The Year in Interventional Cardiology, Volume 3 (The Year in)

THE YEAR IN INTERVENTIONS CARDIOLOGY VOLUME 3

THE YEAR IN INTERVENTIONS CARDIOLOGY VOLUME 3 Edited by

AP BANNING AND C DI MARIO

CLINICAL PUBLISHING OXFORD Distributed worldwide by CRC Press Boca Raton London New York Washington, DC Clinical Publishing an imprint of Atlas Medical Publishing Ltd

This edition published in the Taylor & Francis e-Library, 2006. “To purchase your own copy of this or any of Taylor & Francis or Routledge’s collection of thousands of eBooks please go to http://www.ebookstore.tandf.co.uk/.” Oxford Centre for Innovation Mill Street, Oxford 0X2 OJX, UK Tel: +44 1865 811116 Fax: +44 1865 251550 Web:www.clinicalpublishing.co.uk Distributed by: CRC Press LLC 2000 NW Corporate Blvd Boca Raton, FL 33431, USA Email:[email protected] CRC Press UK 23–25 Blades Court Deodar Road London SW15 2NU, UK Email:[email protected] © Atlas Medical Publishing Ltd 2005 First published 2005 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, without the prior permission in writing of Clinical Publishing or Atlas Medical Publishing Ltd 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 A catalogue record for this book is available from the British Library ISBN 0-203-50019-9 Master e-book ISBN

ISBN 0-203-59807-5 (Adobe e-Reader Format) ISBN 1 904392 33 4 (Print Edition) ISSN 1478-0178 The publisher makes no representation, express or implied, that the dosages in this book are correct. Readers must therefore always check the product information and clinical procedures with the most up-to-date published product information and data sheets provided by the manufacturers and the most recent codes of conduct and safety regulations. The authors and the publisher do not accept any liability for any errors in the text or for the misuse or misapplication of material in this work Project manager: Clive Sparling

Contents Contributors

vii

Preface Adrian Banning, Carlo Di Mario

ix

Part I Strategy 1. Risk stratification in acute coronary syndromes Sunil V Rao, L Kristin Newby 2. Percutaneous coronary intervention for acute ST-elevation myocardial infarction Felix Zijlstra

3 29

Part II Stenting 3. Pressure and flow measurements in the catheterization laboratory Narbeh Melikian, Philip A MacCarthy 4. Drug-eluting stents Italo Porto, Adrian Banning 5. Percutaneous coronary intervention versus coronary artery bypass graft surgery Mark Webster 6. Contrast agents and renal protection during percutaneous intervention Robin Choudhury, Cheerag Shirodaria 7. Advances in antiplatelet therapy Anthony A Bavry, A Michael Lincoff 8. Percutaneous coronary intervention for left main stem disease Neville Kukreja, Leisheng Ru, Carlo Di Mario 9. Percutaneous coronary intervention in diabetic patients Nick E J West

39 60 81

99 117 139 160

Part III New developments 10. Vascular brachytherapy Goran Stankovic, Dejan Orlic 11. Myocardial reperfusion, no-reflow and distal protection Dan Blackman 12. Intravascular ultrasound Paul Schoenhagen 13. Carotid artery stenting Bernhard Reimers, Luca Favero 14. Cell therapy Narbeh Melikian, Carlo Di Mario 15. Invasive assessment of the vulnerable plaque Anitha Varghese, Carlo Di Mario

185 209 231 249 274 295

List of abbreviations

320

Index of papers reviewed

323

General index

335

Contributors ADRIAN BANNING, MD, FRCP, FESC, Department of Cardiology, John Radcliffe Hospital, Oxford, UK ANTHONY A BAVRY, MD, MPH, Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio, USA DAN BLACKMAN MD, MRCP, Department of Cardiology, John Radcliffe Hospital, Oxford, UK ROBIN CHOUDHURY, DM MRCP, Department of Cardiology, John Radcliffe Hospital, Oxford, UK CARLO DI MARIO MD, FACC, FESC, Royal Brompton Hospital, London, UK LUCA FAVERO MD, Cardiovascular Department, Civic Hospital, Mirano, Italy NEVILLE KUKREJA MD, Department of Cardiology, Royal Free Hospital, London, UK A MICHAEL LINCOFF, MD, Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio, USA PHILIP A MACCARTHY BSC, PHD, MRCP, Department of Cardiology, King’s College Hospital, London, UK NARBEH MELIKIAN BSC, MBBS, MRCP, Department of Cardiology, Guy’s, King’s and St Thomas’ School of Medicine, London, UK L KRISTIN NEWBY MD MHS, Duke Clinical Research Institute, Durham, North Carolina, USA DEJAN ORLIC, Klinika za kirurgiju, Klinickibolnicki centar Rijeka, Rijeka, Croatia ITALO PORTO, MD, Department of Cardiology, John Radcliffe Hospital, Oxford, UK SUNIL V RAO MD, Interventional Cardiology Fellow, Duke Clinical Research Institute, North Carolina, USA BERNHARD REIMERS MD, Cardiovascular Department, Civic Hospital, Mirano, Italy LEISHENG RU, Department of Cardiology, Royal Brompton Hospital, London, UK PAUL SCHOENHAGEN, MD, FAHA, Department of Diagnostic Radiology, Cardiovascular Imaging and Department of Cardiovascular Medicine, The Cleveland Clinic Foundation, Cleveland, Ohio, USA CHEERAG SHIRODARIA BSC MRCP, Department of Cardiology, John Radcliffe Hospital, Oxford, UK GORAN STANKOVIC, Institute for Cardiovascular Diseases, Clinical Center of Serbia, Belgrade, Serbia and Montenegro ANITHA VARGHESE MD, Cardiovascular Magnetic Resonance Unit, Royal Brompton Hospital, London, UK

MARK WEBSTER MD, Cardiology Department, Green Lane Hospital, Auckland, New Zealand NICK E J WEST MA MD MRCP, Consultant Cardiologist, Department of Cardiology, Gloucestershire Royal Hospital, Gloucester, UK FELIX ZIJLSTRA, Academisch Ziekenhuis Groningen, Afd Cardiologie, Groningen, The Netherlands

Preface Once again, this has been a monumental year for interventional cardiology. The promise and excitement surrounding the development of drug-eluting stents has been maintained and percutaneous intervention seems poised to make coronary artery bypass surgery redundant. This book has drawn together authors from the USA, Oceania and Europe to reflect on last year. It is the third volume in the series and we hope that it builds on the success of The Year in Interventional Cardiology 2002 and 2003, which have provided focused summaries of the world’s literature. In Part I, Kristin Newby and Sunil Rao discuss the increasingly precise art of risk stratification using blood markers and particularly troponin. The Zwolle clinic in the Netherlands is renowned for its primary angioplasty programme and Felix Zijlstra discusses further exciting data about treatment for acute myocardial infarction. In Part II, the role of pressure and flow measurement is discussed by Philip MacCarthy and Narbeh Melikian from King’s Hospital in London. Dr MacCarthy spent time in Aalst, Belgium and he gives a perspective of how this technology can be integrated successfully into our routine interventional practice. The principal studies that have been published on drug-eluting stents are then discussed and Mark Webster from Green Lane Hospital in Auckland discusses comparisons between bypas surgery and percutaneous coronary intervention. We are all performing increasingly complex procedures, which require larger contrast volumes and many of our patients have fragile renal function. In the next chapter, Drs Shirodaria and Choudhury discuss the increasingly important issue of protecting renal function during percutaneous coronary intervention. Advances in antiplatelet agents are discussed by Dr Bavry and Mike Lincoff from the Cleveland Clinic in the USA. Dr Nick West from Gloucester Hospital in the UK spent time at the Green Lane Hospital collaborating with the Thorax Center in Rotterdam and he reviews issues and complexity of treating patients with diabetes. In Part III, vascular brachytherapy is reviewed by Goran Stankovic and Dejan Orlic. Dr Dan Blackman, currently in Toronto, Canada then reviews the data that have been published in the last year on distal protection and management of the ‘no-reflow’ phenomenon. A review of intravascular ultrasound literature is presented by Dr Schoenhagen from the Cleveland Clinic and Bernhard Reimers and Luca Favero from Italy gives us a thoughtful review of the literature on carotid intervention. Berhard Reimers is an interventional cardiologist and his perspective on peripheral intervention is a valuable one as it seems likely that many of us will be tackling carotid disease in the near future. There are then further chapters on the exciting developments in cell therapy by Dr Melikian and Dr Di Mario, and on vulnerable plaque identification by Dr Varghese and Dr Di Mario.

We hope that, once again, this book will give an up-to-date and thorough review of the interventional cardiology literature. We are grateful to our colleagues for their thoughtful input and enthusiasm. We hope you find the book a stimulating and useful resource. Dr Adrian Banning and Professor Carlo di Mario

Part I Strategy

1 Risk stratification in acute coronary syndromes SUNIL V RAO, L KRISTIN NEWBY © Atlas Medical Publishing Ltd

Introduction Acute coronary syndromes (ACS) range in severity from unstable angina to acute ST segment elevation myocardial infarction (MI). The underlying pathophysiology of the different manifestations of ACS is similar, with coronary artery plaque rupture and platelet adherence, activation and aggregation forming the basis for varying degrees of artery occlusion. Incomplete occlusion results in the clinical syndrome of unstable angina while complete occlusion leads to cardiac myocyte necrosis and ML The variation in presentation mirrors the risk of recurrent infarction or death. Therein lies the importance of risk stratification. It serves to facilitate both communication between the doctor and the patient by providing prognostic information and selection of therapies that maximize benefit and minimize harm. Given that the clinical presentation is what is first encountered, the cornerstone of risk stratification is the history and physical examination. Indeed, the value of baseline clinical characteristics has been confirmed by several investigators |1,2|. Demographic characteristics such as age and previous history of ischaemic heart disease, and presenting characteristics such as blood pressure, heart rate, and Killip class are all critical for the initial risk assessment. After the initial history and physical examination, the 12-lead electrocardiogram (ECG) is the first objective risk stratification tool available. The ECG serves as the basis for the first therapeutic decision point. The presence of ST segment elevation separates patients into a category where the prompt administration of reperfusion therapy, either fibrinolytic medications or primary percutaneous intervention, can improve both longand short-term survival |3,4|. Patients without persistent ST segment elevation fall into the category of non-ST segment elevation ACS. For this heterogeneous group of patients, a combination of ECG findings and laboratory data provide incremental prognostic value above that which is gained from the history and physical. The importance of both baseline and serial measures of markers of myocardial necrosis (particularly creatine kinase [CK]MB and the troponins) in risk stratification of both ST segment elevation MI and non-ST segment elevation ACS patients has been firmly established |5|. New markers of inflammation and thrombosis continue to expand our knowledge of the pathological processes underlying ACS and provide further indicators of outcome. Whether conventional secondary prevention measures and antithrombotic therapies affect outcomes by modifying the levels of these markers is

The year in interventions cardiology

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unknown. In addition, genetic markers—the ‘holy grail’ of risk assessment—have begun to emerge as viable options for evaluating prognosis in patients with coronary artery disease. The following articles published over the past year were selected to highlight recent developments in each of these areas. Their findings may point the way to the prognostic evaluation of the ACS patient in years to come.

Prognostic value of myeloperoxidase in patients with chest pain Brennan ML, Penn MS, Van Lente F, et al. N Engl J Med 2003; 349(17): 1595–604 BACKGROUND. Identifying patients with chest pain who are at high risk for future events is facilitated by the measurement of markers of cardiac myocyte necrosis (CK, CKMB, troponins) and inflammation (C-reactive protein [CRP]). However, many patients with chest pain who have normal levels of these markers at baseline subsequently develop MI, require revascularization, or die within 6 months of presentation. This indicates that current biochemical markers of risk are inadequate for complete risk assessment. Brennan et al. sought to address this issue by evaluating the prognostic value of myeloperoxidase, an enzyme released by leucocytes in response to injury and associated with angiographic coronary artery disease, development of lipid-laden soft plaque, and plaque instability, among patients with chest pain. INTERPRETATION. Myeloperoxidase levels were measured in 604 consecutive patients presenting to the emergency room for evaluation of chest pain of suspected cardiac origin. Outcomes were assessed at 30 days and 6 months, and consisted of major adverse cardiac events (MACE) (MI, reinfarction, need for revascularization, death). A clinical diagnosis of MI was based on troponin T elevation of at least 0.1 ng/ml; unstable angina was defined as the presence of rest angina, accelerated angina, ST segment depression or T-wave inversion on the initial EGG. The diagnosis of an ACS was based on the presence of either an Ml or unstable angina. Outcomes were confirmed by a blinded chart reviewer. The investigators determined the normal range for myeloperoxidase by recruiting 115 healthy volunteers with no history of coronary artery disease. Among the patients with chest pain, 23.5% had a final diagnosis of MI, 17.1% unstable angina, 37.6% suspected ACS, 21.5% non-cardiac chest pain. The median myeloperoxidase level was higher among patients with chest pain than among controls, and was weakly correlated with troponin T, CRP and age. There was no correlation with white blood cell count. Increasing quartiles of myeloperoxidase levels were significantly associated with the development of MI, ACS, 30-day and 6-month MACE in the unadjusted analysis, even among patients with initially undetectable troponin levels (Table 1.1). After adjustment

Risk stratification in acute coronary syndromes

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Table 1.1 Odds ratio for major adverse cardiac events according to the quartile of myeloperoxidase and C-reactive protein level Myeloperoxidase quartile C-reactive protein quartile 1 2 3 4 1 2 3 4 (11.640 pM) 197.9 393.9 pM) mg/l) 5.470 11.640 mg/l) pM) pM) mg/l) mg/l) odds ratio (95% confidence odds ratio (95% confidence interval) interval) Diagnosis at presentation Myocardial infarction All patients 1.0 1.2 (0.7– 2.1 (1.2– 2.3) 3.8)† Patients 1.0 1.0 (0.4– 1.5 (0.6– initially 2.7) 3.9) negative for troponin T Adjudicated acute coronary syndromes All patients 1.0 1.6 (1.0– 3.5 (2.1– 2.7) 5.8)‡ Patients 1.0 2.0 (1.0– 4.6 (2.3– persistently 4.2) 9.2)‡ negative for troponin T Major adverse cardiac event At 30 days All patients 1.0 1.7 3.2 (2.0– (1.02– 5.4)‡ 2.8)† Patients 1.0 2.2 (1.1– 4.2 (2.1– persistently 4.6)† 8.4)‡ negative for troponin T At 6 months All patients 1.0 1.6 (1.0– 3.6 (2.2– 2.7) 5.8)‡ Patients 1.0 1.9 (1.0– 4.4 (2.3– persistently 3.8) 8.4)‡ negative for troponin T

3.9 (2.2– 1.0 6.8)‡∫ 3.7 (1.6– 1.0 8.5)‡∫

1.9 (1.0– 3.6)† 1.6 (0.7– 3.6)

3.1 (1.7– 5.8)‡ 1.7 (0.8– 3.9)

3.0 (1.6– 5.4)†∫ 1.1 (0.5– 2.7)

4.8 (2.9– 1.0 7.8)‡∫ 4.1 (2.0– 1.0 8.5)‡∫

1.7 (1.1– 2.8)† 1.5 (0.8– 2.6)

2.0 (1.2– 3.2)† 1.2 (0.6– 2.1)

1.5 (0.9– 2.3) 0.6 (0.3– 1.3)

4.7 (2.8– 1.0 7.7)‡∫

1.9 (1.2– 1.7 (1.0– 1.6 (1.0– 3.1)† 2.7)† 2.5)

4.1 (2.0– 1.0 8.4)‡∫

1.7 (1.0– 0.8 (0.4– 0.8 (0.4– 3.0) 1.6) 1.5)

4.7 (2.9– 1.0 7.7)‡∫ 3.9 (2.0– 1.0 7.7)‡∫

1.8 (1.1– 2.9)‡ 1.6 (0.9– 2.7)

1.7 (1.1– 2.7)† 0.9 (0.5– 1.7)

1.8 (1.1– 2.8)†§ 1.0 (0.6– 1.9)†

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*In each analysis, the first quartile served as the reference group. Patients initially negative for troponin T had a troponin T level of less than 0.1 mg/ml at presentation, †P