate with respiration. The flow can be modulated by compression proximally or distally to evaluate the patency of lumen. Pressure on the distal limb will increase forward flow in the vein and pressure on the abdomen will cause reversal of flow. The DVT test is negative if complete approximation of the near and far vein wall is achieved without any space seen between the two walls or if there is complete color filling of the lumen without any defects on color duplex exam (Figure 97.1). The veins that have acute thrombus are distended and echolucent with a thin smooth vessel wall. A chronic thrombus
will cause the vein to become contracted and echogenic with a thick and irregular wall. On compressibility exam, the acute clot will be spongy and the chronic one will be firm. Finally on color duplex one may detect confluent flow channels in the acute thrombus versus multiple channels in chronic thrombus. In addition, the fresh clot may have a free-floating tail. Chronic thrombosis will however lead to collateralization which may be visualized (Table 97.1).
Recurrent deep vein thrombosis Patients who have had an episode of DVT are predisposed to developing recurrent DVT. These patients will have a similar risk of PE. In addition they are at six times increased risk of developing PTS. It is therefore necessary to determine if a specific population of patients who develop DVT are at risk for recurrence. Hansen et al. followed 738 patients for 3.7 to 8.8 years. They determined the 5-year incidence of recurrent DVT is 21% after the first episode of DVT and 27% after a second episode of DVT. The cumulative incidence of PE in these patients was 2.6%. Their study showed that proximal DVT, cancer, and history of previous VTE were risk factors for recurrence. In addition they demonstrated that patients with post-operative DVT and longer duration of anticoagulation were at a lower risk of developing DVT.13 Others have confirmed that patients with ilieofemoral DVT are at a two-fold higher risk of developing recurrent DVT compared to patients without ilieofemoral involvement.14 Three DU criteria can be used to diagnose recurrent DVT: extension of the thrombus > 9 cm,15 non-compressibility of a segment of vein that had previously been compressible or had previously recanalized, and an increase in the thickness of the thrombus by 2 mm.16 There is a need to closely follow the patients with a single episode of DVT for recurrence. The patients who are at lower risk should have a repeat DU at 6 months before discontinuation of anticoagulation. Patients at higher risk for recurrence may require longer duration of anticoagulation and should also have a second DU at the 1-year interval. Further studies are needed to determine the optimal duration of anticoagulation for patients who are at higher risk for developing recurrent DVT.
Reflux The reversal of flow in veins of the lower extremity is usually caused by incompetent valves. The tendency of blood is to flow toward more dependent regions due to the gravitational pull. In order to compensate, the lower extremities have unidirectional valves which in combination with the muscular pump action propel blood to the heart. The valves are prone to damage and disruption due to inflammation, thrombosis, and degeneration. Once the valves cease to function correctly, there is a reversal of flow in the vein. Chronic venous disease (CVD) with its sequellae is a significant and costly problem. The varicosities are present in 10–20% of males and 25–33% of females.17–19 The skin changes and eczema due to CVI has a prevalence of 3–11%.20
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(c) Figure 97.1 Ultrasound images of venous reflux in patients with chronic venous disease. (a) The reverse flow in the femoral veins is 520 ms. This is normal as in the femoral and popliteal veins the cut-off for reflux is > 1000 ms. (b) Prolonged reflux in the thigh segment of the great saphenous vein. (c) Duplicated femoral vein with post-thrombotic reflux. Both femoral veins have the same color as the adjacent artery which is in the center. Feeling defects and wall thickening are seen clearly in the deeper vein which is partially recanalized. (See Color plates.)
The prevalence of active and healed ulcers is 1%.21,22 The prognosis of venous ulceration is poor. Only 50% heal at 4 months and 80% at 2 years.23 Annual recurrence rate is 6–15%.24 The distinction between primary and secondary reflux is based on etiology of venous disease. Secondary is the reflux caused by known factors such as previous DVT, congenital venous abnormalities, traumatic injury to vein, and previous venous interventions. In patients who have reflux without the
above causes, the reflux is primary. The latter is the most common cause and occurs most often in the superficial veins.
Duplex ultrasound techniques for evaluation of reflux The best results are obtained if the patient is in the standing position. The weight of the patient should be on the contralateral
Table 97.1 Ultrasound criteria used to determine presence or absence of DVT Criteria that rule out presence of DVT
Criteria that determine presence of DVT
Complete approximation of the opposing walls of vein during manual compression with ultrasound probe Color filling of the lumen from wall to wall without any defects Non-compressible or partially compressible vein Presence of echogenic material in vein lumen Presence of filling defect on color duplex No Doppler signal in the lumen
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Textbook of peripheral vascular interventions Table 97.2 Ultrasound criteria used to differentiate acute versus chronic DVT Characteristics present that indicate acute DVT
Characteristics present that indicate chronic DVT
Vein distention Lumen is partially compressible or non-compressible Lumen is echolucent and homogenous Vein wall is thin and smooth Spongy texture on compression Absence of collateral veins Free-floating tail maybe present Contracted or non-visualized vein segment Bright echoes in the lumen and heterogeneity Partial recanalization with filling defect and reflux Wall thickening with reduction of luminal diameter Firm texture on compression Existence of collateral veins
leg with the leg of interest slightly flexed and externally rotated. For examination of the veins of the calf, the patient could also be in the sitting position with the foot on a stool. There are two ways to elicit reversal of flow and thus evaluate for reflux. The Valsalva maneuver reverses flow in the veins of the lower extremity by increasing the intra-abdominal pressure. This in turn leads to reversal of flow if the valves are incompetent. This method is limited to the proximal valves of the lower extremity. The second method to evaluate for reflux is manual compression distal to the area of imaging followed by sudden release. Once the compression is released, blood flows through incompetent valves back to the more distal region thus resulting in reflux. When precise flow measurements and duration of reflux are required, standard pressure cuffs should be used. The examination initially focuses on the SFJ, common femoral, and the origin of both femoral veins. The veins are evaluated for flow. The femoropopliteal veins are examined next. This is followed by examination of the posterior and anterior tibial as well as peroneal and gastrocnemial veins. The superficial veins are examined. These include the GSV, SSV, their tributaries, and other non-saphenous veins. The perforator veins are assessed as well. These veins are recognized as they pierce the deep fascia which is seen as an echogenic layer because it contains collagen. Reflux in the perforating veins is defined as the reversal of flow in these veins from the deep system towards the superficial system. When indicated, this is evaluated by following the course of SSV and GSV and looking for veins that perforate through the deep fascia. Then using the same techniques and color Doppler examination, one can determine if there is significant reflux (Figure 97.2). Studies indicate that the acceptable physiologic reversal of flow in the vein is different for various venous systems of the lower extremity. Labropoulos and colleagues demonstrated that in the common femoral, femoral, and popliteal veins the best cut-off value was > 1000 ms. These veins are larger and have fewer valves and it may take longer for these valves to close. The cut-off value for reflux in the superficial,
deep femoral, and deep calf axial and muscular veins was > 500 ms and in the perforating vein was > 350 ms.25 It was also shown that the supine position had both false positive and false negative findings when compared to the standing position. The peak vein velocity was not important for the presence or absence of reflux in contrast to earlier studies.25
Chronic venous disease In order to delineate the severity of chronic venous disease (CVD), improve the precision of reporting, and develop uniform treatment plans, the CEAP classification system has been created. The diseased limb is evaluated and categorized according to clinical signs, etiology, anatomy, and pathophysiology (CEAP).26 Clinical symptomatology has been further divided into seven categories. C0 denotes absence of clinical signs and symptoms, C1 telangiectasias and reticular veins, C2 varicose veins, C3 edema, C4 skin changes, C5 healed ulcer, and C6 active ulcer. Eighty percent of the patients with CVD have varicose veins and telangiectasias, 20–25% have skin changes, and 12–14% have active or healed ulceration. The clinical classes are followed by S for symptomatic and A for asymptomatic. Symptoms include ache, burning sensation, heaviness, itching, restless limb and venous claudication. These symptoms are present in up to 80% of the patients.27,28 The pathophysiology of CVD stems from reflux and obstruction. In patients with CVD reflux alone exists in 80% of the limbs, obstruction alone exists in only 2%, and a combination exists in 17%.29 There is a worse prognosis for developing skin damage with the combination of reflux and obstruction.30 The two processes lead to increased pressures in the lower extremity. Venous hypertension in the lower extremities is believed to be linked to ulcerations that develop in CVD. The superficial system is affected in 90% of limbs and the deep system in 30% of limbs with CVD. In addition,
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(c) Figure 97.2 Ultrasound images from patients with deep vein thrombosis. (a) Acute thrombosis of the common femoral, femoral and deep femoral veins. The femoral artery above the veins is patent. (b) Chronic thrombosis in the femoral vein. Echogenic material with similar brightness and the adventitia of the vein is seen in the lumen. (c) Acute chronic thrombosis in a soleal vein in the calf. The vein is dilated with mixed echogenicity. The echolucent part is from the new thrombus and the bright echo is fibrous tissue which was formed from the old thrombosis. (See Color plates.)
the prevalence of reflux increases with worsening CVD.31,32 In the 2–4% of patients who have no demonstrable abnormalities in the venous system, other causes of ulceration should be considered.33,34 Other factors also play a role in CVD, like age, duration of disease, lifestyle, occupation, soft tissue biology, genetics, and calf muscle pump dysfunction.
Complex patterns of reflux are usually seen in patients with ulcerations and skin damage. Regardless of the involvement of perforator or deep system, in > 50% of patients with ulceration, superficial reflux exists. In a prospective randomized trial it was demonstrated that these patients respond well to surgical intervention in the superficial veins.31
REFERENCES 1. 2. 3. 4. 5. 6.
Criado E, Burnham CB. Predictive value of clinical criteria for the diagnosis of deep vein thrombosis. Surgery 1997; 122: 578–83 Nypaver TJ, Shepard AD, Kiell CS et al. Outpatient duplex scanning for deep vein thrombosis: Parameters predictive of a negative study result. J Vasc Surg 1993; 18: 821–6 Markel A, Manzo RA, Bergelin R, Strandness DE. Acute deep vein thrombosis: Diagnosis, localization, and risk factors. J Vasc Med Biol 1991; 3: 432–9 McLachlin JA, Richards T, Paterson JC. An evaluation of clinical signs in the diagnosis of deep venous thrombosis. Arch Surg 1962; 85: 738–44 Sevitt S, Gallagher N: Venous thrombosis and pulmonary embolism: A clinico-pathological study in injured and burned victims. Br J Surg 1961; 48: 475–89 Nordstrom M, Lindblad B, Bergqvist D et al: A prospective study of the incidence of deep-vein thrombosis within a defined urban population. J Intern Med 1992; 232: 155
7. 8.
9. 10. 11. 12.
Fowkes FJ, Price JF, Fowkes FG. Incidence of diagnosed deep vein thrombosis in the general population: systematic review. Eur J Vasc Endovasc Surg 2003; 25: 1–5 Hull RD, Raskob GE, Brant RF et al Low-molecular-weight heparin vs. heparin in the treatment of patients with pulmonary embolism. American–Canadian Thrombosis Study Group. Arch Intern Med 2000; 160: 229–36 Prandoni P, Lensing AW, Cogo A et al. The long-term clinical course of acute deep venous thrombosis. Ann Intern Med 1996; 125: 1–7 Heit JA, Silverstein MD, Mohr DN et al. Risk factors for deep vein thrombosis and pulmonary embolism: A population-based casecontrol study. Arch Intern Med 2000; 160: 809 Heit JA, Silverstein MD, Mohr DN et al. The epidemiology of venous thromboembolism in the community. Thromb Haemost 2001; 86: 452 Kearon C, Julian JA, Math M et al. Noninvasive diagnosis of deep venous thrombosis. McMaster diagnostic imaging practice guidelines initiative. Ann Intern Med 1998; 128: 663–77
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17. 18. 19. 20. 21. 22.
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Textbook of peripheral vascular interventions Hansson PO, Sorbo J, Eriksson H. Recurrent venous thromboembolism after deep vein thrombosis: incidence and risk factors. Arch Int Med 2000; 160(6): 769–74 Douketis JD, Crowther MA, Foster GA, Ginsberg JS. Does the location of thrombosis determine the risk of disease recurrence in patients with proximal deep vein thrombosis? Am J Med 2001; 110: 515–9 Linkins LA, Pasquale P, Paterson S, Kearon C. Change in thrombus length on venous ultrasound and recurrent deep vein thrombosis. Arch Intern Med 2004; 164: 1793–6 Linkins LA, Stretton R, Probyn L, Kearon C. Interobserver agreement on ultrasound measurements of residual vein diameter, thrombus echogenicity and Doppler venous flow in patients with previous venous thrombosis. Thromb Res 2006; 117: 241–7 Weddell JM. Varicose Veins Pilot Study. Br J Prev Soc Med 1966; 23: 179–86 Da Silva A, Widmer LK, Martin H et al. Varicose veins and chronic venous insufficiency: prevalence and risk factors in 4376 subjects in the Basle Study II. Vasa 1974; 3: 118–25 Widmer LK. Peripheral venous disorders: prevalence and sociomedical importance: observations in 4529 apparently healthy persons: Basle III Study. Bern: Hans Huber, 1978: 1–90 Coon MM, Willis PW, Keller JB. Venous thromboembolism and other venous disease in the Tecumseh Community Health Study. Circulation 1973; 48: 839–46 Nelzen O, Bergqvist D, Lindhagen A. Leg ulcer etiology: a cross sectional population study. J Vasc Surg 1991; 14: 557–64 Wille-Jorgensen P, Jorgensen T, Andersen M et al. Postphlebitic syndrome and general surgery: an epidemiologic investigation. Angiology 1991; 42: 397–403
23. 24. 25. 26. 27. 28. 29. 30.
31.
33. 34.
Skene AI, Smith JM, Dore CJ et al. Venous leg ulcers: a prognostic index to predict time to healing. BMJ 1992; 305: 1119–21 Hanson C, Andersson E, Swanbeck G. A follow-up study of leg and foot ulcer patients. Acta Derm Venereol 1987; 67: 496–500 Labropoulos N. Tiongson J. Pryor L et al. Definition of venous reflux in lower-extremity veins. J Vasc Surg 2003; 38(4): 793–8 Porter JM, Moneta LM and an International Consensus Committee on Chronic Venous Disease. Reporting standards in venous disease: An update. J Vasc Surg 1995; 21: 635–45 Kistner RL, Eklof B, Masuda EM. Diagnosis of chronic venous disease of the lower extremities: the “CEAP” classification. Mayo Clin Proc 1996; 7: 338–45 Labropoulos N. CEAP in clinical practice. Vasc Surg 1997; 31: 224–5 Labropoulos N. Hemodynamic changes according to the CEAP classification. Phlebolymphology 2003; 40: 130–42 Johnson BF, Manzo RA, Bergelin RO, Strandness DE Jr. Relationship between changes in the deep venous system and the development of the postthrombotic syndrome after an acute episode of lower limb deep vein thrombosis: a one- to six-year follow-up. J Vasc Surg 1995; 21: 307–12 Barwell JR, Davies CE, Deacon J et al. Comparison of surgery and compression with compression alone in chronic venous ulceration (ESCHAR study): randomised controlled trial. Lancet 2004; 363: 1854–9 Hanrahan LM. Araki CT. Rodriguez AA et al. Distribution of valvular incompetence in patients with venous stasis ulceration. J Vasc Surg 1991; 13: 805–11 Labropoulos N, Manalo D, Patel N et al. Uncommon leg ulcers. J Vasc Surg 2007; 45:568–73
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Contrast imaging studies of the lower extremity GE Pineda and D Mukherjee
Introduction Angiography allows direct visualization of blood vessels by the injection of iodinated contrast agents via catheters placed directly into an artery or a vein. Although non-invasive imaging techniques, including CT and MR angiograms, have made significant strides in recent years, catheter-based angiography has similarly undergone a new level of complexity and sophistication and to date remains the “gold standard” for definitive evaluation of peripheral vascular beds and is a necessary initial step in percutaneous revascularization. The selective intubation and cannulation of lower extremity arteries has been facilitated by the development of multiple catheter shapes now available in catheterization laboratories. In this chapter, we will focus on the angiographic techniques for visualization of the abdominal aorta and its visceral branches, the pelvic aorta, and lower extremity vasculature. We will also discuss the role of new emerging imaging techniques and how they compare to angiography. The primary objective of peripheral arteriography is to identify and characterize the lesions responsible for the patient’s symptoms. Full characterization should include a description of lesion morphology, location within the vessel, extent of disease and the presence of similar disease in adjacent vascular beds. Such characterization will help determine the best treatment option and revascularization strategy if needed. Before performance of contrast angiography, a full history and complete vascular examination should be performed. This is usually followed by the use of non-invasive vascular tests which will optimize decisions regarding the access site, as well as to minimize contrast dose and catheter manipulation. Lower extremity peripheral pulses at the access sites and distal to these sites must be thoroughly evaluated and documented prior to the angiographic study; this includes the calculation of the ankle–brachial index (ABI), which is a simple, accurate, inexpensive, and painless non-invasive test. It may also serve as a reference if complications should occur during the angiographic study. The ABI is calculated by dividing the systolic blood pressure obtained with a handheld Doppler in the ankle by the higher of the systolic blood pressures in the arms. A normal resting ABI is 1.0 to 1.29; generally a resting ABI more than 1.0 is considered normal, 0.91 to 0.99 borderline (equivocal), 0.41 to 0.90 reflects mild to moderate peripheral arterial disease (PAD) and < 0.40 suggests severe arterial occlusive disease.1 A rough correlation can be made between
the symptoms, ABI, and the expected angiographic findings. The result is used to predict the severity of PAD. A decrease in ABI is a sensitive indicator that significant PAD is probably present, as it reflects the overall burden of atherosclerosis. A decrease in resting ABI value is a strong and independent predictor of mortality.2,3 A reduction in post-exercise ABI over baseline readings can identify additional patients (who have a normal ABI values at rest) at increased risk of subsequent mortality.4
Radiographic contrast agents The administration of radiographic contrast agents in the catheterization laboratory is generally well tolerated by patients. There are several types of contrast agent available today for angiography. Before the late 1960s, all iodinated contrast agents used for radiologic imaging were ionic monomers with an ionizing carboxyl group attached to the first carbon of the iodine-containing benzene ring. All such agents were hyperosmolar relative to plasma, – in the range 1500– 1800 mOsm/kg, contributing to several adverse effects. Well-described side-effects of ionic contrast media include peripheral arterial vasodilatation, osmotic diuresis, and transient myocardial dysfunction. In addition, injection into the extremities may be painful and has been associated with transient blindness during cerebral angiography. As a result of this, nonionic monomers were developed (iohexol, iopamidol, ioversol), whose osmolality was substantially lower than previous agents, but they were still hyperosmolar relative to plasma, in the range 600–850 mOsm/kg. As these agents became less expensive, they gained widespread clinical acceptance due to overall fewer adverse effects. Third-generation non-ionic contrast agents reduce osmolality even further by creating a dimer. Iodixanol is a dimeric contrast agent in this class and is iso-osmolal with plasma. Non-ionic, low-osmolal contrast agents are now routinely used for angiography. Besides being safer, newer contrast agents are much better tolerated.5,6 Emerging reports suggest that if adequate hydration can be attained before contrast administration, there may be no significant difference between the low-osmolal and iso-osmolal agents in their incidence of contrast-induced nephropathy. Low-osmolal or preferably iso-osmolal agents are preferred in patients with severe congestive heart failure, hypotension, history of contrast allergy, severe bradycardia, renal insufficiency 841
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Textbook of peripheral vascular interventions 1.5–2.15 cm in diameter, with slight increase in size with age and in males.7 The major branches of the abdominal aorta are listed in Table 98.1. Visceral vasculature Three visceral vessels originate from the abdominal aorta: the celiac, the superior, and the inferior mesenteric arteries. In general, the celiac artery takes origin at the T12–L1 level. This trunk divides within 1 to 2 cm into three branches, the left gastric, splenic and common hepatic artery (Figure 98.2). The splenic branch has a tortuous leftward and posterior course; the common hepatic courses rightward and anteriorly and the left gastric has a superior take-off. The superior mesenteric artery arises at the level of L1 (Figure 98.3) approximately 1 cm below the celiac trunk. It has a steep, inferior course towards the right lower abdominal quadrant. The inferior mesenteric artery arises at the L3–L4 level, in most cases just to the left of the midline. It has a steep, inferior course in the midline, toward the pelvis.
Figure 98.1 Abdominal aortogram showing the origin of renal arteries and common iliac bifurcation. RA: renal arteries; SMA: superior mesenteric artery; CIA: common iliac arteries.
(serum creatinine > 2 mg/dl), and peripheral vascular contrast studies. A history of contrast reaction should be documented prior to the performance of contrast angiography and appropriate pretreatment administered before contrast is given.
Techniques and catheters Clinical anatomy Lower extremity vasculature can be broadly classified into three segments: the inflow vessels, including the common and external iliac arteries; the outflow vessels, including the common femoral, superficial femoral and profunda femoris arteries; and the run-off, including the anterior tibial, posterior tibial, and the peroneal arteries. Based on the territory affected, patients are said to have inflow, outflow, run-off, or multilevel disease if more than one territory is affected. Abdominal aorta This vessel courses left to the spine from the aortic hiatus at the diaphragm (T12) to its bifurcation at the level of L4 into the common iliac arteries (Figure 98.1). It is normally
Table 98.1
Renal arteries These vessels are usually single and arise from the lateral wall of the aorta at the L1–L2 level (Figure 98.4). In up to 30% of patients, accessory renal arteries can be seen arising from the infrarenal aorta or common iliac artery. This is a second, often smaller in caliber, renal artery that arises inferior to the main renal artery. A second anatomic variant is early subdivision of the main renal artery in which the vessel immediately subdivides into segmental branches just beyond its origin. Lumbar and middle sacral vessels Four paired lumbar vessels arise from the posterior lateral wall of the aorta. The middle sacral branch is the terminal branch of the distal aorta. In cases of severe underlying atherosclerosis, the lumbar vessels often remain patent and provide collateral supply to the lower extremities via anastomosis to the superior gluteal, iliolumbar and deep circumflex iliac arteries to provide flow in the internal iliac or common femoral arteries. The iliac vessels The common iliac vessels are the continuation of the aorta with a mean diameter of 1 cm. They provide two terminal branches at the lumbosacral junction, the internal and external iliac arteries. The internal iliac takes off medially and posteriorly, and the external iliac is the in-line continuation of the common iliac artery, traveling anteriorly and laterally to the groin to exit the pelvis just posterior to the inguinal ligament with a mean diameter of ~ 8 mm to become the common
Branches of the abdominal aorta
Dorsal branches
Ventral branches
Terminal branches
Lumbar arteries Inferior phrenic artery Gonadal arteries Middle adrenal artery Renal arteries
Celiac artery Superior and inferior mesenteric arteries
Common iliac arteries Median sacral artery
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Figure 98.2 Celiac trunk angiogram demonstrating the three major branches. SA: splenic artery; CHA: common hepatic artery and LGA: left gastric artery. Branches of common hepatic are also displayed. PH: proper hepatic artery; LH: left hepatic artery; GD: gastroduodenal artery.
femoral artery. The external iliac artery provides two branches, the deep circumflex iliac and the inferior epigastric arteries (Figure 98.5). The femoral vessels The common femoral artery (CFA) is the in-line continuation of the external iliac artery below the inguinal ligament. On average, it is 2.5–4 cm long and 6–8 mm in diameter. The CFA bifurcates into the profunda femoral artery posterolaterally and superficial femoral artery anteromedially, commonly at the level of the mid femoral head; this bifurcation is best visualized
Figure 98.3 (SMA).
Selective superior mesenteric artery angiogram
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Figure 98.4 Selective right renal artery angiogram demonstrating the main renal trunk, segmental, and interlobar arteries.
with an ipsilateral anterior oblique angulation of 30–40° (Figure 98.6). The proximal branches of the profunda and the medial and lateral circumflex are crucial for patients with iliac occlusive disease, by forming collaterals with the internal iliac artery. The distal branches, the perforating arteries, serve as collateral
Figure 98.5 Pelvic aortogram showing common iliac arteries and their bifurcation. The common femoral artery and its bifurcation is also displayed. CIA: common iliac arteries; EIA: external iliac arteries; IIA: internal iliac arteries; CFA: common femoral artery; SFA: superficial femoral artery and PFA: profunda femoral artery.
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Figure 98.6 Right common femoral artery angiogram. Sheath positioned proximal to bifurcation at the level of the middle of the femoral head. CFA: common femoral artery; SFA: superficial femoral artery and PFA: profunda femoral artery.
pathways for patients with superficial femoral artery occlusion by providing collaterals to the popliteal artery via geniculate collaterals. The superficial femoral artery, extends from the common femoral bifurcation to the adductor (Hunter) canal, where it becomes the popliteal artery running posterior to the femur. It provides multiple small muscular branches. The popliteal artery This vessel is the continuation of the superficial femoral artery below the adductor canal. It has a gradual medial to lateral course as it travels through the popliteal fossa and is usually 5– 7 mm in diameter (Figure 98.7). Its branches – the superior, middle, and inferior geniculate arteries – provide collateral flow to reconstitute the popliteal or tibial vessels. The popliteal artery usually bifurcates into the anterior tibialis (AT) and the tibioperoneal trunk (TPT) approximately 5 cm below the tibial plateau. The tibial arteries These vessels are the terminal branches of the popliteal artery which commonly divides below the knee into the AT and the TPT (Figure 98.7). The AT travels laterally and anterior to the tibia towards the foot. The TPT courses for 3–4 cm before it bifurcates into the posterior tibialis (PT) and peroneal (PER) arteries. This branching pattern is seen in over 90% of patients. In the remaining cases, variant branching is observed. The most commonly encountered variants are the trifurcation of the popliteal artery into its terminal branches which includes the AT, PT and PER arteries, and origin of the PER artery from the AT.
Figure 98.7 Digital subtraction angiogram of left popliteal artery (PA) bifurcating into the anterior tibial (AT), and the tibioperoneal trunk (TPT); which then divides into the posterior tibial (PT) and peroneal arteries (PER).
The pedal arteries The AT and PT continue into the foot as the dorsalis pedis and the posterior tibial arteries. The PER artery runs near the fibula between the AT and PT arteries and terminates at the ankle providing terminal branches to the dorsalis pedis and posterior tibialis arteries. The lateral and medial plantar branches of the posterior tibialis and the deep plantar branch of the dorsalis pedis form the primary pedal arch which is a potential pathway linking the ventral and dorsal circulation in the foot. Access for vascular angiography One of the first and crucial steps of any endovascular procedure is determining the most appropriate site for arterial access. Optimal access reduces the likelihood of complications and shortens the duration of the procedure. As a general rule, and for the purposes of endovascular intervention, the location of the lesion determines the access site in most cases. A couple of principles are worth highlighting, and these are outlined below. Vascular anatomy If available, one must be aware of the vascular anatomy of the patient at hand. Previous angiographic studies and noninvasive studies (e.g. CT or MR angiography, ultrasound) must be reviewed. Known occlusions, significant stenosis and severe tortuosity proximal to a potential access site are helpful points to know in advance. Acute angulation of the aortic bifurcation increases the difficulty in performing crossover techniques and severe atherosclerotic disease of aortic arch
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Contrast imaging studies of the lower extremity and great vessels increases the risk of cerebral embolization if upper extremities are utilized for arterial access. In addition it is imperative to carefully document the peripheral pulses as described above. Previous revascularization The timing and nature of previous surgical revascularization must be available, as percutaneous puncture of grafts is generally avoided in the first 6–12 months. It is also crucial to know the direction of flow if a femoral–femoral bypass is present as this will determine the site to be accessed. With this information in mind, the access site that will provide the safest approach for an adequate diagnostic or interventional procedure is determined. For iliac occlusive disease, the ipsilateral femoral artery via retrograde (toward the iliac artery) common femoral artery (CFA) access is usually performed. Lesions on the CFA, however, must be approached from a contralateral-puncture, axillary or popliteal approach. Lesions distal to the CFA are best approached and treated with an antegrade (towards the foot) CFA approach. Common femoral artery (CFA) access The retrograde CFA is the most common access site used for diagnostic angiography and intervention. It is centrally located to all vascular arterial systems and provides greater distance from the x-ray source and more spacious workplace compared to the arm. The puncture of the CFA should be performed proximal to its bifurcation using the front wall technique (Figure 98.6). The site should be checked under fluoroscopy prior to arterial puncture as its bifurcation usually occurs at the level of the mid-femoral head. In patients with absent or weak pulses, an ultrasound-guided approach or an alternative access site should be used. The SmartNeddle (Escalon Vascular Access Inc., New Berlin, WI) is a percutaneous Doppler-guided vascular access device that is often helpful in patients with weak pulses. Although many operators use crossover techniques from the contralateral CFA, antegrade puncture via the ipsilateral CFA is an effective approach to superficial femoral artery, popliteal or infrapopliteal disease. It is technically more challenging and limits angiography to the ipsilateral leg but offers a stable platform for interventions. As in retrograde access, the desired site of entry is the CFA below the inguinal ligament. Under continuous fluoroscopic guidance, the skin puncture is made at or above the top of the femoral head aiming at the mid or upper portion of the femoral head. A less acute angle (< 45°), facilitates catheter and sheath insertion and avoids the kinking associated with a steeper angle entry. Upper extremity: brachial and radial artery access This site offers the advantage of early ambulation and reduced risk of bleeding complications. It is generally considered in individuals with bilateral iliac artery or distal aortic occlusions and in patients with severe downward angulation of aortic visceral branches. This approach makes selective cannulation easier. The left brachial approach is preferable since instrumentation and passage of equipment across the origin of the vertebral and right common carotid artery exposes the patient to a risk of cerebral embolization when the right-sided vessels are used.
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Diagnostic catheters Knowledge of appropriate catheters, angulations, and injection rates is of vital importance in performing safe and optimal vascular angiography. Several catheter shapes have been designed, which ultimately determine a specific function. They fall into these general families: ●
●
Side-hole catheters. These allow for large volumes of contrast to be infused safely in large vessels at a rapid rate via power injection. By having multiple side-holes along the distal shaft of the catheter, the likelihood of catheter whipping or subintimal dissection is decreased. End-hole, simple curve, and complex reverse curve catheters permit selective angiography by manual injection of contrast material into a specific vessel.
The use of digital subtraction angiography permits the use of 5-French catheters with excellent angiographic results. A general recommendation for catheter selection and injection rates in different vascular territories is displayed in Table 98.2.8 Some of the most commonly used catheters for abdominal aorta and lower extremity angiography are shown (Figure 98.8a–g). Abdominal aortography As a general rule, an abdominal aortogram should be performed with a straight pigtail or an Omniflush catheter placed at the level of L1 vertebrae. Digital subtraction angiography (DSA) is used and a total of 10–15 cm3 of contrast is injected at a rate of 20 cm3/second (Figure 98.1). When performing arteriography with known or suspected aneurysmal disease, care should be taken to avoid dislodgement of mural thrombus or plaque resulting in distal embolization. The operator should be able to visualize and comment on its major branches which include the celiac trunk, superior mesenteric artery (SMA), renal arteries and accessories if present, inferior mesenteric artery (IMA), and aortic bifurcation. If the origins of the mesenteric vessels are being evaluated, a lateral aortogram is indicated. Pelvic and lower extremity angiography With advancements in non-invasive imaging, angiography is usually reserved for patients in whom endovascular interventions are contemplated. The diagnostic lower extremity arteriogram should image the iliac, femoral, and popliteal trifurcation in profile without vessel overlap. The indications for pelvic and lower extremity angiography include ischemia (either resting or exertional) owing to atherosclerosis, embolism, thrombosis, and vasculitis.9 Other potential indications include peripheral aneurysms, vascular tumors, trauma, and extrinsic compression. The preliminary pelvic aortogram is obtained by placing a multiholed catheter (straight pigtail or Omniflush) at the level of L3 slightly above the aortoiliac bifurcation (usually the aorta bifurcates at the L4–L5 level) (see Figure 98.5). Digital subtraction pelvic aortogram at 4 frames/second is performed with 20–25 cm3 of contrast at a rate of 15 cm3/second. This allows excellent visualization of the distal aorta, common iliacs, external iliacs, and the common femoral arteries.
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Textbook of peripheral vascular interventions Table 98.2
Catheters for peripheral angiography
Artery
Catheter
Angulation
Injection
Abdominal aortogram for suspected mesenteric ischemia Abdominal aortogram for suspected renal artery stenosis Pelvic/abdominal aortogram Distal aorta for bolus chase and run-offa Renal arteries
5-F straight pigtail between T12 and L1
Biplane or lateral
20 ml/s for 2 s
5-F straight pigtail between T12 and L1
Anteroposterior
20 ml/s for 1 s
5-F straight pigtail between L1 and L2 5-F straight pigtail between L2 and L3 JR4, renal double curve or SOS catheter
Anteroposterior
15 ml/s for 1 s
Anteroposterior
8 ml/s for 10 s using DSA Hand injection with DSA
Celiac trunk
JR4, SOS, IMA or Cobra catheter JR4, SOS, IMA or Cobra catheter
Superior and inferior mesenteric artery
Anteroposterior and ipsilateral oblique at 10–15° Anteroposterior Anteroposterior
10 ml/s for 1 s 8 ml/s for SMA and 3 ml/s for IMA
a
The volume should be reduced by 50% if each leg is injected separately. DSA: digital subtraction angiography; JR4: Judkins right; IMA: internal mammary artery.
(a)
(b)
(c)
(e)
(f)
(g)
(d)
Figure 98.8 Commonly used catheters for abdominal aorta, its branches and lower extremity angiography. Side-hole catheters: (a) pigtail; (b) Omniflush. End-hole catheters: (c) Cobra; (d) Judkins right (JR); (e) internal mammary (IMA); (f) renal double curve (RDC) and (g) SoS Omni.
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Contrast imaging studies of the lower extremity Following adequate visualization of the inflow vessels with the pelvic aortogram, run-off angiography with digital subtraction angiography with moving table and bolus chase technology is performed. Contrast material is injected at a rate of 7–10 cm3/second for a total of 10–12 seconds (i.e. 70– 100 cm3). Filming is begun after a 2 second delay and the bolus of contrast is then chased from the pelvis to the feet. The transit of contrast material is dependent on the patient’s cardiac output and severity of underlying vascular disease. Selective angiography of the iliac arteries can also be achieved via the brachial or femoral approach. With a brachial artery access, a multipurpose catheter is used to selectively engage each common iliac vessel. The ipsilateral femoral artery can be used (retrograde approach) and contrast injected directly through the arterial sheath or via a short catheter (MP, pigtail) placed in the external iliac or common iliac artery. An alternative and commonly used approach is from the contralateral femoral artery which requires crossing the aortic bifurcation and engagement of the opposite common iliac artery. To accomplish this, catheters commonly used are an internal mammary, Cobra or the SOS-OMNI (Angiodynamics Inc.). Alternatively, the common iliac artery can also be engaged by unfolding a pigtail or Omniflush catheter using an angled guidewire at the aortic bifurcation, and advancing the catheter as described above. An angulated view (contralateral left anterior oblique 30–40° degrees) allows visualization of the common iliac bifurcation without overlap. Hand or power injection at 10 ml/second for a total of 10 ml is sufficient for adequate visualization. Pressure gradients across iliac artery stenosis aid in determining the hemodynamic significance of common iliac stenosis. A pressure gradient of > 15 mmHg is typically considered significant. Selective lower-extremity arteriography is commonly performed using the ipsilateral common femoral artery via an antegrade approach or utilizing the aortic crossover technique described above if the contralateral lower extremity is to be imaged. The CFA can be imaged in the anteroposterior projection; however, if stenosis of the SFA or PFA is suspected, the optimal view for the common femoral artery bifurcation is the ipsilateral 30–40° oblique angulation. Using DSA at 4 frames per second, hand injection of 6–8 ml is enough for adequate visualization. Run-off of lower extremities is performed with a single angiographic run and bolus chase or using sequential stations. The use of sequential stations allows for better resolution and angulated views if stenosis is suspected. If DSA is used, an image rate of 4 frames/second is used for above the knee and 2 frames/second for below the knee.
Complications Contrast-induced nephropathy (CIN) CIN is usually defined as an acute decline in renal function, expressed as a relative increase in serum creatinine concentration of at least 25%, or an absolute increase in serum creatinine of 0.5 mg/dl (44.2 µmol/l) in the absence of other etiologies.10 Nephropathy induced by contrast medium remains one of the most clinically important complications of the use of iodinated contrast medium.11 At 12% of cases, it is the leading cause of hospital acquired acute renal failure and
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is associated with a 34% mortality in patients who require in-hospital dialysis with 19% survival at 2 years.12 The use of intravenous fluids for hydration remains crucial in the prevention of CIN; this approach is simple and carries minimal risks of adverse effects if appropriate care is taken.13 Access site complications One of the most common complications of diagnostic and interventional angiograms involves the vascular access site and is an important cause of procedure-related morbidity and mortality. Currently, there is a 0.1–2% rate of significant local vascular complications after diagnostic transfemoral catheterization, and 0.5–5% after interventional transfemoral treatment but may be as high as 14% after complex and prolonged procedures. Following transbrachial and transradial catheterization, local vascular complications amount to 1–3% after diagnostic and 1–5% after interventional procedures. The most common vascular access site is the common femoral artery. This vessel is reasonably large, superficial, and hemostasis can be achieved by compressing it against the femoral head. An arteriotomy below the distal common femoral bifurcation or above the inguinal ligament increases the risk of access site complications. These are sites where the femoral artery is poorly compressible.14 Risk factors for femoral access complications include female gender, older age, uncontrolled hypertension, high or low body mass index, high level of anticoagulation, prolonged sheath duration, larger arterial sheaths, presence of peripheral vascular disease, and location of the arteriotomy.15,16 Complications of femoral artery vascular access site include hemorrhage (hematoma or retroperitoneal bleeding), peripheral embolization, thrombosis, dissection, aneurysm, AV fistula, pseudoaneurysm, infection, and injury to other local structures. Emerging non-invasive modalities Digital subtraction angiography (DSA) is still considered the reference standard technique in the assessment of aortoiliac and lower extremity arteries; with the advantage that performing therapeutic interventions is possible during the examination. Its main drawbacks, however, are invasiveness which requires catheterization and intra-arterial injection of iodinated contrast medium, high cost, patient discomfort, post-procedural patient observation and a complication rate of approximately 1%. The assessment of peripheral arterial disease by non-invasive imaging techniques has undergone substantial changes over the past decade. Recent advances in multi-detector CT angiography (CTA) and contrast-enhanced magnetic resonance angiography (MRA) provide the basis for using these imaging modalities in the anatomic evaluation of central and peripheral vascular beds. Both MRA and CTA have been shown to be sensitive and specific techniques for the evaluation of peripheral arteries.17,18 Reports of comparative studies have indicated that multi-detector row CTA has sensitivity for the evaluation of the complete peripheral arterial system that ranges from 91% to 92%; a specificity that ranges between 92% and 97%; and an agreement with DSA that ranges between 78% and 92%.18 Contrast-enhanced three-dimensional MRA is increasingly being used in patients with PAD of aortoiliac and lower extremity arteries, especially those with chronic renal insufficiency.
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Gadolinium, the most commonly used contrast agent for this purpose, has no nephrotoxicity, as compared with the iodinated contrast agents used for CTA and DSA. Acquisition time is fast; with high performance systems, it may be as short as a breath hold. For a complete peripheral MRA study, imaging is sequentially performed on three overlapping fields: the aortoiliac region, the femoropopliteal region and below-the-knee run-off vessels. The contrast agent is chased down the arterial tree by synchronizing table translation and image acquisition with arterial transit time. Using the current technology of contrast enhanced MRA, sensitivities of 77–99% and specificities of 84–100% in the detection of hemodynamically significant arterial stenosis have been reported.19,20
●
●
●
●
● ●
Key points ●
The patient history, clinical examination, and non-invasive imaging allow a targeted approach to peripheral angiography.
●
Review non-invasive tests beforehand. It provides critical information of the vasculature to be imaged. This forward planning will help ensure that the right access site is used and the necessary equipment is at hand for the successful completion of study. Adequate intravenous hydration and contrast dosage limitation can reduce the morbidity and mortality associated with contrast-induced nephropathy. Use of non-ionic, iso-osmolal radiocontrast agents in patients with underlying impaired renal function is indicated. For vascular access, use a cautious and sensitive puncture technique. Always advance catheters and sheath over a wire. For diagnostic angiography, obtain orthogonal views of suspected lesions, and identify the view that produces the least foreshortening of the lesion. Newer imaging modalities provide a quick, safe, reliable and non-invasive means for the initial detection of PVD.
REFERENCES 1. 2. 3.
4. 5. 6. 7. 8.
9. 10. 11.
Hiatt WR. Medical treatment of peripheral arterial disease and claudication. N Engl J Med 2001; 344(21): 1608–21 Criqui MH, Langer RD, Fronek A, et al. Mortality over a period of 10 years in patients with peripheral arterial disease. N Engl J Med 1992; 326(6): 381–6 Newman AB, Siscovick DS, Manolio TA, et al. Ankle-arm index as a marker of atherosclerosis in the Cardiovascular Health Study. Cardiovascular Heart Study (CHS) Collaborative Research Group. Circulation 1993; 88(3): 837–45 Feringa HH, Bax JJ, van Waning VH, et al. The long-term prognostic value of the resting and postexercise ankle-brachial index. Arch Intern Med 2006; 166(5): 529–35 Aspelin P, Aubry P, Fransson SG, et al. Nephrotoxic effects in high-risk patients undergoing angiography. N Engl J Med 2003; 348(6): 491–9 Sandler CM. Contrast-agent-induced acute renal dysfunction — is iodixanol the answer? N Engl J Med 2003; 348(6): 551–3 Horejs D, Gilbert PM, Burstein S, et al. Normal aortoiliac diameters by CT. J Comput Assist Tomogr 1988; 12(4): 602–3 Mukherjee D. Diagnostic catheter-based vascular angiography. In: Rajagopalan S, Mukherjee D, Mohler E, eds. Manual of Vascular Diseases, first edition. Philadelphia: Lippincott Williams & Wilkins, 2005 Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 Practice Guidelines for the management of patients with peripheral arterial disease. Circulation 2006; 113(11): 463–654 Murphy SW, Barrett BJ, Parfrey PS. Contrast nephropathy. J Am Soc Nephrol 2000; 11(1): 177–82 Rihal CS, Textor SC, Grill DE, et al. Incidence and prognostic importance of acute renal failure after percutaneous coronary intervention. Circulation 2002; 105(19): 2259–64
12. 13.
14. 15. 16.
17.
18.
19. 20.
Levy EM, Viscoli CM, Horwitz RI. The effect of acute renal failure on mortality. A cohort analysis. JAMA 1996; 275(19): 1489–94 CIN Consensus Working Panel. Report on Strategies to Reduce the Risk of Contrast-Induced Nephropathy. Contrast-Induced Nephropathy: Clinical Insights and Practical Guidance. Am J Cardiol 2006; 98(6, suppl. 1): 59–77 Lumsden AB, Miller JM, Kosinski AS, et al. A prospective evaluation of surgically treated groin complications following percutaneous cardiac procedures. Am Surg 1994 60(2): 132–7 Waksman R, King III SB, Douglas JS, et al. Predictors of groin complications after balloon and new-device coronary intervention. Am J Cardiol 1995 75(14): 886–9 Sherev, DA, Shaw RE, Brent BN. Angiographic predictors of femoral access site complications: implication for planned percutaneous coronary intervention. Catheter Cardiovasc Interv 2005; 65(2): 196–202 Ouwendijk R, de Vries M, Pattynama P, et al., Imaging peripheral arterial disease: A randomized controlled trial comparing contrast-enhanced MR angiography and multi-detector row CT angiography. Radiology 2005; 236(3): 1094–103 Martin ML, Tay KH, Flak B, et al. Multidetector CT angiography of the aortoiliac system and lower extremities: a prospective comparison with digital subtraction angiography. AJR Am J Roentgenol 2003; 180(4): 1085–91 Swan JS, Carroll TJ, Kennell TW, et al. Time-resolved Threedimentional Contrast-enhanced MR Angiography of the peripheral vessels. Radiology 2002; 225(1): 43–52 Bezooijen R, van den Bosch HC, Tielbeek AV, et al. Peripheral arterial disease: sensitivity-encoded multiposition MR angiography compared with intraarterial angiography and conventional multiposition MR angiography. Radiology 2004; 231(1): 263–71
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Interventional therapy for pulmonary embolism S Faintuch, FB Collares, and GM Martinez Salazar
Introduction Pulmonary embolism (PE) contributes to 50,000–200,000 deaths per year in the US. As PE can be notoriously difficult to diagnose, its true incidence is unknown, but it is estimated that there are more than 600,000 cases each year in the US.1–3 The mortality rate from recognized PE varies from 2.3 to 28%.4,5 Two out of three deaths occur in the first hour, thus rapid approach to diagnosis and treatment; that is, recovery of pulmonary flow, can change the outcome.2,5 The principal criterion for characterizing acute massive PE is systemic arterial hypotension (systolic blood pressure < 90 mmHg).4 Hemodynamic decompensation in the form of arterial hypotension and right ventricular dysfunction is caused not only by the embolus, but also by the release of humoral factors such as serotonin and histamine. Hypoxia is a result of ventilation and perfusion mismatches, as well as vasoconstriction. The role of humoral factors and reactive vasoconstriction explains why the size of the emboli, as seen on CT, does not necessarily correlate to the severity of the clinical presentation.6 The most common clinical symptoms of PE are sudden onset of dyspnea along with tachycardia and pleuritic or nonpleuritic chest pain. Fever, diaphoresis, and coughing with or without hemoptysis are other clinical manifestations. Classic symptoms and signs are not present in many cases and findings may be subtle in young, previously healthy patients with excellent cardiac reserve, or mimic other illnesses such as acute coronary syndrome or exacerbation of chronic obstructive pulmonary disease in older patients.3 Thus, the interventionalist may be involved in the decision of when and how to treat. This chapter will therefore include segments on diagnosis and non-interventional treatment options.
similar clinical presentation, such as myocardial infarction, pneumonia, pneumothorax, rib fracture, and congestive heart failure. ECG abnormalities in patients with massive PE include incomplete or complete right bundle-branch block, T-wave inversion in leads V1 to V4, an S wave in lead I, and both a Q wave and an inverted T wave in lead III on the electrocardiogram. Pulmonary artery enlargement and oligemia of the embolized lung on the radiograph have been described, but present low sensitivity.7 Note that elevated troponins can be present in the setting of PE; therefore, care should be taken to rule out a diagnosis of myocardial infarction.8 Traditionally, the imaging test for suspected PE was the ventilation/perfusion lung scan. Normal studies and highprobability lung scans are well validated with paired pulmonary arteriograms, which are considered the gold standard for the diagnosis of PE. However, the main difficulty with ventilation/perfusion scans is that most cases are considered of intermediate or indeterminate probability.9 Contrastenhanced chest CT is fast (less than 30 seconds, with a single breath-hold sequence); it can directly visualize the thrombus, and can evaluate other structures for differential diagnoses (lung parenchyma, heart, aorta). Thus, this modality has been rapidly replacing nuclear scanning as the main diagnostic imaging test for suspected PE.3 In the PIOPED II trial, CT angiograms had a sensitivity of 83% and a specificity of 97% for the diagnosis of acute PE.10 Consequently, pulmonary arteriography should no longer be indicated as a primary diagnostic tool – the angiographic access site has been a source of hemorrhagic complications in patients who were diagnosed with PE and anticoagulated.11 Therefore, percutaneous access should only be recommended on an intent-to-treat basis, rather than intent-to-diagnose.
Diagnosis
Treatment
The patent’s history may reveal predisposing factors such as deep venous thrombosis or stasis (immobility, long-haul air travel, large varicose veins, surgery), obesity, pregnancy, oral contraceptive use, hormone replacement therapy, cigarette smoking, hypertension, cancer, and the hypercoagulable states or thrombophilias (factor V Leiden, antithrombin III deficiency, protein C deficiency, protein S deficiency, and antiphospholipid antibody syndrome).3 Initially an electrocardiogram and chest x-ray, and possibly a CT scan, are performed to exclude other disease entities with
The traditional therapeutic options for PE are anticoagulation, systemic thrombolysis, and surgical thrombectomy. Recently, however, minimally invasive procedures such as catheter-directed thrombolysis, percutaneous embolectomy and embolus fragmentation techniques have been introduced as treatment options.12 The key to appropriate therapy is risk stratification, since low-risk patients have an excellent prognosis with anticoagulation alone and high-risk patients benefit from anticoagulation and thrombolysis or embolectomy.3 Aggressive intervention for PE treatment is indicated when at 849
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least one of the following criteria is present: arterial hypotension (< 90 mmHg systolic or drop of > 40 mmHg); cardiogenic shock with peripheral hypoperfusion and hypoxia; circulatory collapse with need for cardiopulmonary resuscitation; echocardiographic findings indicating right ventricular afterload stress and/or pulmonary hypertension, with a contraindication to anticoagulation or systemic thrombolytic therapy.12–14 Anticoagulation Heparin anticoagulation prevents formation of new thrombus and facilitates endogenous fibrinolytic mechanisms to lyse clot that has already formed. This therapy, therefore, does not directly dissolve formed thrombus, but prevents its progression and recurrence.3,12 There is an 18–30% chance of recurrent lethal PE if the patient survives an acute PE episode and no anticoagulation therapy is initiated.15–17 Traditionally, anticoagulation therapy uses unfractionated heparin in an initial bolus of 5000–10,000 units followed by a continuous intravenous infusion of 1250 units/hour to maintain a partial thromboplastin time in the target range of 60– 80 seconds, but this strategy may not achieve anticoagulation rapidly.18 More recently, low-molecular-weight heparins (LMWH) have been used to achieve an immediate anticoagulant effect. LMWH provide high and sustained plasma antithrombin activity, and the use of reviparin or tinzaparin once daily has proven to be effective and safe as a bridge to oral anticoagulation with vitamin K antagonists such as warfarin.19–21 LMWHs offer several advantages over unfractionated heparin including a longer half-life, increased bioavailability, and a more predictable dose response. In addition, LMWHs are dosed by weight, administered subcutaneously, and usually do not require dose adjustments or laboratory monitoring. Whereas unfractionated heparin is largely cleared by the liver, LMWHs are cleared by the kidneys. Fondaparinux is an LMWH approved by the FDA for the initial treatment of PE. In hemodynamically stable patients with
Table 99.1
acute symptomatic PE, it is as safe and effective as intravenous unfractionated heparin.22 Fondaparinux is administered subcutaneously, once a day, in fixed doses of 5 mg for body weight < 50 kg, 7.5 mg for body weight between 50–100 kg, and 10 mg for body weight > 100 kg. Unlike intravenous unfractionated heparin, it does not require dose adjustment with laboratory coagulation tests and does not cause heparin-induced thrombocytopenia. However, as fondaparinux is cleared through the renal route, it is contraindicated in patients with severe renal disease.22,23 Warfarin is usually initiated at a dose of 5 mg and takes at least 5 days of therapy to achieve full efficacy; thus, during this period, heparin and oral anticoagulation are administered concomitantly. The dose is adjusted to the prothrombin time, and the target INR value is between 2.0 and 3.0. Warfarin is typically used for 3–6 months after an acute episode of PE, although some patients may benefit from indefinite-duration anticoagulation (Table 99.1).3,12,24 Systemic thrombolysis Systemic fibrinolysis is generally considered to be a lifesaving intervention in patients with massive PE; nonetheless, the extent of the clinical benefit remains unclear.4 A dose of 100 mg of tPA (alteplase), for IV infusion over 2 hours, is approved by the FDA for treatment of massive PE. The risk of bleeding complications increases significantly with the use of thrombolytics: up to 3% incidence of intracranial hemorrhage has been reported.23 In a recent analysis of the International Cooperative Pulmonary Embolism Registry data, fibrinolytics did not reduce the rate of mortality or recurrent PE at 90 days. Among 2,392 patients with acute PE, 33 received systemic thrombolysis. Mortality was 46.3% in the thrombolysis group versus 55.1% in the anticoagulation group. Recurrent PE within 90 days was 12% for both groups.4 The combination of urokinase and therapeutic doses of heparin is safe, which is not usually true for tPA.12 Heparin
Comparison of systemic treatments and proposed regimens4,12,19,22,23
Mortality Recurrence of PE Incidence of bleeding complications Proposed regimes
Systemic thrombolysis
Anticoagulation treatment
5–46% 8–12% 22% (3% intracranial)
11–55% 12–19% 8%
Urokinase: 4500 IU/kg (loading dose) followed by 4,500 IU/kg/h for 12–24h, with full heparin dose tPA: 100 mg continuous peripheral IV infusion over 2 h; or 50 mg over 2 h + 40 mg over 4 h; or 100 mg over 7 h, with low heparin dose (100–300 IU/h)
Heparin: 5000–10,000 IU (IV bolus) followed by 1,000–1,250 IU/h Fondaparinux: Fixed dose, once daily (SC): 5 mg (body weight < 50 kg), 7.5 mg (body weight 50–100 kg) or 10 mg (> 100 kg) Warfarin: 5–10 mg/day PO, typically used for 3–6 months
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Interventional therapy for pulmonary embolism is withheld during the administration of tPA for PE and is not restarted until the activated partial thromboplastin time has fallen to less than twice the upper limit of normal (Table 99.1).13 Surgical embolectomy Surgical pulmonary embolectomy is performed through sternotomy and direct clot retrieval from the pulmonary artery with a forceps.12 It represents a major surgical challenge for patients who are very unstable hemodynamically. However, it has some advantages, such as the removal of the entire embolus burden and preservation of maximal pulmonary arterial area for reperfusion. It has been classically associated with high peri-operative morbidity and mortality.25 However, a recent retrospective series presented favorable follow-up data on 47 patients who underwent emergency surgical embolectomy. Peri-operative mortality was 6% and late mortality was 12%. Actuarial survival was 86 and 83%, at 1 and 3 years, respectively. These data, however, represent experience of a single tertiary care center, with renowned expertise in this technique.26 Catheter-based therapies Catheter-based therapies are based on three conceptual frameworks: (1) to bring lytic agents directly into the clot, therefore decreasing their systemic distribution and side effects (bleeding); (2) to fragment the clot and/or displace it from a central location in the pulmonary artery towards the periphery and thereby enlarging the perfusion surface; and (3) to remove the clot. The means of treatment will depend on the availability of equipment, and also on severity of signs/symptoms and thus time left to achieve reperfusion. Catheter-directed thrombolysis Catheter-directed thrombolysis involves positioning of a catheter via femoral or jugular access into the pulmonary artery, for targeted infusion of thrombolytics. It aims at a faster clot lysis, leading to early reperfusion of the pulmonary circulation. The catheter is wedged within the clot, and a bolus injection of thrombolytic drug is followed by continuous infusion for 12–24 hours, in association with systemic heparinization, if using urokinase (Table 99.2). Note that the presence of the infusion catheter in the pulmonary artery can lead to massive arrhythmia. Association with other techniques, such as
Table 99.2
mechanical thrombus fragmentation, balloon catheter angioplasty, or other devices that increase clot surface by fragmentation, may increase the velocity of thrombolysis. Hemorrhagic complications are theoretically less likely with this alternative technique than with systemic infusion of thrombolytic agents, due to the smaller dose and targeted delivery. However, fibrinogen levels should be monitored at 4–6 hour intervals. Infusion may need to be stopped or reduced if fibrinogen falls to less than 30–40% of the initial measurement or below 100–150 mg/dl, since this is a predictor of increased bleeding complications.12,28,29 Percutaneous embolectomy When there is no response or contraindication to the chemical thrombolytic therapy, patients may benefit from percutaneous embolectomy, a treatment option that uses mechanical devices designed to remove or promote fragmentation, maceration or aspiration of the clot.12 Fragmentation techniques Many techniques do not attempt to eliminate the clot completely, but rather to fragment thrombus into small parts that migrate peripherally into the pulmonary circulation. The distal dispersion of a proximal embolus promotes the opening of the main pulmonary artery improving lung perfusion.30,31 The rationale for this approach is the knowledge that the cross-sectional area of the distal arterioles is more than four times that of the central pulmonary circulation. Chemical thrombolytic therapy may facilitate and complement the action of thrombectomy devices by helping and speeding the process of fragmentation.32 This association is desirable and has potential to improve treatment outcome.31,33 The main purpose of percutaneous embolectomy and catheter fragmentation is the rapid restoration of pulmonary blood flow and perfusion, improving oxygenation, decreasing pulmonary pressure, and preventing cardiac failure, especially when pharmacologic thrombolysis and open surgery are contraindicated. These minimally invasive procedures have better results with recent embolus compared to older and more organized clots. Generally, 3 weeks is the time limit to indicate mechanical thrombectomy.12 Clots causing massive pulmonary embolism have been described typically as long, cohesive, worm-shaped segments that can be removed in intact segments as long as 15–50 cm with surgical instruments, suction cups, or embolectomy catheters. The histologic finding of a fibrin mesh indicates that
Catheter-directed thrombolytic regimens12,27
Agent
Administration
Urokinase
Infusion of 250,000 IU/h mixed with 2000 IU of heparin over 2 h, followed by an infusion of 100,000 IU/h of urokinase for 12–24 h Bolus of 10 mg, followed by 20 mg/h over 2 h (total of 50 mg); or 100 mg over 7 h Infusion of 1000 IU/h, keeping the partial thromboplastin time at 1.5–2.5 times the upper normal limit
tPA Heparin (in association with urokinase)
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Textbook of peripheral vascular interventions Table 99.3
Advantages and disadvantages of different catheter-based devices used for PE*12
Device
Advantages
Disadvantages
Greenfield suction cup34
Available for more than 30 years Effective in 76% of cases Rapid reperfusion Available for several years Rapid reperfusion Effective in 87.5% of cases Potential reperfusion Aspiration and fragmentation of clot Effective in peripheral branches Potential reperfusion Aspiration and fragmentation of clot Effective in peripheral branches Rapid fragmentation
Multiple passes may be required Difficult manipulation Arrhythmias Moderate morbidity
Balloon angioplasty and fragmentation35 Hydrolyser/Oasis36 Angiojet37 Rotatable pigtail catheter38 Arrow-Trerotola39 Amplatz (ATD)14
Rapid fragmentation Effective in old organized clots Rapid fragmentation
Wallstent/Z stent40
Rapid reperfusion
Low power Low efficacy in larger vessels Moderate efficacy Potential trauma to vessel Potential trauma to vessel Limited experience Potential trauma to vessel Difficulty in steerability Potential trauma to vessel Displacement
*Note: Most of these devices are not FDA-approved for use in the pulmonary artery, and were reported as anecdotal or small case series.
the clot arose, maturated, and embolized from a distant site. One may speculate that massive pulmonary emboli that cause hypotension, severe hypoxemia, or cardiac arrest tend to be more cohesive, whereas emboli that induce less severe symptoms tend to fragment. The firm consistency of massive central pulmonary emboli facilitates removal by suction.32 The selection of the device and technique to be used in the treatment of PE depends on the equipment availability and the expertise of the interventional radiologist. As seen in Table 99.3, each procedure/technique has particular advantages and disadvantages and there is no universal best option. The ideal thrombectomy catheter should be low-cost, easy to use and to position, and able to promote adequate removal or fragmentation of emboli. Greenfield, in 1969, developed the first prototype device for catheter embolectomy. This device is commercially available, and consists of a 10-French steerable catheter with a 5–7 mm plastic cup attached to its tip. Through manual suction with a large syringe, it allows removal of clot, but this usually requires several passages. In a series of 46 patients treated with this device, rapid hemodynamic improvement was seen in most patients, with 70% survival rate after 30 days.34 The rotatable pigtail catheter is a custom-made, hightorque device for clot disruption that employs a 5-French pigtail catheter with a radio-opaque tip and 10 side-holes used for angiographic contrast material injection. There is also an oval side-hole in the outer aspect of the beginning of the pigtail curve for passage of the guidewire, which serves as a central axis around which the catheter rotates. The pigtail catheter is introduced into a flexible 5.5-French sheath with a radioopaque tip and used with a 0.035-inch J wire with a movable core. The pigtail catheter is rotated around the guidewire
using an electric motor or manually with a handle connected to the proximal end of the catheter, and can be advanced or withdrawn over the wire that serves as a guide rail.38 The Arrow-Trerotola device is a low-speed mechanical thrombectomy system that uses a self-expandable metal basket measuring 9–15 cm in diameter when expanded. It is placed over a 0.035-inch guidewire and has an 8-French constraining catheter. This device is potentially more useful for treating older and more organized clots where other devices show decreased success rates; however, a case report demonstrating its clinical usefulness reported difficulties in directing the catheter into some target vessels, and the safety of this device in native vessels is unproven.12,39 Stent placement for pulmonary artery recanalization in the PE setting has been suggested in two case reports. This appears to be an option when chemical thrombolysis is contraindicated and mechanical fragmentation/removal does not lead to satisfactory results, especially with organized thrombi.40 Percutaneous suction thrombectomy Many different techniques and devices have been designed to remove and fragment clot, but they may not be technically easy or accessible in various hospitals and practice settings. Two-thirds of patients who die of pulmonary embolism, do so within 1 hour.2,5 If emergency embolectomy is to be effective, it must be widely and immediately available. One type of percutaneous pulmonary suction thrombectomy technique, published originally in 1997, uses readily available components and is capable of rapidly removing large amounts of clot. A 16-French, 40-cm-long Check-Flo II Introducer sheath (Cook), designated as a stationary sheath, is advanced through a transfemoral venous access. A 14-French, 90-cm-long
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Interventional therapy for pulmonary embolism Ultrathane non-tapered catheter (Cook) is used as the suction catheter. It is mounted coaxially over a 6-French, 97-cm multipurpose C Envoy guiding catheter (Cordis) to provide the stiffness and stepwise taper necessary for advancement past the pulmonary valve. Points of resistance to clot removal can be encountered at the pulmonary valve, at the entry into the stationary sheath and, most pronounced, at the valve of the stationary sheath. To minimize this problem a 14-French peelaway introducer sheath (Braun) is inserted coaxially into the stationary sheath, until the hubs of the peel-away and stationary sheath touch. Therefore, the peel-away sheath is only used to overcome the friction at the hub of the stationary sheath, and to prevent amputation of the clot piece which is being removed. Thus, it is not peeled away. Clot is aspirated with a 50-ml syringe and removed with the peel-away sheath to prevent clot amputation at the hub of the stationary sheath (Figure 99.1).32,41 The recommended step-by-step sequence for suction thrombectomy is: 1. dilation of the femoral access tract over a guidewire in the inferior vena cava, and insertion of the 16-French stationary sheath; 2. placement of a pulmonary angiographic catheter proximal to the clot; 3. over-the-wire exchange of the coaxial peel-away sheathguiding catheter-suction catheter assembly; 4. engagement of a Glidewire in a segmental pulmonary artery; 5. telescopic advancement of the guiding catheter and suction catheter over the Glidewire; 6. suction with the guiding catheter; 7. suction with suction catheter once the guiding catheter has been retracted (Figure 99.2). To avoid the risk of air embolism, the suction catheter is halted in the most distal portion of the peel-away sheath, during removal, and the sheath and suction catheter are removed as a unit from the stationary sheath. Initial peripheral compacting of clot, for example with an angioplasty balloon, can be useful in producing long cohesive retrievable pieces. Additionally, suction thrombectomy may be
Figure 99.2
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Figure 99.1 Suction catheter assembly: guidewire, guiding catheter (6 French), suction catheter (14 French), peel-away sheath (14 French) and stationary sheath (16 French).
associated with pharmacologic lysis and clot fragmentation or maceration, at the operator’s discretion. Of note, the authors recommend that suction thrombectomy be done while patients are on a pacing pad, in order to easily manage arrhythmias. Further experience with pulmonary suction thrombectomy in 11 hemodynamically unstable patients has been reported. Results included an average decrease in pulmonary artery pressure of 6 mmHg, increase in paO2 of 54 mmHg, and decrease in paCO2 of 3 mmHg. Adjunct tPA lysis was used in half of the cases, with an average dose of 4 mg (range: 2–8). Survival was 90% after 2 months.42 Inhaled nitric oxide: a powerful adjuvant to suction thrombectomy There are no specific imaging guidelines regarding endpoints for transcatheter therapy, and procedures are typically ended when oxygenation, systemic blood pressure, heart rate, and pulmonary arterial pressures improve.12,32 With suction thrombectomy, blood pressure and peripheral oxygenation usually improve relatively quickly after a few larger clots have
In-vitro model showing sequential clot suction with the guiding catheter (6 French) and suction catheter (14 French).
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Figure 99.3 36-year-old man presented hemodynamically unstable to the emergency department after a motor vehicle accident. (a) CT angiogram showing clot in both pulmonary arteries and a left pleural effusion. (b) Angiogram before clot removal. Clot is outlined by contrast material in the right descending pulmonary artery. Note the clot in the truncus anterior and hypoperfusion of the right upper lobe. (c) Clot fragments removed by suction thrombectomy. (d) Final left-sided pulmonary angiogram after the catheter moved from the right to the left pulmonary artery shows a cleared left pulmonary artery and improved but patchy perfusion of the right lung. (Reprinted with permission from reference 41.)
been removed. Usually, end-tidal CO2 tends to normalize compared with partial arterial CO2 pressure. However, a long duration of pulmonary artery occlusion may precipitate microcirculatory vasoconstriction that persists even after removal of the originally causative clot (Figure 99.3). This is analogous to what is encountered in advanced coronary and peripheral thrombotic arterial ischemia. In these situations, despite clot removal, vasodilators may be needed to improve flow through the microcirculation. The clinical value of intravenous vasodilators such as nitroglycerin and sodium nitroprusside is limited in the setting of pulmonary embolism and hemodynamic instability, as a result of their predominant systemic vasodilatory effects, which would worsen hypotension. When clot removal alone does not produce sufficient hemodynamic and respiratory improvement, inhaled nitric oxide (iNO) should be considered as a possible adjunct treatment alternative. iNO has received attention as a selective
pulmonary vasodilator, improving blood gases in different types of lung injury, including acute respiratory distress syndrome, primary pulmonary hypertension, and chronic pulmonary thromboembolism.41 iNO acts as a selective pulmonary vasodilator because of its rapid inactivation by binding with hemoglobin, which limits potential systemic effects. Moreover, it causes specific vasodilation in the well-ventilated segments of the lung, not only decreasing pulmonary arterial pressure but also improving the ventilation/perfusion relationship. iNO binding to hemoglobin leads to formation of methemoglobin, which, although not directly toxic, cannot carry oxygen. Its accumulation can significantly reduce the oxygen-carrying capacity of blood. Methemoglobin formation is minimal at iNO levels as high as 100 ppm; however, monitoring of its levels is mandatory. iNO doses used in association with suction thrombectomy have been reported in the 20–40 ppm range.41
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Figure 99.4 61-year-old man presented with PE, after a plane trip. A conventional arteriogram of the right pulmonary artery demonstrates subsegmental filling defects in the right upper lobe artery with complete occlusion of the right middle and lower lobe arteries with an associated sharp meniscus. Pathologic analysis of the aspirated thrombus revealed extensive intraluminal extension of bronchogenic carcinoma, which had only a relatively small extraluminal component. (Reprinted with permission from reference 43.)
Tumor thromboembolism: an important differential diagnosis Despite the inevitable decline in the use of conventional pulmonary arteriography for diagnostic purposes and the increased use of CT pulmonary angiography, it is crucial that interventional radiologists maintain a critical diagnostic eye. Not all filling defects within the pulmonary arterial circulation represent bland thromboembolism, but may represent tumor emboli (Figure 99.4). This may go undiagnosed unless the interventional radiologist recognizes this and sends a sample of the thrombus for pathologic examination. The identification of tumor thromboemboli may serve to alter future workups, provide crucial prognostic information to the patient and family, and invariably affect treatment options. Indeed, tumor
thromboembolism may be the presenting sign of an underlying malignancy. The inability to obtain a significant amount of thrombus despite aggressive pulmonary suction thrombectomy, difficulty performing mechanical clot disruption secondary to adherence to the vessel wall, and prevention of guidewire passage beyond the filling defect should raise flags and should lead to sending a sample of the clot to pathology to exclude an underlying neoplastic thrombus (Figure 99.5). The presence of a tumor clot within the pulmonary artery may necessitate more aggressive techniques to ensure vessel patency such as stent placement.43 In conclusion, the value and efficacy of anticoagulation and thrombolysis in the setting of PE is clear. Nonetheless, some patients who present with massive PE are hemodynamically unstable, and cannot afford to wait for the slow restoration of pulmonary flow achieved with those approaches. In this setting, fast interventional techniques are clearly indicated.
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Figure 99.5 51-year-old man referred for suction thrombectomy: (a) pulmonary CT angiogram demonstrates large bilateral pulmonary emboli; (b) histopathologic analysis with cytokeratin staining of thrombus removed from the pulmonary arteries revealed atypical cells of epithelial origin (renal cell carcinoma). (Reprinted with permission from reference 43.) (See Color plates.)
REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9.
10. 11.
12. 13.
14. 15. 16. 17.
Giuntini C, DiRicco G, Marini C et al. Pulmonary embolism: epidemiology. Chest 1995; 107: 3S–9S Wood KE. Major pulmonary embolism: review of a pathophysiologic approach to the golden hour of hemodynamically significant pulmonary embolism. Chest 2002; 121: 877–905 Goldhaber SZ. Pulmonary embolism. Lancet 2004; 363: 1295–305 Kucher N, Rossi E, De Rosa M et al. Massive pulmonary embolism. Circulation 2006; 113: 577–82 Donaldson GA, Williamson C. A reappraisal of application of the Trendeleburg operation to massive fatal embolism. N Engl J Med 1963; 268: 171–4 Goldhaber SZ, Elliott CG. Acute pulmonary embolism: part I: epidemiology, pathophysiology, and diagnosis. Circulation 2003; 108: 2726–9 Worsley DF, Alavi A, Aronchick JM et al. Chest radiographic findings in patients with acute pulmonary embolism: observations from the PIOPED Study. Radiology 1993; 189: 133–6 Fromm RE Jr. Cardiac troponins in the intensive care unit: common causes of increased levels and interpretation. Crit Care Med 2007 (in press) PIOPED Investigators. Value of the ventilation/perfusion scan in acute pulmonary embolism: results of the prospective investigation of pulmonary embolism diagnosis (PIOPED). JAMA 1990; 263: 2753–9 Stein PD, Fowler SE, Goodman LR et al. Multidetector computed tomography for acute pulmonary embolism. N Engl J Med 2006; 354: 2317–27 Stein PD, Hull RD. Relative risks of anticoagulant treatment of acute pulmonary embolism based on an angiographic diagnosis versus a ventilation/perfusion scan diagnosis. Chest 1994; 106: 727–30 Uflacker R. Interventional therapy for pulmonary embolism. J Vasc Interv Radiol 2001; 12: 147–64 Konstantinides S, Geibel A, Olschewski M et al. Association between thrombolytic treatment and the prognosis of hemodynamically stable patients with major pulmonary embolism: results of a multicenter registry. Circulation 1997; 96: 882–8 Uflacker R, Stange C, Vujic I. Massive pulmonary embolism: preliminary results of treatment with the Amplatz thrombectomy device. J Vasc Interv Radiol 1996; 7: 519–28 Dalen JE, Alper JS. Natural history of pulmonary embolism. Prog Cardiovasc Dis 1975; 17: 259–70 Barritt DW, Jordan SE. Anticoagulant drugs in the treatment of pulmonary embolism: a controlled trial. Lancet 1960; i: 1309–12 Jones TK, Barnes RW, Greenfield LJ. Greenfield vena cava filter: rationale and current indications. Ann Thorac Surg 1986; 42: S48–55
18. 19. 20. 21. 22.
23. 24. 25. 26.
27. 28. 29. 30. 31. 32. 33.
Hirsh J, Anand SS, Halperin JL et al. Guide to anticoagulant therapy – heparin; a statement for health care professionals from the American Heart Association. Circulation 2001; 103: 2994–3018 Agnelli G, Iorio A, Renga C et al. Prolonged antithrombin activity of low-molecular-weight heparins: clinical implications for the treatment of thromboembolic diseases. Circulation 1995; 92: 2819–24 Columbus Investigators. Low-molecular-weight heparin in the treatment of patients with venous thromboembolism. N Engl J Med 1997; 337: 657–62 Simonneau G, Sors H, Charbonnier B et al. A comparison of lowmolecular-weight heparin with unfractioned heparin for acute pulmonary embolism. N Engl J Med 1997; 337: 663–9 Buller HR, Davidson BL, Decousus H et al. Subcutaneous fondaparinux versus intravenous unfractionated heparin in the initial treatment of pulmonary embolism. N Engl J Med 2003; 349: 1695–702 Piazza G, Goldhaber SZ. Acute pulmonary embolism: part II: treatment and prophylaxis. Circulation 2006; 114: e42–7 Ridker PM, Goldhaber SZ, Danielson E et al. Long-term low-intensity warfarin therapy for the prevention of recurrent venous thromboembolism. N Engl J Med 2003; 348: 1425–34 Jamieson SW, Auger WR, Fedullo PF et al. Experience and results of 150 pulmonary thromboendarterectomy operations over a 29-month period. J Thorac Cardiovasc Surg 1999; 40: 135–7 Leacche M, Unic D, Goldhaber SZ et al. Modern surgical treatment of massive pulmonary embolism: results in 47 consecutive patients after rapid diagnosis and aggressive surgical approach. J Thorac Cardiovasc Surg 2005; 129: 1018–23 Goldhaber SZ. Thrombolitic therapy for pulmonary embolism. Semin Vasc Surg 1992; 5: 69–75 The STILE investigators. Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischemia in the lower extremity. The STILE trial. Ann Surg 1994; 220: 251–8 Trouillas P, Derex L, Philippeau F et al. Early fibrinogen degradation coagulopathy is predictive of parenchymal hematomas in cerebral rt-PA thrombolysis: a study of 157 cases. Stroke 2004; 35: 1323–8 Brady AJ, Crake T, Oakley CM. Percutaneous catheter fragmentation and distal dispersion of proximal pulmonary embolus. Lancet 1991; 338: 1186–9 Fava M, Loyola S, Flores P et al. Mechanical fragmentation and pharmacologic thrombolysis in massive pulmonary embolism. J Vasc Interv Radiol 1997; 8: 261–6 Lang EV, Barnhart WH, Walton DL et al. Percutaneous pulmonary thrombectomy. J Vasc Interv Radiol 1997; 8: 427–32 Tajima H, Murata S, Kumazaki T et al. Hybrid treatment of acute massive pulmonary thromboembolism: mechanical fragmentation
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34. 35. 36.
37. 38.
with a modified rotating pigtail catheter, local fibrinolytic therapy, and clot aspiration followed by systemic fibrinolytic therapy. AJR 2004; 183: 589–95 Greenfield LJ, Proctor MC, Willians DM et al. Long-term experience with transvenous catheter pulmonary embolectomy. J Vasc Surg 1993; 18: 450–8 Handa K, Sasaki Y, Kiyonaga A et al. Acute pulmonary thromboembolism treated successfully by balloon angioplasty: a case report. Angiology 1988; 8: 775–8 Michalis LK, Tsetis DK, Rees MR. Case report: percutaneous removal of pulmonary artery thrombus in a patient with massive pulmonary embolism using the Hydrolyser catheter: the first human experience. Clin Radiol 1997; 52: 158–61 Koning R, Cribier A, Gerber L et al. A new treatment for severe pulmonary embolism. Circulation 1997; 96: 2498–500 Schmitz-Rode T, Gunther RW, Pjeffer JG et al. Acute massive pulmonary embolism: use of a rotatable pigtail cathter for diagnosis and fragmentation therapy. Radiology 1995; 197: 157–62
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41. 42.
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Rocek M, Peregrin J, Velimsky T. Mechanical thrombectomy of massive pulmonary embolism using an Arrow-Trerotola percutaneous thrombolitic device. Eur Radiol 1998; 8: 1683–5 Haskal ZJ, Soulen MC, Huetti EA et al. Life-threatening pulmonary emboli and cor pulmonale: treatment with percutaneous pulmonary artery stent placement. Radiology 1994; 191: 473–5 Faintuch S, Lang EV, Cohen RI et al. Inhaled nitric oxide as an adjunct to suction thrombectomy for pulmonary embolism. J Vasc Interv Radiol 2004; 15: 1311–5 Faintuch S, Lang EV. Percutaneous pulmonary suction thrombectomy: further experience and lessons learned. Proceedings of the 29th Annual Scientific Meeting of the Society of Interventional Radiology,Phoenix, March, 2004. J Vasc Interv Radiol 2004; 15: S152–3 Brecher CW, Lang EV. Tumor thromboembolism masquerading as bland pulmonary embolism. J Vasc Interv Radiol 2004; 15: 293–6
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Superior and inferior vena cava thrombosis J Pisco and M Duarte
First described by William Hunter in 175,1 superior vena cava (SVC) syndrome is an uncommon but serious condition that requires immediate intervention. The typical symptoms of SVC obstruction are dyspnea, cough, and (less commonly) pain, syncope, dysphagia, and hemoptysis. The most important physical findings are the increased collateral veins covering the anterior chest wall and the dilated neck veins, with edema of the face, both arms, and chest. The chest x-ray film usually shows widening of the superior mediastinum. SVC syndrome rarely is life threatening; however, it is often associated with distressing complications and cognitive dysfunction due to cerebral venous hypertension.2
Causes Obstruction of the SVC has a variety of malignant and benign entities. Most cases (> 85%) are associated with advanced malignancy, either a primary thoracic malignancy (lung or mediastinal cancer), lymphoma, or metastatic tumor with obstruction caused by tumor invasion or extrinsic compression of the SVC.3–5 Lung cancer is the most frequent malignant cause (80%), with superior vena cava syndrome (SVCS) in 3–4% of these patients.6 Up to 15% of patients with bronchogenic carcinoma develop SVC syndrome, and usually small cell carcinoma is the cytopathologic diagnosis.7 SVC syndrome is estimated to occur in 3–8% of lymphoma cases, with symptoms secondary to extrinsic compression of the cava by enlarged anterior mediastinal lymph nodes. Metastatic disease to the thorax is seen in a variety of solid tumors, with breast and testicular cancer having the highest frequency. Symptomatic SVC obstruction also may occur from benign conditions that may not change life expectancy.8 SVCS has a benign cause in 5–15% of cases, with the frequency increased recently due to the more frequent use of vascular access devices for infusion of fluids and antibiotics, chemotherapy, and alimentation. Other benign causes of SVC obstruction are compression from mediastinal fibrosis, thoracic aortic aneurysm and iatrogenic etiologies secondary to invasive monitoring devices (cardiac pacemaker electrodes, pulmonary artery, and central venous monitoring catheters).4 In the pediatric population SVCS is a rare entity, usually in association with previous cardiac surgery or external compression and with congenital SVC obstruction.9 858
SVC obstruction types were described by Stanford:10 type I – partial SVC obstruction up to 90%, with patency of the azygos vein; type II – near complete to complete obstruction with patency and antegrade flow in the azygos vein; type III –near complete to complete obstruction with reversal of blood flow in the azygos vein; type IV – complete obstruction in one or more of its major tributaries, including the azygos system.
Causes of IVC obstruction Obstruction of the inferior vena cava (IVC) may result from intrinsic and extrinsic factors: thrombus, extension of a tumor, extrinsic compression, or intrinsic caval disease. Thrombus is a major cause of obstruction11,12 often by superior extension of idiopathic thrombophlebitis in the lower extremities or pelvis. Thrombus can also be secondary to more generalized conditions such as dehydration, sepsis, localized inflammation, pelvic inflammatory disease, coagulopathy, congestive heart failure, immobility, trauma (direct on indirect) or severe exertion.11,13 Iatrogenic thrombosis may be due to surgery in the lower extremities or to direct caval manipulation.11,13 Tumor invasion is most frequently associated with renal tumors,14 more commonly from the right kidney, presumably because of the shorter renal vein length on that side. Tumor thrombus from a renal carcinoma usually extends in a superior direction, not infrequently into the right atrium, but thrombosis of the IVC below the renal veins can occur. Other tumors that can extend into the IVC include adrenal, pancreatic, and hepatic carcinoma; Wilms tumor; and metastatic disease in the retroperitoneal lymph nodes (often from ovarian, cervical or prostatic carcinoma).11,13 Extrinsic compression is usually due to retroperitoneal adenopathy and is most frequently involved at the L2–L3 level.11 Adenopathy may be due to metastatic disease, lymphoma, or granulomatous diseases such as tuberculosis. Other sources of external compression include hepatic masses or hepatomegaly; pancreatic, renal, and adrenal tumors or masses; aortic aneurysms; retropenitoneal hematomas or neoplasms and retroperitoneal fibrosis. Ascites has been shown to compress the suprahepatic IVC directly. VCI can be evaluated with cavography, magnetic resonance imaging and computed tomography (CT). Although magnetic resonance offers multiplanar imaging, cavography is often necessary to exclude intraluminal tumor extension. CT is sen-
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Superior and inferior vena cava thrombosis sitive for intracaval thrombus and compression. Venography demonstrates well the resultant collateral pathways. Congenital caval anomalies, such as caval interruption with azygos continuation, can be diagnosed as acquired cava disease. With obstruction of normal flow in the IVC, blood from the lower extremities and pelvis returns to the right side of the heart through deep and superficial venous collateral vessels. The common resulting venous collateral pathways can be divided into four groups: deep, intermediate, superficial, and portal.15 These pathways are well visualized with venography, but certain rare congenital anomalies of the IVC may mimic their appearance.
Treatment Even in patients with limited life expectancy, palliation of SVC syndrome is required to achieve comfort and improve the patient’s quality of life. Five types of treatment are available for patients with SVC syndrome: medical therapy, radiotherapy, chemotherapy, surgical bypass, and endovascular techniques. General medical therapies are bed rest, elevation of the head, systemic anticoagulation, steroids to relieve laryngeal and cerebral edema and diuretic therapy to relieve peripheral edema. They have limited clinical benefit and are usually a last-resort attempt to alleviate symptoms after other treatments have been unsuccessful.16,17 Radiation therapy is widely advocated for SVC syndrome caused by radiosensitive tumors and, when effective, provides considerable symptom relief2 by reducing tumor volume18 in up to 80% of patients; however, relief of symptoms may not be achieved for up to 4 weeks. Common side effects include dysphagia, nausea, and vomiting or may result an immediate and dramatic progression of SVCS due to tumor edema. The benefits are often temporary, however, with most patients developing recurrent symptoms before dying of the underlying disease.17 If symptoms recur, further radiation therapy is not an option and patients will require another type of treatment. With chemotherapy, SVC syndrome may recur after initial treatment owing to tumor regrowth. Non-small cell cancers usually do not respond well to chemotherapy. The venous engorgement may increase due to hyperhydration.19 Before the development of endovascular techniques for treating SVC syndrome, the only remaining treatment option (particularly in patients with benign disease) was surgical bypass. Surgical palliation by means of a venous bypass graft is difficult to justify in those patients because it involves a major intervention, with sternotomy. There are limited indications for surgery, while radiation therapy and chemotherapy are not completely or promptly effective.20 Refractory cases have a serious prognosis particularly when airway obstruction or brain edema persists.2 Balloon angioplasty does not provide long-term palliation in venous stenosis,21 because they are resistant to dilation and have a high recurrence rate due to elastic recoil and tumor evolution. The use of endovascular methods has become increasingly important. Catheter-directed thrombolysis and/or endovascular stent placement to treat SVCS are used in malignant and
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benign diseases.22 Thrombolytic treatment was initially suggested in 1974 to treat pacemaker-wire-induced SVC thrombosis.23 Since then, many investigators have documented the efficacy of this treatment.24–26 Performing catheter-directed thrombolysis before stent deployment has many benefits such as the reduction the thrombus volume, reduction of the amount of potential embolic material that may be released after decompression of the venous system by the stent placement; reduction of the length of the obstruction, and reduction of the length or the number of stents required (thus decreasing the amount of potentially thrombotic foreign material placed in the vessel). A smaller thrombus volume also allows incremental stent expansion to a greater diameter in the vessel. Contraindications to thrombolysis are: contraindication to anticoagulation, bleeding disorder, pregnancy or recent delivery (< 2 weeks), metastatic cancer with brain or spinal cord involvement or history of hemorrhagic stroke.22 Endovascular stents have been proposed and tested with success, as a mechanical support introduced percutaneously to normalize the SVC circulation (19).19 Several studies have investigated stent placement in the SVC to treat malignant disease.27–33 Stent placement can be performed with four types of stents. The first studies used Gianturco stents. Later, Palmaz stents, Wallstents and nitinol stents were used. The Gianturco Z-stent has excellent radial expansible strength and is commonly used in large-diameter vessels. The Palmaz balloonexpandable stent can be positioned accurately and has a high radial force when inflated in strictures caused by tumors or those associated with radiation fibrosis.34,35 They are usually placed through a 9- to 10-F sheath. The main disadvantages of the Palmaz stent are its short length and lack of flexibility. Wallstents and nitinol stents are longer than Palmaz stents but have less radial strength and are somewhat more difficult to position precisely.36,37 The disadvantage of the Wallstent endoprosthesis is the lower radio-opacity and the susceptibility to retraction after placement, thus the stent may be misplaced. This endoprosthesis, however, is flexible and can be withdrawn if misplacement occurs and removed through the femoral sheath if complete deployment has not been achieved. Nowadays nitinol stents are the most frequently used. Chest computed tomography (CT) must be performed before stent placement to determine: the nature of the obstruction, the length of the stenoses, the presence of a simple compression of the SVC or a direct tumor invasion, the pattern of collateral return, and the confluence of the brachiocephalic veins.19
Endovascular treatment procedures for SVCS Endovascular procedures are performed in one angiography unit with local anesthetic, without sedatives or general anesthesia. Superior vena cavography, using intravenous digital subtraction angiography, is obtained to document the extent and degree of stenosis or occlusion. If the SVC is the only vein involved, the right femoral vein is punctured and attempts are made to cross the stenosis or occlusion with fluoroscopy control. If it is impossible to cross the SVC with a guidewire by the femoral route, the wire is advanced across the stenoses
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Figure 100.1 (a) Phlebography of right axillary vein by right brachial approach shows: occlusion of right subclavian vein and superior vena cava; (b) Superior vena cava phlebography by right femoral vein shows severe stenosis of SVC; and (c) superior vena cava phlebography following stenting shows normal calibre of SVC.
by an arm access. A 4-French diagnostic catheter introduced via venous brachial access, generally on the right side, is placed at the caudal extremity of the right brachiocephalic vein, which allows opacification to control the confluence of the brachiocephalic veins during the stent deployment. A 0.035inch hydrophilic angled guidewire, supported by a multipurpose or Cobra 6-French catheter is used to cross the stricture (Figures 100.1 and 100.2). In patients with occlusion of the SVC and no contraindication to thrombolysis, a multi-side-hole catheter can be placed in the thrombus for a catheter-directed thrombolysis. A solution prepared with 500,000 IU of urokinase in 250 ml of 0.9% NaCl is delivered in the catheter (50,000–100,000 IU/hour). Thrombolysis is performed within 24–48 hours, and controlled by venography. Before the procedure, heparin is
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administered (5,000 IU) in the SVC through the catheter. Lesions that involve the brachiocephalic veins, which are more peripheral and tortuous, are commonly treated by an arm access with a self-expanding stainless-steel Wallstent or a nitinol stent. Angiography of the final stent placement is then performed. Technical success is defined as successful manipulation of a guidewire across the venous stenosis. Clinical success is the complete or partial resolution of edema and the return of cognitive functions. After the procedure, the patients continue the treatment with intravenous heparin and antiplatelet agents or warfarin. Patients with underlying malignancy receive anticoagulation for as long as clinically feasible. In patients with benign disease, anticoagulation is discontinued at 6-month follow-up if clinical patency persists. A second vena cavogram is obtained to confirm the absence of thrombus.
(c)
Figure 100.2 (a) Right axillary phlebography by right femoral vein showing occlusion of right subclavian vein and SVC; (b) SVC phlebography following stenting; (c) nitinol stent in place.
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Figure 100.3 (a) Right subclavian phlebography shows extensive collateral circulation due to occlusion of SVC; (b) following stenting the collateral circulation is not shown.
When it is impossible to cross the stenosis from bottom to top, the guidewire can be placed by a brachial approach through the stenosis, in the direction of the inferior vena cava, where the guidewire can be caught by a snare and withdrawn through the 9-French femoral sheath. In this way, all stents could be implanted via femoral access (Figures 100.3 and 100.4). Selection of the correct stent size is the major determinant of Wallstent or nitinol stent patency. For implantation in the SVC, the stent diameter must be 2 mm greater than that of the SVC, to prevent stent migration and to compensate for neointimal growth. The stent length must be adapted to the length of the stenosis to cover the entire lesion. If necessary, more than one stent may be used. The cephalic stent is placed first, followed by the caudal one and the two overlap each
(a)
other to cover the entire lesion. When implanted, if the stent shows a mild residual stenosis balloon angioplasty should be performed to complete the expansion. The persistence (or the recurrence) of a stenosis within the stent creates a high risk of thrombosis or restenosis by intimal hyperplasia. In a stenosis near the confluence with the SVC, sometimes is necessary to cover the ostium of one brachiocephalic vein to preserve the other one (Figure 100.5). The patency of one of two brachiocephalic veins is generally sufficient to avoid recurrence of the SVCS. Placement of two stents in a Y shape could also represent a solution for this problem. Placement of a stent both in the left brachiocephalic vein and in the SVC may be difficult, particularly when the left brachiocephalic vein runs at a right angle to the SVC or when its
(b)
Figure 100.4 (a) Superior vena cava phlebography: stenosis of the upper-third of the SVC and occlusion of the distal end; (b) after stent placement, the caliber of the SVC is normal.
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(b)
Figure 100.5 (a) Phlebography showing stenosis at the ostium of the left brachiocephalic vein; (b) following stent placement, the stenosis is not shown.
caudal portion has a stenosis. Because of its flexibility, the Wallstent or a nitinol stent provides coverage of the two vessels in a single procedure, usually by means of one long stent only.19
Results In patients with IVC, although the improvement starts the next day, the complete relief takes 3–4 days. The most satisfying aspect of the endovascular treatment of SVCS is the almost universal relief of symptoms experienced by the patients, once endovascular decompression occurs they notice clinical improvement, often while still on the angiographic table. These treatments can be used also with success in benign causes of SVCS.38 In these non-neoplastic diseases, such as fibrosing mediastinitis or post-irradiation fibrosis, the challenge is to maintain a long-term patency in patients with an otherwise normal life expectancy. They may need further follow-up maintenance therapy19 and when recurrence occurs, repeated stenting can be performed successfully.38
Complications Some physiologic complications have been reported in stent treatment of SVCS. The rapid increase in venous return influences the circulatory system hemodynamic. The reperfusion achieved after stent placement might precipitate cardiac failure and/or pulmonary edema.39 This complication
is rare and is easily managed with diuretics, dopamine, steroids and oxygen. Electrocardiographic changes, blood pressure, oxygen content, respiratory sounds, and other physical signs should be monitored. The stent-treated vessel might be narrowed by a fibroproliferatory reaction, with inflammatory cells.40,41 Antiplatelet therapy decreases this unfavorable reaction.42 SVC perforation may cause mediastinal hemorrhage or hemopericardium with cardiac tamponade. Restenosis or reocclusion within the stent is usually due to tumor ingrowth, secondary thrombosis, or both. Thrombosis can be successfully treated with selective thrombolysis or clot aspiration. Tumor ingrowth may be managed by balloon angioplasty or a second stent within the first.19 Other complications of stent placement in the SVC are not specific and are due to the invasive percutaneous procedure, for example hematoma at the puncture site, infection, and transient exacerbation of chronic renal insufficiency.
Conclusion SVCS is an extremely debilitating disorder. Endovascular thrombolysis or percutaneous stent placement are safe and effective to treat this syndrome and can be considered the first choice of treatment due to the immediate and sustained symptomatic relief.22,32,43–45 Stents as a palliative treatment are very effective, because these patients with a limited life expectancy can return home to their families, with improved cognitive function, normal facial appearance, relief of severe headaches, full mobility of the upper extremities, and usually stay free of symptoms until death.
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REFERENCES 1. 2. 3. 4. 5. 6. 7. 8. 9.
10. 11. 12. 13. 14. 15. 16. 17. 18. 19. 20. 21. 22. 23. 24.
Hunter W. History of aneurysm of the aorta with some remarks on aneurysm in general. Med Observation Inquiries 1757: 1: 323 Lochnidge 5, Knibbe W, Doty D. Obstruction of superior vena cava. Surgery 1979; 85: 14–24 Mahajan V, Striznlan V. Van Ordstrand HS, Loop FD. Benign superior vena cava syndrome. Chest 1975; 6: 32–5 Chen JC, Bongard F, Klein SR. A contemporary perspective on superior vena cava syndrome. Am J Surg 1990; 160: 207–11 Comes MN, Hufnagel CA. Superior vena cava obstruction. Ann Thorac Surg 1975; 20: 344–51 Zollikofer CL, Antonucci F, Stuckmann C. Use of the Wallstent in the venous system including haemodialysis-related stenoses. Cardiovasc Intervent Radiol 1992; 15: 334–41 Scherck J, Kerstein MD, Stansel HC. The current status of vena caval replacement. Surgery 1974; 76: 209–33 Sheikh MA, Fernandez BB Jr, Gray BH. Endovascular stenting of nonmalignant superior vena cava syndrome. Catheter Cardiovasc Interv 2005; 65(3): 405–11 Ro PS, Hill SL, Cheatham. Congenital superior vena cava obstruction causing anasarca and respiratory failure in a newborn: successful transcatheter therapy. Catheter Cardiovasc Interv 2005; 65(1): 60–5 Stanford W, Jolles H, Ell 5, Chiu LC. Superior vena cava obstruction: venographic classification. AJR 1987; 148: 259–62 Kadir S. Diagnostic Angiography. Philadelphia: Saunders, 1986 Neiman HL, Yao JS. Angiography of Vascular Disease. New York: Churchill Livingstone, 1985 Harris RD. The etiology of inferior vena caval obstruction and compression. Crit Rev Clin Radiol NucI Med 1976; 8: 57–86 McCullough DL, Talner LB. Inferior vena caval extension of renal carcinoma: a lost cause? AJR 1974; 121: 819–26 Sonin AH, Mazer MJ, Powers TA. Obstruction of the inferior vena cava: a multiple-modality demonstration of causes, manifestations, and collateral. Radiographics 1992; 12: 309–22 Escalante CP. Causes and management of superior vena cava syndrome. Oncology 1993; 7: 61–8 Baker G, Barnes H. Superior vena cava syndrome: etiology, diagnosis, and treatment. Am J Crit Care 1992; 1: 54–64 Levitt S, Jones I, Kilpatnick S. Treatment of malignant superior vena cava obstruction: a randomized study. Cancer 1969; 24: 447–51 Hennequin LM, Fade O, Fays JG. Superior vena cava stent placement: results with the wallstent endoprosthesis. Radiology 1995; 196: 353–36 Chen JC, Bongard F, Klein SP. A contemporary perspective on superior vena cava syndrome. Am J Surg 1990; 160: 207–11 Elson JD, Becker CJ, Wholey MH. Vena caval and central venous stenoses: management with Palmaz balloon-expandable intraluminal stents. JVIR 1991; 2: 215–23 Kee ST, Kinoshita L, Razavi MK. Superior vena cava syndrome: treatment with catheter directed thrombolysis and endovascular stent placement. Radiology 1998; 206: 187–93 Williams D, Demos N. Thrombosis of superior vena cava caused by pacemaker wire and managed with streptokinase. J Thorac Cardiovasc Sung 1974; 68: 134–7 Mico G, Robles I, Catalan M et al. Superior vena cava syndrome caused by a pacemaker cable, treated with streptokinase. Rev Clin Esp 1985; 177: 358–61
25. 26. 27. 28. 29. 30. 31. 32. 33. 34. 35. 36. 37. 38. 39. 40. 41. 42. 43. 44. 45. 46.
Montgomery J, D’Souza V, Dyer R et al. Nonsurgical treatment of the superior vena cava syndrome. Am J Cardiol 1985; 56: 829–30 Blackburn T, Dunn M. Pacemaker-induced superior vena cava syndrome: consideration of management. Am Heart J 1988; 116: 893–6 Gaines PA, Belli AM, Anderson PB et al. Superior vena caval obstruction managed by the Gianturco Z stent. Clin Radiol 1994; 49: 202–8 Irving J, Dondelinger R, Reidy J et al. Gianturco self-expanding stents: clinical experience in the vena cava and large veins. Cardiovasc Intervent Radiol 1992; 15: 328–33 Rosch J, Uchida B, Hall L et al. Gianturco-Rosch expandable Z-stents in the treatment of superior vena cava syndrome. Cardiovasc Intervent Radiol 1992; 15: 319–27 Oudkerk M, Kuijpers TJ, Schmitz P1 et al. Self-expanding metal stents for palliative treatment of superior vena caval syndrome. Cardiovasc Intervent Radiol 1996; 19: 146–51 Shah R, Sabanathan S, Lowe RA et al. Stenting in malignant obstruction of superior vena cava. J Thorac Cardiovasc Sung 1996; 112: 335–40 Kazushi K, Sonomura I, Mitsuzane K et al. Self-expandable metallic stent therapy for superior vena cava syndrome: clinical observations. Radiology 1993; 189: 531–5 Dyet JF, Nicholson AA, Cook AM. The use of the Wallstent endovascular prosthesis in the treatment of malignant obstruction of the superior vena cava. Clin Radiol 1993; 48: 381–5 Palmaz J. Balloon expandable intravascular stent. AJR 1988; 150: 1263–9 Solomon N, Holey M, Janmolowski L. Intravascular stents in the management of superior vena cava syndrome. Cathet Cardiovasc Diagn 1991; 23: 245–52 Antonucci F, Salmonowitz E, Stuckmann G et al. Placement of venous stents: clinical experience with a self-expanding prosthesis. Radiology 1992; 183: 493–7 Watkinson AF, Hansell DM. Expandable Wallstent for the treatment of obstruction of the superior vena cava. Thorax 1993; 48: 915–20 Courtheoux P, Alkofer B, Al Refai M. Stent placement in superior vena cava syndrome. Ann Thorac Surg 2003; 75(1): 158–61 Yamagami T, Nakamura T, Kato T, Hemodynamic changes after self-expandable metallic stent therapy for vena cava syndrome. AJR Am J Roentgenol 2002; 178(3): 635–9 Palmaz JC. Intravascular Stents. RSNA 1991 Chansangavej C, Carrasco CH, Wallace 5 et al. Stenosis of the vena cava: preliminary assessment of treatment with expandable metallic stents. Radiology 1986; 161: 295–8 Kubota Y, Kichikawa K, Uchida H. Pharmacologic treatment of intimal hyperplasia after stent placement in the peripheral arteries: an experimental animal study. RSNA 1992 Beran S. Superior vena cava syndrome: potential of the intervention therapy. Cas Lek Cesk. 2006; 145(5): 349–52 Kim YI, Kim KS, Ko YC. Endovascular stenting as a first choice for the palliation of superior vena cava syndrome. J Korean Med Sci 2004; 19(4): 519–22 Garcia Monaco R, Bertoni H, Pallota G. Use of self-expanding vascular endoprosthesis in superior vena cava syndrome. Eur J Cardiothorac Surg 2003; 24(2): 208–11 Rousseau HP, PuelJ, Joffre FC et al. Self expanding endovascular prosthesis: an experimental study. Radiology 1987; 164: 709–14
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Introduction The hallmarks of venous insufficiency, varicose veins, and telangiectasias are exceedingly common. A San Diego epidemiological study has shown that more than 20% of women and half that number of men had signs of venous insufficiency.1 Presence of telangiectasias varied by gender, ethnicity, and age but prevalence of varicose veins varied only by gender and were more common in women. These conditions are termed primary venous insufficiency. When edema, hyperpigmentation, and venous ulcers or the scars of healed ulcers are present the applied term is chronic venous insufficiency. The prevalence of severe chronic venous insufficiency (CVI) is acknowledged to be 1–2% in Western civilization.2,3 Discarded theories of causation of CVI include stagnant blood pooling (stasis)4 and deprivation of skin oxygenation.5 Venous pressure is linked both to causation of CVI and varicose veins. It has been linked to cutaneous microangiopathy,6 and in the dermis and epidermis to the chronic changes of CVI.7 More importantly, venous hypertension is linked to valve failure and even valve destruction. This may eventually provide the medical community with a target for therapy.8 A focused approach using pharmacologic principles would be quite acceptable in the future to physicians and patients alike. Varicose veins (Figure 101.1) and telangiectasias (Figure 101.2) do not bother everyone. Men under age 60 often have no symptoms, even in the face of large varicosities. In contrast, young females with or without symptoms may be quite disturbed by the appearance of small telangectasias. Apart from appearance, dilated veins of any size may bother their owners because of the true symptoms. Characteristic symptoms include aching pain, burning pain, and itching easy leg fatigue and leg heaviness. All of these often poorly described symptoms worsen as the day progresses causing the victim to sit down in the late afternoon to elevate the leg for symptom relief. The anatomy of veins that are tributary to the great saphenous vein places them in an unsupported position under the skin, superficial to the superficial fascia (tela aponeurotica). This is in contrast to the great saphenous vein, which, in its saphenous compartment, is strongly supported between the superficial fascia and the deep fascia.9 The subcutaneous position of tributary veins renders them vulnerable to high venous pressure, which causes their elongation and dilation. It is the elongated and dilated tributary veins and even telangiectasias that press on somatic nerves and cause the well-known symptoms of aching and heaviness. Pressure on cutaneous nerves produces the burning pain of venous neuropathy and inflammation associated with the varices causes the itching 864
that may precede an eczematoid dermatitis. Indications for intervention for telangiectasias and varicose veins are listed in Table 101.1.
Varicose veins: surgical principles Principles guiding treatment of varicose veins were laid down in the 1950s by Mayo Clinic surgeons dedicated to full-time care of varicose veins.10 These principles were three in number: (1) to remove the great saphenous vein from ankle to groin; (2) to perform a thorough dissection of the venous tributaries to the saphenous vein at the saphenofemoral junction; and (3) to disconnect perforating veins from existing varicosities. The need to remove the saphenous vein from the circulation was confirmed by many prominent surgeons.12–14 The operations
Figure 101.1
Varicose veins.
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It remains important despite the lack of popularity of great saphenous stripping. Vein stripping is a somewhat morbid operation with a sometimes considerable painful hematoma and prolonged recovery time. The morbidity of great saphenous stripping can be avoided by destroying the vein in situ by using energy from electromagnetic waves. The energy can be derived from radiofrequency waves (VNUS Closure, Figure 101.3) or shorter laser light waves (endovenous laser therapy (EVLT), Figure 101.4). Both are delivered by an endovenous catheter, usually placed percutaneously. Both techniques result in greater than 90% success in ablation of the saphenous vein and can be considered standard techniques at this time. These techniques are described elsewhere in this volume.
Superficial venous ablation Figure 101.2
Telangectasias.
performed according to these principles led to long, anticosmetic scars, external skin sutures which were also anticosmetic, and a painful post-operative course with extended morbidity.15 In time, it was learned that the saphenous vein from ankle to knee need not be removed in all cases and that groin-to-knee stripping of the saphenous vein prevented nerve injury encountered in ankle-to-groin stripping. Thus, the first principle laid down by surgeons of the early 1950s was successfully challenged. The second principle of careful dissection and disconnection of tributaries to the saphenofemoral junction is violated when endovenous management of saphenous vein reflux is done by laser or VNUS Closure. The tributaries are left in the circulation but the saphenous vein is removed from the circulation.16,17 Leaving the saphenofemoral junction tributaries intact has not proven to lead to varicose recurrence. In fact, meticulous dissection of the saphenous tributaries has never been subjected to rigorous scrutiny. Thus, the second principle of varicose vein surgery appears to have been refuted. The third principle of careful perforator vein dissection and removal of varicose vein clusters is currently under challenge.
Varicose vein surgery today Removing the saphenous vein from the circulation has been the keystone in the arch of treating primary venous insufficiency.
Table 101.1 veins
Indications for intervention in varicose
Aching pain Leg heaviness Leg fatigue Superficial thrombophlebitis External hemorrhage General appearance
Removal of the saphenous vein from the circulation is an important first step in treating varices. Removing, obliterating, or destroying the varicosities themselves is the second step. It is something of a paradox that the patient’s complaint is the varicose veins and the treating physician’s interest is in taking from the circulation a structure that is invisible to patients and physician alike. The situation becomes especially stressful when a non-comprehending patient recovers from a well-performed saphenous ablation, removes the pressure dressing or stocking, looks down and sees that the varicose veins are still there. Varicose veins are most often treated by physical removal or phlebectomy. In the recent past, general and vascular surgeons favored using mosquito clamps for the removal of the varicose veins but for many the crochet hook came in vogue during the 1980s. At about the same time, dermatologists, under the influence of Robert Mueller began using specially designed and dedicated hooks. Descriptions of the crochet hook technique followed word-of-mouth information18,19 and by the time published descriptions appeared, specialized instrumentation had been developed to make the crochet hook obsolete.
Hook phlebectomy The technique of mini-phlebectomy using specialized instrumentation was developed by the Swiss dermatologist, Robert Muller, in the mid-1950s.20 He designed his own instruments and presented his techniques in 1966. Since that time, others have suggested modifications of the procedure and instrumentation.21–23 There are many advantages to varicose vein removal using variations of the Muller technique. The surgery, often referred to as ambulatory phlebectomy, is entirely outpatient, often done in a physician’s office. It is very simple, free of thromboembolic risks, and can be applied to all types of varicose veins. There is economy to the technique because there is a very simple infrastructure, little loss of patient work time, and careful extirpation of the varicose veins allows healthy vein trunks to be conserved. The scars can be practically invisible. In surgery as practiced by general surgeons and vascular surgeons, the mini-phlebectomy of Muller is a complement to saphenofemoral junction stripping and to
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(a)
(b) Figure 101.3
(a) RFA Generator; and (b) 6-French and 8-French RFA catheters.
endovenous techniques of saphenous ablation. Ramelet, a dermatologist from Lausanne, Switzerland, has said: “The drawbacks are minimal: The usual complications of any surgical technique and too easy accessibility to the poorly trained practitioner.”24 A number of terms have been applied to this technique including microsurgical phlebectomy, minisurgical phlebectomy, office phlebectomy, ambulatory stab avulsion phlebectomy, ambulatory phlebectomy, and Muller’s phlebectomy. The performance of this technique involves several steps. First, the varicose veins must be very carefully marked with the patient in the standing position using indelible ink. After adequate skin preparation and draping, local or tumescent anesthesia can be used or intravenous sedation combined with local or tumescent anesthesia. Through 2–3 mm stab incisions, the vein is grasped using a phlebectomy hook. It is then brought to the surface, secured with clamps, and extracted until it breaks off. The vein should be harvested completely, and the incisions need no suture if they are 1–2 mm in length.
A simple absorbable monofilament suture inverted under the skin can be used for incisions that stretch to 3–4 mm. Reinforcement with surgical tape and infiltration with longacting local anesthesia adds elegance to the procedure.
Post-operative compression After minisurgical ambulatory phlebectomy, post-operative compression becomes an important part of the operation. Areas that are difficult to compress include the dorsum of the foot, the popliteal fossa, and the proximal edge of the bandage. Post-operative pain is usually due to too much compression on the dorsum of the foot and yet a loose bandage in this area allows edema to develop. Careful bandaging will allow uniform pressure. This is also true at the knee where flexion and extension during ambulation may cause painful skin rubbing and blistering. The knee area should be protected carefully by appropriate padding.
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Figure 101.4
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EVLT generator.
Prevention of slipping of the proximal edge of the bandage can be achieved by adhesive. However, care must be taken to avoid skin irritation and blistering. Some operators use an elastic stocking applied over a stocking donner, and every surgeon practicing this technique uses his own method. Duration of compression depends upon the individual case and ranges from 48 hours for small superficial varicosities to 7–10 days for large varicose veins or persistent post-operative swelling or pain. Following removal of the compression dressing, an elastic stocking may be worn until all post-operative symptoms disappear. Claude Garde has described his results of ambulatory phlebectomy using the technique described above.25 The technique was utilized in 900 patients who were evaluated after 6 months, paying attention to scars, therapeutic results, neoangiogenesis, recurrence of varicose veins, symptom relief, and new signs of venous insufficiency. Brown hyperpigmentation was seen along the skin closure strips or as a result of hematoma inadequately controlled by compression bandaging in 7.2%. Recurrence of new varicose veins was seen in 3% of limbs, and this recurrence was defined as a vessel appearing in the same location with the same appearance as the extracted vessel as assessed by preoperative mapping. New varicose veins outside of this definition occurred in 1% of patients. Neoangiogenesis, or the appearance of blue or red capillaries (telangiectatic matting) around an incision or along the pathway of an extracted vessel occurred in 3.7% of cases. Edema occurred in a very few patients but deep venous thrombosis developed in five individuals, all of whom had popliteal fossa exploration, small saphenous vein surgery with or without gastrocnemius vein surgery. Paresthesias lasting longer than 6 months were seen in 0.6% of patients and these were limited to the external aspects of the foot. Stefano Ricci, whose book, Ambulatory Phlebectomy is available in English, has detailed his complications.16,17 His complications in 300 limbs were as follows: lymphocele: 1.6%, sensitive nerve damage: 0.9%, and persisting foot
edema, hemorrhage at home, and hematoma in the lower leg: 0.3% each.
Tumescent anesthesia Local and tumescent anesthesia are an important part of ambulatory phlebectomy. The technique is not native to general and vascular surgeons but has been used to a great extent by dermatologic surgeons and plastic surgeons.28 The tumescent technique becomes especially valuable in endovenous saphenous vein ablation described elsewhere in this volume. The anesthetic solution is comprised of 0.2% lidocaine in normal saline buffered with 1 mEq of sodium bicarbonate per 100 ml of solution. Goldman has described leaving epinephrine out of the solution29 in 100 cases prior to 1997 and then modified the technique to add epinephrine 1:100,000. The addition of epinephrine proved safe and reduced the incidence of hematoma and hyperpigmentation.30 Although Klein,28 who is the father of the technique, uses a microcannula less than 2.0 mm in diameter, his technique is more applicable to liposuction. For varicose vein surgery, it is well to perform the infiltration with 3-inch spinal needles of 22– 25 gauge. The anesthetic solution can be delivered through 20–50 cm3 syringes or more easily by using a peristaltic pump. The standard dosage of lidocaine with epinephrine for infiltration anesthesia is stated to be 7 mg/kg in the Physician’s Desk Reference and in the Astra/Merck Maximum Recommended Dosage Statement. There is no scientific publication that supports this dose and an experimental study has shown that toxicity of subcutaneous lidocaine is inversely proportioned to drug concentration. This supports the use of extremely dilute solutions. The dilute anesthetic agent combined with epinephrine causes peak levels of anesthetic agent to occur many hours after surgery is completed. Klein has stated that the safe dose of lidocaine is 35 mg/kg as used in tumescent anesthesia.
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In studying lidocaine levels using the technique described above, Goldman has found that “despite variability, the serum levels of lidocaine remain well within safety limits during infusion of tumescent solution and the first hours of surgical procedures.”31
Sclerotherapy No discussion of techniques of minimal invasion in varicose vein surgery would be complete without mentioning sclerotherapy. The fundamental principle of sclerotherapy is obliteration of the lumen of the vein so that no blood can flow through it. Injection sclerotherapy has been used for all sizes of varicose veins ranging from protuberant saccular varicosities to minute telangiectasias. Gradually, principles have been developed which allow the successful performance of sclerotherapy as well as satisfactory performance of ambulatory phlebectomy. In general, the first principle is that the smaller the vessel to be destroyed, the greater the success of sclerotherapy. A second principle is that varicose veins treated by sclerotherapy will recur if axial reflux through the great and small saphenous vein is not controlled first. This principle is currently being challenged. Sclerotherapy of varicose veins is most applicable in varicose veins persistent after ambulatory surgery, recurrent varicose veins following ambulatory surgery, and varicose veins in the aged or infirm when these veins are symptomatic. The fundamental mechanism of action of sclerotherapy is fibrotic obliteration of the vein lumen. The detergent sclerosants in use today denude the endothelium. If blood is present in the vein lumen, thrombus may form and this thrombus may defeat the objectives of complete fibrosis. Such postinjection thrombosis is best referred to in the presence of the patient as trapped blood. It is the most common side-effect of sclerotherapy and is a causative factor in development of postinjection pigmentation. Veins larger than 1 mm are particularly prone to thrombosis. When this occurs, the vein becomes black, raised and tender. In veins larger than 1 mm, an 18gauge needle can be introduced to allow expression of the trapped blood. Other complications of the procedure include post-injection hyperpigmentation which is a product of the inflammatory process that obliterates the injected veins. There is no treatment for post-injection hyperpigmentation but 90% of this will disappear within 1 year. Other side-effects, including skin ulceration and post-inflammatory telangiectatic matting, are less commonly seen. For most injections, a 3–5 ml plastic syringe can be used and this should be coupled to a 30- or 32gauge hypodermic needle. The syringes are filled from vials of 1–3% solution and diluted to appropriate strength. For FDAapproved sodium tetradecyl sulfate, this is 0.25% for telangiectasias and 0.5% for varices 1–3 mm in diameter. There is much dogma surrounding the practice of sclerotherapy, most of which is untrue. For example, there is no evidence for the dogmatic statement that crossing the legs brings on telangiectasias. Similarly, the instruction for patients to walk around the clinic for 15–30 minutes and then come back for an evaluation is unnecessary. Most practitioners of the art of sclerotherapy believe that external compression is essential to the process, and a small but growing number of
physicians believe that compression after injection of telangiectasias is totally unnecessary. An exception to this is the fact that large truncal varicose veins should be compressed with 20–30 mmHg stockings or elastic bandages. There is no agreement on duration of compression for these vessels. However, 24–72 hours is commonly the time allotted. Foam sclerotherapy Sclerosant foam has gradually come into use because it is effective, quick, efficient, and cheap. It is estimated to be 5–10 times more effective than sclerotherapy using identical concentrations.32 Its complications are identical to those of liquid sclerotherapy and are detailed above. The agent must be a detergent. Saline and dextrose will not foam and must be diluted to a proper strength for each patient and then foamed with unfiltered room air using the Tessari technique.33 The ratio of air to liquid sclerosant should be 4:1. Vascular access/treatment Vascular access for foam injection for varicose veins is usually through percutaneous access to the great saphenous vein above or below the knee. Direct cannulation of the saphenous vein as reported by other investigators34,35 can be omitted in favor of direct puncture of a varix.36 Using ultrasound guidance the foam is guided to the saphenofemoral junction (SFJ) by external massage pressure. Then firm digital or transducer pressure is applied to the SFJ to halt proximal passage of the foam. It is desirable to obtain a solid core of foam surrounded by a vein in complete spasm. Stimulation of venous spasm is aided by brief intermittent transducer pressure. The usual amount of microfoam injected into a varix is 5–10 ml. After proximal injection of foam, the foot and leg are elevated 45∞ and an additional 3–5 cm3 of foam is injected and guided in a distal direction to fill incompetent varices and pathologic perforating veins. The deep veins are then visualized by ultrasound and searched for evidence of foam particles. If any are present, they are cleared by rapid ankle flexion and extension maneuvers. Adverse events thought to be due to the passage of foam particles through a patent foramen ovale have been reported in 2–3% of cases.37,38 Experience teaches us that holding the leg in a 45∞ elevated position for 10 minutes after foam injection fixes the foam distally and allows reversion of foam to its original liquid state thus completely preventing any adverse events. A firm elastic stocking and a compression bandage over-wrap with focal compression over large varices and the saphenous vein is then applied. This completes the procedure. The posttreatment bandage is replaced with a fitted class 3 stocking after 48 hours and this is worn in the daytime for 14 days.
Conclusion Varicose veins, a common malady with real symptoms, are being treated today using the principles of minimal invasion, little trauma, and decreased morbidity. Principles that governed care of venous insufficiency for 100 years have been successfully challenged so that present day care has become simplified while remaining effective.
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Langer RD, Criqui MH, Denenberg J, Fronek A. The prevalence of venous disease by gender and ethnicity in a balanced sample of four ethnic groups in Southern California. Phlebology 2000; 15: 99–105 Callam MJ, Ruckley CV, Harper DR, Dale JJ. Chronic ulceration of the leg: Extent of the problem and provision of care. Br Med J 1985; 290(22): 1855–56 Evans CJ, Fowkes FG, Ruckley CV, Lee AJ. Prevalence of varicose veins and chronic venous insufficiency in men and women in the general population: Edinburgh vein study. J Epidemiol Community Health 1999; 53: 149–53 Homans J. The etiology and treatment of varicose ulcer of the leg. Surg Gynecol Obstet 1917; 24: 300–11 Schmeller W, Roszinski S, Tronnier M, Gmelin E. Combined morphological and physiological examinations in lipodermatosclerosis. In: Raymond-Martimbeau P, Prescott R, Zummo M, eds. Phlebologie 92. Paris: John Libbey Eurotext, 1992: 172–4 Van Cleef JF, Desvaux P, Hugentobler JP. Venous endoscopy. J Mal Vasc 1991; 116: 184–87. Partsch H. Das offene Bein. Klinische Pathophysiologie Ther Umsch 1984; 41: 825–33 Bergan, JJ, Schmid S, Coleridge SP, Nicolaides AN, Boisseau MR, Eklof B. NEJM 2006 to be published about June 18 Caggiati A, Bergan JJ. The saphenous vein: derivation of its name and its relevant anatomy. J Vasc Surg 2002; 35(1): 172–5 Myers TT. Results and technique of stripping operation for varicose veins. JAMA 1957; 163: 87–92 Rivlin SR. The surgical cure of primary varicose veins. Br J Surg 1975; 62: 913–17 Jacobsen BH. The value of different forms of treatment for varicose veins. Br J Surg 1979; 66: 182–84 Koyano K, Sakaguchi S. Selective stripping operation based on Doppler ultrasonic findings of primary varicose veins of the lower extremities. Surgery 1988; 103: 615–19 Samuels PB. Technique of varicose vein surgery. Am J Surg 1981; 142: 239–44 Manfrini S, Gasbarro V, Danielsson G et al. Endovenous management of saphenous vein reflux. J Vasc Surg 2000; 32: 330–42 Chandler JG, Pichot O, Sessa C et al. Treatment of primary venous insufficiency by endovenous saphenous vein obliteration. Vasc Surg 2000; 34: 201–14 Martin AG, Wainwright AM, Lear PA. Crochet hooks in varicose vein surgery. Ann R Coll Surg Engl 1995; 77(18): 460–61 Waddell BE, Harkins B, Lepage PA, Modesto VL. The crochet hook method of stab avulsion phlebectomy for varicose veins. Am J Surg 1996; 172: 278–80
20. 21. 22. 23. 24. 25. 26. 27. 28. 29. 30. 31.
32. 33. 34. 35. 36. 37.
38.
Muller R. Traitement des varices par la phlébectomie ambulatoire. Société de Phlébologie 1966; 4: 277–79 Dortu J, Raymond-Martimbeau P, eds. Ambulatory Phlebectomy/ Phlébectomy Ambulatoire. Houston: PRM Editions, 1993 Ramelet A-A. Die behandlung der besenreisvarizen: Indikationen der phlebektomie nach Muller. Phlebologie 1993; 22: 163–67 Varady Z. Erfahrungen mit der minichiururgischen operationstechnik in der varizenchirurgie. Phlebology 1993; 18: 200–5 Ramelet A.-A. La phlébectomie ambulatoire selon Muller: Technique, avantages, désavantages. J des Mal Vasculaires 1991; 16: 119–22 Garde C. Ambulatory phlebectomy. Dermatol Surg 1995; 21: 628–30 Ricci S, Georgiev M, Goldman MP. Ambulatory Phlebectomy: A Practical Guide to Treating Varicose Veins. St. Louis: CV Mosby, 2006 Ricci S. Ambulatory phlebectomy: Principles and evolution of the method. Dermatol Surg 1998; 24: 459–64 Klein JA. Tumescent technique chronicles: Local anesthesia, liposuction, and beyond. Dermatol Surg 1995; 21: 449–57 Smith SR, Goldman MP. Tumescent anesthesia in ambulatory phlebectomy. Dermatol Surgery 1998; 24: 453–6 Keel D, Goldman MP. Tumescent anesthesia in ambulatory phlebectomy: Addition of epinephrine. Dermatol Surg 1999; 25: 371–2 Butterwick KJ, Goldman MP, Sriprachya-Anunt S. Lidocaine levels during the first two hours of infiltration of dilute anesthetic solution for tumescent liposuction: Rapid versus slow delivery. Dermatol Surg 1999; 25: 681–5 Hamel-Desnos C, Desnos P, Ouvry P. Nouveautes therapeutiques dans la prise en charge de la maladie variqueuse: echosclerotherapie et mousse. Phlebologie 2003; 56: 41–8 Tessari L. Nouvelle technique d’obtention de la scléro-mousse. Phlebologie 2000; 53: 129–33 Sica M, Benigni JP. Écosclérosea la mousse: trois ans d’expérience sur les axes saphéniens. Phlébologie 2000; 53: 339–42 Monfreux A. Traitement sclerosant des troncs sapheniens et leurs collaterales de gros calibres par la methode MUS. Phlebologie 1997; 50: 351–3 Bergan J, Pascarella L, Mekenas L. Venous disorders: treatment with sclerosant foam. J Cardiovasc Surg 2006; 47: 9–18 Guex JJ, Allaert FA, Gillet JL, Chleir F. Immediate and midterm complications of sclerotherapy: report of a prospective multicenter registry of 12,173 sclerotherapy sessions Dermatol Surg. 2005 Feb; 31(2): 123–8 Guex JJ. Foam sclerotherapy: an overview of its use for primary venous insufficiency. Semin Vasc Surg 2005; 18: 25–9
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Introduction Varicose veins occur because of the malfunction of venous valves in superficial veins of the leg. As a result of this blood pools in these veins which then enlarge and become dilated and tortuous (varicose veins). They often cause symptoms of fatigue, pain, sweating, pigmentation, or ulceration in the leg. Venous insufficiency from superficial reflux through varicose veins is usually progressive if left untreated. When refluxing circuits involve failure of primary valves at the saphenofemoral junction, treatment options are limited and early recurrence is a rule rather than exception.1 Limited treatment options, frequent recurrences, and multiple complications have led to searches for newer treatment options, of which endovenous laser therapy (EVLT) has been suggested as a less invasive and relatively safer therapy. The recurrence rate of EVLT is less than 7% after 2 years which is comparable or superior to that reported for surgery, ultrasound-guided sclerotherapy, and radio-frequency ablation.2 This article focuses on this newer modality of treatment. Elastic compression bandages and stockings, crossectomy and stripping, TRIVEX, VNUS Closure, Chiva clip and cryoablation are some of the other techniques which have been tried for treating venous in competence.
to the leg and upper calf (Figure 102.1). An appropriate entry point is selected just above or just below the knee at a point that permits cannulation of the vessel with a standard or micropuncture needle introducer. The course of the vein, the saphenofemoral junction, and the anticipated entry point is marked on the skin with a surgical marker. The leg is prepared and draped, and a local anesthetic agent (lidocaine) is used to numb the site of cannulation. The Seldinger technique is used to get venous access. (Figure 102. 2) Under ultrasonographic guidance, a dilute local anesthetic agent is injected into the tissues surrounding the greater saphenous vein within its fascial sheath. In most patients, 60–120 ml of lidocaine is sufficient. Delivering the anesthetic in the correct interfascial location with a volume sufficient to compress the vein and dissect it away from other structures along its entire length is important. Some interventionalists prefer a local anesthetic with epinephrine. Ultrasonography is used to guide needle puncture of the vein. A 0.035-inch guidewire is passed through the sheath and advanced across the saphenofemoral junction into the common femoral vein. A long introducer sheath (25–45 cm) with a radio-opaque marker is introduced over the guidewire and parked about 2 inches below the saphenofemoral junction. A 400–1000 µm sterile, bare-tipped laser fiber is measured and
Ablation of veins by endovenous laser therapy (EVLT) ELVT works by means of thermal destruction of varicose veins. Laser energy is delivered to the desired location inside the vein through a laser fiber.3 When the laser is fired, it delivers thermal energy to the blood and the varicose veins, causing instant blood clotting and irreversible localized venous tissue damage. Permanent ablation of the vein is caused by thermal injury to the entire circumference of the vessel. ELVT is of value in the treatment of truncal varicose veins and treatment of large branches and tributaries.
The procedure of EVLT For treatment of the great saphenous vein and saphenofemoral junction, ultrasonography is used to confirm and map all areas of reflux and to trace the path of the refluxing great saphenous vein from the saphenofemoral junction down 870
Figure 102.1 Duplex guided mapping of great saphenous vein and saphenofemoral junction.
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Necessary accessories for treatment ● EVLT diode laser ● Duplex ultrasound ● 16-inch needle ● EVLT treatment kit 䊊 0.0035-inch J-tip Glidewire 䊊 5-French introducer sheath 䊊 EVLT 600–810 µm fiber
Figure 102.2
Post EVLT
Pre EVLT
(a)
(b)
Varicose vein: (a) post-EVLT; and (b) pre-EVLT.
advanced through the sheath until it protrudes 1–2 cm from the tip of the sheath. Neither the fiber tip nor the laser beam should extend into the femoral vein because injury to the femoral vein may cause deep vein thrombosis. To prevent the laser fiber from slipping back into the sheath, the fiber is secured to the introducer by using Steri-Strips or a clamp. When the laser console is switched on, a red aiming beam is visible through the skin at the level of the saphenofemoral junction. Failure to observe this beam is a reliable indicator of malpositioning. For treatment using intermittent pulsation, the console is set to deliver 12 J per pulse in 1-second pulses. The laser can be fired manually, but most often it is controlled by a foot pedal with automatic pulses at 1 second intervals (Figure 102.2). Manual pressure is applied to achieve venous wall apposition around the tip of laser fiber when the laser is fired. The sheath and the laser fiber are pulled back approximately 3 mm, manual pressure is again applied, and the laser is fired again. This procedure is repeated along the entire length of vessel to be treated. With pulses delivered once per second at 3-mm intervals, an entire 30 cm greater saphenous vein can be treated in 90 seconds. Except when used by experts, wrapped bandages do not provide a safe or effective means of compression. Bandages may slip spontaneously, or the patient may remove them and reapply them incorrectly. The loss of graded compression with the development of the tourniquet syndrome can increase the patient’s risk for distal venous stasis and venous thrombosis. In the US, graded compression is most often applied by using surgical compression stockings. At least 30–40 mmHg of compression is necessary for effective compression of the superficial veins.
Immediately after the procedure, ultrasonography shows a patent vessel that is in spasm through most or all of its length and immediate clotting of blood. This is also demonstrated on contrast venography (Figure 102.3). Follow-up ultrasonography at 1 week demonstrates nearly 100% early closure of vessels. Post-operative bruising can be significant after EVLT. Bruising may be completely absent in patients who wear compression stockings continuously during the first 3 days after treatment. Post-operative tenderness after day 3 has also been reported, which may be related to the amount of intravascular coagulant in the closing vessel. Tenderness is not usually observed in patients who wear compression stockings. The patients are re-evaluated on third and seventh days, at which time ultrasonography should demonstrate a closed vein and no evidence of thrombus in leg veins. If vessel is still patent at seventh day the procedure can be repeated.4
Further applications of EVLT These are outlined as follows: ● ● ● ● ●
recurrence after surgical stripping; lasering the remaining veins after an operation; prevention of ulcers; saphena magna; telangiectasia or spider veins.
Figure 102.3 EVLT.
Immediate clotting of the blood in GSV after
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Table 102.1
EVLT parameters
Pulse length Pulse interval Vein diameter Power (Watts) (seconds) (seconds) > 8 mm 6–8 mm 4–6 mm Lasering time 3–5 minutes
9–10 8–9 7–8
2.5–3 2.5–3 2–2.5
1 1 1
Advantages of EVLT These are outlined as follows: ● ● ● ● ● ● ●
outpatient procedure; quick and easy to perform; minimally invasive and less traumatic; no scarring; excellent clinical and cosmetic result; reduced procedure cost; recurrence of 7% over 2 years (less than surgical stripping).5
Discussion Min et al. reported 3 years data of EVLT in 499 limbs using 810 nm diode laser energy delivered intraluminally.
They reported 98% success (490/499 limbs). At follow-up of 3, 6, 9, 12, and 24 months, recurrence was 0.7, 1.5, 2.2, 2.5, and 6.6%, respectively.6 Navarro et al. reported a 4-year follow-up of 200 limbs treated by EVLT and reported a success rate of 95%. They noted that recurrences were due to recanalization and not to neovascularization.7 Some centers have now started using laser assisted distal stripping (LADS). This hybrid technique is useful when the GSV leaves the saphenous canal in the thigh and courses superficially under the skin up to the leg. Worldwide experience with this procedure is limited because it is relatively new. Fewer than 10,000 cases are reported. In this limited population, only a single skin burn has been reported, and no other significant complication has been reported to date.
Conclusion In the last 7 years, there has been a dramatic improvement in the treatment of varicose veins by endovenous techniques. Although EVLT procedure is new, published results show a high success rate with low subsequent recurrence rate as long as 48 month after treatment. This procedure is of particular importance because it is cheap, very effective, and is almost an OPD procedure. It is easily accepted by the patient because of its simplicity, cosmetic value, and good results. However, larger studies are required for standardizing the intraoperative energy doses, pullback rates and treatment of perforators, and saphenopoplitial reflux.
REFERENCES 1. 2. 3. 4. 5.
Feied CF. Peripheral venous disease. In: Rosen P, Barkin RM, eds. Emergency Medicine: Principles and Practice, fourth edition. Mosby Year Book, 1998 Weiss RA, Feied CF, Weiss MA. Vein Diagnosis & Treatment: A Comprehensive Approach. New York: McGraw-Hill, 2001: 1–304 Jung DS, Jang HS, Kwon KS. Endovenous laser surgery of the incompetent greater saphenous vein with a 980-nm diode laser. Dermatol Surg 2003; 29 (11): 1135–40 Min RJ, Khilani N, Zinuued SE. Endovenous laser treatment of saphenous vein reflux: long-term results. J Vasc Interv Radio1 2003; 14(8): 991–6 Perkowski P, Ravi Gowda RC et al. Endovenous laser ablation of the saphenous vein for treatment of venous insufficiency and
6. 7. 8. 9.
varicose veins: early results from a large single-center experience. J Endovasc Ther 2004; 11(2): 132–8 Min RJ, Khilnani N, Zimmet SE. Endovenous laser treatment of saphenous vein reflux: long term results. J Vasc Intervent Radiol 2003; 14: 991–6 Navarro L, Bone C. Endolaser: four years of follow-up evaluation (abstract). UIP World Congress, 2003 Fischer R, Linde N, Duff C et al. Late recurrent saphenofemoral junction reflux after ligation and stripping of the greater saphenous vein. J Vasc Surg 2001; 34: 236–40 Pichot O, Kabnick LS, Cretor D et al. Duplex ultrasound scan findings two years after great saphenous vein radiogrequency endovenous obliteration. J Vasc Surg 2004; 39: 189–95
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Background Deep vein thrombosis (DVT) is one of the most commonly missed diagnoses. DVT and pulmonary embolism (PE) represent two extremes of a single disease process. The annual reported incidence of DVT in the US is 20 million cases, out of which approximately 10% require hospitalization. Most commonly, DVT occurs in the deep veins of lower extremities but it can also arise in the veins of the pelvis and that of superior extremities. A triad of venous stasis, intimal injury, and a hypercoagulable state (Virchow’s triad) is usually the cause in most of the patients of DVT. Risk factors for DVT and subsequent pulmonary embolism are: ● ● ● ●
● ● ●
prolonged immobilization (due to illness, surgery, travel); pregnancy; malignancy; hypercoagulable states (lupus anticoagulant, anti thrombin III deficiency, protein C and protein S deficiency, polycythemia rubra vera); factor V Leydin mutation; genetic predisposition; age > 50 years.
Pulmonary embolism is the most dreaded complication of DVT and is the third-leading cause of cardiovascular deaths in the US (approximately 120,000–150,000 deaths per year). Massive pulmonary embolism has a mortality of 50% while recurrent pulmonary embolism is associated with pulmonary arterial hypertension and is associated with right ventricular dilatation and failure. Systemic anticoagulation by oral or intravenous (IV) route is the mainstay for the treatment of DVT and subsequent prevention of pulmonary embolism. However, studies have shown that as many as one-third of patients develop recurrent pulmonary embolism even when they are on adequate anticoagulation therapy. In many patients of DVT, anticoagulation is contraindicated because of high risk of bleeding or fetal abnormalities (when used in pregnant females, as warfarin crosses the blood–placenta barrier). In these patients, mechanical interruption of the flow through the inferior vena cava (IVC) is recommended. The concept of mechanical interruption of the IVC to prevent pulmonary embolism has been practiced since late 1930s and involves a major retroperitoneal surgical procedure to clamp/ligate the IVC (12–15% mortality, 10–16% patients had immediate lower extremity swelling).1 Therefore, in the mid-1960s, various methods were
used to partially interrupt IVC flow. This allowed the clots to be trapped in the IVC, yet it did not lead to venous stasis and reduced the immediate post-operative limb edema. These methods were suture plication of IVC or clipping the IVC with Moretz, Miles, or Adams-DeWeese clips. However, despite the fact that these procedures only partially interrupted the flow of IVC, caval occlusion still occurred in 30–40% patients on long-term follow-up. In 1967, the Mobin-Uddin umbrella filter was developed and replaced surgical procedures for IVC interruption.2 The relative simplicity of the device and the placement procedures has revolutionized the strategy of prevention of PE in cases of DVT by IVC interruption.3 These filters are now used as an alternative to anticoagulation therapy for preventing PE in patients of DVT.4 This article briefly reviews various types of IVC filters on the market, indications of their use and future trends in the prevention of pulmonary embolism.
Vena caval filters Vena caval filters are mechanical devices placed in the IVC (or sometimes in the SVC) to trap any major thrombus which is likely to embolize to the pulmonary artery. They are made up of stainless steel or other non-ferromagnetic alloys. They are self-expanding devices with hooks to fix the filter to the walls of the IVC. They are designed for maximal clot trapping, flow preservation and ease of placement. Of the currently available filters, each design achieves varying degrees of the following desired properties. Desired qualities of IVC filters ● maximum clot trapping; ● stability; ● non-thrombogenicity; ● biocompatibility; ● non-corrosiveness; ● long durability; ● low profile; ● ease of deployment; ● filter should not migrate after deployment; ● filter should not perforate IVC after deployment; ● non-ferromagnetic to allow MRI in future; ● retrievability; ● ability to be delivered from a femoral/jugular/antecubital approach. 873
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Types of IVC filters After the successful implantation of the Mobi-Uddin umbrella filter in 1967, more than a dozen filters have been made available on the market, all of which are US FDA approved. These are outlined below.
● ● ● ● ● ●
Permanent filters ● Kimray–Greenfield filter ● Titanium Greenfield filter ● Percutaneous Greenfield filter ● Bird’s nest filter ● Trap-Ease filter ● Simon nitinol filter ● Vena Tech-LGM filter ● Vena Tech-LP filter. Optional or retrievable filters Retrievable filters are sometimes refereed as optional filters because they can either be retrieved after a fixed period of time following implantation or can be left in the patient as a permanent device. The following retrievable/optional filters are available. ● ● ●
Gunther–Tulip filter Opt-Ease filter Recovery filter.
Technique of filter implantation The IVC filters can be implanted using the jugular or common femoral approach, or sometimes by the antecubital approach. This involves getting percutaneous venous access and then doing a venogram with a pigtail catheter to locate the level of the renal veins. The filter is placed just below the level of lowest renal vein. It is delivered over a 0.035-inch guidewire by withdrawing the delivery sheath over the filter. In cases of retrievable filters, a cavogram is first done to assess the burden of thrombus. Filter is not retrieved if the entrapped thrombus occupies more than 25% of the volume of the filter. In experienced hands the success rate of deployment is > 97%. Anatomic variations of the IVC are fairly common (3–15%) and this reflects the variation in the involution and the persistence of the cardinal veins. These assume importance because they may alter the location of the filter deployment. The common anatomic variations of the IVC are duplication of the IVC, transposition of IVC, and the presence of circum aortic and retro aortic renal veins. Duplication of the IVC occurs in about 0.2–3% of the population. In this anomaly, the left IVC is usually smaller and subsequently drains into the right IVC. In the presence of this anomaly the filter placement in the right IVC alone is not enough to prevent pulmonary embolism and the filters are placed in both the left and right IVC.
●
2 Complications of anticoagulation therapy This indication accounts for 6–18% of IVC filter placements. The main complications of anticoagulation therapy are hemorrhage and immune-mediated heparin-induced thrombocytopenia (HIT) 3 Failure of anticoagulation therapy Patients who have ● ●
●
4 5 6 ●
● ●
●
● ●
●
recent surgery;
new onset of pulmonary embolism; extension of DVT while on optimal doses of anticoagulation therapy; new deep vein thrombosis. Free-floating ileofemoral thrombus IVC thrombus Prophylactic placement to prevent PE patients with DVT who are undergoing major orthopedic surgery, abdominal surgery, or neurosurgery; patients with polytrauma; patients with severe head injury on prolonged ventilator dependence; patients with head injury and multiple lower extremity fractures or pelvic fracture; patients with spinal injury with or without paralysis; major abdominal and pelvic penetrating injuries.
Contraindication to IVC filter placement Although IVC filter placement has been shown to be very safe there are a few contraindications. These are: ●
● ●
thrombus between the venous access and expected site of deployment; IVC fully laid-in with thrombus; septicemia/bacteremia.
Complications of IVC filters There are a number of complications associated with filter placement, but the overall incidence is less than 3%.7 These are outlined below. Short-term complications contrast reaction; ● malplacement; ● tilting and angulation; ● filter migration (3–69%); ● embolization of filter to the right side of heart and lungs (2–5%); ● fracture of the filter; ● contrast induced renal dysfunction; ●
Indications for IVC filters 1 Contraindications to anticoagulation therapy This accounts for 38–77% of patients undergoing IVC filter implantation.5,6 The common contraindications to anticoagulation therapy are:
hemorrhagic stroke; active internal bleeding; trauma; intracranial neoplasm; bleeding diathesis; pregnancy; patients with an unsteady gait or tendency to fall.
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insertion site thrombosis; infection.
Long-term complications ● migration; ● perforation of IVC; ● IVC occlusion; ● vena caval syndrome; ● increased risk of subsequent DVT. Post-implantation care and follow-up Usually patients with IVC filter implantation are put on oral anticoagulation.8–10 In these patients it is important to keep the INR between 2.5 and 3.5. Clinical success is defined as technical success without pulmonary embolism, filter migration, IVC thrombosis, or any other complication. In the follow-up, the following tests are done. Venous duplex scan The purpose here is to look for recurrent deep vein thrombosis and chronic venous insufficiency. One should also look for thrombosis of the IVC and the degree of clot entrapment. CT Scan/MRI The purpose here to look for the stability and patency of the filter. We also look for the occasional perforation of IVC and the reduction of the diameter at the base of the filter which suggests caval stenosis or occlusion. Superior vena caval filters The overall incidence of DVT in the upper limb is 4%. The increased incidence is mainly due to central venous line insertion. Upper limb DVT is more likely to lead to pulmonary embolism. Underlying malignancy, hypercoagulable states and congestive heart failure are predisposing factors for upper extremity DVT. Percutaneous placement of vena cava filters in the SVC is a potentially attractive method of preventing pulmonary embolism. However it is technically more challenging than IVC filter implantation because of the relatively small area for filter placement. The complications are also high and potentially more dangerous.11–18 A superior vena cavogram is done to determine the SVC diameter, and to exclude caval stenosis, anomalies and SVC thrombosis. A femoral insertion kit is used if the filter is placed from the jugular approach and jugular insertion kit is used if the filter is inserted from the femoral approach, so as to keep the cone of the filter directed towards the heart. The filter is placed immediately below the confluence of both brachiocephalic veins. Sometimes in the presence of upper limb and lower limb DVT both IVC and SVC filters are implanted. The Greenfield filter is the filter of choice. The Birds Nest filter is not preferred because of its long length (7 cm). Spence et al. published the results of 41 cases of acute upper extremity DVT who underwent SVC filter implantation. The indication of filter implantation was failure of or contraindication to therapeutic anticoagulation. The Greenfield filter was implanted in 33 patients (86%), the Simon nitinol filter was used in 5 patients and the Vena Tech filter was used in 2 patients. There was no clinical evidence of SVC occlusion,
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venous gangrene, or exacerbation of upper extremity symptoms. PE occurred in only one patient in whom it probably originated from the lower limb DVT. In some of these cases, a central venous line or Swanz Ganz catheter was also placed through these filters. However this was done using a straight guidewire under fluoroscopic guidance. Individual types of vena caval filters Mobin-Uddin umbrella filter This was originally introduced in 1967 and released for general use in 1973. It could only be introduced through the right internal jugular vein after surgical venisection. It was a 27-French device and was associated with many complications like wound hematoma, sepsis, filter migration, IVC thrombosis, limb edema, and retroperitoneal hemorrhage. It was withdrawn in 1986. Kimray Greenfield filter (KGF) This was introduced in 1973 by Greenfield. It is a stainlesssteel filter which is conical in shape and consist of six stands of stainless steel legs in a radial array with hooks attached at the end of each leg. The filter is loaded into a 24-French delivery sheath and is placed via surgical cut-down of common femoral or internal jugular vein. Due to the design of the filter, even if 80% of the filter is filled with thrombus the effective reduction of cross-sectional diameter of IVC flow is 64%. In a 20-year experience of Greenfield filters, the overall rate of recurrent pulmonary embolism was only 4.9%. The long-term patency rate was as high as 96%. Titanium Greenfield filter (TGF) This was introduced in 1989 and is made up of titanium alloy with elastic properties allowing the filter to be delivered in a 12-French sheath as opposed to 24-French in the Kimray Greenfield filter. It is similar in design but because of the material it is resistant to fatigue and corrosion. It is nonthrombogenic and non-ferromagnetic. It has a greater radial force at the base than the Steel Greenfield Filter (SGF). It has high incidence of IVC penetration, is similar in performance and has a 97.8% long-term patency. Percutaneous Greenfield filter (PSGF) (Figure 103.1) This received FDA approval in 1995 and is a truly percutaneous stainless steel Greenfield filter which is delivered through a 12-French sheath. Here a guidewire is used during deployment to provide centering effect during deployment. This eliminates tilting. The hooks are improved to prevent the migration of filters. It has a similar design – a conical shape with six zig-zig radiating legs of 316L-grade stainless steel. In 2000, Greenfield et al. reported the results of 600 PSGFs. The filter tilt was present only in 0.4% of patients and migration was seen in < 2% of the patient. Recurrent PE was present in 2% and IVC patency was seen in 98%. The rate of IVC filter thrombosis was 4.3%. Bird’s Nest filter (BNF) (Figure 103.2) This is made up of a network of four biocompatible stainless steel wires of 0.18 mm in diameter and 25 cm length. The wires are fixed at each end to V-shaped struts which are connected at an acute angle. The BNF has a unique design and can be used even in megacavas (diameter > 28 mm).
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Figure 103.1
Percutaneous stainless steel Greenfield filter.
It has been used in IVCs with diameter as large as 42 mm. IVC thrombosis is reported in 2.9–17% of patients and recurrent pulmonary embolism is reported in 1–7% of cases. Trap-Ease filter (Figure 103.3) The Trap-Ease filter was approved by the FDA in 2000. It is a laser cut nitinol tube with a symmetrical trapezoid doublebasket design and self-centering characteristics. The two baskets are connected by six side struts each of which has proximal and distal hooks for anchoring. The filter is 65 mm
Figure 103.3
Trap-Ease filter.
in length in its undeployed condition and 50 mm in length when expanded to a diameter of 35 mm. It is recommended in IVCs with a diameter of 18–30mm. The unique symmetrical design of this filter allows placement from both a jugular or femoral approach using the same 55 cm package. There is another 90-cm-length package which is suitable for an antecubital approach. The filter is deployed by a pusher through an 8-French delivery system. It has the smallest profile among the available filters, but it has the most clot-trapping potential. Simon nitinol filter (Figure 103.4) This is made up of nitinol (nickel, titanium. and cobalt alloy). It has a thermal memory and it takes its preformed shape at body temperature. It is non-ferromagnetic and resistant to corrosion. It is 3.8 cm long and consists of seven overlapping loops of nitinol wires fused together at two points. It was approved by the FDA in 1990. Because of its unique design it can trap emboli larger than 5 mm in diameter. Its clot trapping capability is not affected by the filter tilt. It can be placed using femoral, jugular, or antecubital approaches. In a study by Athanas Oulis et al. comparing different filters of the last 26 years, the Simon nitinol filter had the lowest rate of recurrent pulmonary embolism (3%) and fatal pulmonary embolism (2%). The rate of IVC thrombosis was 3.5%. The rate of filter migration and perforation is extremely low. Strut fracture and axial deviation of filter have been reported with the Simon nitinol filter but none of these complications appear to adversely affect the filter function.
Figure 103.2
Birds Nest filter.
Vena-Tech LGM filter (Figure 103.5) This was first used in France and received FDA approval in 1989. It is made up of an alloy called Phynox (cobalt, chromium, iron, nickel, and molybdenum). It is conical in shape with six radiating legs joining at a central apex. It is delivered through a 12-French sheath using either a jugular or femoral approach. There have been reports of incomplete
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which is a non-ferromagnetic material. It is conical in design with a hook at the apex. It has four legs of 44 mm length with barbed hooks for anchoring. Four wires are wrapped around the primary legs to form a tulip petal-like conical structure with a total of 12 wires for clot trapping. It can be used for IVCs of a diameter of up to 30 mm. The introducer system is 8 French and is different for femoral and jugular approaches. It comes with a retrieval sheath which is 11 French in diameter. The recommended retrieval time is 2 weeks but the filter has been retrieved up to 4 weeks later. A vena cavogram must be performed before filter retrieval to access the amount of the trapped clot. If the amount of clot trapped in the cone is more than 25%, it is a relative contraindication for retrieval.
Figure 103.4
Simon nitinol filter.
opening of this filter which has adversely affected its clottrapping ability. The reported rate of pulmonary embolism with its use is 6%. There are reports of a higher rate of filter thrombosis and lower rates of IVC patency at 2 years and 6 years follow-up.
Opt-Ease filter (Figure 103.7) The Opt-Ease filter is similar in design to the permanent TrapEase filter. It is cut from a single nitinol tube and has a sixsided conical shape and dual-level clot-trapping ability. It can be placed from both femoral or jugular approaches, but because of placement of the hook at the caudal end it can be retrieved only from the femoral approach. It was approved by the FDA in 2002 and can be retrieved up to 23 days later by a 10-French retrieval system.
Optional filters Gunther–Tulip filter (Figure 103.6) This filter became FDA approved for permanent use in 2000 and for retrievable use in 2003. It is made of Conichrome
Recovery nitinol filter (Figure 103.8) This was approved by FDA as a permanent device in 2002 and as an optional filter in 2003. It is made up of nitinol and is MRI compatible. It has two levels of filtration and has six radiating arms and legs each made up of 0.13-inch wires. The legs have hooks for anchoring. It is delivered through a 9-French sheath using a femoral approach and is recommended to be used in IVCs of up to 28 mm in diameter. The recovery kit is 12 French in diameter.
Figure 103.5
Figure 103.6
Vena-Tech LGM filter.
Gunther Tulip filter.
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Figure 103.7
Opt-Ease filter.
Figure 103.8
Recovery filter.
REFERENCES 1. 2. 3. 4. 5. 6. 7.
8. 9. 10.
Kempczinski RF. Surgical prophylaxis of pulmonary embolism. Chest 1986; 89: Suppl: 384s–8 Mobin-Uddin K Smith PE, Martinez LO, Lombardo CR, Jude JR. A vena caval filter for the prevention of pulmonary embolus. Surg Forum 1967; 18: 209–11 Greenfield LJ, Proctor MC. Current indications for caval interruption: should they be liberalized in view of improving technology? Semin Vasc Surg 1996; 9: 50–8 Becker DM, Philbrick KT, Selby JB. Inferior vena cava filters: indications, safety, effectiveness. Arch Intern Med 1992; 152: 1985–94 Arnold TE, Karabinis VD, Mehta V et al. Potential of overuse of the inferior vena cava filter. Surg Gynecol Obstet 1993; 177: 763–7 Davidson B. Vena cava filters: indications and issues. Thromb Forum 1996; 2: 1–6 Decousus H, Leizorovicz A, Parent F et al. A clinical trial of vena caval filters in the prevention of pulmonary embolism in patient with proximal deep-vein thrombosis. N Engl J Med 1998; 338: 409–15 Hull RD, Carter CJ, Jay RM et al. The diagnosis of acute, recurrent, deep-vein thrombosis: a diagnostic challenge. Circilation 1983; 67: 901–6 Meissner MH, Caps MT, Bergelin RO, Manzo RA, Strandness DE Jr. Propagation, rethrombosis and new thrombus formation after acute deep venous thrombosis. J Vasc Surg 1995; 22: 558–67 Schulman S, Rhedin A-S, Lindmarker P et al. A comparison of six week with six month of oral anticoagulant therapy after a first
11. 12. 13. 14. 15. 16.
17. 18.
episode of venous thromboembolism. N Engl J Med 1995; 332: 1661–5 Monreal M, Lafoz E, Ruiz J, valls R, Alastrue A. Upper extremity deep venous thrombosis and pulmonary embolism: a prospective study. Chest 1991; 99: 280–3 Black MD, French GJ, Rasuli P, Bouchard AC. Upper extremity deep venous thrombosis: underdiagnosed and potentially lethal. Pa: Saunders, 1990; 115–27 Campbell CB, Chandler JG, Tegmeyer CJ, Berbstein EF. Axillary, subclavian, and brachiocephalic vein obstruction. Surgery 1977; 82: 812–26 Langham MR Jr, Etheridge JC, Crute SL, Greenfield LJ. Experimental superior vena caval placement of the Greenfield filter. J Vasc Surg 1985; 2: 794–8 Ascer E, Gennaro M, Lorensen E, Pollina RM. Superior vena caval Greenfield filters: indications, techniques, and results. J Vasc Surg 1996; 23: 498–503 Hoffman MJ. Greenfield LJ. Central venous septic thrombosis managed by superior vena cava Greenfield filter and venous thrombectomy: a case report. J Vasc Surg 1986; 4: 606–11 Pais SO, De Orchis DF, Mirvis SE. Superior vena caval placement of a Kimray-Greenfield filter. Radiology 1987; 165: 385–6 Owen EW, Schoettle GP, Harrington OB. Placement of a Greenfield filter in the superior vena cava. Ann Thorac Surg 1992; 53: 896–7
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Foam treatment of varicose veins JI Greenberg, N Angle, and J Bergan
Introduction Once a disease treated only with operation by surgeons, varicose veins are now treated with minimal invasion by radiologists, dermatologists, and other specialists. This has undoubtedly benefited many patients by increasing access to care for a painful, unsightly, and sometimes disabling disease process. It remains important that every clinician who treats varicose veins be well informed about venous pathophysiology, treatment strengths and limitations, and the importance of a multi-modality approach with rigorous follow-up. Such information is often lacking in primary specialty training. In this chapter, we will briefly describe the historical background, anatomical considerations, and current theory of chronic lower extremity venous insufficiency (CVI). We will subsequently focus on proven treatment options for the percutaneous management of this disease before concluding with a contemporary treatment algorithm.
Background History The history of totally percutanous treatment of varicose veins is essentially that of sclerotherapy. After invention of the syringe by Rynd in 1845 and Pravaz in 1851, sclerotherapy entered an era of trial and error with many sclerosants being tried and found wanting. Among these were carbolic acid and quinine. Liquid sclerosants were first injected into varicose veins as an attempt at “conservative management” by Paul Linser in 1911 with variable success.1 Liquid sclerotherapy was subsequently modified into foam sclerotherapy by Stuart McAusland in 1939, when he used sodium morrhuate froth from a shaken bottle aspirated into a syringe.2 In 1944, Egmont James Orbach envisioned the underlying mechanism of the “air block technique” and the displacement of blood that would revolutionize phlebology. Orbach injected liquid sclerosant into a vein collapsed between two tourniquets and released the proximal tourniquet to allow proximal passage of the material in the direction of blood flow.3 In order to generate prolonged and more intimate contact between the sclerosant and the endothelium, he devised the “air-block” technique by injecting air prior to the sclerosant to prevent dilution of the agent and prolong contact with the endothelium. This discovery is relevant because foam acts through a similar mechanism in a process that has been called “foam-block” (Figure 104.1).
After 1944, a number of techniques and devices were proposed to facilitate the genesis and safe use of this “extemporary” foam. In 1956, Peter Flückinger described the role of “retrograde injection” and leg elevation wherein a proximal vein was injected and passage of the sclerosant could be directed in a distal direction rather than in the direction of blood flow. Thus the sclerosant would pass into dysfunctional veins with incompetent valves while competent valves in normal veins would block the flow of foam. In the absence of ultrasound imaging monitoring of treatment was by palpation of crepitus as foam was guided by massage.4 In this way, Flückinger also invented the aspiration technique, in which a needle bevel was partially submerged in a vial of Varsyl thereby generating an air–liquid interface and resultant foam.5 In 1957 Mayer and Brücke described the double-piston syringe (DPS) which contained two plungers, one served as the main plunger and the other contained numerous small holes.6 They used Phlebocid, a detergent, for the generation of foam by excursion of the smaller plunger against the air–liquid interface in the syringe. The truly modern age of foam sclerotherapy was ushered in by Juan Cabrera Garrido who first described the use of sclerosant “microfoam” generated by a novel rotating brush and a carbon dioxide carrier.7 The half-life of the foam was found to be dependent upon the content of carbon dioxide. An increased carbon dioxide to sclerosant ratio resulted in faster degradation of the foam. Cabrera used the foam to treat the great saphenous vein, varicosities, and venous malformations with dramatic success. Anatomical considerations Comprehensive discussion of the variable anatomy of CVI can be found in a number of articles and textbooks.8,9 For the most part, two patterns are present. The patient seeks relief from the varicose clusters. The physician seeks to relieve gravitational pressures by removing the saphenous vein from the circulation. Often both maneuvers need to be done either simultaneously or at separate settings. Here we emphasize the anatomy relevant to the safe performance of percutaneous venous interventions. The revised CEAP classification (Clinical–Etiology–Anatomy– Pathophysiology) is presented in Table 104.1 along with important definitions. For the interventionalist, the CEAP classification can be a valuable instrument to formulate a diagnosis, guide treatment, and assess prognosis. The classification should not be used as a measure of success of treatment. 879
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Textbook of peripheral vascular interventions Table 104.2 Interrogation points in the venous reflux examination Common femoral vein
(a)
Femoral vein Upper third Lower third Popliteal vein Sural veins Saphenofemoral junction* Saphenous vein, above the knee Saphenous vein, below the knee Saphenopopliteal junction† Mode of termination, lesser saphenous veins
(b) Figure 104.1 Orbach’s theory was simple but elegant. (a) Air injected into a small vein will “block” the dilution of a liquid introduced thereafter; (b) it was subsequently discovered that foam has the ability to generate an analogous effect termed “foamblock.”
The clinical classification (C) is derived from the history and physical examination while the E, A, and P categories are assigned according to findings on duplex scanning. The term “chronic venous insufficiency” is generally restricted to diseases involving classes C4 to C6. The minimal anatomic landmarks for interrogation during a preprocedural venous duplex examination are tabulated in Table 104.2.
Table 104.1
*Record diameter of refluxing long saphenous vein. †Record
distance from floor.
The greater saphenous vein is identified on the basis of its relation to the deep and superficial fascia that ensheathe it to form the saphenous compartment. This has come to known as the saphenous eye (Figure 104.2). The saphenous eye is a constant marker, clearly demonstrable in transverse sections of the medial aspect of the thigh that serves to differentiate the saphenous vein from varicose tributaries and other superficial veins.
Revised CEAP classification for chronic venous disorders10
Clinical classification
Etiologic classification
Anatomic classification
Pathophysiologic classification
C0: no visible or palpable signs of venous disease
Ec: congenital Ep: primary Es: secondary (post-thrombotic) En: no venous cause identified
As: superficial veins Ap: perforator veins Ad: deep veins An: no venous location identified
Pr: reflux Po: obstruction Pr,o: reflux and obstruction Pn: no venous pathophysiology identifiable
C1: telangiectasies* or reticular vein† C2: varicose veins; distinguished from reticular veins by a diameter of 3 mm or more. C3: edema C4a: pigmentation or eczema C4b: lipodermatosclerosis§ or atrophie blanche‡ C5: healed venous ulcer C6: active venous ulcer S: symptomatic, including ache, pain, tightness, skin irritation, heaviness, and muscle cramps, and other complaints attributable to venous dysfunction A: asymptomatic
*Telangiectasia is a confluence of dilated intradermal venules less than 1 mm in caliber. Synonyms include spider veins, hyphen webs, and thread veins; †reticular vein is a dilated bluish subdermal vein, usually 1 mm to less than 3 mm in diameter. Usually tortuous. Excludes normal visible veins in persons with thin, transparent skin. Synonyms include blue veins, subdermal varices, and venulectasies; atrophie blanche (white atrophy)‡ is localized, often circular whitish and atrophic skin areas surrounded by dilated capillaries and sometimes hyperpigmentation; lipodermatosclerosis (LDS)§ Localized chronic inflammation and fibrosis of skin and subcutaneous tissues of lower leg, sometimes associated with scarring or contracture of Achilles tendon.
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(a)
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(b)
Figure 104.2 Shown are ultrasonographic images of the so-called saphenous eye. Correct identification of this marker is crucial to correct performance of the preoperative ultrasonographic reflux examination. (a) Transverse sonography of the medial thigh demonstrating the boundaries of the saphenous compartment and the saphenous ligament (black arrows); (b) note the superficial course of a collateral vessel placed just below the dermis (*). MF – Muscular fascia.
Casual examination of the thigh often reveals an elongated, dilated vein that is incorrectly assumed to be the great saphenous vein. This mistaken assumption can be corrected by means of ultrasound scanning using the saphenous eye as an anatomic marker. Pathophysiology The pressure in the veins of the leg is determined by two components: a hydrostatic component related to the weight of the column of blood from the right atrium to the foot and a hydrodynamic component related to pressures generated by contraction of the skeletal muscles of the leg and the pressure in the capillary network. Competent venous valves ensure that venous blood flows toward the heart, thereby emptying the deep and superficial venous systems and reducing venous pressure, usually to less than 30 mmHg.11 If valves in the perforator veins are incompetent, the high pressures generated in the deep veins by calf muscle contraction can be transmitted to the superficial system and even to the microcirculation of the skin. A hypertensive subcutaneous venous circulation is the most likely cause of venous ulceration (Figure 104.3). Venous hypertension promotes an insidious cascade of events resulting in valvular distortion, inflammation, capillary leakage, edema, and ultimately ulceration of the skin.
When a patient is seen in the office on referral for varicose veins, a focused history and physical examination is performed. A standing venous reflux Doppler examination is documented according to a previously published protocol.13 Diameters of refluxing venous segments and exit and re-entry perforating veins are recorded. In cases of venous ulceration, the relationship between pathological perforating veins and ulceration is documented and the size of the ulcer in three dimensions is recorded. In decision making regarding the treatment of the patient with varicose veins, one must consider not just one finding, but the entirety of the patient’s history, physical
Techniques The successful management of varicose veins once consisted of two surgical interventions, which are now often accomplished with specialized instruments. First, the refluxing saphenous vein must be excluded from the circulation. Second, varicose veins must be removed from their source of venous hypertension. The same principles can be applied to a venous ulcer which, for a sustained cure, must be excluded from its hypertensive microcirculatory bed. Percutaneous techniques for saphenous vein ablation are not just cosmetically attractive, but hold potential for eliminating the neovascularization thought to be responsible for varicose vein recurrence after groin surgery.12
Figure 104.3
Active venous ulceration (CEAP class C6).
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examination, and standing venous reflux Doppler examination in the context of evidence-based guidelines (Table 104.3). Foam sclerotherapy Sclerosants cause irreversible damage to the vascular endothelium by disrupting cell membranes resulting in vasospasm and denudation of the venous endothelial monolayer. The end result is fibrous obliteration of the vessel lumen. Available evidence suggests that the mechanism is the same whether the physical phase of the inciting agent is liquid or foam.14 Prospective randomized outcome data support the hypothesis that foam sclerotherapy is superior to liquid sclerotherapy.15–17 The reason for this appears to be two-fold. First, the physical properties of foam afford more efficient contact with its target: the venous endothelium. Second, because the local efficiency of sclerosant is increased, less volume of the agent may be given. The result appears to be few local and systemic complications. The three current methods in use for foam preparation were refined and published by Alain Monfreux, Lorenzo Tessari, and Hamel-Desnos. The Tessari technique has gradually become dominant. In 1997, Alain Monfreux devised the “Methode MUS” using a negative pressure system in which a piston draws subatmospheric air into a syringe through small gaps between the piston and syringe.18 There is significant variability in the resultant foam depending on the type of syringe and the mode of pulling back the piston. The Tessari technique (or Tourbillon technique) was first described in 1999 and uses two syringes varying from 2–10 cm3 in capacity connected by a three-way stop-cock (Figure 104.4).19,20 Only sodium tetradecyl sulfate was used by Tessari et al. Today, many use polidocanal but this agent is not FDA approved in the US. Air and liquid sclerosant were mixed by Tessari in 20 passages while the aperture in the three-way stop cock was decreased to generate a microfoam. It was noted that over 20 passages did not alter foam architecture, that using saline instead of sterile water created larger bubbles, and a higher concentration of sclerosant produced a less stable foam. Foam lasting less than 2 minutes is considered less stable as 2 minutes marks the usual time required to perform an injection. In Tessari’s 2001 report, no mention was made of the ratio of air to liquid; but subsequent reports proposed 5:2 or 4:1 air–liquid ratios.21
Table 104.3
EVLT
The known variability in foam produced by different syringe types and needle sizes prompted Hamel-Desnos to propose the double-syringe system (DSS) technique in 2001. She published this technique in a case series in 2003.17 The required method included a 10-ml Omnifix syringe, a 10 ml injection syringe (each with a Luer-Lock connection), a Combidyn adaptor, and a 0.2 µm filter. A total of 8 ml of air was drawn into the injection syringe before 2 ml of 3% polidocanol was used to fill the Omnifix syringe. The connector was used to join both syringes. A total of five pumps was employed with additional pressure to mix both solutions followed by seven pumps without additional pressure. The effective delivery of foam sclerotherapy is easy. Depending on local availability, a procedure room in a quiet office is best for injecting foam sclerosant. Other than the drug and the consumable supplies described earlier, other necessary equipment includes a high-quality color duplex ultrasound (5–15 Mhz) transducer unit and emergency equipment. The latter is indicated in rare cases of drug reaction to STD foam. Polidocanol, being a mixture of fatty acids, does not induce an allergic reaction. It can be purchased from licensed compounding pharmacies in the US and compounded into
Evidence-based indications:* foam sclerotherapy, RFO and EVLT
Foam sclerotherapy
RFO
Figure 104.4 Tessari’s technique is so simple that it has become dominant in foam generation. Syringe contents are passed from one syringe into the other. Note angulation of the connector lock to reduce the size of the foam bubbles.
Strong (Level 1A)
Intermediate (Level 1C)
Anecdotal (Level 2C)
Long saphenous reflux C2–C6 varicose veins Recurrent varicose veins
Venous ulcers Lipodermatosclerosis Short saphenous reflux Venous malformations 23
Varicocele 41 Angiodysplasia Vascular tumors
Long saphenous reflux Short saphenous reflux C1–C3 varicose veins
42
C4 varicose veins (single modality) Long saphenous reflux Short saphenous reflux
*Assigned based on guidelines for assigning quality of evidence from: Guyatt G et al. Grading Strength of Recommendations and Quality of Evidence in Clinical Guidelines: Report from an American College of Chest Physicians Task Force. Chest 2006; 129; 174–81.
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Foam treatment of varicose veins 1–3% solutions according to guidelines published by the American College of Phlebology. Once a decision is made to proceed with foam sclerotherapy, we use polidocanol in a 1–3% dilution. The ability to use the proper concentration of foam in the right vein requires training and experience but there is broad latitude of safety. Foams with greater viscosity (i.e. more concentrated) are best used in larger veins. High viscosity foams are more powerful than low viscosity foams, which, in turn, are more powerful than liquid sclerosants. There is extensive evidence that relates high-viscosity foam to more complications in smaller diameter veins.14 A deliberate choice must be made between ultrasound cannulation of the great saphenous vein and simple cannulation of an available varix. In the latter case, a varicose vein tributary to the greater saphenous vein is identified. Under direct ultrasonographic observation, the foam is injected toward the saphenofemoral junction (usually about 5 ml). Firm pressure against the groin may be maintained with the ultrasound transducer to prevent central migration of the foam. This may be unnecessary. Next, the extremity is elevated 45∞ and a bolus is injected to fill distal incompetent veins (usually about 3 ml). Foam flows through incompetent valves and is blocked from passing into normal veins by competent valves. The deep venous system is carefully interrogated with the ultrasound probe. In case of foam migration to the deep system, vigorous ankle flexion/extension will dissipate the foam fragments. The question naturally arises: how much volume should be used in a foam injection? A number of animal and human studies confirm that a remarkable amount of air is tolerated within the circulatory tree. Indeed, Juan Cabrera used volumes upwards of 20 ml and more for his injections, though he reported a DVT rate of 6%.22 The question of optimal injection volume was addressed at the European Consensus Meeting in 2003.14 We generally use 8–15 ml of foam for the treatment of each leg. The aftercare of a patient treated with foam sclerotherapy is quite simple. Focal compression over varicose clusters is supplemented by a class III 30–40 mmHg stocking and further aided by appropriate elastic bandages. The objective of this treatment is to avoid blood trapping and maintain vein wall apposition so that the vessels, now stripped of their endothelium, will undergo fibrosclerotic healing. We recommend 48–72 hours of initial firm compression although 7–10 days might be better. Juan Cabrera Garrido and his colleagues in Granada, Spain, reported their experience with the rotating brush foam technique to treat great saphenous veins and venous malformations.22,23 STD foam was used in concentrations up to 3% and volumes up to 20 ml. After 5 years of follow-up, 81% of treated veins showed complete fibrosis. It was notable that their early experience with foam volumes of 20 ml or greater resulted in deep venous thrombosis in 6% of patients.18 At least five randomized controlled trials (RCTs) have demonstrated the efficacy of foam sclerotherapy. The most robust RCTs include the VEDICO trial and the more contemporary trial from Bountouroglou et al.15,24 Both trials enrolled a matched set of patients and treated primary varicose veins with similar techniques. They both sought to make important comparisons and generate new observations. At 3 months, both trials demonstrated comparable efficacy and safety when comparing liquid versus foam and SFJ
883
ligation and foam versus SFJ ligation/stripping. A trend towards hyperpigmentation was seen with foam treatment and saphenous nerve injury with vein stripping. Bountouroglou also showed that the hybrid procedure (SFJ ligation and foam) improves efficiency, cost, and time to normal activities. The VEDICO trial provides the longest available prospective randomized data involving foam sclerotherapy. It overwhelmingly confirmed the safety of foam, but the long-term efficacy data on foam as a single modality is less exciting. The data suggests that substantially more veins are present at 10 years when foam is used as a single modality when compared to surgery or surgery plus foam. If true, this still provides an important place for foam in the treatment of primary varicose veins in older patients and in all patients undergoing concomitant or sequential SFJ ligation or ablation. In the year 2001, the cost associated with severe venous insufficiency and venous leg ulceration in the US was over $1 billion.25 While evidence for the utility of foam sclerotherapy was developing, we used ultrasound-guided sclerosant foam injection to treat severe chronic venous insufficiency, varicose veins, venous angiomata and recurrent varicose veins after standard surgery.26 Foam generation was performed using the Tessari technique and access was nearly always through a varicose tributary to the great saphenous vein. Polidocanol was compounded to 1, 2, or 3% strength in a ratio of air to liquid sclerosant of 5:2. In the CVI group of patients, we identified 39 limbs of 29 patients to compare with a matched conservative treatment cohort (compression therapy only). Our analysis revealed that sclerosant foam healed ulcers faster and was more effective when compared with compression at 2 weeks. At 4 weeks, foam-treated patients were more likely to have less pain and to have healed ulcers. Immediate complications included one acute DVT (in a muscular vein) and two iatrogenic ulcers. There was only one treatment failure in a patient with well-established chronic venous insufficiency and occult femoropopliteal arterial occlusive disease. We believe that venous ulcers are perpetuated and lipodermatosclerotic skin is inflamed because of local venous hypertension transmitted from incompetent perforating veins and refluxing superficial veins. Using ultrasound examination it is possible to see a tangle of small venules under venous leg ulcers. This cluster of interwoven venules is also seen under lipodermatosclerosis and is in direct connection with incompetent and refluxing superficial veins as well as outflowing perforating veins. Foam sclerotherapy affords access to this microcirculation, which is otherwise inaccessible by surgical techniques. Superficial vein stripping or removal of refluxing superficial veins as well as interruption of perforating veins has an indirect influence on local venous hypertension while foam sclerotherapy has a direct effect in closing or obliterating the venular caput medusa that underlies lipodermatosclerosis and venous leg ulcers. Endovenous radio-frequency obliteration Endovenous radio-frequency obliteration (RFO) known as the “closure procedure” (VNUS Medical Technologies Inc., San Jose, CA), was introduced into Europe in 1998 and the US in 1999. Thermal occlusion of either saphenous veins results
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in fibrosis and exclusion from the circulation. This procedure can be performed in the interventional suite or in a properly equipped physician’s office under local anesthesia and is described in detail elsewhere in this volume. The Endovenous Radiofrequency Obliteration (Closure Procedure) Versus Ligation and Stripping (EVOLVeS) study showed significant early advantages for radio-frequency ablation over conventional vein stripping, with earlier return to work and normal activities, less pain, and better cosmesis.28 The 5-year results of registry patients (1,222 limbs) who received RFO are also quite impressive. Cumulative vein occlusion and absence of reflux at 5 years was 87% and 84%, respectively.29 The percentage of limbs exhibiting pain decreased from 85.3% pretreatment to 29.9% by 1 week, 10.0% by 6 months, and 8.5% by 5 years after RFO. Limb fatigue was improved from 78.6% of limbs before RFO to 7.3% at 1 week and 3.9% at 6 months after treatment. Of the limbs that met pre-established anatomic criteria for failure, 50% were closed with sclerotherapy. Endovenous laser therapy In endovenous laser therapy (EVLT), laser energy (most commonly from an 810-nm diode laser) is delivered to the desired location of either saphenous vein through a bare laser fiber passed through a sheath. Most published laser outcomes involve the Diomed 810-nm laser. Analogous to RFO, thermal ablation of the vein is induced as the laser fiber is slowly withdrawn. Venous ablation procedures have also been performed with 940-nm, 1064-nm, and 1320-nm lasers. These are described elsewhere in this volume. EVLT is often employed with adjunctive procedures, similar to the trends seen in the RFO experience. Huang et al. recently reported on 208 consecutive patients treated with EVLT combined with surgical strategies.31 In this study, EVLT was used as a single modality in only 15 patients. EVLT was combined with high ligation of the GSV and open ligation of perforators in 5 patients; with high ligation of the GSV in 76 patients; and with external banding of the first femoral venous valve and high ligation of the GSV in 112 patients. The authors noted that only three patients had recurrent varicose veins (1.4%) during a 2- to 27-month follow-up. Clinical CEAP classes significantly improved across all groups. No post-procedural symptomatic deep venous thromboses were reported.
Table 104.4
Contraindications
Foam Sclerotherapy Known allergy to local anesthetic Known allergy to sclerosant agent Acute DVT Coagulopathy Peripheral vascular disease (ABI < 0.8) Pregnancy Patent foramen ovale History of severe migraines May-Thurner syndrome (relative) Klippel-Trenaunay syndrome (relative) RFO Known allergy to local anesthetic Acute DVT Coagulopathy Peripheral vascular disease (ABI < 0.8) Pregnancy Aneurysmal section of the vein EVLT Same as RFO.
Very severe complications of foam sclerotherapy have not been reported. The largest published experience with complications of foam injection comes from Henriet in France.33 He describes more than 10,000 treatment sessions using 5% polidocanol over a 3-year period (average patient age was 51). Eighty percent of these were injections into reticular varicosities and frank varicose veins. Nine patients had immediate visual disturbances, eight had blurred vision lasting several minutes, one had monocular blindness which lasted 2 hours. Other immediate complications included vomiting in one patient and migraine in seven patients. All complications resolved.
Contraindications and adverse effects Table 104.4 summarizes the current contraindications to foam sclerotherapy, RFO, and EVLT. It is important to note three groups of patients in whom one must use judicious volumes of foam sclerosant. First, patients with a history of severe migraine might be more susceptible to transient migraineaura symptoms. Second, patients with a patent foramen ovale are more susceptible to systemic dissemination of foam. Finally, patients with May-Thurner or Klippel-Trenaunay syndrome, often have coagulation abnormalities after treatment of venous malformations.32 This predisposes them to both bleeding and thrombosis due to an underlying consumption coagulopathy.
Figure 104.5 Endovenous laser therapy (EVLT) is demonstrated as the diode is withdrawn along the length of the proximal saphenous vein (Copyright © evlt.ca, 2003).
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Figure 104.6 Successful EVLT duplex examinations (longitudinal views) of the great saphenous vein (GSV) at the saphenofemoral junction (SFJ). (a) Pretreatment scan demonstrated an incompetent SFJ after augmentation; (b) intraoperative color duplex interrogation showed successful occlusion of the GSV with a patent, 3-mm proximal stump (arrow 1) and absence of flow within the treated segment (arrow 2). From Puggioni et al. J Vasc Surg 2005; 42: 488–93.
Another report on the safety of sclerotherapy comes from Guex of Nice.34 He reported 12,173 sessions of sclerotherapy, 5,434 with liquid, 6,395 with foam, and 344 using both. Fourthousand and eighty-eight (33.9%) sessions were carried out with ultrasound guidance. Forty-nine incidents or accidents (0.4%) occurred, of which 12 were with liquid and 37 with foam. These were reported during the time of the study and an additional 1-month follow-up. Most numerous were 20 cases of visual disturbances (in 19 cases, foam or air block was used);
all resolved shortly, without any after-effects. A femoral vein thrombosis was the only severe adverse event in this study. Foam sclerotherapy does produce a definite trend toward more transient visual disturbances and migraine in pre-disposed individuals when compared to liquid.34 This is most probably due to passage of foam particles through a patent foramen ovale. Other complications observed in larger series and clinical trials include superficial thrombophlebitis, cough, and skin discoloration. Skin necrosis from foam injection into
Lower Extremity CVI
Standing Duplex
FS/EVLT/RFO
Primary Varicose Veins (C2-C4) GSR
LSR
RFO/ EVLT
Telaniectasias/Reticular veins (C1) GSR
LSR
FS
GSR
LSR
FS
Reassess 6 months
Cosmetic Result No symptoms
Venous Ulcer(C5-C6) GSR
FS/EVLT/RFO + Local FS
LSR
RFO/EVLT + Local FS
Reassess Frequently Symptomatic Persistence or Recurrence Failure to Heal
No Axial Reflux
Arteriora gm
Resolution
Repeat Venous Duplex Arterial Waveforms
Arterial insufficiency
Figure 104.7 Treatment algorithm. GSR – greater saphenous reflux; LSR – lesser saphenous reflux; FS – foam sclerotherapy; RFO – radio-frequency obliteration, EVLT – endovenous laser therapy. It is imperative to note that not all patients fall into a predefined treatment strategy, emphasizing the importance of clinical judgment and follow-up.
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small caliber reticular veins and telangiectasias are also a rare but clearly documented complication.35 Based on 5-year registry data, complications related to RFO include deep vein thrombosis (0.9%), skin burn (1.2%), clinical phlebitis (2.9%), and access site infection (0.2%).29 A single pulmonary embolism was reported in the VNUS registry. It is important to note, however, that the incidence of post-RFO deep venous thrombosis has been reported as high as 16%.36
Multi-modality treatment The morbidity of saphenectomy (excision of either saphenous vein) with its 40% incidence of sensory abnormalities is not trivial.38 Noting that most patients enrolled in RFO and EVLT registries underwent adjunctive treatments, such as sclerotherapy and stab avulsion phlebectomy, a recent focus of inquiry surrounds whether these procedures are even necessary. Indeed, Nicolini for the closure procedure investigators examined RFO-only patients versus RFO and stab avulsion patients and found no difference in symptom severity at 3 years.39 Monahan sought to investigate this same question by prospectively studying a group of patients with greater saphenous reflux and symptomatic varicose veins subjected to RFO.40 He carefully documented all varicose veins but did not directly treat them for a period of 6 months (only axial reflux was treated). Forty-two percent of the varicose veins resolved spontaneously after greater saphenous vein ablation during
this period. The resolved above-knee varicose veins were medially located, suggesting a direct relationship to the ablated saphenous vein. Posterior varicose veins were less prone to resolve spontaneously, whether the location was above or below the knee. The vast majority of the remaining veins were subsequently closed with sclerotherapy. Despite these interesting points raised by a number of investigators, the dogma behind 100 years of phlebology that calls for the extirpation (or ablation) of symptomatic varicose veins has not been rigorously overturned. The burden of proof will ultimately rest on multicenter, prospective randomized trials. Until such data becomes available, we propose an algorithm outlined in Figure 104.7 that calls for single modality treatment and watchful waiting for less severe venous disease (i.e. C1–C3) and multi-modality treatment for cases of severe CVI (i.e. C4–C6).
Conclusion Peripheral vascular interventionalists are amply trained in the technical maneuvers required for the percutaneous management of varicose veins. Whether employing foam sclerotherapy, RFO, EVLT, or a combination thereof, the careful appraisal of every new patient coupled with generous post-procedural follow-up is critical for positive patient outcomes. It is an exciting time for the safe and effective incisionless treatment of a wide variety of venous disorders.
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Linser P. Über die conservative Behandlung der Varicen. Med Klin 1916; 12: 897–8 McAusland S. The modern treatment of varicose veins. Med Press Circular 1939; 201: 404–10 Orbach EJ. Sclerotherapy of varicose veins: utilization of an intravenous air block. Am J Surgery 1944; LXVI(3): 362–6 Flückiger P. Nicht-operative retrograde Varicenverödung mit Varsylschaum. Schweiz Med Wochenschr 1956; 48: 1368–70 Wollman JC. The history of sclerosing foams. Dermatol Surgery 2004; 30(5): 694–703 Mayer H, Brücke H. Angiologie – Zur Ätiologie und Behandlung der Varizen der unteren Extremitäten. Chir Prax 1957; 4: 521–8 Cabrera J, Cabrera Garcia-Olmedo JR. Nuevo metodo de esclerosis en las varices tronculares. Patol Vasc 1995; 4: 55–73 Caggiati A. The saphenous vein compartments. Surg Radiol Anat 1999; 21: 29–34 Bergan, JJ. Etiology and Surgical Management of Varicose Veins in Vascular Surgery: Principles and Practice. Hobson, AW, Wilson, SE, Veiths, FJ, eds. New York: Marcel Dekker, 2004 Eklöf B, Rutherford RB, Bergan JJ et al. for the International Ad Hoc Committee of the American Venous Forum, Revision of the CEAP classification for chronic venous disorders: Consensus statement. J Vasc Surg 2004; 40: 1248–52 Bergan JJ, Schmid-Schönbein GW, Coleridge Smith PD et al. Chronic venous disease. N Engl J Medicine 2006; 355: 488–98 Nyamekye I, Shephard NA, Davies B, Heather BP, Earnshaw JJ. Clinicopathological evidence that neovascularization is a cause of recurrent varicose veins. Eur J Vasc Endovasc Surg 1998; 15: 412 Mekenas L, Bergan JJ. Venous reflux examination: Technique using miniatured ultrasound scanning. J Vasc Tech 2002; 26: 139–44 Breu F-X, Guggenbichler, eds. European Consensus Meeting on Foam Sclerotherapy, April, 4–6, 2003, Tegernsee, Germany. Dermatol Surg 2004; 30: 709–17 Belcaro G, Cesarone MR, Di Renzo A et al. Foam sclerotherapy, surgery, sclerotherapy, and combined treatment for varicose veins: a 10-year, prospective, randomized, controlled, trial (VEDICO Trial). Angiology 2003; 54: 307–15
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Alòs J, Carreóo P, López JA et al. Efficacy and safety of sclerotherapy using polidocanol foam: a controlled clinical trial. Eur J Vasc Endovasc Surg 2006; 31: 101–7 Hamel-Desnos C, Desnos P, Wollmann JC et al. Evaluation of the efficacy of polidocanol in form of foam compared to liquid form in sclerotherapy of the greater saphenous vein: intial results. Dermatol Surg 2003; 29: 1170–5 Monfreux A. Traitement sclérosant des troncs saphéniens et leurs collatérales de gros calibre par la méthode mus. Phlébologie 1997; 50: 351–3 Tessari L. Nouvelle technique d’obtention de la scléro-mousse. Phlébologie 2000; 53: 129 Tessari L, Cavezzi A, Frullini A. Preliminary experience with a new sclerosing foam in the treatment of varicose veins. Dermatol Surg 2001; 27: 58–60 Tessari L, Cavezzi A, Frullini A. Preliminary experience with a new sclerosing foam in the treatment of varicose veins. Dermatol Surg 2001; 27: 58–60 Cabrera J, Cabrera Jr A, Garcia-Olmedo A. Treatment of varicose long saphenous veins with sclerosant in microfoam form: Long-term outcomes. Phlebology 2000; 15: 19–23 Cabrera, J, Cabrera, J Jr. Garcia-Olmedio, MA, Redondo, P. Treatment of venous malformations with sclerosant in microfoam form. Arch Derm 2003: 139: 1409–16 Bountouroglou DG, Azzam M, Kakkos SK et al. Ultrasound-guided foam sclerotherapy combines with sapheno-femoral ligation compared to surgical treatment of varicose veins: early results of a randomized controlled trial. Eur J Vasc Endovasc Surg 2006; 31: 93–100 Margolis DJ, Bilker W, Santanna J, Baumgarten M. Venous leg ulcer: incidence and prevalence in the elderly. J Am Acad Dermatol 2002; 46: 381–6 Pascarella L, Bergan JJ, Mekenas LV. severe chronic venous insufficiency treated by foam sclerosant. Ann Vasc Surg; 20: 83–91 Welch HJ. Endovenous ablation of the great saphenous vein may avert phlebectomy for branch varicose veins. J Vasc Surg 2006; 44(3): 601–5
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Bergan JJ, Weiss RA, Goldman RP. Extensive tissue necrosis following high-concentration sclerotherapy for varicose veins. Dermatol Surgery 2000; 26: 535–42 Hingorani AP, Ascher E, Markevich N et al. Deep venous thrombosis after radiofrequency ablation of greater saphenous vein: A word of caution. J Vasc Surg 2004; 40: 500–4 Agus GB, Mancini S, Magi G; Italian Endovenous Working Group. The first 1000 cases of Italian Endovenous-laser Working Group (IEWG). Rationale, and long-term outcomes for the 1999–2003 period. Int Angiol 2006; 25(2): 209–15 Subramonia S, Lees T. Sensory abnormalities and bruising after long saphenous vein stripping: Impact on short-term quality of life. J Vasc Surg 2005; 42: 510–4 Nicolini P. Closure Group. Treatment of primary varicose veins by endovenous obliteration with the VNUS closure system: results of a prospective multicentre study. Eur J Vasc Endovasc Surg 2005; 29: 443–9 Monahan DL. Can phlebectomy be deferred in the treatment of varicose veins? J Vasc Surg 2005; 42(6): 1145–9 Lord DJ, Burrows PE. Pediatric varicocele embolization. Tech Vasc Interv Radiol 2003; 6(4): 169–75 Vogel H, Niemeier J. Indications, procedures and choice of embolization material in transcatheter vascular occlusion. Rontgenblatter 1985; 38(8): 265–9
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Index Page numbers in italic denote figures or tables. PVI = peripheral vascular interventions abciximab in CAS 341 in endovascular revascularization 390 in intracranial stenting 252 in PAD 817 in stroke 271 acute ischemic 293 in vertebral artery PTAS 379 abdominal angina 553 abdominal aorta branches 842 duplex ultrasound 457 focal stenosis 590 inflammatory arteritis 737 abdominal aortic aneurysms (AAAs) in Behçet’s disease 744 CECTA imaging 496 duplex ultrasound 457 endografts 445, 445, 446 endoluminal exclusion 449–55 aneurysm shrinkage 452 encapsulation of stent 452 endograft breakdown/migration 453 endograft occlusion 453 endoleaks coil embolization 453 type I/III 452 type II 452–3 future perspectives 454 historical perspective 449–54 neck dilatation 451–2 supported vs non-supported devices 454 video-assisted clipping of vessels 453 imaging 476 Parodi endograft 449–50 treatment branched grafts 477–8 interventional 475–8 Vanguard endograft 449, 450–1 complications 452–3, 454 see also thoracoabdominal aneurysms abdominal aortic dissections 459 clinical presentation 461–2 complications 462 diagnosis 461–2 radiologic 462 follow-up 465 imaging 462, 465 indications for intervention 462 isolated 461 management 465 malperfusion syndrome 462, 465 pathogenesis 461 rupture 461–2 treatment medical 462, 464, 465 surgical 464–5
see also infrarenal aortic dissection abdominal aortic occlusive disease 467–72 complete aortic calcification 470 treatment 467–8 complications 469–70 PTA 467 results 470 stenting 467–8 surgery 467 technical considerations 468–9 abdominal aortography 845 catheters 846 Absolute Stent System 133–4, 636 ACAS (Asymptomatic Carotid Atherosclerosis Study) 200, 300 access see under specific access sites, conditions and interventions Acculink 328 Acculink for Revascularization of the Carotids in High-Risk Patients (ARCHER) trial 160, 314, 336, 337 AccuNet Filter 328, 753 AccuNet system 160, 160, 314 acetazolamide test see Diamox test n-acetylcysteine (NAC) 803, 804, 806 ACSRS (Asymptomatic Carotid Stenosis and Risk of Stroke) study 225–6 acute aortic syndrome 440 acute cerebrovascular ischemia 190 acute ischemic stroke (AIS) 288, 295–6 combinational IA–IV thrombolysis 293–4, 296 diagnosis 289 intervention treatment 288–99 evaluation 289 grading 289–90 literature review 289–90 recanalization rates 288 intra-arterial (IA) thrombolysis future directions 296–7 imaging developments 296–7 mechanical 294–6 pharmacologic 290, 292–4 vs intravenous (IV) 288–9 recanalization rates 289 acute limb ischemia (ALI) 648–55 categories, clinical 649, 650 causes 648 classification 649 clinical presentation 649 epidemiology 648–9 6 p’s 652 tissue/limb loss 648–9 treatment 649–54 algorithms 651 chemical thrombolysis 650 CIS power-pulse spray 651–4, 652 case studies 651–2
protocol 651 femoral-popliteal bypass graft 653 surgery, open 650 acute lower limb ischemia 595 acute mesenteric ischemia (AMI) angiography 558–9 clinical presentation 557–8 signs 558, 558 symptoms/diagnosis 557, 557 diagnosis 558–9 non-occlusive 555 pathophysiology 555 radiographic findings 558 thumb printings 558 treatment endovascular therapy 574–5 general measures 574 surgical revascularization 584 advantages 582 indications 584 adenomyosis 693, 696 adenopathy 858 adenoviral vectors 782, 783 Advanta stent 143 age and ARAS 487, 491 and atherosclerosis 190 in carotid angioplasty/stenting 302 in PAD 822 Alberta Stroke Program early CT score (ASPECTS) 289 ALI see acute limb ischemia (ALI) Allen’s test 22 in thromboangiitis obliterans 664 ALLHAT (Antihypertensive and Lipid Lowering to Prevent Heart Attack Trial) 813 alteplase (Activase) 817 in acute limb ischemia 650 in DVT 122 in pulmonary embolism 850 in thoracic outlet syndrome 412 Alteplase Thrombolysis for Acute Neuro-interventional Therapy in Ischemic Stroke (ATLANTIS) 263 ambulatory phlebectomy 866, 867 AMI see acute mesenteric ischemia (AMI) amlodipine 802 Amplatz Clot Buster 113 Amplatz gooseneck snare 179, 180 Amplatz thrombectomy device (ATD) 852 Amplatzer occluders 709–10, 709 amputation in CVM 717 in thromboangiitis obliterans 664, 666, 668 anastomoses, stenotic 707 anastomotic graft marker (AGM) 642, 653
889
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anatomy aortic arch 192, 192 carotid arteries 195, 196 common 192 internal 193, 194–6, 194 cerebral circulation anterior 192–6, 195 posterior 196–7, 196, 197 neuroradiological 192–8 anesthesia, tumescent 867–8 aneurysms with aortic dissection 461 in Behçet’s disease 743, 744–5, 744 complications 4 covered stents for 150, 153 definition 432 formation 4 intracranial 182 stent-assisted coiling 249 after stent placement 145 in stroke 279, 280–1 wide-necked 249 see also abdominal aortic aneurysms; iliofemoropopliteal aneurysms (IFPAs); peripheral aneurysms; pseudoaneurysms; thoracic aortic aneurysms angina abdominis 553 Angio-Seal 173–4 complications retroperitoneal hemorrhage 176 thrombosis 175 angiogenesis 182–3, 867 angiogenic growth factors 782–4 angiography access 844–5, 847 arterial 29, 169 in Budd–Chiari syndrome 729 contrast agents 564–5 failing infraingual vein graft 659, 659 in fibromuscular dysplasia 732–3 iliac occlusive diseases 607 infraingual vein graft, failing 657 intra-arterial 605 lower extremity arterial disease 596, 597, 598, 604 markers 10–11 quantitative online angiographic analysis 564 transient ischemic attack 230 Angioguard filters in internal carotid artery stenting 753 in renal angioplasty/stenting 534 Angioguard XP 160, 160 Angiojet 101, 105, 107, 113, 852 in ALI 653 in DVT 121–2 in pulmonary embolism 114 in stroke 294 AngioLink 174 angioplasty 39 in Budd–Chiari syndrome 728, 729 for chronic total occlusions 94 inflammatory arteritis 737 peripheral 165 popliteal approach 30 stent-assisted in intracranial stenosis 238–46 history 238–9 medical treatment 240–1 outcomes 242–3 patient selection 239 preoperative assessment 240 procedure 241–2 superficial femoral artery 32 see also balloon angioplasty; subintimal angioplasty; vibration angioplasty
angiotensin-converting enzyme (ACE) 490 angiotensin-converting enzyme (ACE) inhibitors 490 in intracranial atherosclerosis 385 ankle–brachial pressure index (ABPI) 595, 601 exercise ABPI 595 antecubital fossa 24 antegrade femoral artery access 15–16 complications 16 indications/contraindications 15 landmarks 15, 16 antegrade percutaneous popliteal access 29–30 antegrade popliteal puncture 30–1 anterior cerebral artery (ACA) 194, 195 anterior descending artery 756 anterior tibial artery lesions, Rotablator in 60 anticoagulation 850, 850 Antihypertensive and Lipid Lowering to Prevent Heart Attack Trial (ALLHAT) 813 antioxidants 803 antiplatelet drugs 306, 338, 813 aorta digital subtraction angiography 498, 499 see also abdominal aorta; thoracic aorta aortic aneurysms 620, 623 treatment 619 endovascular aortic aneurysm repair (EVAR) 800–1 see also abdominal aortic aneurysms (AAAs); thoracic aortic aneurysms aortic arch anatomic variations 192, 192, 193, 301 anatomy 192, 192 bovine-type 423, 424 double 424 embolic potential 358 imaging 422 right-sided 424, 425 see also thoracic aorta aortic endartectomy 467, 468 aortic pseudoaneurysms 427, 428 aortic transection 429 aortoarteritis see Takayasu’s disease aortocoronary bypass grafting 752 aortography abdominal aortic dissections 462 thoracic aortic aneurysms 434–5 aortoiliac lesions classification 40 management guidelines 39–40, 40 aortorenal bypass 540 aortorenal graft thrombosis 112 ARAS see atherosclerotic renal artery stenosis (ARAS) ARCHER (Acculink for Revascularization of the Carotids in High-Risk Patients) trial 160, 314, 336, 337 Arrow-Trerotola device 852 Arteria system 327–8 arterial access 15–33 femoral artery 168–70 “safe zone” 168, 169, 170 see also specific approaches arterial fibrodysplasia see fibromuscular dysplasia arterial occlusion following PTA 103 as indication for CDTT 103 Rotablator, use of 60 arterial occlusive lesion (AOL) recanalization score 290, 291 arterial pressure, ankle vs brachial 591 arterial spasm 66 arterialization of venous circulation 666, 667
arteriography cerebral 390 classification of cerebrovascular disease 388–9 renal 503 arteriosclerosis and aneurysm rupture 420 arteriovenous dialysis studies 780 arteriovenous fistulae duplex ultrasound 458, 459 as PVI complications 793–4, 793 stent-assisted angioplasty 249–51 arteriovenous malformations (AVM) AV shunting malformation 716 embolization therapy 689–90, 690, 713, 714 therapy approach 717 arteriovenous shunting 832 arteriovenous shunting malformation (AVM) 716, 718 ascending phlebogram 120 ASian Paclitaxel-Eluting stent Clinical Trial (ASPECT) trial 253 ASPECT (ASian Paclitaxel-Eluting stent Clinical Trial) trial 253 ASPECTS (Alberta Stroke Program early CT score) 289 aSpire covered stent 142–3, 151 aspirin in arterial access 30 for CAS 306, 338 in CDTT 103 in endovascular revascularization 390 in endovascular stent placement 576 in failing infraingual vein graft 658 in infra-popliteal disease 635 in intracerebral hemorrhage 268 for intracranial atherosclerosis 385 intracranial stenosis treatment 240, 243 in intracranial stenting 252 in limb salvage 633 in PAD 814, 817 plus warfarin 658 in RAS 504 in renal angioplasty/stenting 532 in stent-assisted angioplasty 390 for stent reocclusion 153 in subclavian artery PTA 361 in thromboangiitis obliterans 664, 666 in vertebral artery PTAS 379 asymmetric dimethylarginine (ADMA) 813 Asymptomatic Carotid Atherosclerosis Study (ACAS) 220, 300 Asymptomatic Carotid Stenosis and Risk of Stroke (ACSRS) trial 220, 222, 223–4, 225–6 atherectomy debulking 74–5, 77–8 in femoropopliteal disease 628 history 69 atherectomy systems Rotablator 59–68 SilverHawk® atherectomy device 50–8 see also Rotablator; Rotarex system atheroembolism in angioplasty 527 clinical presentation 527–8 diagnosis 528 in PTRA 526, 534 in RAS 521–2 and renal function 528 atherogenesis 3 atherosclerosis 3 in cardiac artery 187 gene therapy for 785–6 in iliofemoropopliteal lesions 675 in lower extremity arterial disease 589
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Index atherosclerosis (Continued) natural history 5 plaques see plaques stent-assisted angioplasty 247–9, 248 staged 249 subclavian artery lesions 354 atherosclerotic renal artery disease 539 atherosclerotic renal artery stenosis (ARAS) 487–93, 502 and age 487, 488, 491 antioxidant therapy 491 complications 489 in end-stage renal disease 539 epidemiology 487–8 incidence 487–8, 488 and ischemic nephropathy 491 pathophysiology 490–1 risk factors 488–90, 491 treatment algorithm 499 vascular co-morbidity 488–90, 489 atherothrombosis 4 atherotomes 46 see also cutting balloons (CB) ATLANTIS (Alteplase Thrombolysis for Acute Neuro-interventional Therapy in Ischemic Stroke) 263 atrial natriuretic peptide 801 atrial septal defect (ASD) closure 709, 711 autologous vein graft 642 Avitene 683 axillary artery thrombosis 102, 104 Axiom Artis dBA system 10 balloon(s) balloon catheters 181 coated 773 cutting see cutting balloons (CB) balloon angioplasty coated balloons 773 failing infraingual vein graft 659–60, 659 femoropopliteal arteries 41–2 fibromuscular dysplasia 733 iliac occlusive diseases 610–11 iliac PTA 40–1 inflammatory arteritis 736 intracranial atherosclerosis 388–9 pulmonary embolism 852 risks/complications 389 stent-assisted 247–9 failing infraingual vein graft 659, 660 tibial lesions 642 see also cutting balloon angioplasty balloon-expandable stents 132, 133–8 in CAS 323 crashed/thrombosed stent 627 in iliac occlusion 611 see also Advanta; Jostent balloon protection device see embolic protection devices (EPDs), distal occlusion basic fibroblast growth factor (bFGF) in gene therapy 782 in PAD pathogenesis 4 basilar artery 196, 196 basilar artery disease 189 PTA in 274 stenting 242, 243 vessel rupture during angioplasty 392 basilar trunk aneurysm 250 Behçet’s disease 743–7 abdominal aortic aneurysms 744 clinical presentations 743 description 743 diagnosis/diagnostic criteria 743, 744
epidemiology 743 pathology/pathogenesis 743–4 treatment endovascular 745 medical 744 surgical 744–5 Belgian Netherlands Stent Study (BENESTENT) 764 Below-The-Knee Chill trial 646, 772 Bentsen guidewires 38 beta-blockers 464, 465, 481 beta radiation 776 catheter-based 777 Beta Radiation following balloon angioplasty for improving life pan of recurrent failed ArterioVenous fistulae (BRAVO) study 777, 780 BetaCath system 777, 778 bicarbonate 802, 806 “Big Chill” trial 646, 772 biliary stents 133–4 biotape retrieval system 181 Bird’s Nest filter (BNF) 875, 876 bivalirudin 93, 338, 504 Blalock–Taussig anastomosis 705 bleeding complications of PVI 792–3, 793 blood flow energy losses 590–1 blood flow velocity infrarenal aorta 5 in PAD pathogenesis 4 blood pressure stroke 258 see also hypertension blood viscosity and cerebrovascular resistance 229 in PAD 824 and plaque deposition 4 and Raynaud’s syndrome 402 and serial stenoses 590–1 blue toe syndrome 103, 608, 656 BM stent 329 bone marrow-derived mononuclear cells (BM-MNCs) 183 Boomerang Closurewire 173, 173 bovine-type aortic arch 423, 424 brachial access 23–4, 845 carotid angioplasty/stenting 310 in CAS 310 contraindicated 30 limitations 33 renal angioplasty 503, 506–7 subclavian artery PTA 355, 355, 359 brachial arteriography 718 AV shunting malformation 718 brachial artery complications 23–4 indications 23 thromboaspiration in 115 brachial artery thrombosis 104 brachial–radial artery bypass 405 brachiocephalic vein stenosis 862 brachytherapy 771–2, 776–81 limitations 780 and probucol 780 and restenosis 780 of renal arteries 780, 780 brain hemorrhage 331 brain infarcts, silent 303 branch vessel dissections 480 branched grafts 477–8 CT imaging 477 gold markers 477 helical 477, 479
891
implantation 477 BRAVO (Beta Radiation following balloon angioplasty for improving life pan of recurrent failed ArterioVenous fistulae) study 777, 780 bronchial embolization 685, 686 Budd–Chiari syndrome 725–31 abdominal wall appearance 726 clinical experience 727–30 compensatory circulation 727 description 725 diagnosis 725–6 differential diagnosis 725 endovascular treatment 725 epidemiology 725 imaging 725–6 inferior vena cava obstruction 726 management 726–7 balloon angioplasty 729 with stenting 727, 728 clinical experience 728–30 Buerger’s disease see thromboangiitis obliterans bupropion, sustained-release 811, 812 buttock claudication 593 Buttoned devices 709–10 Bx Velocity stents 753, 755, 757 bypass grafts durability 630 mesenteric ischemia 581 occluded cutting balloon angioplasty in 47–8 as indication for CDTT 103 stenosis 637 for SVC occlusion 859 in thromboangiitis obliterans 666 vein 47–8 CABERNET (Carotid Artery Revascularization Using the Boston Scientific Filter Wire EX/EZ and the Endo Tex Nex Stent Trial) 337 calcitonin gene-related peptide (CGRP) 342 calcium channel blockers 464, 802–3 calf claudication 593 calf DVT 124–6 CAMPER trial 814 CAPRIE (Clopidogrel Versus Aspirin in Patients at risk of Ischemic Events) trial 814–15 captopril renography 499, 500, 503 carbamazepine 269 carbon dioxide as contrast agent 564–5 cardiovascular disease and PAD 822 CARESS (Carotid Revascularization Using Endarterectomy or Stenting Systems) trial 330, 337–8 carotid angioplasty/stenting (CAS) 165, 309, 322, 338 access site location 338, 338 angiography, periprocedural 307 assessment, preprocedure 301 B-mode imaging 200 catheters 306–7, 308 co-morbidities 304 complications 336–44, 338, 345 avoidance 343 preprocedural 338, 343 intraprocedural 339–41, 343 postprocedural 341–2, 343 delayed 342–3, 343 from registries/trials 336–8 current status 345, 346 in elderly patients 345 follow-up 204
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carotid angioplasty/stenting (CAS) (Continued) future directions 346 indications/contraindications 301–4 conventional 302 emerging parameters 302–3 outcomes 327 long-term 332 patient selection 338 practical advice 304–5 predilatation, with/without 324–5 under protection 300–35, 345 access 306–7, 310, 310 site assessment 321 angioplasty 340–1 circulation assessment 321 clinical experience 325–6 delayed embolic events 331 lesion site assessment 321, 323 medication 306 outcomes 327 with different stents 329 high-/low-risk patients 327, 329 morbidity/mortality 328, 329, 330, 331 symptomatic/asymptomatic patients 327 protection devices 304–5, 310–14, 316–21 choice of 321, 323 complications 340, 341 distal occlusion 311–14, 340 filters 316–20, 326–7, 339 flow reversal technique 320–1 in place 341, 342 placement 339, 340 proximal occlusion 340 sizing 339, 340 stents implantation 324–5 selection 323–4, 327 sizing 340 techniques 305–7, 310 restenosis rates 346 selection criteria general 302–3 specific 303–4 after stent placement 342 team 304 techniques 307, 309 learning curve 305 new 304 timing 338 ultrasound before 201–2, 202 ultrasound during 203 ultrasound after 203–4, 204–5 vs CEA 345, 346 carotid arteries 187 access see direct internal carotid artery puncture anatomy 195, 303–4 dissection 189 duplex ultrasound 458, 458 inflammatory arteritis 737, 740 restenosis 767 stents/stenting 132, 135, 139 duplex ultrasound 458 embolic protection device 165 see also common carotid artery; internal carotid artery carotid artery disease 187–8, 200 characterization, standardization of 201 CT imaging 197, 198, 235, 236 differential diagnosis 190 spontaneous dissection 189 stenosis quantification 199–201 anatomic quantification 199
area reduction 200, 200 degree 199 diameter reduction 199–200, 200 morphological approach 200 see also carotid plaque; carotid stenosis Carotid Artery Revascularization Using the Boston Scientific Filter Wire EX/EZ and the Endo Tex Nex Stent Trial (CABERNET) 337 carotid endartectomy (CEA) 187, 345 and CAS 336–8, 341–2, 343, 345, 346, 346 without stenting 345–7 patient selection 346 carotid plaque hemorrhage 212 hyperechoic 211, 214 hypoechoic 211, 214 and stenosis 219–20, 222, 224 stroke, risk of 214 ulcerated 219 ultrasound characterization 211–28 analysis image 215 B-mode imaging 200, 212 normalization 214–17, 215, 223, 225 black area near lumen 225, 226 classification (types) 211–12, 218 follow-up comparisons 219, 223 and neurological events 223 stenosis and risk of stroke 223–4, 224 visual vs computer classification 218 vs risk 213, 220, 222, 224 discriminant function analysis 225 echodensity and structure 217–19 cross-sectional studies 217 prospective studies 217–19 echogenicity 212 future perspectives 225–6 histology, correlation with 212–17 natural history studies 213–14, 222 shape 212 texture analysis 225–6 carotid pseudoaneurysm 10 Carotid Revascularization Using Endarterectomy or Stenting Systems (CARESS) trial 30, 337–8 carotid siphon stenosis 385–6 carotid stenosis asymptomatic 188 natural history studies 222 common carotid artery 388 and plaque 219–20, 222, 224 and risk of stroke 223–4, 224, 225 symptomatic 188–9 carotid–subclavian artery bypass 404 CAS see carotid angioplasty/stenting (CAS) CASPAR trial 814 Catheter-Based Plaque Excision with SilverHawk® in Critical Limb Ischemia 640 catheter-based radiation systems 777 catheter-directed intra-arterial thrombolytic therapy (CDTT) 99–110 adjunctive technique 101, 103 agents 99–101 clinical experience 108–9, 109 complications 105–6, 109 contraindications 105 delivery systems 101 disadvantages 111 dosage 101 for DVT 122 technical aspects 123–4 follow-up/monitoring 108, 109 goals 99 indications 103–5
patient preparation 108 patient selection 106–8 percutaneous intra-arterial thrombolysis 109 technique 108 catheter suction thromboembolectomy see thromboaspiration catheters ablation 866 angiographic/diagnostic 17, 34–6, 845, 846 shapes 35, 36 sizes 36 end-hole 846 guide 36–7, 37 infusion 38 internal mammary artery (IMA) 17 microcatheters 38 for peripheral angiography 845, 846 side-hole 846 suction 852–3, 853 CAVATAS trial 328, 331 CB see cutting balloons (CB) CDTT see thrombolytic therapy, catheter-directed intra-arterial CECTA see contrast-enhanced computed tomography angiography celiac artery 843 anatomy 562 atherosclerosis 553 compression 554, 554 stenosis 564 stents/stenting 567 celiac artery stenosis 572, 573 celiac axis compression syndrome 554 cellular proliferation in restenosis 766 cerebral arteries anterior 194–6, 195 elective endovascular revascularization 382–97 posterior 195, 196–7 urokinase treatment 267 cerebral arteriography 390 cerebral artery stenosis 243 cerebral autoregulation 229 impairment 229 stroke and 258 cerebral blood flow (CBF) determination 229 thresholds in ischemia 232 cerebral embolism prevention 305–7, 310 cerebral infarcts 275, 280 cerebral perfusion 229 cerebral perfusion imaging 229–37 in acute ischemic stroke 233–4 in chronic ischemia 235 methods 229 in revascularization therapy 235–6 transient ischemic attack 230–1 cerebral perfusion pressure 229 cerebrovascular disease (CVD) 589 cerebrovascular reserve 303 cerebrovascular resistance 229 CFA see common femoral artery (CFA) CHARISMA (Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Management and Avoidance) trial 814, 815 chemotherapy 859 Chinese Acute Stroke Trial 271 cholesterol embolization 797 cholestyramine 812 chronic limb ischemia see critical limb ischemia (CLI) chronic mesenteric ischemia (CMI) 553 access
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Index chronic mesenteric ischemia (CMI) (Continued) brachial artery 578 retrograde CFA 577 clinical presentation 558, 559 diagnosis 559–60 functional assessment 558–9 pathophysiology 555–6 survival rates 577 tonometry 558–9 treatment 582 endovascular therapy 575–8, 576 medical therapy 575 percutaneous transluminal angioplasty 575, 576, 577, 578 stents/stenting 575–6, 576, 577, 578 surgical revascularization 582 indications 584 results 582, 583 vs endovascular therapy 583 chronic obstructive pulmonary disease (COPD) 420, 432 chronic renal failure, contrast-induced 805 chronic total occlusions (CTOs) angioplasty/stenting 94 complications 94–6 future technologies 96 medical management 96–7 recanalization 92–8 crossing CTOs 93 devices 94–6 thrombolytic therapy 96 chronic venous disease (CVD) 838–9 classification 880 chronic venous insufficiency 832–3, 864, 881 cigarette smoking see smoking cilostazol 664, 815 Cimino-Brescia AVF 699 malfunctioning 700 CIN see contrast-induced nephropathy circle of Willis 193, 194, 194, 229 patency 202 circumferential artery occlusion 385 CIS power-pulse spray 651–4, 652 in ALI 652–4 case studies 651–2 protocol 651 citicoline 274 claudication 593 femoropopliteal disease 625 with hypogastric artery stenosis 614, 615 in iliac occlusive diseases 606 intermittent see intermittent claudication SilverHawk® for 50, 52 therapy 815–17 thigh/limb 590, 593 CLI see critical limb ischemia; critical limb ischemia (CLI) clofibrate 812 clonidine 811 clopidogrel arterial access 30 for CAS 306, 338 in endovascular revascularization 390 in intracerebral hemorrhage 268 intracranial stenosis treatment 240, 243 in intracranial stenting 252 in PAD 814 in RAS 504 in renal angioplasty/stenting 532 in stent-assisted angioplasty 390 for stent reocclusion 153 in subclavian artery PTAS 361
in thromboangiitis obliterans 664 in vertebral artery PTAS 379 Clopidogrel for High Atherothrombotic Risk and Ischemic Stabilization, Management and Avoidance (CHARISMA) trial 814, 815 Clopidogrel Versus Aspirin in Patients at risk of Ischemic Events (CAPRIE) trial 814–15 closed-cell stents 323, 323, 324 CMI see chronic mesenteric ischemia (CMI) coarctation of aorta 427–8, 429 pseudocoarctation 427–8 transluminal balloon angioplasty 704 stenting 704, 704 coated balloons 773 coated stents see stents/stenting, covered/coated Cobra catheter 619 for peripheral angiography 846, 847 for SVC occlusion 859 Cockroft–Gault formula 800, 801 coil embolization 181–2, 714 coils 181, 684 in congenital vascular malformation 714 in CVM 714 hypogastric artery 616–18, 618, 619, 620, 621, 623 bilateral 622 choice of coils 617 internal iliac artery 673 pulmonary arteriovenous malformation 690 colestipol plus niacin therapy 812 Collaborative Rotablator Atherectomy Group (CRAG) study 64, 66, 67, 628 collagen, microfibrillar 683 collateral circulation and autoregulation 229 in stroke treatment 274 collateral vein, intrahepatic 726, 727 common carotid artery anatomy 192 PTAS 348–52 surgical options 350 common femoral artery (CFA) 844 access 845 safety in 168, 169 see also antegrade femoral artery access; contralateral iliofemoral artery access minimal luminal diameter 172, 172 common femoral artery lesions 51, 53, 55 common hepatic artery atherosclerosis 553 common iliac arteriovenous fistula 617, 622 common iliac artery 843 aneurysms 617, 619–20, 623 bifurcated graft 623 stenosis 597, 608 completed stroke, definition of 189 complications of PVI 791–8 angioplasty site 794–6 abrupt closure 796 dissections 794 perforation/dissection 795 stent thrombosis 796 thromboembolism 795 thrombosis 796 systemic 796–7 cholesterol embolization 797 contrast-related 796–7 radiation injuries 797 vascular access site 792–3 arteriovenous fistulae 793–4, 793 bleeding complications 792–3, 793 dissections 794 hematomas 792–3 infection 794
893
pseudoaneurysms 793, 793 thromboembolism 794 vascular closure devices 794 see also under specific conditions and interventions compression stockings 124 compression syndromes 408–16 Compressor 169 computed tomography (CT) for abdominal aortic aneurysms 476 for abdominal aortic dissections 462, 463 for acute ischemia stroke 297 for aortic disease 422–3, 423, 426, 433–4 for DVT 121 in neuroradiological anatomy 197–8 for RAS 503 for thoracic aortic aneurysms 476 for thoracic aortic dissections 480 computed tomography angiography (CTA) contrast agents 565–6 lower extremity arterial disease 598, 598, 604, 605 mesenteric arteries 564, 565–6, 566 multi-detector 847 in neuroradiological anatomy 197 rendering (post-processing) 566 scanning/reconstruction parameters 567 visualization techniques 566 vs magnetic resonance angiography 568 computed tomography perfusion 297 conduit stenting 706–7 Conformexx Biliary Stent 136 congenital aortic valve stenosis 704–11 congenital heart diseases 704–6, 705 congenital vascular malformation (CVM) 712 AV shunting malformation 716, 718 classification 712 diagnosis 712 endovascular treatment 712–21 access 713–14 adjunctive therapy 713 clinical experiences 714, 716 coil/glue embolotherapy 713, 714 ethanol sclerotherapy 714, 717–18 independent therapy 713 indications 713, 713 selection of treatment 713–14 follow-up 712–13 imaging 712 lymphatic malformation 714, 716, 717–18 management 712 venous malformation 714, 715–16 congestive heart failure 785–6 continuous infusion method 101 contralateral iliofemoral artery access 16–18 indications/contraindications 17, 17, 30 contrast agents 841–2 conventional angiography 564–5 volumes in PVI 801 contrast-enhanced computed tomography angiography (CECTA) pelvic artery stenosis 497 renal arteries 495 stenosis 496, 497, 499, 500 contrast-enhanced imaging 841–8 catheters, diagnostic 845 clinical anatomy 842–4 complications access site complications 847 contrast-induced nephropathy 847 contrast agents 841–2 emerging non-invasive modalities 847–8 patient history 844–5
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contrast-enhanced imaging (Continued) revascularization, previous 844–5 vascular anatomy 844 vascular access 844–5, 847 contrast-enhanced magnetic resonance angiography (CEMRA) 496, 496, 497, 497, 499, 500 contrast-induced nephropathy (CIN) 797, 799–807 clinical presentation 801 definition 799 epidemiology 799 future directions 805–6 outcomes 801 pathogenesis 799 prevention 801–5 antioxidants 803 diuretics 803 fluid administration 802 prophylactic strategies 802 renal replacement therapies 803–5 vasodilators 802–3 renal replacement therapies 806 risk factors 797, 800–1, 800 contrast injectors 435 Cook retrieval forceps 180, 181 Cordis biopsy forceps 181 Cordis nitinol stent 143, 151 Corinthian stent 360 in lower limb artery stenting 757 in renal artery stenting 755 in vertebral artery occlusion/stenosis 374 Corona system 777 coronary arteries inflammatory arteritis 740 stenting 753, 756 coronary artery bypass graft (CABG) 753, 756, 816 coronary artery disease (CAD) 589–90 coronary–cardiac fistulae 707, 710 coronary heart disease (CHD) 488, 489, 490 coronary steal syndrome 354, 365 coronary stents intracranial use 389 for peripheral arteries 132, 139 Corvita Endoluminal Graft 141, 141 clinical experience 148, 148–9 follow-up, long-term 151 lesion characteristics 150 iliofemoropopliteal lesions 671, 673, 673, 674, 674, 677, 678 coumarin in CAS 341 in limb salvage 633 COVENT study 151 covered stents see stents/stenting, covered/coated CRAG (Collaborative Rotablator Atherectomy Group) study 64, 66, 67, 628 Cragg Endopro System 1/Passager 140–1, 141 clinical experience follow-up, long-term 147, 147 lesion characteristics 146 lesion locations 146 restenosis 147 results 146 iliofemoropopliteal lesions 671, 673, 674, 675, 677 locations 141, 144–5 Cragg infusion wires 38 CREST trial 330 critical limb ischemia (CLI) 639–47 classification 640 clinical presentation 639–40
diagnosis 641 epidemiology 639 femoropopliteal disease 625–6 mortality 589 pathophysiology 639–40 plaque excision 643 risk factors 640 SilverHawk® for 50, 52, 53, 56 stenting 139, 634 symptoms/diagnosis 640 treatment 589, 640–4, 646 cryotherapy 644, 644, 645, 646 laser 640, 643, 644 prostaglandins 816 PTA vs PTAS 643 surgical bypass 642–3 see also thromboangiitis obliterans (Buerger’s disease) critical stenosis 590 Crosser system 95, 96 cryoplasty 628, 772 cryotherapy 644, 644, 645, 646 CTOs see chronic total occlusions cutting balloon angioplasty 45–9 clinical experience in hemodialysis fistula 48 in-stent restenosis 47–8 lower extremity arteries 47 lower limb vein bypass graft 47–8 pulmonary artery stenosis, peripheral 48 pulmonary vein stenosis 48 Takayasu’s disease 46–7 complications 48 device description 45 hemodialysis access problems 700, 701 mechanism 45 technical aspects 45–6 cutting balloons (CB) inflated 46 mechanism of action 45 selection 45–6 CVM see congenital vascular malformation (CVM) cyanotic congenital heart disease 707 Cypher stent 753, 754, 755, 756 Dacron grafts 676 danaparoid 270 DeBakey classification 439 deep vein thrombosis (DVT) 121 acute left leg 127 acute lower extremity 125 calf 124–6 chronic lower extremity 119–31 clinical appearance 119 clinical experience 127–30 compressibility test 836 diagnosis 119 work-up 120–1 iliofemoral/iliocaval obstruction 127–30 long-term sequelae 120 recurrent 130 risk/contributing factors 835 symptomatic 119 tibial thrombus 124, 125 treatment 873 endovenous therapy 121 mechanical thrombectomy 121–2 stenting 125, 126–7 understenting 127 thrombolysis 122–3, 125 catheter-directed 123–4 flow-directed 124–6, 125
depressive hemicraniectomy 275–6 Dextran 390 dextrans, low-molecular 664 Diabetes Control and Complication Trial 812 diabetes mellitus and ARAS 489–90 foot infections 633 and hemodialysis access problems 702 in PAD 4, 5, 812, 823 and SIA complications 90 dialysis access grafts, thrombosed 104 Diamox (acetazolamide) test 207, 208, 235 dietary interventions 491 diffusion-weighted imaging (DWI) see under magnetic resonance imaging (MRI) digital subtraction angiography (DSA) 8, 10, 498, 499 aorta 497, 498 for aortic disease 424, 434 cerebral artery occlusion 267 focal/multifocal stenoses 261 ischemic stroke 262, 271 renal artery stenosis 497, 498 transient ischemic attack 272 diltiazem 802 dimethyl sulfoxide (DMSO) 684 dimethylamine hydrolases (DDAH) 813 dipyridamole 390, 658, 814 direct internal carotid artery puncture 307, 310, 310 directional atherectomy 773 directional coronary atherectomy (DCA) 112 device 69 dissections propagation, iatrogenic 630 as PVI complications 794, 794, 795 with Rotarex system 73–4 see also abdominal aortic dissections; thoracic aortic dissections distal bypass surgery (DBS) 642–3 distal embolic protection devices see embolic protection devices (EPDs) diuretics 803 DMSO (dimethyl sulfoxide) 684 dopamine 803 Doppler echocardiography (echo Doppler) 29 Doppler equation 570 Doppler flow pattern, arterial 456 Doppler shift 570, 571 Doppler ultrasound 456–60 abdominal aorta 456 advantages 456 contrast-enhanced 457 flow pattern in peripheral vessels 456 future directions 459 lower extremity arterial disease 602 mode of action 456 renal arteries 495 spectral analysis 570, 571 technical aspects 456 transcranial see transcranial Doppler see also duplex ultrasound Dormia stone catheter 180 dorsal penile artery 614, 615, 616 Dotter retrieval catheter 180 double aortic arch 424 DRASTIC (Dutch Renal Artery Stenosis Intervention Cooperative) study 490 drug delivery catheters 101 drug-eluting stents 132 in femoropopliteal disease 627 in infra-popliteal disease 635 and restenosis 770, 771
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Index Duett 172–3, 173, 795 duplex ultrasound abdominal aorta 457 arteriovenous fistulae 459 B-mode imaging 570, 570 Budd–Chiari syndrome 726 carotid arteries 458 carotid stenosis quantification 199 for DVT 120 iliac arteries 457 incidental/reflected wave formation 570 infraingual vein graft, failing 656–7 lymphatic malformation 717, 718 mesenteric arteries 570–3 application 570–1 clinical studies 572 procedure 571–2 peripheral veins 459 principles 570 pseudoaneurysms 458 renal arteries 494–5 upper/lower limb arteries 457 dural sinus thrombosis 249 Dutch Renal Artery Stenosis Intervention Cooperative (DRASTIC) study 490 DVT see deep vein thrombosis Dynalink Stent System 133–4 dynamic contrast-enhanced CT 232–3, 297 dyslipidemia 812, 823 E (ECST) (European) method see European Carotid Surgery Trial (ECST) (E) method ECASS (European Cooperative Acute Stroke Study) 263 Echelon microcatheter 38 echo Doppler see Doppler echocardiography (echo Doppler) EC–IC (Extracranial–Intracranial) Bypass study 238, 385, 386–7, 388 ECST (E) (European) method see European Carotid Surgery Trial (ECST) (E) method ectopic pelvic kidney 498 Edinburgh Vein Study 831 effort thrombosis of subclavian vein 412 Ehlers–Danlos syndrome 419, 433 EKOS system 118 elastic recoil 89–90 embolectomy MR RESCUE trial 295–6 percutaneous 851 pulmonary 851 superior mesenteric artery 581 surgical 851 see also thromboaspiration (catheter suction thromboembolectomy) embolic agents 713 embolic particles from angioplasty 300, 305 from atherectomy 80 filter particle size 319 in plaque 202 embolic protection devices (EPDs) 156–67, 157 aspiration catheters 515 in renal angioplasty/stenting 531, 532 choice of device 165, 321, 323 advantages/disadvantages 164, 321 distal occlusion 311 advantages/disadvantages 159, 313–14 complications 314 devices 156–9, 311–12 limitations 535 in RAS 511, 515
in renal angioplasty/stenting 528, 528, 529, 530–1, 532 technique 312–13 efficacy 300–1 filters 159–63, 314, 315, 316–17 advantages/disadvantages 161, 162–3, 317–19, 535 characteristics 159–60 clinical experience 326–7 devices 160–1, 314 new generation 163, 319–20 particle size 319 in RAS 515, 528, 530, 531–3, 534 flow reversal technique 163, 320–1 occlusion balloons 528 placement 339, 340 proximal flow blockage devices 164–5 SilverHawk®, used with 55 sizing 339, 340 see also specific devices embolisms arterial, in acute mesenteric ischemia 555 cerebral, prevention of 305–7, 310 distal 674 peripheral, with subintimal angioplasty 88 risks with filters 318 with protective balloon 313 thromboaspiration in 115 transcranial Doppler detection 207 embolization therapy 181–2 coil embolization 181–2 embolic agents 683 biodegradable particles 683 mechanical agents 683, 684 permanent particles 683–4 occlusive agents 182 peripheral 683–91 see also transcatheter peripheral embolization Emboshield 161, 161, 314, 317–18, 753 Emboshield Pro 314 embospheres (microspheres) 684, 687 Emergency Management of Stroke (EMS) Bridging Trial 293 end-stage renal disease (ESRD) ARAS as cause 487, 488 in infra-popliteal disease 634–5 after transplantation 547 endartectomy see aortic endartectomy; carotid endartectomy; endovascular endartectomy; renal endartectomy Endograft Registry 482 endografts abdominal aortic aneurysms 445, 445, 446 branched 478 fenestrated 475–6, 476, 477, 482 reinforced fenestration 477 occluding 442, 443–4, 444 Parodi 449–50, 452 complications 451, 452, 453–4 PTFE 627, 676–7, 699, 701 Vanguard 449, 450–1 complications 452–3, 454 endoleaks abdominal aortic aneurysms coil embolization 453 type I/III 452 type II 452–3 hypogastric artery aneurysm 616 endoluminal graft placement, iliofemoropopliteal 676 Endopro System see Cragg Endopro System 1/Passager
895
Endotex prosthesis 671, 673–4 endothelial dysfunction 188 in restenosis 767 endovascular aortic aneurysm repair (EVAR) 800–1 endovascular endartectomy 53 see also aortic endartectomy; carotid endartectomy endovascular equipment 11–12 basic necessities 11 equipment carts 9 lead shields 9 see also fluoroscopy equipment Endovascular Photo Acoustic Recanalization (EPAR) laser system 294 endovascular revascularization 388–9 imaging, pre-procedural 390 endovascular suite 7–11, 8 anesthesia requirements 7 control/observation room 8, 10 fluoroscopy equipment 7–8, 10 operating table 8 procedure room design 7 endovenous laser therapy (EVLT) 865 duplex-guided mapping 870 further applications 871–2 in great saphenous vein 871, 885, 886 parameters 872 varicose veins 870–2, 884, 885 advantages 872 before/after therapy 871 contraindications 885 duplex-guided mapping 870, 885 indications 882 parameters 872 procedure 870–1 technique 885 Endovenous Radiofrequency Obliteration Versus Ligation and Stripping (EVOLVeS) study 884 endovenous therapy for DVT 121 enalapril 258 EPAR laser system 294–5 EPI filter 318 in CAS 316, 317 in internal carotid artery stenting 753 retrieval 317 Epiclose Plus 174 epidural blockade in thromboangiitis obliterans 664 eptifibatide 817 equipment arterial access antegrade femoral artery access 15 contralateral iliofemoral artery access 16–18, 17 endovascular 9, 15 fluoroscopy 7–8, 9, 10, 10, 11–12 erectile dysfunction 614 estrogens and fibroids 692 ethanol as embolic agent 684, 713, 714 sclerotherapy 714, 717–18 ethylene vinyl alcohol copolymer (onyx) 684, 714 etomidate 391 European Carotid Surgery Trial (ECST) method 220 carotid stenosis quantification 200 and event-free survival 224, 225 as marker for surgery 224 and neurological events 222 vs NASCET method 222 European Cooperative Acute Stroke Study (ECASS) 263 EUROSTAR 482
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EVA 3S study 330 EVOLVeS (Endovenous Radiofrequency Obliteration Versus Ligation and Stripping) study 884 excimer laser angioplasty (ELA) 644, 772–3 for chronic total occlusions 94–5 in critical limb ischemia 640, 643, 644 in femoropopliteal disease 628 Excluder stent-graft 752 exercise ABPI 595 exercise rehabilitation therapy 817 exercise treadmill testing 602–3 ExoSeal 173, 173 Exponent 328 Express Biliary Stents 136, 360 external beam radiation 776–7 in restenosis 771–2 external iliac artery angioplasty/stenting 609–10 obstruction 590 occlusion 604, 609 stenosis 31 stenting 32 extracellular matrix (ECM) in restenosis 764, 765, 766–7 Extracranial–Intracranial (EC–IC) Bypass study 238, 385, 386–7, 388 factor V Leiden mutation 119 factor VIIc 824 factor VIII 824 Fallot’s tetralogy 705 false lumens abdominal aortic dissections 461, 462, 464–5 thoracic aortic dissections 439, 480, 481 endovascular treatment 441 adjunctive procedures 442, 443–5, 444–5, 446 femoral access 845 carotid angioplasty/stenting 306–7 landmarks 169–70, 170 lower extremity contrast studies 847 renal angioplasty 503, 504–6, 504, 505, 506 “safe zone” 168, 169, 170 subclavian artery PTA 355, 355, 356–9 vertebral angioplasty/stenting 373 femoral artery lesions aneurysms 676 cutting balloon angioplasty, before/after 47 duplex ultrasound 457 subintimal angioplasty 84–5 femoral artery stenting 132 femoral closure devices, iatrogenic lesions from 53, 54 femoral-popliteal bypass graft (FBG) 653 femoral vein thrombosis 839 femoral venogram in DVT 119, 120 femoral vessels 843–4 femoropopliteal aneurysms 674 femoropopliteal disease 625–9 claudication 625 critical limb ischemia 625–6 SFA stenting technique 629 TASC recommendations 626 treatment 625–6 endovascular 626–9 surgical 630–2 femoropopliteal lesions balloon angioplasty 41–2 CDTT in 102 chronic total occlusions 96 classification 42 subintimal angioplasty 84–5, 85, 87 treatment 630, 631
FemoStop 169 fenestrated endografts reinforced fenestration 477 thoracic aortic dissections 482 thoracoabdominal aneurysms 476, 476, 477 fenoldopam 803 fever after stent placement 147, 153, 674 FiberNet 163, 319–20, 319, 515 efficacy 328 in RAS 515, 531, 532–3, 533, 534 fibrinogen 822, 824 fibrinolysis 850 fibrinolytic system defects 824 fibrinolytics 306 fibroids 692 diagnosis 692 giant 692 imaging 692–3, 696, 696 pathophysiology 692 and pregnancy 697 prevalence 692 therapies 693 see also uterine artery embolization fibromuscular dysplasia (FMD) 544–5, 544, 732–3 after balloon angioplasty 44 branch-vessel dissections 544 indications for revascularization 539–40 renal arteries 495, 496, 496, 498, 498, 502, 513 treatment options 511, 514, 540 “string of beads” 544 Filter Wire EZ 160–1, 160, 314, 328 Finale see Mynx Fisher grading scale 281, 281 flexion angiography 628, 628, 636 Flexor introducer sheaths 34 Balkin Up and Over Contralateral Sheath 34 Check-Flo II 34, 35 with Keller–Timmerman valves 34, 35 Shuttle Select 34, 35 flow-directed thrombolysis areas treated 124, 125 for DVT 124–6 Fluency stent 143 fluid administration in CIN 802 fluid attenuated inversion recovery (FLAIR) imaging 231 fluoroscopic aortography 434–5 fluoroscopy 168 fluoroscopy equipment 7–8, 10 fixed vs mobile 8, 10 flat-panel detectors 8, 9, 10, 10, 11 operating table 8 single vs bi-plane systems 8 Flushcath 313 FMD see fibromuscular dysplasia (FMD) foam sclerotherapy 868, 882 congenital vascular malformation 713 varicose veins 879–86 classification 879, 880 contraindications/adverse effects 884, 884 “foam block” 880 history 879 indications 882 Orbach’s “air block technique” 879, 880 technique 881–3 Tessari (Tourbillon) technique 868, 882, 882, 883 Fogarty thrombectomy balloon catheter 642 fondaparinux 850, 850 Fontaine classification 594, 663 foot claudication 593 Formula 418 Stent 136
fragmentation 851–2, 852 Framingham Study 3, 823 Frankfurt brachytherapy trials 778 Frontrunner catheters 95, 95 furosemide 275, 803 gadolinium 499, 848 in computed tomography angiography 564–5 in magnetic resonance angiography 567 gamma radiation 776 catheter-based 777 gangrene, toe 663, 663 GDC coils 617 gelfoam 683, 685 gene therapy 782 adenoviral delivery 782, 783 angiogenic growth factors 783 atherosclerosis/restenosis/congestive heart failure prevention 785–6 characteristics of various vectors 783 clinical trials 784–5, 785 delivery routes 784 diagrammatic representation 783 hazards, potential 785 patient selection 784 plasmid “naked” DNA delivery 782, 783 in thromboangiitis obliterans 666 Genesis stent 322, 506, 755 in renal artery stenting 755 GFX stents 389 giant cell arteritis 403, 732–3 see also Takayasu’s disease (Takayasu’s arteritis) (aortoarteritis); temporal arteritis Gianturco coils 617, 709 Gianturco Z stents 852, 859 Glasgow coma scale 281 Glasgow outcome score 283 Glidewire 93 glucose intolerance 823 glue embolotherapy 713, 714, 811 glyceryl trinitrate (GTN) 89 glycoprotein IIb/IIIa inhibitors 817 for CAS 306 in critical limb ischemia 641 in intracranial stenting 252 in RAS 504 in stroke 271 GnRH agonists 693 Gore TAG device 432, 436 Gore Tri-lobed Balloon 436, 437 graded infusion method 101 graft thrombus extraction 642, 654 grasping retrieval forceps 181 grayscale median (GSM) 214, 217, 303 great saphenous vein endovenous laser therapy 871, 884, 885 identification 829 GREAT study 510 Greenfield suction cup 852, 852 GRIP registry 96 Grollman catheter 35 growth factors, angiogenic 783–4 Guard Dog 157, 158, 312 GuardWire see Percusurge GuardWire guide catheters 36–7, 37 intracranial 391 guidelines aortoiliac lesion management 39–40, 40 PAD management guidelines 41 Guidelines for the Management of Patients with Peripheral Arterial Disease 648 guidewires 37–8 components 37
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Index guidewires (Continued) size/shape 37 steerable 15, 18 guiding systems 18, 18 Gunther–Tulip filter 877, 877 H&L-B introducer system 476, 476 Hamburg classification 712 Headhunter catheter 309 Heart and Estrogen/Progestin Replacement Study (HERS) 813 Heart Protection Study 812 helical branched grafts 477, 479 hemangiomas 712 hematomas as PVI complications 792–3 in stroke 277–80, 280 hemicraniectomy, depressive 275–6 Hemobahn/Viabahn 141–2, 677 clinical experience 148–9 in critical limb ischemia 640 in femoropopliteal disease 627 iliofemoropopliteal lesions 672 in restenosis 771 hemodiafiltration 804, 806 hemodialysis 804, 806 hemodialysis access problems 699–703 anastomosis problems 699 complications early 699–701 late 701–2 covered/coated stents 153 cutting balloon angioplasty 48 inflow problems 700–1 kink 699 outflow problems 700, 700, 701–2 hemodynamics of PAD 590–1 hemofiltration and CIN 804–5, 805, 806 extracorporeal circuit 804 hemoptysis control 685, 686 hemorrhagic stroke 276–8, 280–3 after aneurysm 281 before/after PTAS 276 causes 278 in CDTT 105–6 in cerebral venous thrombosis 283 classification 260 management 283 algorithm 282 in spinal cord 282–3 hemorrhagic transformation 270 heparin arterial access 30 atherectomy 72 Budd–Chiari syndrome 728 CAS 338, 341 catheter-based thrombolysis 851 CDTT 103 DVT 124 endovascular revascularization 390 endovascular stent placement 576 intracranial stenting 252 PAD 817 pulmonary embolism 850–1, 850, 851 RAS 504, 532 stroke 270–1 acute ischemic 290, 292 subclavian artery PTA 361 heparin-induced thrombotic thrombocytopenia (HITT) 103 hepatic malignancy chemoembolization 687–8, 688 hepatocellular carcinoma (HCC) 730
Hi-Torque Spartacore guidewires 38 high-intensity transient signals (HITS) 199, 203, 203 high-speed rotation in imaging 11 HMG-CoA reductase inhibitors see statins homocysteine 4, 822, 823–4 hook phlebectomy 865–7 post-operative compression 866–7 HOPE study 813 horseshoe kidneys 494 HOT study 813 Hunt and Hess scale 281, 283 hydantoin 269 Hydrolyser 103, 112–13, 852 hypercholesteremia 490 hyperechoic plaque definition 211 risk of stroke 214 hyperglycemia 4 hyperhomocysteinemia 813, 823, 824 hyperperfusion syndrome 341–2 hypertension and abdominal aortic dissections 461 and aneurysm rupture 420, 432 in aortic dissection 439 and ARAS 489 in fibromuscular dysplasia 544, 545, 546 in PAD 4–5, 813, 824 and renal aneurysm 545, 546 in renal angioplasty/stenting 533, 535 renovascular 502, 525 venous 120, 832 see also vasorenal hypertension hypertensive hematomas 277 hyperthermia 258–9 hypervascular tumor embolization 687, 687 hypobaric oxygen therapy 274 hypoechoic plaque 211, 214 hypogastric artery 620 hypogastric artery aneurysm 621 hypogastric artery disease 614–24 aneurysms 621 visualization 614 hypogastric artery embolization 616–18, 618, 620, 622, 623 indications 618 hypoglycemia 258 hypoperfusion 264 hypothenar hammer syndrome 402, 404 hypothermia 274 hypoxia of kidney 799 in stroke 257, 257 in venous insufficiency 832 ICA see internal carotid artery ICAROS study 303 IFPAs see iliofemoropopliteal aneurysms iliac aneurysms 673, 676, 677 before/after PTAS 672 iliac arteries duplex ultrasound 457 perforation, treatment of 611 restenosis 767 iliac compression 127 iliac occlusive diseases 606–13 diagnosis 606 revascularization, selection of 607, 610 medical considerations 608 vascular access 607 iliac vein recanalization 129–30, 129 iliac vessels 842–3 inflammatory arteritis 740 lesion dilation 40
897
PTA in 39–41 stent placement 41 iliac vessel lesions classification 610 Corvita Endoluminal Graft in 148–9, 150 Cragg/Passager stent in 144 Hemobahn/Viabahn in 148–9 Rotablator in 63 subintimal angioplasty 86, 88, 89 surgical options 618 iliofemoropopliteal aneurysms (IFPAs) lesion characteristics 670–1, 670 percutaneous endovascular treatment complications 673–4 follow-up 674 long-term 675, 675–6 restenosis 675 results arterial diameter 674 immediate 672–3, 674 prosthesis lengths 672–3, 672 stent types 671, 671 image reproduction/storage 11 imaging equipment, fluoroscopy 7–8, 10 imaging techniques 10–11 in-stent restenosis (ISR) 47–8 balloon angioplasty, before/after 75, 76 and brachytherapy 780, 780 in CAS 342–3, 346 CCR2/CD18 inhibition of 767 cutting balloon angioplasty, before/after 46, 47 prevention 767 Rotarex angioplasty, before/after 75, 76 SilverHawk® atherectomy device 55 subclavian artery 363 ultrasound 204, 205 infantile/neonatal hemangiomas 712 infection in Behçet’s disease 743 as PVI complication 794 with vascular closure devices 174 infective aneurysms 425 inferior epigastric artery 182 inferior mesenteric artery (IMA) 572 anatomy 562 duplex ultrasound 570, 571 inferior vena cava (IVC) clipping 873 inferior vena cava (IVC) filters see vena caval filters inferior vena cava (IVC) occlusion 120, 130, 130, 858 causes 858–9 duplex ultrasound 459 treatment 859 inflammation/inflammatory factors and plaque stability 188 in restenosis 764, 766 and smoking 823 in thromboangiitis obliterans 662, 665 in venous insufficiency 833 inflammatory arteritis 736–42 interventions 736–40, 741 abdominal aorta 737 angioplasty 737 coronary arteries 740 crossing lesions 736–7 iliac vessels 740 innominate/carotid arteries 737, 739, 740 lesions at specific sites 737, 739–40 mesenteric arteries 740 outcome, factors affecting 737 preprocedural evaluation 736 renal arteries 739, 740
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inflammatory arteritis (Continued) revascularization 736 subclavian artery 737, 739 technical aspects 736–7 thoracic aorta, descending 737 before/after aortoplasty 738, 739 vascular access 736 pathology 736 see also Takayasu’s disease (Takayasu’s arteritis) (aortoarteritis) infragenicular PTA 633, 634 infraingual vein graft, failing 656–60 diagnosis 656–7 duplex ultrasound 656–7 critical parameters 657 vs angiography 657 incidence rates 657, 657 risk factors 656 surveillance 656–7, 659 treatment 657–60 antithrombotics/antiplatelets 657–8 endovascular 658–60, 659–60 roadmap-assisted 660 surgical 658 thrombolytic 658 infrapopliteal arterial diseases 633–7 and critical limb ischemia 639 PTA 635–7 PTAS 636, 637 stenosis/thrombolysis 636 treatment options 635–7 infrarenal aorta 5 infrarenal aortic aneurysms CECTA imaging 496 repaired with branch grafts 479 treatment 475 complications 477 infrarenal aortic dissection 463 infrarenal aortic occlusion 468, 469 infusion catheters 38 infusion wires 38 inguinal crease as landmark 169–70 innominate artery 737, 739, 740 innominate artery lesions 404 treatment 404–5 angioplasty/stenting 405 stenting 404, 405 INSTEAD (INvestigation of STEnt grafts in patients with type B Aortic Dissection) trial 432, 441, 465, 482 Interceptor Plus 161, 162, 316 intermittent claudication 5, 589, 593 internal carotid artery (ICA) 194 in acute ischemic stroke 291, 292 recanalization rates 289 anatomy 193, 194–6 direct puncture 307, 310, 310 stenting in ischemic heart disease 753, 753 internal carotid artery pathology with ischemic heart disease 751, 752, 753–4 occlusion 264, 272 stenosis 754 with EPI filter 316 imaging 202, 276 transcranial Doppler findings 394 treatment 752–3, 753 stent-assisted angioplasty 394, 758 internal iliac artery aneurysm 676 internal mammary artery (IMA) catheter 846, 846, 847 International Cooperative Pulmonary Embolism Registry 850
International Registry of Acute Aortic Dissection (IRAD) on abdominal dissections 462 on thoracic dissections 439, 440, 461 International Stroke Trial (IST) study 270 International Subarachnoid Aneurysm Trial (ISAT) 281, 283 intra-arterial angiography 605 intra-arterial (IA) thrombolysis future directions 296–7 imaging developments 296–7 mechanical 294–6 pharmacologic 290, 292–4 vs intravenous (IV) 288–9 see also catheter-directed intra-arterial thrombolytic therapy (CDTT); percutaneous intra-arterial thrombolysis (PIAT) intracerebral hemorrhage management 269 predictors 267 after thrombolysis 263, 265 intracranial atherosclerosis 382 cerebral artery thrombosis mechanisms 384–5 imaging 390 prognosis 385 symptomatic stenosis 387–8 restenosis 394 stroke 383–8 perfusion failure 383–4 stenosis-related pathology small artery occlusion 385 thrombosis 384–5 transcranial Doppler findings 394 treatment endovascular revascularization 388–9 follow-up 393, 394 medical 388 post-procedural care 393–4 revascularization with craniotomy 388 stent-assisted angioplasty 389, 393, 394 surgical 388 angioplasty 391–3 guide catheter 391 lesion navigation 391–3 patient preparation 390 patient selection 389–90 premedication/anesthesia 390–1 stenting 392, 393 vessel rupture 392 intracranial carotid siphon stenosis 385–6 intracranial circulation 165 intracranial stenosis 382 classification, angiographic access 240, 240 Mori 239–40 as dynamic lesion 382 hemodynamic effects 383 pathophysiology 239 stent-assisted angioplasty 238–46 complications 242–3 history 238–9 medical treatment 240–1 outcomes 242–3, 242, 243 patient selection 239 preoperative assessment 240 procedure 241–2 intracranial stenting 247–54 arteriovenous fistulae 249–51 atherosclerosis 247–9, 248 staged 249 caveats 253 future directions 252–3
medical management, periprocedural 251–2 stent placement 252 venous occlusions 249–51 intramesenteric steal 555–6 intramural hematoma 440 Intrastents 640 intravascular ultrasound (IVUS) for aortic disease 426, 435, 436 in fibromuscular dysplasia 733 lower extremity arterial disease 598, 599 introducer sheaths 29, 34 INvestigation of STEnt grafts in patients with type B Aortic Dissection (INSTEAD) trial 432, 441, 465, 482 ipsilateral iliofemoral artery access 17, 17 IRAD (International Registry of Acute Aortic Dissection) on abdominal dissections 462 on thoracic dissections 439, 440, 461 IS see ischemic stroke ISAT (International Subarachnoid Aneurysm Trial) 281, 283 ischemia in aortic dissection 462 pathophysiologic mechanisms 480 of brain tissue 229, 232 CBF thresholds 232 critical limb 4, 639–47 classification 640 clinical presentation 639–40 diagnosis 641 epidemiology 639 femoropopliteal disease 625–6 mortality 589 pathophysiology 639–40 plaque excision 643 risk factors 640 SilverHawk® for 50, 52, 53, 56 stenting 139, 634 symptoms/diagnosis 640 treatment 589, 640–4, 646 cryotherapy 644, 644, 645, 646 laser 640, 643, 644 prostaglandins 816 PTA vs PTAS 643 surgical bypass 642–3 see also thromboangiitis obliterans (Buerger’s disease) in hemodialysis access problems 702 of kidney 799 ischemic colitis 579 ischemic gastropathy 578 ischemic heart disease with ICA pathology 751, 752, 753–4 with lower limb ischemia 757, 758, 759 with vasorenal hypertension 754–7, 755 ischemic nephropathy 491 ischemic rest pain 594 ischemic stroke 263, 264, 265 12 hours after onset 277 acute see acute ischemic stroke angioplasty/stenting 272 cerebral perfusion imaging 233–4 classification 260 correlation with neuroimaging 234 as indication for CDTT 104 magnetic resonance imaging/angiography 234 management algorithm 278 pathophysiology 239 thrombolysis 263 unstable 262 n-isobutyl cyanoacrylate (NBCA) 684 isosorbide dinitrate 27, 390
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Index IST (International Stroke Trial) study 270 Ivalon 683–4 Joint Study of Extracranial Arterial Occlusion 377 Jomed stent 153 Jostent 142 clinical experience 150–1, 152 iliofemoropopliteal lesions 672 in lower limb artery stenting 757 Judkins catheter 309 Judkins right catheter 17, 846 Katzen infusion wires 38 Kawasaki’s disease 548, 734 Keller–Timmerman valves 34, 35 Kensey catheter 30, 75 kidney angiomyolipoma embolization 687 Kimny catheters 22 Kimray Greenfield filter (KGF) 875 kissing balloons technique 88, 132, 497, 608 abdominal aortic occlusive disease 468 Budd–Chiari syndrome 728 inflammatory arteritis 739 renal artery stenosis 498 subclavian artery stenosis/occlusion 361 vertebral artery 375 kissing stents 518 abdominal aortic occlusive disease 469, 469 iliac occlusive diseases 608 labetalol 258 LACI (Laser Angioplasty for Critical Limb Ischemia) trial 67, 94, 95, 640, 643 and restenosis 772–3 large aorto–pulmonary collateral artery (LAPCA) embolization 708–9 stenting 706, 708 Laser Angioplasty for Critical Limb Ischemia (LACI) trial 67, 94, 95, 640, 643 and restenosis 772–3 laser recanalization 32 laser therapy 643, 644 Latis laser device 294 left heart hypoplasia syndrome 706 left iliac compression 127 lenticulostriate artery occlusion 385, 388 levocarnitine 815–16 lidocaine 867–8, 870 Life Stent NT 771 limb salvage 31, 52, 631, 633–4 lipoproteins 3 liquid embolic agents 684 liver status in Budd–Chiari syndrome 727, 729, 730 lobar hematoma 277, 280 location of lesions 31 long segment lesions 630–1, 636–7 long segment retro/infragenicular stenting 636–7 loop-snare retrieval systems 179–80, 181 lower extremity angiography 845, 847 lower extremity arterial disease assessment 593–600, 601–5 intraoperative 598, 599 non-invasive 602 “triple” 598–600 case example 598–600 clinical examination auscultation 595 inspection 594 palpation 594–5 clinical history 593–4 epidemiology 589–90 etiology 589 imaging modalities 603, 605
investigations clinical 595 invasive 596, 598–600 non-invasive 595–6 pathophysiology 590–1 physiologic testing 601–3 ulceration sites 595 lower limb ischemia acute 757, 759 with ischemic heart disease 757, 759 stent-assisted angioplasty 758 lumbar vessels 842 Luminexx Biliary Stent 136 lung cancer 858 lymphatic malformation (LM) 714, 716, 717–18 Magnetic Resonance and Recanalization of Stroke Clots Using Embolectomy (MR RESCUE) 295–6 magnetic resonance angiography (MRA) contrast agents 567 ischemic stroke 234 lower extremity arterial disease 596, 597, 604, 605 mesenteric arteries 566–8, 567, 568 for RAS 503 renal arteries 496–9 contrast-enhanced MRA 496–9, 496 three-dimensional contrast-enhanced 847–8 vs computed tomography angiography 568 magnetic resonance imaging (MRI) for abdominal aortic dissections 462 for aortic disease 423, 424, 426 diffusion-weighted imaging (DWI) 233 ischemic stroke 234 perfusion-weighted imaging (PWI) 233 PWI– DWI mismatch 233, 234, 234 transient ischemic attack 230 magnetic resonance venography (MRV) 121 malperfusion syndrome 462, 465, 480 Mani-Vitek catheter 309 Marfan syndrome 419–20 MAST (Multicentre Acute Stroke Trials) 263 MAUDE database review 173 May–Thurner syndrome 127 Mechanical Embolus Removal in Cerebral Ischemia (MERCI) retrieval system 295, 295 mechanical thrombectomy 101, 103, 121–2 medial dysplasia/fibroplasia/hyperplasia 544 median perforating artery occlusion 385 membranous obstruction of vena cava (MOVC) 725, 726, 730 MERCI retrieval system 295, 295 mesenteric arterial circulation 562 mesenteric arteries anatomy 562, 563 imaging computed tomographic angiography 564, 565–6 scanning/reconstruction parameters 566 visualization techniques 566 conventional angiography 562–5, 564 procedure 565 duplex ultrasound 570–3 application 570–1 clinical studies 572 procedure 571–2 magnetic resonance angiography 566–8 inflammatory arteritis 740 mesenteric artery occlusion 572 mesenteric artery stenosis 572 mesenteric ischemia 462, 553–6 assessment 557–61
899
clinical presentation acute disease 557–8, 557, 558 chronic disease 558, 559 diagnosis acute disease 558–9 chronic disease 559–60 endovascular therapy 574–80 etiology 553–4 natural history 554 pathophysiology acute disease 555 chronic disease 555–6 physiology 554–5 prevalence 553 therapy 574–80 endovascular 574–8 complications 578 PTA 576 stent placement 577, 578 vs surgical revascularization 583 general measures 574 medical 575 surgical revascularization 581–3 indications 584 vs endovascular therapy 583 metabolic risk factor treatment 812–13 metallic stents 126–7 see also nitinol stents metastatic disease 858 Mewissen infusion catheter 38 microbubbles 118 microcatheters 38 intracranial 391 microembolization 379 “microfoam” 879 MicroLys US infusion catheter device 295 MicroMewi infusion catheter 38 MicroSelectron HDR system 777, 777, 778, 779 microspheres (embospheres) 684, 687 middle cerebral artery (MCA) 194–6, 195, 196 recanalization rates in IS 289 stenosis 382 prognosis for 386–7 stent-assisted angioplasty 393 middle sacral vessels 842 mini-basket 180 misery perfusion 232, 247, 383 mitral valve replacement 759 MOBILE study 777 Mobin-Uddin umbrella filter 873, 875 “modification of diet in renal disease” equation (MDRD) 800, 801 modified (Quereshi) TIMI score 289, 290, 291 modified Rankin scale 283 molsidomine 27, 72 MOMA device 164–5, 320–1 MOMA trial 330 morphine sulfate 464 MR RESCUE (Magnetic Resonance and Recanalization of Stroke Clots Using Embolectomy) 295–6 Multicentre Acute Stroke Trials (MAST) 263 mycotic aneurysms 425 Mynx 173, 173 myocardial infarction 118 n-acetylcysteine (NAC) 803, 804, 806 n-butyl cyanoacrylate (NBCA) 713, 714 n-isobutyl cyanoacrylate (NBCA) 684 N (NASCET) (North American) method see North American Symptomatic Carotid Endarterectomy Trial (NASCET) method naftidrofuryl 815
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NASCET (N) (North American) method see North American Symptomatic Carotid Endarterectomy Trial (NASCET) (N) method NASCET trial 283, 300 National Health and Nutrition Examination Survey (NHANES) studies 817, 823 National Institute of Health Stroke Scale (NIHSS) 259, 259 National Institute of Neurological Disorders and Stroke (NINDS) Interventional Management of Stroke (IMS) trials 294, 295 Recombinant Tissue Plasminogen Activator Stroke study 263, 288 National Venous Registry 128 NBCA (n-isobutyl cyanoacrylate) 684 neonatal hemangiomas see infantile/neonatal hemangiomas nephrectomy, primary 540 nephropathy, ischemic 491 Nester coils 181 neural injury with vascular closure devices 176 neurofibromatosis 548 neuroradiological anatomy 192–8 Neuroshield 328 neurovascular disease differential diagnosis 190 epidemiology 187 pathophysiology 187–90 basilar artery disease 189 carotid artery disease 187–8 spontaneous dissection 189 carotid stenosis asymptomatic 188 symptomatic 188–9 risk factor modification 190 stroke prevention 190 vertebral artery disease 189 spontaneous dissection 189 “vulnerable” plaque 188 Nexstent 328 NHANES (National Health and Nutrition Examination Survey) studies 817, 823 niacin plus colestipol therapy 812 nicotine replacement therapy 811–12 nimodipine in endovascular revascularization 390 intracranial stenosis treatment 241 NINDS 288–99 nitinol stents 136, 323 CAS outcomes 328, 329 characteristics 324, 327 Cordis 143 Cragg Endopro/Passager 140 in critical limb ischemia 640 geometric effects 325, 326 Hemobahn/Viabahn 141 in infrapopliteal PTA 635–6 in limb salvage 634 for SVC occlusion 859, 860, 861, 862 nitinol vena caval filters 877, 877, 878 nitrates 258 nitrendipine 803 nitroprusside 258 non-atherosclerotic renovascular disease 544–50 North American Symptomatic Carotid Endarterectomy Trial (NASCET) (N) method 220, 283, 300 carotid stenosis quantification 199 as marker for surgery 224 and neurological events 222, 223 vs ESDT method 222 nortriptyline 811
Oasis thrombectomy catheter 113, 852 Oasis thrombectomy system 102, 113 obliterative endarteritis. see thromboangiitis obliterans (Buerger’s disease) obstructive sleep apnea 276 occlusive agents 182 omental transplantation 666 Omniflush catheter 35, 845, 846, 846 Omnilink Stent System 133–4, 136 onyx (ethylene vinyl alcohol copolymer) 684, 714 open-cell stents 323, 323, 324 Opt-Ease filter 877, 878 optic coherence reflectometry 96, 96 Orbach’s “air block technique” 879, 880 Orbital atherectomy system (OAS) 79–82 complications 80–1 components 79, 80 crown sizes available 80 description 79 downstream particle size 80 studies case study 81, 82 clinical 81–2 preclinical 79–81 osmotherapy 275 Outback catheter 93–4, 94 oxygen extraction fraction (OEF) 382, 384 PACCOCATH ISR balloon catheter 773 paclitaxel-coated stents 253, 770 PAD see peripheral artery disease (PAD) Paget–Schroetter syndrome 412, 412 pain ischemic rest pain 594 after stent placement 147, 153, 674 see also claudication palmar arch anatomy 22 Palmaz stent 32 in critical limb ischemia 640 crushing/redilatation 322 follow-up 770 in iliac occlusion 611 in iliofemoropopliteal lesions 676 in internal carotid artery stenting 753 in lower limb artery stenting 757 in subclavian artery occlusion/stenosis 360, 361, 367, 859 in vertebral artery occlusion/stenosis 374, 375 panvasculitis 743 papaverine 615 Paris Radiation Investigation Study (PARIS) 771–2, 778, 779–80 Parodi antiembolization catheter (PAEC) 163–4, 164, 320, 320, 330 Parodi endograft for abdominal aortic aneurysms 449–50 complications 451, 452, 453–4 endoluminal exclusion 452 particles see embolic particles PARTNERS study 3, 822 Passager see Cragg Endopro System 1/Passager patent ductus arteriosus stenting 709 transcatheter closure 709–10 PATRIOT (Peripheral Approach To Recanalization In Occluded Totals) study 95 peak systolic velocity ratio 199 pedal arteries 844 PELA (Peripheral Excimer Laser Angioplasty) trial 772 pelvic angiography 845, 847 pelvic artery stenosis 497 pelvis transcatheter embolizations 684
penetrating thoracic ulcer 426–7 penile arterial reconstruction 614, 615 pentoxifylline 664, 815 Perclose 174, 176 Percusurge GuardWire 156–7, 157, 311, 328 in internal carotid artery stenting 753 in RAS 511, 514 in renal angioplasty/stenting 528, 528, 534 results 532 technique 529, 530–1 technique 325–6 Percutaneous Greenfield filter (PSGF) 875, 876 percutaneous intentional extraluminal recanalization (PIER) see subintimal angioplasty percutaneous intra-arterial thrombolysis (PIAT) 109 percutaneous metal arterial closure devices 174 percutaneous popliteal access 18–19 antegrade 29–30 endovascular techniques with 29 complications 19, 31, 33 indications/contraindications 19, 30–1, 33 retrograde 29, 31 Percutaneous Transluminal Angioplasty for Treatment of “Below-the-Knee” Critical Limb Ischemia 640 percutaneous transluminal angioplasty (PTA) 39–44 for abdominal aortic occlusion 467 basilar artery 274 chronic mesenteric ischemia 575, 576, 577, 578 critical limb ischemia 643 for hypogastric artery stenosis 615 iliac occlusive diseases 610 indications 39 infragenicular 633, 634 infrapopliteal arterial diseases 635 mechanism/technique 39 in subclavian arteries 353–71 indications 354–5 techniques 355–61 brachial approach 355, 355, 359 femoral approach 355, 355, 356–9 radial approach 355 vascular territories 39–44 iliac vessels 39–41 renal arteries 43–4 superficial femoral artery 41–2 tibioperoneal arteries 42–3 vertebral artery 273 percutaneous transluminal angioplasty with stenting (PTAS) 267–8 common carotid artery 348–52 outcomes 348–9, 348 restenosis/treatment 350 technique 349–50, 349, 350, 351 in DVT 643 subclavian arteries 358–63, 366 cerebral protection 360 complications 362, 366 discussion 363–4, 366–8 follow-up 361, 362–3, 363 medication 360–1 patients 361–2 recanalization/restenting 360–1, 364, 366 restenosis 360–1, 364, 366 results 361–3, 364–5, 366–8, 367 immediate technical 362 techniques 356, 357, 358, 358, 359–60, 362 vertebral artery stenosis, extracranial 371–81 access 373 clinical findings 372
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Index percutaneous transluminal angioplasty with stenting (PTAS) (Continued) complications 376 controversial issues 379 diagnostic imaging 372 discussion 377–9 evaluation of results 375–6 follow-up 377, 378–9 indications 372–3 medication 373–6 microembolization 379 patient selection 376 predilatation 375 protection devices 376 results 376–7, 377 stent choice/placement 378 techniques 373–7 percutaneous transluminal renal angioplasty (PTRA) 502 advantages 526 atheroembolism during 526 before/after 43 bilateral 513, 514 complications 515–17, 526 dissections 516–17, 518 pseudoaneurysms 516 renal artery thrombosis 517, 518 renal function deterioration 515–16 renal rupture/perforation 516, 516 stent-related 517 with cutting balloon 512 distal embolization 504, 511, 514, 515, 521 drug-eluting stents 510 in fibromuscular dysplasia 540 indications/contraindications 503, 504 see also renal artery stenosis, angioplasty/stenting medication 504 mortality 517, 522 ostial/non-ostial lesions 508, 508, 509 patient preparation/surveillance 504 protected stenting 506, 509, 510 under protection 521–2 devices 511, 515 with Percusurge 514 vulnerable patients 504 in RAS 525, 534, 540 and renal function 520–2, 520, 526 results 519–22, 519 blood pressure 519–20, 520 long-term patency 519, 519 patient survival 522 technical aspects 519 special cases 511 techniques 504–11, 515 access 503, 505–7 angioplasty 507–8 coaxial technique 505–6, 508 stenting 508–10 Perflex stent 755, 757 perforation as PVI complication 795 with Rotablator 60, 62, 66 with Rotaflex 72, 74, 77, 78 with subintimal angioplasty 88–9 perfusion see cerebral perfusion perfusion CT (PCT) cerebral perfusion imaging 232–3 dynamic 232–3, 297 transient ischemic attack 230 perfusion-weighted imaging (PWI) see under magnetic resonance imaging (MRI) periarteritis nodosa see polyarteritis nodosa
perimedial fibroplasia 544 peripheral aneurysms embolization therapy 688 percutaneous endovascular treatment 670–80 methods 670–2 patient selection 670 techniques 670 see also iliofemoropopliteal aneurysms Peripheral Approach To Recanalization In Occluded Totals (PATRIOT) study 95 peripheral artery disease (PAD) arteries involved 648 concomitant vascular diseases 589 concomitant with ARAS 488–9, 490 exercise rehabilitation therapy 817 hemodynamics 590–1 incidence/prevalence 3 lower extremities epidemiology 589–90 etiology 589 pathophysiology 590–1 morbidity/mortality 3 multilevel 590–1, 591 pathophysiology 4–5 pharmacological treatment 811–21 antiplatelet therapy 813–15, 817 claudication therapy 815–17 thrombolytics 817 prevalence 656 risk factors 822–6 age 822 cardiovascular disease 822 dyslipidemia 823 fibrinogen/blood viscosity 824 gender 822 glucose intolerance/diabetes 823 homocysteine 823–4 hypertension 824 modification 811–13 diabetes mellitus 812 dyslipidemia 812 hypertension 813 metabolic risk factors 812–13 smoking 811–12 smoking 822–3 see also peripheral vascular disease (PVD) Peripheral Brachytherapy Centering Catheter 777 Peripheral Excimer Laser Angioplasty (PELA) trial 772 peripheral stents 136 peripheral vascular disease (PVD) classification 594 risk factors 594 see also peripheral artery disease (PAD) peripheral venous disease see venous disease peroneal artery angioplasty, before/after 43 persantine 634 pharmacomechanical thrombolysis 118 phlebectomy ambulatory 866, 867 hook 865–7 post-operative compression 866–7 Phlebocid 879 PIAT (percutaneous intra-arterial thrombolysis) 109 picibanil 718 picotamide 814 pigtail catheters 35, 36, 845, 846, 847 rotatable 852, 852 Pinnacle Destination renal guide sheath 34 Pioneer catheter 93, 94 plaques carotid artery 187–8, 188
901
debulking 74–5, 77–8 echodensity 211 vs particle numbers 202, 202 vs particle size 202 vs stenosis 217 echogenicity vs homogeneity 212 excision in CLI 643 features 383 morphology 383 morphology as cerebral risk factor 200 tissue samples from SilverHawk® 50, 54, 56–7, 57 ulcerated 200–1, 201, 219 “vulnerable” 188, 211 plaque fatigue/rupture 217 plaque formation 4 susceptibility 5 vascular effects 3–4 plaque regression 5 Plaque Removal Versus Open Bypass Surgery for Critical Limb Ischemia (PROOF) study 56 plasmin 118 plasminogen activator inhibitor (PAI) 824 plasminogen activator (PA) 817 see also recombinant tissue plasminogen activator (rtPA); tissue plasminogen activator (tPA) platelet activation 4 platelet-derived growth factor (PDGF) 764 Poiseuille’s law 590–1 PolarCath 644, 644, 645, 646 polidocanol 884 polyarteritis nodosa 548, 733–4 polychondritis, relapsing 734 polymyalgia rheumatica 733 polyvinyl alcohol (PVA) particles 683–4, 685, 685 pons hematoma in stroke 278 popliteal aneurysm thrombosed, as indication for CDTT 103 treatment with Cragg Endopro 674 popliteal artery 18, 19, 844, 844 access see percutaneous popliteal access anatomic variations 19 stenting 132 popliteal artery lesions aneurysms 675–6 CDTT in 102, 105 Corvita Endoluminal Graft in 149 Cragg/Passager stent in 145 failed percutaneous interventions 630 long segment disease 630–1 Rotablator in 60 SilverHawk® in 53, 55, 56 subintimal angioplasty 84–5 surgery 630–1 thromboaspiration 116 see also infrapopliteal arterial diseases portal hypertension 728 positron emission tomography (PET) 232 Possis Angiojet see Angiojet post-embolization syndrome 688 post-thrombotic syndrome 128, 129 posterior cerebral artery (PCA) 195 power-pulse spray (P-PS) 651–4, 652 in ALI 652–4 case studies 651–2 protocol 651 Precise stent 754, 758 in internal carotid artery stenting 753 pregnancy after UAE 697 pressure gradients, translesional 503 PREVENT III trial 656 primary venous insufficiency 831–2, 864
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PROACT (Prolyse in Acute Cerebral Thromboembolism) 267 probucol 780 intracranial stenosis treatment 241 profunda femoral artery lesions 53, 55 progenitor cell transplantation 182 progesterone and fibroids 692 Progetto Lombardo Athero-Thrombosis study 824 Prolyse in Acute Cerebral Thromboembolism (PROACT) 267 prolyse in acute cerebral thromboembolism (PROACT) studies 290, 292–3 PROOF (Plaque Removal Versus Open Bypass Surgery for Critical Limb Ischemia) study 56 proprionyl levocarnitine 815–16 prostaglandins and CIN 803 in PAD 816 in thromboangiitis obliterans 665 ProStream infusion wires 38 protection balloons see embolic protection devices (EPDs), distal occlusion Protegé stents 636 prothrombin gene mutation 128 pseudoaneurysms duplex ultrasound 457, 458, 458 embolization therapy 688 as PVI complications 793, 793 after stent placement 147 thrombin injection for 793 see also aortic pseudoaneurysms; carotid pseudoaneurysm pseudocoarctation of aorta 427–8 PTA see percutaneous transluminal angioplasty (PTA) PTAS see percutaneous transluminal angioplasty with stenting (PTAS) PTFE endografts 627, 676–7 hemodialysis access 699, 701 pulmonary artery atresia 708–9 pulmonary artery recanalization 107 pulmonary artery stenting 705 pulmonary edema 525 pulmonary embolectomy 851 pulmonary embolism 849–57 acute massive 849 Angiojet thrombectomy in 114 anticoagulation 850, 850 catheter-based therapies 851–4, 851 advantages/disadvantages 852 CDTT in 107 diagnosis 849 embolectomy, percutaneous 851 fragmentation 851–2 as indication for CDTT 104–5 prevention 873 surgical embolectomy 851 systemic thrombolysis 850–1, 850 therapy, interventional 849–54 thrombectomy, percutaneous suction 852–3, 853 catheter assembly 852–3, 853 with inhaled nitric oxide 853–4, 854 thrombolysis 118 catheter-based 851, 851 pulsatility index 207 pulse-generated run-off 596 pulse oximetry 596 pulse spray thrombolysis 101, 104 in DVT 121–2 in hemodialysis access problems 702 pulse volume recordings 602, 603 PVA particles see polyvinyl alcohol (PVA) particles
quantitative online angiographic analysis 564 Quereshi grading scheme (modified treatment score) 289, 290, 291 Quickcross catheter 93 radial access 845 renal angioplasty 503 subclavian artery PTA 355 see also transradial access radial artery thrombosis, CDTT in 104 Radiance balloon system 777 radiation radiation injuries in PVI 797 safety 11 training 11 radiation arteritis 548–9 radiation therapy peripheral vascular system 776 catheter-based beta radiation 777 gamma radiation 777 clinical trials 777–80 Frankfurt experience 777, 778 PARIS trials 778, 779–80 Vienna trials 778–9, 779 MicroSelectron HDR system 777, 777 SVC occlusion 859 radio-frequency ablation/obliteration (RFA/RFO) for chronic total occlusions 96, 96 generator 866 for varicose veins 865 see also VNUS closure radioactive stents 253 radionuclide captopril renography 499, 500 Radius stent 636 Rankin scale, modified 283 rapamycin-coated stents 253, 770 see also sirolimus-coated stents Rapamycin-Eluting Versus Plain Polymer Stents (RAVEL) study 253 RAS see renal artery stenosis RAVEL (Rapamycin-Eluting Versus Plain Polymer Stents) study 253 Raynaud’s syndrome 401, 402 causes 402 primary vs secondary 402 treatment 404 re-entry devices 93 recanalization 129–30, 129 definition 289 lesion assessment 92 patient selection 92–3 recanalization devices 92–8 recombinant plasminogen activator (rPA) 817 recombinant pro-urokinase (r-proUK) 290, 292–3 recombinant tissue-type plasminogen activator (rtPA) in acute ischemic stroke 296 in CDTT 99, 100–1, 100, 101 in PAD 817 Recovery nitinol filter 877, 878 reflux in chronic venous disease 836–8, 839 duplex ultrasound in 837–8 in perforating veins 838 primary vs secondary 837 relapsing polychondritis 734 renal arteries 842, 843 anatomy 494 brachytherapy 780 digital subtraction angiography 498, 499 imaging 494–501 CECTA imaging 496
contrast-enhanced CT angiography 495, 497 contrast-enhanced MRA 496–9, 496, 497 digital subtraction angiography 499 duplex ultrasound 494–5 ideal modality 494 radionuclide captopril renography 500 renal vein renin 499 inflammatory arteritis 739, 740 multiple 494 PTA in 43–4 stenting 132, 139, 526, 526 renal arteriography 503 renal artery aneurysms 511, 545, 546 renal artery angioplasty/stenting 526, 755 bilateral 513, 514 complications 515–17 dissection 516–17 dissections 518 pseudoaneurysms 516 renal artery thrombosis 517, 518 renal function deterioration 515–16 renal rupture/perforation 516, 516 stent-related 517 contraindications 503 with cutting balloon 512 distal embolization 504, 511, 514, 515, 521 drug-eluting stents 510 indications 502, 504 medication 504 mortality 517, 522 ostial/non-ostial lesions 508, 508, 509 patient preparation/surveillance 504 protected stenting 506, 509, 510 under protection 525–38, 531 devices 531 see also embolic protection devices (EPDs) discussion 534–6 EPI filter 530 indications 535 limitations 534–5 medication 532 renal function, effects on 526–8 results 532–4 follow-up 533 particulate analysis 532–3 urea/creatinine levels 533 surveillance 532 techniques 528, 530–2 see also renal artery angioplasty/stenting protection, distal see under percutaneous transluminal renal angioplasty (PTRA) in RAS 547, 548 and renal function 533, 534–6, 534 restenosis 767 results 519–22, 519 blood pressure 519–20, 520 long-term patency 519, 519 patient survival 522 renal function 520–2, 520 technical aspects 519 special cases 511 Takayasu’s disease 546 techniques 504–11, 515 access 503, 505–7 angioplasty 507–8 coaxial technique 505–6, 508 stenting 508–10 renal artery dissection 795 renal artery occlusion 511 renal artery reimplantation 540 renal artery rupture 516, 516 renal artery stenosis (RAS) 502–24 at bifurcation 511, 512
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Index renal artery stenosis (RAS) (Continued) causes 502 CECTA imaging 496 covered/coated stents 153 cutting balloon angioplasty, before/after 46 diagnosis 503 screening tests 503 digital subtraction angiography 498 embolic protection device 165 in fibromuscular dysplasia 732 imaging 503 inflammatory disease 511 multiple stenoses 511 natural history 525 prevalence 502 restenosis 511, 513 after transplantation 546, 547, 548 treatment 502, 525–6 under protection 529, 530, 531 surgical 540–2 indications 540–1, 542 referral for 539–43 see also percutaneous transluminal renal angioplasty (PTRA); renal artery angioplasty/stenting renal artery stenting 132, 526, 526 renal artery thrombosis 517, 518 renal double curve (RDC) catheter 846 Renal Double Curve (RDC) guiding catheter 505 renal endartectomy 540 renal failure and aneurysm rupture 420, 432–3 hemodialysis access intervention 699–703 renal fibromuscular dysplasia 545 renal function and atheroembolism 528 and PTRA 526 in renal angioplasty/stenting 533, 534–6, 534 in renal artery stenting 526, 526, 527 renal function reserve 536 renal replacement therapies 803–5, 806 renal revascularization with aortic aneurysm repair 541, 541 disadvantages 541 indications 539–42, 542 surgical techniques 540, 540 see also percutaneous transluminal renal angioplasty (PTRA); renal artery angioplasty/stenting renal vein renin 503 renal arteries 500 renovascular disease see atherosclerotic renal artery disease; non-atherosclerotic renovascular disease; specific disorders renovascular hypertension 502, 525 reperfusion 289 reperfusion injury syndrome 269 RESILENT trial 771 rest pain 594 causes 594 definition 589 restenosis 811 acute gain 763 and brachytherapy 780, 780, 781 clinical 763 definition 763 in femoropopliteal disease 628–9 gene therapy for 785–6 in-stent 47–8 balloon angioplasty, before/after 75, 76 and brachytherapy 780, 780 in CAS 342–3, 346 CCR2/CD18 inhibition of 767
cutting balloon angioplasty, before/after 46, 47 prevention 767 Rotarex angioplasty, before/after 75, 76 SilverHawk® atherectomy device 55 subclavian artery 363 ultrasound 204, 205 incidence based on anatomic bed 767–8 interventions 770–5 late loss 763 loss index 763 pathophysiology 763–9 cellular proliferation 766 endothelial dysfunction 767 extracellular matrix 766–7 inflammation 766 mechanisms 764–7 thrombosis 764–5 risk factors 763–4 surrogate measures 763 reteplase (Retavase) 817 in acute ischemic stroke 293 for DVT 122 reticular varicosities 833 retrieval devices 179–81 baskets 180–1 biotape 181 grasping forceps 181 loop-snare systems 179–80, 181 Retriever snare 179, 180 retrograde femoral artery access 16, 30 retrograde percutaneous popliteal access 29, 31 retroperitoneal hemorrhage with subintimal angioplasty 88 treatment 182 with vascular closure devices 174, 176 Reuter Tip Deflecting Wire 38 rheopolyglucinum 664 rheumatoid disease 734 ribs in thoracic outlet syndrome 409, 410, 411 right-sided aortic arch 424, 425 right ventricular outflow tract stenting 706–7, 710 road-mapping 11 in arterial access 29 failing infraingual vein graft angioplasty 660 Rochester trial 109 Rotablator 59–68 approaches 59, 60, 62 burr sizes 59 clinical experience 60–2 approaches used 62 lesion lengths treated 62 lesion locations treated 61, 62 lesion types treated 61, 61, 62 comparison with other devices 67 complications 61–2, 66, 67 arterial spasm 66 by lesion location 66 slow/no-reflow 67 thrombosis/embolism 66 description 59 endothelial damage 62 in femoropopliteal disease 628 follow-up 62, 67 indications/contraindications 64 outcomes 61 at bifurcation 64 distal to graft 64 multiple severe stenoses 63 in SFA/popliteal arteries + 64 with/without balloon dilatation 65 patient selection 61, 61 in RAS 511
903
restenosis rates 62, 63, 66 techniques 59–60, 61 special scenarios 60 treatment with/without balloon dilatation 63, 63, 65 vs Rotarex system 67, 77 vs SilverHawk® 67 vs transluminal extraction catheter 67 Rotarex system 69–78, 70, 111–12 advantages/disadvantages 77 angiographic results 76 as atherectomy device 69, 72–4, 73 lesion characteristics 72 catheter and motor drive 70 catheter head draining 70 competing systems 69 complications 73–4, 77 description 69–70 electronic control unit 70 follow-up 74 hematocrit/hemoglobin effects 74, 77, 77 mechanism of action 69–70, 70 restenosis rates 77 studies clinical 71–4 preclinical 70–1 technique 71 adjunctive medical therapy 71–2 debulking 73 optimal atherectomy 73 as thrombectomy device 69, 71–2 vs Rotablator 67, 77 rotational atherectomy/ablation 59 devices see Orbital; Rotablator; Rotarex Rubicin Filter 161, 162, 317 Rutherford–Becker classification 640 RX Acculink Carotid Stent System 135 RX Herculink Stent System 133–4 saddle embolism 106, 107 Safe-Cross system 96, 96 SafeGuard 169 Saint Thomas Trial 812 saphenofemoral junction endovenous laser therapy 870, 870, 871 foam sclerotherapy 883 incompetent 459 Rotablator 886 saphenous eye 829, 880, 881 saphenous vein grafts disadvantages 83 stenosis 637 saphenous vein tributaries 829, 830 SAPPHIRE (Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy) trial 314, 330, 331, 336, 337 scalene anticus syndrome 408 Scandinavian Simvastatin Survival Study 812 scleroderma 548 sclerotherapy 868 seatbelt and airbag technique 164, 320–1 segmental pressure examination 601–2, 603 self-expanding stents 133–8 in carotid artery stenosis 151, 323 in iliac occlusion 611 uses 132 see also Cordis nitinol stent; Corvita Endoluminal Graft; Cragg Endopro System; Fluency; Hemobahn; Wallgraft endoprosthesis Sentinol Stent System 136–8 sequential stenoses 590–1
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serum creatinine in RAS 521, 535, 536 and renal function reserve 536 SFA see superficial femoral artery (SFA) shear stress 4 sheaths see introducer sheaths Shuttle guiding sheaths 307 SIA see subintimal angioplasty Sidewinder catheter 309 silent brain infarcts 303 SilverHawk® atherectomy device 50–8, 51 for CLI 50, 52, 53 future studies 56 clinical outcomes 50–2 limb salvage 52 in common femoral artery 51, 53, 55 complications 55 in critical limb ischemia 640, 643 description 50 future studies 55–7 iatrogenic lesions removal 53, 54 in popliteal artery 53, 55, 56 in profunda femoral artery 53, 55 special applications 52–3, 55 in superficial femoral artery 55, 56 and tissue analysis 50, 54, 56–7, 57 types available 50, 52 vs Rotablator 67 Simon nitinol filter 877, 877 simvastatin 812 single photon emission CT (SPECT) 232 SIROCCO studies 379, 627 restenosis in 770–1, 772, 773 sirolimus-coated stents 253, 510, 770 see also rapamycin-coated stents skin changes in venous insufficiency 831, 832, 833, 836 Slip-Cath 34, 35 SmartNeedle 29, 845 Smart stents 636, 758 Control Stents 136 in critical limb ischemia 640 in femoropopliteal disease 627 Hepatic Stents 136 in internal carotid artery stenting 753 in lower limb artery stenting 757 and restenosis 770 smoking in abdominal aortic occlusive disease 467 and aneurysm rupture 420 in ARAS 491 in carotid occlusive disease 343 in mesenteric ischemia 575 and PAD 5, 811–12, 822–3 lower extremities 589, 594, 594 upper extremities 403 in restenosis 767 and SIA complications 88 in thromboangiitis obliterans 661, 662, 663, 664, 666, 667, 668, 669 sodium bicarbonate 802, 806 sodium nitroprusside 464, 481 SOS Omni catheter 846, 847 SPACE trial 330 Spectranectics CVX-300 94 Spider RX 161, 161, 314, 316, 317–18 spider veins 831 spinal cord stimulation 666 splanchnic arterial circulation see mesenteric arterial circulation splanchnorenal bypass, extra-anatomical 540 splenic embolization 686
in hypersplenism 685, 687 in trauma 685 Spongostan 453, 453 SSYLVIA (Stenting of SYmptomatic atherosclerotic Lesions in the Vertebral or Intracranial Arteries) 238, 242, 379 Stanford classification 425, 425, 439 STAR registry 42 StarClose 174 stasis dermatitis 832 stasis ulcer 832 statins in intracranial atherosclerosis 385 in peripheral artery disease 488, 812 STD foam 882, 883 stenoses assessment methods 220 critical 590 in hemodialysis fistula 48 sequential 590–1 see also carotid stenosis; in-stent restenosis (ISR); renal artery stenosis stenotic anastomoses 707 Stent Anticoagulation Restenosis study 252 stent-assisted angioplasty aneurysm management 249 atherosclerosis 248–9, 248 staged 249 failing infraingual vein graft 660 intracranial atherosclerosis 389 intracranial stenosis 238–46 history 238–9 medical treatment 240–1 outcomes 242–3 patient selection 239 preoperative assessment 240 procedure 241–2 see also percutaneous transluminal angioplasty with stenting (PTAS) stent-grafts/stent grafting abdominal aortic dissections 464 in Behçet’s disease 744 hemodialysis access 699 in hypogastric artery disease 618 and hypogastric artery embolization 616 thoracic aorta 429 thoracic aortic dissections 481–2 see also endografts; stents/stenting, covered/coated stents Stent Restenosis Study (STRESS) 764 stent thrombosis 796 Stenting and Angioplasty with Protection in Patients at High Risk for Endarterectomy (SAPPHIRE) trial 314, 330, 331, 336, 337 Stenting of SYmptomatic atherosclerotic Lesions in the Vertebral or Intracranial Arteries (SSYLVIA) 238, 242, 379 stents/stenting 94, 132–9, 133–8, 608 for abdominal aortic occlusion 467–8 bare metal stents in aortic dissection 441, 442–4, 445, 446 in iliofemoropopliteal lesions 671, 677 biodegradable stents 379 within branched endografts 478 carotid artery, ultrasound in 201–4 characteristics open-/closed-cell 323, 324 rigid/flexible 324, 326 straight/tapered 324, 324 chronic mesenteric ischemia 575–6, 576, 577, 578 common iliac artery 608 covered/coated stents 140–55, 145
advantages/disadvantages 153 complications 144, 147–8 descriptions 140–3 implantation techniques 140–3 indications 143–4, 147–53, 154 in limb salvage 634 locations 143–4, 147–53 carotid 151–2 iliofemoropopliteal 143–4, 147–51 subclavian/vertebral 152–3 reocclusion 153 in restenosis 771 techniques/treatment 153–4 in critical limb ischemia 640 in DVT 125, 126–7, 128, 128 endothelialization 126 migration 126 rethrombosis 129 stent characteristics 126, 132 stents available 126 technical aspects 127 understenting 127 external iliac artery 609 fenestrated devices 476 iliac occlusive diseases 611 iliac vessels 41, 609 intracranial see intracranial stenting; stentassisted angioplasty, intracranial stenosis kissing stents 518 abdominal aortic occlusive disease 469, 469 iliac occlusive diseases 608 migration 126, 700 open-/closed-cell stents 323 spot stenting 635–6 in stent-assisted angioplasty 252 stent characteristics 133–8, 323–5 geometric effects 325, 326 stroke 251 for SVC occlusion 859 in thoracic aortic aneurysms 441–6 ultrasound in 201 see also specific types of stent stepwise infusion method 101 STILE (Surgery vs Thrombolysis for Ischemia of the Lower Extremity) study 101, 106, 109 stone basket retrieval catheter 181 Straub-Rotarex system see Rotarex system Strecker stent 360 streptokinase (STK) in acute limb ischemia 650 in CDTT 99–100, 100, 101 “string of beads” sign 544 stroke 256–7 biomolecular changes 256, 256 blood pressure 258 and cerebral autoregulation 258 classification 259, 259 subgroups 260 completed 189 as complication of CAS 338, 339 complications management 277 medical 274–5, 277 neurological 275–6, 277 prophylaxis 277 cord sign 260 cost implications 187, 255 definition 189 differential diagnosis 257 epidemiology 187 focal/multifocal stenoses 261 follow-up 283 hemorrhagic 105–6
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Index stroke (Continued) hypoxia in 257, 257 incidence 255 management 266 0-3 hours after onset 265–6 3-8 hours after onset 266–7 algorithm 265 ancrod 273 antiaggregation 271, 273 anticoagulation 270–1 endovascular treatment 267–70 hemodilution 273 in-hospital 258–9 neuroprotection 273–4 prehospital 257–8 tissue plasminogen activator (tPA) in 263, 265, 267 intra-arterial 268 intravenous 266 urokinase 269 minor 189 neuroimaging 259–60, 262–3 bolus tracking 262 computed tomography 260, 260 magnetic resonance imaging 260 magnetic resonance imaging (MRI) 261 ultrasound 262, 263 prevention 190 risk factors 190 modification 190 stent-assisted angioplasty 251 with subclavian artery lesions 353 swallowing assessment 259 thrombolysis 118 time of onset 257 see also hemorrhagic stroke; ischemic stroke stroke-in-evolution 189 stroke teams 255 stroke units 255–87 classification 255, 256, 256 equipment 255 public awareness 256 subarachnoid hemorrhage Fisher grading scale 281, 281 Hunt and Hess scale 281, 283 in stroke 279, 280, 281 subclavian arteries 737, 739 subclavian artery aneurysms 406 subclavian artery compression 408, 410 see also compression syndromes, superior thoracic aperture subclavian artery stenosis/occlusion 353 causes 354 clinical signs 353–4 diagnosis 354 imaging 354 in-stent restenosis 363 proximal 404 restenosis 767 stenting 132 thrombus above stenosis 367 treatment 356, 359 balloon angioplasty 357 indications 354–5 PTA 353–71, 404 indications 354–5 techniques 355–61, 362 PTAS 358–63, 358, 360, 361 complications 362, 366 discussion 363–4, 366–8 follow-up 361, 362–3, 363 recanalization/restenting 360–1, 364, 366 restenosis 360–1, 364, 366
results 361–3, 364–5, 366–8, 367, 375 techniques 356, 357, 358–60, 358, 362 stenting 359–60 with vertebral artery stenosis 359 subclavian steal syndrome 353, 353, 354, 360, 365 vertebrobasilar insufficiency 403, 403 subclavian vein compression, chronic 412–14, 413 subclavian vein, effort thrombosis of 412 subclavian vein occlusion 860 subintimal angioplasty (SIA) 83–91 advantages 83 for chronic total occlusions 93 complications 88–9 diagrammatic representation 84 indications 83–4 infrapopliteal arterial diseases 635 outcomes 90 technique femoropopliteal lesions 84–5, 85, 87 iliac lesions 86, 88 tibial lesions 85–6 sulfinpyrazone 814 sulodexide 816–17 Super Arrow-Flex introducer sheath 34 Super Stiff Amplatz Guidewires 38 Super Stiff Glidewires 38 superficial femoral artery (SFA) 74 angioplasty, before/after 43 balloon angioplasty, before/after 75, 76 cutting balloon angioplasty in 47 Oasis thrombectomy 113 partial thrombosis 30 plaque formation in 5 PTA in 41–2 Rotarex, before/after 75, 76 superficial femoral artery (SFA) lesions CDTT in 102 Corvita Endoluminal Graft in 149 Cragg/Passager stent in 144, 145 long segment disease 630–1 MRA 597, 604 Orbital in 81, 81 PTA in 41–2 radiation therapy 778–9 SilverHawk® in 55, 56 stents/stenting crashed/thrombosed stent 627 long segment 628 technique 629 subintimal angioplasty in 84–5, 85, 87 surgery 630 thromboaspiration 116 Wallgraft endoprosthesis in 151 superior mesenteric artery (SMA) 572, 843 anatomy 562 duplex ultrasound 570–1 embolectomy 581 flow velocities after food 554 magnetic resonance angiography 567 occlusion 567 stenosis 564 Doppler ultrasound 572 stents/stenting 567 superior thoracic aperture anatomy 409 compression syndromes 408–16 superior vena cava (SVC) occlusion 858, 860 before/after stenting 860, 861 collateral circulation 861 causes 858 endovascular procedures 859–62 complications 862 results 862
905
superior vena caval filters 875 suprahepatic inferior vena cava occlusive disease see Budd–Chiari syndrome Surgery vs Thrombolysis for Ischemia of the Lower Extremity (STILE) study 101, 106, 109 Sutura SuperStitch 174 Swiss 4 arm brachytherapy study 778 sympathectomy 666 systemic lupus erythematosus 734 Syvek patch 173 TAG device 432, 436 Takayasu’s disease (Takayasu’s arteritis) (aortoarteritis) 348, 403, 545, 546, 736 aortic anatomy 428 cutting balloon angioplasty 46–7 renal artery rupture 516 renal artery stenosis 497 surgical reconstruction in 733 thoracic aortic aneurysms 419 see also giant cell arteritis TALON (Treating Peripherals with SilverHawk®: Outcomes Collection) study 50–1, 52, 643, 773 tantalum powder 684 TASC see TransAtlantic Inter-Society Consensus (TASC) telangiectasias 831, 831, 833, 864, 865 temporal arteritis 733 see also giant cell arteritis tenecteplase 122 in acute limb ischemia 650 in thoracic outlet syndrome 412 Terumo guides 627, 629 Tessari (Tourbillon) technique 868, 882, 882, 884 Tetra stents 753, 755, 757 thalamogeniculate artery occlusion 385 thalamus hematoma 278 theophylline 803 thienopyridines 814 thigh claudication 590, 593 thoracic aorta anatomic variations 423–4 anatomy 422, 423–30 blunt trauma 427 coarctation 424, 427–8 embryology 423–4 imaging 422–3 post-operative 429–30 inflammatory arteritis 737 before/after aortoplasty 738, 739 physiology/pathophysiology 418–19 stent-grafting 429 stenting 132 ulcer, penetrating 426–7 see also aortic arch thoracic aortic aneurysms 417–22, 432–8 anatomy 424–5 dissecting 418, 425–6 epidemiology 417–18 etiology 418, 419–20 metabolic/genetic predictors 419 physical/clinical factors 419–20 familial 419 imaging 433–5, 476 pseudoaneurysms 427, 428 rupture, risk of 432 treatment branched grafts 477–8, 477, 478 endovascular intervention 433, 434 clinical results 436–7 customized devices 433, 433
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thoracic aortic aneurysms (Continued) fenestrated/branched grafts 434 TAG device 432, 436 interventional 475–8 medical 417 thoracic aortic dissections 425–6, 439–46 antegrade 439 chronic dissections 482–3 class 1 425–6 class 2 426 classification 425–6, 439, 480 DeBakey classification 439 proximal/distal 439 Stanford classification 425, 425, 439 clinical features 439–40 diagnosis 480 endovascular fenestrations 482 malperfusion syndrome 480 mortality 440, 441, 479 progression 441 pulse deficits 439–40, 440 related conditions 440 treatment 480–3 adjunctive procedures 442–5 occluding endograft 442, 443–4, 444 uncovered stenting of end organ 442–3, 443, 444 endovascular 441, 481 recent advances 441–5 entire descending thoracic aorta 441 immediate 440 interventional 479–83 medical 481 modifications design 441–2 indications 442 technique 442 stent grafting 481–2 surgery, open 481 traditional 440–1 thoracic inlet compression syndromes 411–14 chronic obstruction of subclavian vein 412–14 Paget–Schroetter syndrome 412, 412 thoracic outlet compression syndrome 408–11 diagnostic work-up 409 findings 409 results 411 symptoms/diagnosis 408 treatments 409–11, 413 incision 411 patient positioning 411 thoracoabdominal aneurysms 475–9 repaired with branch grafts 479 see also abdominal aortic aneurysms; thoracic aortic aneurysms thrombectomy devices 111–14 mechanical 101, 103 in acute limb ischemia 650–1 for DVT 121–2 in hemodialysis access problems 702 mechanism of action 111 percutaneous suction 852–3, 853 catheter 853 with inhaled nitric oxide 853–4, 854 Thrombectomy in Middle Cerebral Artery Embolism (TIME) trial 294 thrombin injection for pseudoaneurysm 793 thromboangiitis obliterans (Buerger’s disease) 402, 403, 661–9 classification 663 clinical features 662–3 definition 661
diagnostic criteria 663–4 differential diagnosis 664 imaging 663–4 laboratory findings 664 disease progression 663 epidemiology 661 etiology 661 pathogenesis 661–2 prognosis 666, 668 toe gangrene 663, 663 treatment 664–6 amputation, determination of level 668 venous arterialization 666, 667 before/after therapy 667 of vessels 662, 662 thromboaspiration (catheter suction thromboembolectomy) 114, 116–17 as adjunct to CDTT 101, 103, 114 clinical experience 116–17, 116 disadvantages 111 femoropopliteal lesions 116 technique 114 thromboembolism as cause of PAD 4 CDTT in 103, 106 as PVI complication 794, 795 tumor 855, 855, 856 thrombolysis in acute limb ischemia 650 catheter-based 851, 851 clinical experience 112 complications 124 for DVT 122–3, 125 future of 118 in hemodialysis access problems 702 for ischemic stroke 263 acute 288–99 mechanical 292–4 microbubbles 118 percutaneous intra-arterial thrombolysis (PIAT) 109 perioperative 103 pharmacologic 290, 292–4 pharmacomechanical 118 pulse spray 101, 104, 702 systemic 850–1, 850 see also flow-directed thrombolysis thrombolysis in brain ischemia (TIBI) score 289–90, 290 thrombolysis in cerebral infarction (TICI) score 290, 291 thrombolysis in myocardial infarction (TIMI) score modified (Quereshi) 289, 290, 291 original 289, 289 Thrombolysis or Peripheral Arterial Surgery (TOPAS) trial 100, 106, 109 thrombolytic agents 99–101, 267 thrombolytic therapy for arterial thrombosis/graft occlusions 817 for chronic total occlusions 96 infusion methods 101 see also catheter-directed intra-arterial thrombolytic therapy (CDTT) thrombosing agents 172 thrombosis arterial, in acute mesenteric ischemia 555 in Behçet’s disease 743 deliberate, in aortic dissection 443 of femoral veins 839 of prosthesis in IFPAs 673–4 as PVI complication 796 in restenosis 764–5
after stent placement 144, 147 with vascular closure devices 174 thrombotic thrombocytopenia see heparininduced thrombotic thrombocytopenia (HITT) thromboxane A2 blockers 814–15 thrombus formation 4 occlusive 107 see also graft thrombus extraction thrombus formation after aortic angioplasty 469 carotid artery 188 THUNDER trial 773 TIBI score 289–90, 290 tibial arteries 844 tibial lesions subintimal angioplasty 85–6, 88, 89 surgery 631 tibial thrombus 124, 125 tibioperoneal arteries 42–3 TICI score 290, 291 ticlopidine in arterial access 30 in endovascular revascularization 390 in infra-popliteal disease 635 in PAD 814 in RAS 504, 532 in stent-assisted angioplasty 390 for stent reocclusion 153 in subclavian artery PTA 361 in thromboangiitis obliterans 664 in vertebral artery PTAS 379 TIME (Thrombectomy in Middle Cerebral Artery Embolism) trial 294 TIMI score modified (Quereshi) 289, 290, 291 original 289, 289 TIPS (transjugular intrahepatic porto-systemic shunt) 727, 728 tissue plasminogen activator (tPA) 290, 851 catheter-directed 120, 129 intra-arterial 268 intravenous 266 in pulmonary embolism 850, 850, 851 in stroke 255, 263, 265, 266, 267, 268 ischemic 270, 288 with mechanical thrombolysis 293–4 Titanium Greenfield filter (TGF) 875 TLBAP see transluminal balloon angioplasty TOAST (Trial of ORG 10172 in Acute Stroke Treatment ) 270 tobacco use see smoking toe–brachial index (TBI) 601 toe gangrene 663, 663 toe pressures 595–6 toe pulse oximetry 596 Tolazoline 89 TOPAS (Thrombolysis or Peripheral Arterial Surgery) trial 101, 106, 109 total occlusions pathology 92 see also chronic total occlusions Tourbillon (Tessari) technique 868, 882, 882, 883 tPA see tissue plasminogen activator (tPA) Trac-Wright see Kensey catheter transarterial lung perfusion scintigraphy (TLPS) AV shunting malformation 718 venous malformation 715 TransAtlantic Inter-Society Consensus (TASC) on acute limb ischemia 648, 650 Iliac Stenotic Lesions, Classification of 610
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Index on Management of Peripheral Arterial Disease 626 on aortoiliac lesions 39–40, 40 femoral popliteal lesions 41, 41 transcatheter peripheral embolization 684–5, 687–8, 690 transcranial Doppler (TCD) angioplasty/stenting 306 preprocedural evaluation 303 in carotid disease angioplasty/stenting 201, 202–5 before procedure 201–2 during procedure 203 after procedure 203–4 endartectomy 207–10 before procedure 208 during procedure 208 after procedure 208 embolism detection 207 high-intensity transient signals (HITS) 199, 203, 203 in intracranial stenosis 382 tests 207 transcutaneous oximetry 603 transesophageal echocardiography 462 transient ischemic attack (TIA) 189 angioplasty/stenting 272 cerebral perfusion imaging 230–1 transjugular intrahepatic porto-systemic shunt (TIPS) 727, 728 transluminal balloon angioplasty (TLBAP) atrial septal defect closure 709, 711 coarctation/recoarctation of aorta 704 stenting 704, 704 false aneurysm after 704 conduit stenting 706–7 in congenital aortic valve stenosis 704–11 coronary–cardiac fistula 707, 710 cyanotic congenital heart disease 707 large aorto–pulmonary collateral artery (LAPCA) embolization 708–9 stenting 708 large aorto–pulmonary collateral artery (LAPCA) stenting 706 left heart hypoplasia syndrome 706 patent ductus arteriosus stenting 709 transcatheter closure 709–10 pathological communications, closure of 711 pulmonary artery atresia 708–9 pulmonary artery stenting 705 right ventricular outflow tract stenting 706–7, 710 stenotic anastomoses 707 in thromboangiitis obliterans 666 ventricular septal defect closure 708, 710–11 transluminal extraction–endartectomy catheter (TEC) 67, 69, 112 transplantation bone marrow-derived mononuclear cells 183 progenitor cells 182 transradial access 21–3, 26–8 Allen’s test 22 complications 27 indications/advantages 27 procedural success 21–2 right vs left 22, 26 safety 21 sheath removal/hemostasis 27 technique 26–7 Trap-Ease filter. 876, 876 trash foot 103
Treating Peripherals with SilverHawk®: Outcomes Collection (TALON) study 50–1, 52, 643, 773 Trellis device 118, 121 Trerotola device 113–14, 852, 852 Tri Active FX 157, 157, 311 Tri-lobed Balloon 436, 437 Trial of ORG 10172 in Acute Stroke Treatment (TOAST) 270 triplex ultrasound 456 tumescent anesthesia 867–8 tumor embolization 687, 687 tumor thromboembolism 855, 855, 856 Twin-One 157–9, 158, 312 two-vessel coronary disease 754 UK Endograft Registry 482 UK Prospective Diabetes Study (UKPDS) 812 ulcerated plaque 200–1, 201, 219 ulceration lower extremity arterial disease 595 stasis ulcer 832 venous 830, 881 venous insufficiency 837 ulnar artery thrombosis 104 ultrasound carotid plaque 199–206 before angioplasty/stenting 201–2, 202 during angioplasty/stenting 203 after angioplasty/stenting 203–4, 204–5 B-mode imaging 200, 212 normalization 214–17, 215 software package 215–17, 216, 217 characterization 211–28 classification 211–12 echodensity and structure 217–19 future perspectives 225–6 histology, correlation with 212–17 natural history studies 213–14 standardization of 201 follow-up 204 quantification of stenosis 199–201 carotid stenting 201–3 fibroid imaging 692 ulcerated plaque 200–1, 201 Ultrasound Thrombolytic Infusion Catheter 295 unstable plaques see plaques, “vulnerable” upper extremity arterial disease 401–7 aneurysmal disease 403, 406 clinical presentation 401 diagnosis 403 etiology 402 large artery disease 402–3 distal disease 405–6 proximal disease 404–5 treatment 404–6 small artery disease 401–2 treatment 403–4 treatment 403–6 urokinase 851, 851 in acute limb ischemia 650 in CDTT 99, 100, 100, 101 in DVT 122, 124, 127, 128 intra-arterial 269 in PAD 817 in pulmonary embolism 850, 850, 851, 851 in stroke, acute ischemic 290, 293 see also recombinant pro-urokinase in thoracic outlet syndrome 412 uterine arteries 693 uterine artery embolization (UAE) 614–16, 617, 684–5, 685, 692–8 in adenomyosis 696 before/after 694–5
907
complications 696–7 contraindications 694 follow-up 696 protocols 695–6 patient evaluation 693–4 preprocedural 692 patient selection 693–4 periprocedural care 694 pregnancy after 697 procedure 694–5 results 696 side effects 695 uterine fibroids see fibroids Vanguard endograft (VE) for abdominal aortic aneurysms 449, 450–1 complications 452–3, 454 varicose veins 831, 831, 833, 864–9, 864, 865 anatomical considerations 879, 881 endovenous laser therapy 870–2, 884, 884 advantages 872 before/after therapy 871 contraindications 885 duplex-guided mapping 870 duplex ultrasound 885 in great saphenous vein 871 indications 882 parameters 872 procedure 870–1 technique 885 foam sclerotherapy 879–86 classification 879, 880 contraindications/adverse effects 884, 884 “foam block” 880 history 879 indications 882 Orbach’s “air block technique” 879, 880 technique 881–3 Tessari (Tourbillon) technique 868, 882, 882, 883 multi-modality treatment 886 pathophysiology 881 post-operative compression 866–7 radio-frequency ablation/obliteration 865, 884 contraindications 885, 886 generator 866 indications 882 Rotablator 885 sclerotherapy 868 access 868 surgery current status 865 hook phlebectomy 865–6 indications 865 principles 864–5 superficial venous ablation 865 tumescent anesthesia 867–8 treatment algorithm 885 treatment techniques 881–4 vascular access see under specific access sites, conditions and interventions vascular brachytherapy treatment (VBT) see brachytherapy vascular closure devices 168–78 advantages/disadvantages 176 approximators active 170, 173–4, 174 passive 170, 172–3, 173 classification 170, 171, 172 closure devices 170, 172 complications 174–6 analysis 175 techniques avoiding 168–9
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vascular closure devices (Continued) cost implications 177 femoral angiography, importance of 176 manual compression 168, 170 mechanical compression 169 and peripheral vascular interventions 176 vascular access 168–70 vascular endothelial growth factor (VEGF) in gene therapy 782, 785, 785 in PAD pathogenesis 4 vascular endothelium in CDTT 187 vascular occlusion 174 vascular shields 168 vascular smooth muscle cells 418–19 vasculogenesis 182 vasodilators in CIN 802–3 in PAD 815 vasorenal hypertension 754–7, 755 VasoSeal 168, 172, 173 vasospasm with Rotablator 66 with Rotarex system 72, 74 in stroke 281–2 vazaprostan 665 VEDICO trial 884 vein bypass grafts 47–8 Vein Graft Surveillance Randomized Trial (VGST) 656 vena cava occlusion see inferior vena cava (IVC) occlusion; superior vena cava (SVC) occlusion vena caval filters 873–8 complications 874–5 desired qualities 873 implantation techniques 874 indications/contraindications 874 permanent 874 post-implantation care/follow-up 875 retrievable/optional 874 types available 874, 875 Vena-Tech LGM filter 876–7, 877 venous ablation, superficial 865 venous arterialization 666, 667 venous disease 829–34 classification 880 diagnostic evaluation 835–40 chronic 838–9 vs acute 838 deep vein thrombosis 835, 839 recurrent 836 duplex ultrasound 835–6, 837–8, 837 criteria 837–8 reflux 836–8, 880 epidemiology 830, 831 pathophysiology insufficiency 832 chronic 832–3 primary 831–2 reversal of flow 838 risk factors 831, 832 venous hypertension 120, 832 venous insufficiency chronic 832–3, 864, 880 primary 831–2, 864
venous malformation (VM) 714, 715–16 venous occlusions stent-assisted angioplasty 249–51 thrombolysis 118 venous reflux examination 836–8, 880 venous stasis disease 832 venous system anatomy 829–30 physiology 830 venous thrombosis 743 venous ulceration 830, 881 venous valves 830, 836 ventricular septal defect (VSD) closure 708, 710–11 Venture 38 verapamil 27, 802 vertebral artery anatomy 196, 196 embolic protection device 165 vertebral artery disease 189 spontaneous dissection 189 vertebral artery stenosis, extracranial access 373 balloon angioplasty 371 location 371, 371 PTA 273 PTAS 361, 364, 371–81 access 373 before/after 373 clinical findings 372 complications 376 controversial issues 379 diagnostic imaging 372 discussion 377–9 evaluation of results 375–6 follow-up 377, 378–9 indications 372–3 medication 373–6 microembolization 379 patient selection 376 predilatation 375 protection devices 376 results 375, 376–7, 377 stent choice/placement 378 techniques 373–7 and subclavian artery occlusion 359 vertebral angioplasty/stenting 374 vertebrobasilar insufficiency (VBI) 187, 189, 371, 377 revascularization 384 vertebrobasilar stenoses, intracranial 387 Veterans Administration Cooperative Study 606 Viabahn see Hemobahn/Viabahn VIBRANT trial 771 vibration angioplasty 95–6 vibration injury 402 Vienna trials 778–9, 779 Vienna-2 628, 771 Vienna-V 771 visceral vasculature 842 Vista Brite Tip guiding sheath 506, 507 vitamin C 491 vitamin E 491 vitamin K antagonists (VKA) 658
Vitek catheter 308, 309 VIVEXX Carotid Stent 135 VNUS closure 865, 884 generator 866 see also radio-frequency ablation von Willebrand factor 824 “vulnerable” plaque 188 Wallenberg syndrome 189 Wallgraft endoprosthesis 142, 151 in carotid artery stenosis 151 clinical experience 149–50, 151 iliofemoropopliteal lesions 671, 677 Wallstent 136 in Budd–Chiari syndrome 728 in CAS 317, 318 outcomes 328, 329 characteristics 324, 327 in critical limb ischemia 640 in femoropopliteal disease 626–7 follow-up 770 geometric effects 325, 326 in hemodialysis access 701 Magic Wallstent 249 in pulmonary embolism 852 in subclavian artery occlusion/stenosis 361, 375 for SVC occlusion 859, 861, 862 for venous stenting 126 warfarin in Budd–Chiari syndrome 728 for DVT 124 for intracranial atherosclerosis 385 plus aspirin 658 in pulmonary embolism 850, 850 Warfarin Aspirin Symptomatic Intracranial Disease (WASID) 238, 242, 387 “watermelon seeding”, avoidance of 341 Welter retrieval loop catheter 179, 180 whole body blood pool scintigraphy (WBBPS) AV shunting malformation 718 lymphatic malformation 717 venous malformation 715–16 Wingspan stent system 239 Xact Carotid Stent 135, 328 Xceed Biliary Stent 133–4 xenon-enhanced computerized tomography (XeCT) 846 cerebral perfusion imaging 232 Xpert Biliary Stent 133–4, 636 in hemodialysis access problems 700 xxxK stents 627 Z stents 852, 859 Zenith device 476 Zilver Stents 136 in critical limb ischemia 640 in internal carotid artery stenting 753 Zilver Ptx trial 771 Zyban 811