An Atlas of Contrast-Enhanced Angiography

An Atlas of CONTRAST-ENHANCED ANGIOGRAPHY THE ENCYCLOPEDIA OF VISUAL MEDICINE SERIES An Atlas of CONTRASTENHANCED AN...

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An Atlas of CONTRAST-ENHANCED ANGIOGRAPHY

THE ENCYCLOPEDIA OF VISUAL MEDICINE SERIES

An Atlas of CONTRASTENHANCED ANGIOGRAPHY THREE-DIMENSIONAL MAGNETIC RESONANCE ANGIOGRAPHY Nicholas Bunce St. George’s Hospital London, UK and Raad H.Mohiaddin National Heart and Lung Institute London, UK Foreword by

Professor Sir Magdi Yacoub Royal Brompton Hospital London, UK

The Parthenon Publishing Group International Publishers in Medicine, Science & Technology

A CRC PRESS COMPANY BOCA RATON LONDON NEW YORK WASHINGTON, D.C.

Published in the USA by The Parthenon Publishing Group 345 Park Avenue South, 10th Floor New York , NY 10010 USA Published in the UK and Europe by The Parthenon Publishing Group 23–25 Blades Court Deodar Road London SW 15 2NU UK Copyright © 2003 The Parthenon Publishing Group Library of Congress Cataloging-in-Publication Data Bunce, Nicholas An atlas of contrast-enhanced angiography/Nicholas Bunce and Raad Mohiaddin p.; cm.—(The encyclopedia of visual medicine series) Includes bibliographical references and index. ISBN 1-84214-081-7 (alk. paper) 1. Angiography—Atlases. 2. Contrast media. I. Mohiaddin, Raad H. II. Title. III. Series. [DNLM: 1. Coronary Angiography—methods—Atlases. 2. Cardiovascular Diseases—physiopathology—Atlases. WG 17 B9422a 2003] RC691.6.A53 B864 2003 616.1'307548–dc21 2002042501 British Library Cataloguing in Publication Data Bunce, Nicholas An atlas of contrast-enhanced angiography.—(The encyclopedia of visual medicine series) 1. Angiography 2. Blood vessels—Diseases—Diagnosis I. Title II. Mohiaddin, Raad H. 616.1'3'07572 ISBN 0-203-00891-X Master e-book ISBN

ISBN - (Adobe e-Reader Format) ISBN 1-84214-081-7 (Print Edition) First published in 2003 This edition published in the Taylor & Francis e-Library, 2005. “To purchase your own copy of this or any of Taylor & Francis or Routledges’s collection of thousands of eBooks please go to www.eBookstore.tandf.co.uk.” No part of this book may be reproduced in any form without permission from the publishers except for the quotation of brief passages for the purposes of review

Composition by The Parthenon Publishing Group

Contents

1 2 3 4 5 6 7 8

Foreword Preface Acknowledgements

ix xi xii

Introduction and methods Principles of magnetic resonance angiography Magentic resonance of the aorta Carotid artery disease Magnetic resonance angiography of the pulmonary vessels Magnetic resonance angiography of the coronary arteries Magnetic resonance angiography of the renal vessels Magnetic resonance angiography of the peripheral vessels

1 10 18 39 46 62 79 91

Conclusion Index

102 104

Foreword Decision-making in surgery of the aorta and peripheral vessels is almost totally dependent on accurate three-dimensional localization and characterization of the abnormalities concerned. Advances in different forms of non-invasive imaging, particularly those utilizing magnetic resonance, have had a massive impact on this field. The authors of this Atlas have made or contributed to many of these advances. The authors draw on their vast experience in the field and provide an extremely valuable resource for all clinicians involved in the specialty or those trying to gain knowledge about the subject. I am confident that this book will contribute to both the practices of vascular surgery as well as research in this rapidly evolving area. Professor Sir Magdi Yacoub Royal Brompton Hospital London, UK

Preface Magnetic resonance of the cardiovascular system is a rapidly developing technique that can provide anatomical and functional information to assist the clinician in the diagnosis and management of patients with cardiovascular disease. Contrast-enhanced magnetic resonance angiography is a recently developed method of producing high quality three-dimensional images of the vascular system with the peripheral injection of a non-toxic gadolinium-based contrast agent. In this book, we provide a basic introduction to magnetic resonance angiography with a step-wise guide to imaging each section of the vascular system; including anatomical drawings to orientate the reader. We have also included annotated images illustrating typical pathology that may affect the cardiovascular system; and provide evidence to support the increasing referrals for magnetic resonance angiography. With this text, which will appeal to all physicians with an interest in the cardiovascular system as well as physicians primarily focusing on magnetic resonance; it is hoped that an increasing number of patients will benefit from the rapidly developing technique of magnetic resonance angiography. Raad H.Mohiaddin and Nicholas Bunce November 2002

Acknowledgements The authors would like to thank their clinical and technical colleagues at the Cardiovascular Magnetic Resonance Unit for their assistance with the preparation of this manuscript. The authors acknowledge the support provided by the clinicians at the Royal Brompton Hospital. In addition, the authors are grateful for the generous support of the British Heart Foundation, CORDA The Heart Charity; and Imperial College.

1 Introduction and methods STATIC MAGNETIC FIELD The core of an atom is made up of positive and neutral particles. Nuclei with an uneven atomic mass or number possess angular momentum that is termed magnetic spin. This induces a magnetic field with an axis coincident with the axis of spin and the magnitude and direction proportional to the magnetic moment (µ). At rest, these atomic moments are lined up randomly, but, when placed in a static magnetic field (β0), the moments line up parallel or anti-parallel to the field. It is more efficient for these nuclei to line up parallel with the field and this results in a net magnetization parallel to the field (M). This is proportional to the temperature and magnetic field strength. These orientations correspond to specific quantum mechanical energy states determined by the spin quantum number (I). However; the alignment of the atomic nuclei is not exact after the application of the field β0 and the nuclei precess about an axis (Larmor precession). The Larmor frequency (ω) is related to the field strength by the equation ω=γβ0 where γ is the gyromagnetic ratio specific to a particular nucleus and β0 the magnetic field strength in Teslas.

EXCITATION-RELAXATION The net magnetization (M) has two parts, Mxy in the transverse axis and Mz in the longitudinal axis. At rest, the net magnetization vector (M) is static with zero current detectable in a receiver coil. To induce a signal, it is necessary to excite nuclei with a radiofrequency (RF) pulse with a frequency matching the Larmor frequency for a particular nucleus. The angle of rotation (θ) about the secondary gradient (β1) is a function of the amplitude and duration of the applied radiofrequency pulse, related by the equation θ=γβ1t where θ is the angle of rotation or radiofrequency flip angle, γ the gyromagnetic ratio; β1 the amplitude of the radiofrequency pulse; and t the duration. The maximal signal that can be obtained is following a 90° RF pulse. Nuclei return to an equilibrium state by emitting electromagnetic radiation and by transferring energy between themselves and the surrounding molecular lattice. This relaxation begins at the end of the radiofrequency pulse as Mz increases and Mxy reduces. However; the increase of Mz and reduction of Mxy are influenced by independent factors. The longitudinal-relaxation (spin-lattice) is related to the molecular structure of a substance, which determines the ability of molecules to exchange discrete quanta of

An atlas of contrast-enhanced angiography

2

energy during collisions. The return of Mz to normal occurs in an exponential manner, reflecting the statistical probability of molecular collisions. The T1 of a substance is defined as the time for Mz to return to 63% of its original value. The T1 of a substance is related to its molecular size, the presence of macromolecules such as proteins with hydrophilic bonding sites and whether a substance is a solid or a liquid. The process of transverse-relaxation (spin-spin) is due to the presence of local magnetic field variations between adjacent molecules. These affect the precessing molecules; leading to de-phasing and decay in Mxy. The T2 is defined as the time for Mxy to fall by 63% of its original value. The T2 of a substance is related to its molecular size, whether the

Figure 1.1 Nuclei with an odd atomic number possess angular momentum or spin that induces a magnetic field

Figure 1.2 At rest, the nuclei are distributed randomly, but application of a static magnetic field β0 causes the nuclei to line up parallel or antiparallel to the field

Introduction and methods

3

Table 1.1 The T1 and T2 values in milliseconds for different tissues within the human body

T1

T2

Skeletal muscle

870

47

Liver

490

43

Kidney

650

58

Spleen

780

62

Fat

260

84

Lung

830

79

Gray matter

920

101

White matter

790

92

>4000

>2000

1200

300

850

60

Cerebrospinal fluid Blood Myocardium

substance is a solid or a liquid and the presence of macromolecules. Although T2 is independent of field strength; spin coherence is affected by inhomogeneities in the applied field that result in an effective transverse relaxation time of T2*. The excitation-relaxation sequence produces a detectable signal in the transverse (Mxy) plane. The signal is due to the free precession of Mxy and is termed the free induction decay (FID) signal. The FID oscillates at the Larmor frequency of the excited nuclei and its magnitude is proportional to the density of nuclei within the tissue measured. Fourier transformation of the FID yields the frequency-based nuclear magnetic resonance spectrum used to form magnetic resonance images.

PULSE SEQUENCES There are two basic methods of producing a magnetic resonance signal—the spin-echo (SE) and the gradient-echo (GRE) sequence. With a SE sequence, a 90° pulse is administered followed by a 180° refocusing pulse, which occurs after the phase-encoding gradients are applied. The 180° refocusing pulses cancel out field inhomogeneities. With a GRE sequence; an additional gradient is applied for a limited period of time in the readout direction. The magnetic spins precess out of phase and the signal reduces, then a reverse gradient leads to rephasing and an echo signal can be detected. GRE sequences are affected by local field inhomogeneities. GRE imaging allows the use of lower flip angles; shorter TEs and TRs, and a subsequent reduction in imaging time. Additional prepulses can be used with both SE and GRE sequences to produce an image that is more


4

T1- or T2-weighted.

Figure 1.3 After the application of a static magnetic field, the nuclei precess around the central axis, producing a magnetic moment


5

IMAGE FORMATION To obtain a magnetic resonance image, it is necessary to spatially encode a signal to detect the type and

Figure 1.4 The net magnetization M has two components: Mxy in the transverse plane and Mz in the longitudinal plane. At rest, Mxy is zero. Application of a 90° pulse flips the magnetization into the Mxy plane such that Mz is zero and Mxy is equal to M. The nuclei return to the resting state by emitting electromagnetic radiation

Figure 1.5 Longitudinal relaxation. The T1 of a substance is the time taken for Mz to return to 63% of its original value

location of nuclei in a structure. Two processes occur—slice selection and spatial encoding, and both rely on the fact that the resonant frequency is proportional to the


6

magnetic field. A thin slice selection can be obtained by the application of a radiofrequency pulse with a narrow range of frequencies (narrow bandwidth), which excites only a thin slice of the tissue in which the radiofrequency pulse matches the Larmor frequency. Additional spatial encoding is obtained by the application of a second gradient Gx (frequencyencoding gradient), orthogonal to slice selection, which relates frequency to the position along the Gx axis. A third gradient Gy (phase-encoding gradient), perpendicular to Gx, enables complete spatial encoding. The raw data obtained (k-space) is then transformed into a two-dimensional spectrum by two-dimensional fast Fourier transformation, to obtain a gray-level image. Repeating the measurement Ny times for different values of the Gy gradient will produce a matrix of Nx×Ny. For a three-dimensional volume slab, an additional secondary phase-encoding gradient is applied in the required slice direction, with the number of phase-encoding steps determining the number of slices within a volume.

IMAGE QUALITY Each magnetic resonance image obtained consists of multiple gray-scale pixels. The matrix of the image is the multiple of the number of read-encoding steps (Nx) by the number of phase-encoding steps (Ny). The voxel size (spatial resolution) of the image is determined by the equation:

It can be seen from this equation that an improved resolution can be obtained by using a smaller field of view, although this will reduce the signal intensity of the image. Alternatively, the number of Nx or Ny steps acquired can be increased, although this will prolong scan time. Signal-averaging may reduce motion artefacts and improve the signalto-noise ratio (SNR) of an image but also prolongs scan acquisition. Using a sequence with a short repeat time (TR) will reduce scan time but reduces SNR. This can be offset by imaging at higher field strength, or by using local surface coils.

MAGNETIC RESONANCE CONTRAST AGENTS The contrast agents used in magnetic resonance are either paramagnetic or superparamagnetic substances. Extravascular contrast agents are small molecules that rapidly transfer from the blood pool to the extravascular compartment and so have a limited duration of action. In cardiac magnetic resonance, they are typically used as ‘firstpass’ agents to produce signal enhancement of blood in magnetic resonance angiography, or myocardium in myo-cardial perfusion imaging. These agents interact with a body tissue to reduce its T1 and/or T2 relaxation times. The most widely used agents are gadolinium


7

Figure 1.6 Transverse relaxation. The T2 of a substance is the time taken for Mxy to fall by 63% of its original value

Figure 1.7 In order to obtain a magnetic resonance image, it is necessary to apply additional gradients (frequency and phase-encoding gradients) to spatially locate the tissue. In addition, a slice-selecting pulse is applied to image a thin slice of tissue

chelates which reduce the T1 of blood according to the equation:

The arterial concentration of a gadolinium chelate is affected by the infusion rate and the cardiac function of a subject, as indicated in the equation: [Gd] arterial=Gd infusion rate/cardiac output1. Contrast between the tissue of interest and its surroundings can be obtained using several methods. The first method, suitable for angiography of stationary structures such as the aorta or renal arteries; uses non-cardiac-gated sequences with ultra-short TE and TR. The rapid sequence prevents recovery of signal from the background structures with relatively long T1 values, but signal is regained from the blood vessels because of the T1 shortening effects of the contrast agents. Contrast can be improved if the acquisition of k-


8

space is coordinated with the peak T1 shortening effects of the contrast agent. This can be predicted using the following equation:

where Ts is the time to the start of the scan, Td is the time to arterial enhancement, Tg is the duration of arterial enhancement or the duration of the gadolinium infusion; and Ta is the duration of sequence acquisition) 1. Timing of the enhancement can be coordinated with the arterial or venous phase, depending upon the region of interest required. The short TE and TR employed in these sequences allow the acquisition of a three-dimensional data set that can be reformatted using the maximum intensity projection or the multi-planar reformatting techniques. The second method of obtaining contrast, suitable for coronary angiography and myocardial perfusion, uses an additional suppression or inversion pulse to null the background tissue. Before the arrival of contrast, no signal is obtained if the tissue is sufficiently nulled and only when the contrast arrives and shortens T1 can signal be regained and a structure imaged. This type of sequence is frequently used with cardiac gating in cardiac magnetic resonance. Unlike extravascular contrast agents that rapidly transfer from the intravascular compartment into the surrounding tissues, intravascular contrast agents remain within the blood pool, so increasing the duration of arterial enhancement. Current clinical trials are evaluating two types of agents—paramagnetic gadolinium chelates that bind in vivo to albumin (e.g. MS-325/AngioMARK2,3) and ultra small super para-magnetic iron oxide particles (e.g. NC100150 injection/Clariscan4,5).

INSTRUMENTATION There are three types of commercially available magnets: resistive magnets with coils that create a magnetic field when current is applied, permanent magnets that are very heavy and have a maximum field strength of 0.3 T but with low running costs, and superconducting magnets that have magnetic windings in liquid helium to enable superconductivity and persistence of a magnetic field once applied. Shimming of the magnet is performed to improve field homogeneity. To produce the magnetic field gradients (Gx, Gy and Gz) that allow the creation of spatial information requires separate coils (x, y and z), each with their own power supply. The radiofrequency coils produce the radiofrequency pulses to excite nuclei and, in some magnets, additionally receive the signal. The coils are tuned to match the resonant frequency of the nuclei studied. The computer(s) are responsible for execution of magnetic resonance programs, acquisition and demodulation of magnetic resonance signals, reconstruction and display of images, and image processing. The magnet is shielded to prevent the field from damaging watches; credit cards, pacemakers, etc. The shield consists of passive shielding made up of iron plating and active shielding consisting of an outer superconducting coil set. There is additional radiofrequency shielding to prevent signals coming in or out of the magnet environment.


9

REFERENCES 1. Prince MR. Gadolinium-enhanced MR aortography. Radiology1994; 191:155–64 2. Li D, Dolan RP, Walovitch RC, Lauffer RB. Three-dimensional MRI of coronary arteries using an intravascular contrast agent. Magn Reson Med 1998; 39:1014–18 3. Li D, Zheng J, Bae KT, Woodard PK, Haacke EM. Contrast-enhanced magnetic resonance imaging of the coronary arteries. Invest Radiol1998; 33:578–86 4. Bunce NH, Moon JC, Bellenger NG, et al. Improved cine cardiovascular magnetic resonance using Clariscan (NC100150 injection). J Cardiovasc Magn Reson2001; 3:303–10 5. Bunce NH, Keegan J, Gatehouse PD, et al. Initial experience with the intravascular contrast agent NC100150-Injection (Clariscan) for breath-hold and navigator-gated magnetic resonance coronary artery imaging. J Magn Reson Imag2002; 16:217–223

2 The principles of magnetic resonance angiography PRACTICAL MAGNETIC RESONANCE ANGIOGRAPHY Magnetic resonance is able to image the arterial and venous systems, and is increasingly used for the investigation of patients with suspected vascular disorders. In this chapter, the practical aspects of contrast-enhanced magnetic resonance angiography (CE-MRA) will be described, using the thoracic aorta as an example. Initial steps The initial step in performing a CE-MRA scan is to obtain intravenous access using a 16– 18-gauge cannula positioned within a large peripheral vessel1. Examinations of the head, thorax and abdomen may be performed with a cannula placed in the arm, but, for venous examination of the legs, a leg cannula may be required. The cannula must be secured and connected to a power or hand injector using a long extension line located outside the magnet bore. Piloting Correct piloting is then required to position the region of interest within the center of the magnet bore. For a thoracic aortogram, the aortic arch is located using coronal, sagittal and transverse pilot scans. Figure 2.1 shows some examples of piloting. Positioning From these pilot scans, the three-dimensional CE-MRA slab is positioned so that it includes the anatomical structure of interest. A baseline unenhanced three-dimensional CE-MRA slab is acquired for use in image subtraction. For imaging of structures within the thorax and abdomen, breath-holding is required to reduce respiratory artefacts and blurring. The length of the breath-hold is determined by the temporal resolution of the CE-MRA sequence (ideally as fast as possible); the spatial resolution required; and the ability of the patient to co-operate with the demands for breath-holding. For imaging of the coronary arteries and bypass-grafts, cardiac gating for suppression of cardiac motion may increase the duration of the breath-hold. For improved spatial resolution, a small field of view is recommended but may produce image wrapping in the phase-encode direction. Anatomical positioning of the patient’s arms outside the field of view; or performing repeated acquisitions of separate parts of the structure of interest e.g. one

The principles of magnetic resonance angiography

11

sagittal slab for each lung during pulmonary angiography may reduce this wrap. For the thoracic aorta, the un-enhanced three-dimensional CE-MRA slab is acquired during a breath-hold of 20–30 s, usually performed in inspiration for maximum duration (see Figure 2.2).

Figure 2.1 Transverse (a), coronal (b), and sagittal (c) images are used to pilot the MRA volume slab. It is important to center the region of interest within the three-dimensional slab

Optimal enhancement of the vascular structure For optimal enhancement of the vascular structure of interest, it is necessary to accurately co-ordinate the contrast enhancement with the time of acquisition of the center of kspace2. This can be done by using a ‘best-guess’ approach; e.g. a 15-s delay from the start of contrast injection until scan acquisition for a pulmonary artery angiogram versus 25 s for a descending thoracic aortogram, although the exact duration will be affected by cardiac output and the position of the peripheral cannula. A more recent method available with some scanners uses a rapid automated sequence, which automatically detects a change in signal intensity in a sector upstream from the region of interest and then triggers scan acquisition3–5. At hird method that is simple to acquire utilizes a timing bolus6 of 2 ml of contrast injected with 10 ml of saline flush, and an inversion recovery sequence acquiring images at 1 s intervals, which can be used to determine peak vascular enhancement (see Figure 2.3).


12

Figure 2.2 To enable subsequent image reconstruction and three-dimensional reformatting of the volume slab, it is essential to perform a baseline acquisition prior to contrast administration. In this slab, the vascular blood pool appears black due to the rapid gradient-echo sequence; whereas the surrounding fat layers are visible due to the short T1 of the fat relative to the blood

Time to vascular enhancement Once the time to vascular enhancement has been obtained, the time to the start of the scan can be determined from the following equation from Prince7.

where Ts is the time to the start of the scan, Tdis the time to vascular enhancement, Tg is the duration of vascular enhancement or the duration of the gadolinium infusion, and Ta is the duration of sequence acquisition. This is illustrated graphically in Figure 2.4.

CE-MRA Using this equation; the CE-MRA can be performed, acquiring both an early and a late volume slab. For a


13

Figure 2.3 Accurate co-ordination of the sequence acquisition and the peak of vascular enhancement can be performed using a test bolus. Administering a small volume of contrast and acquiring one image per second of the vessel of interest allows the delay to peak vascular enhancement to be determined. In these images (a-d), the initial vascular structures appear black. Arrival of the gadolinium within the right ventricle and then the right ventricular outflow tract produces arterial enhancement (b). The contrast then circulates to the aortic root (c) and then the descending thoracic aorta (d)

gadolinium-chelate agent, between 0.2 and 0.4 mmol/kg can be used for a threedimensional CE-MRA, with a similar volume of saline used as a flush8 (see Figures 2.5 and 2.6). The vascular enhancement can be imaged using repeated volume slabs with relatively low spatial resolution to produce a dynamic series of the same structure of interest or; following modifications to the scanner table, it is possible to track the contrast from the aorta to the peripheral vascular tree.


14

Figure 2.4 Determination of the time Ts to the start of the scan. Td is the time to vascular enhancement, Tg is the duration of vascular enhancement and Ta is the duration of sequence acquisition

Postprocessing With the data stored on the computer hardware; the patient can be removed from the magnet bore and post-processing performed. The initial step is to subtract the unenhanced CE-MRA from the early and late CE-MRA datasets, which reduces the amount of stationary non-vascular background structures that are contained within the final image9. It is then possible to perform maximum-intensity projection, multi-planar reformatting, and surface rendering on the three-dimensional CE-MRA slab. In addition, when reporting the CE-MRA, it is important to review the raw datasets, to eliminate artifacts that may be introduced in the postprocessing phase (see Figure 2.7). The adverse effects of MRA During the CE-MRA scan, the patient will hear the knocking sounds of the magnet gradient coils. In addition; the patient may experience a warm flushing sensation or a mild headache with the gadolinium contrast agent. Anaphylaxis is uncommon with these agents; but facilities should be available for resuscitation10–12. Allergic reactions appear more common in atopic individuals and those with a prior allergic reaction to contrast media; including iodine-based agents13.


15

Figure 2.5 Because of the high temporal resolution of the gradient-echo sequences used in MRA, it is possible to acquire multiple 3D-volume slabs of the region of interest during one examination. In this aortic dissection study, initially the enhancement is maximal within the true lumen of the aortic root

Figure 2.6 In the same patient as Figure 2.5, within seconds the arterial


16

enhancement passes into the false lumen of the descending thoracic aorta

Figure 2.7 Postprocessing of the raw data acquired can be performed. This can include maximal intensity projection and surface rendering. This produce true three-dimensional images that can help the clinician to diagnose and manage medical conditions

REFERENCES 1. Grist TM. MRA of the abdominal aorta and lower extremities. J Magn Reson Imag 2000; 11:32–43 2. Maki J, Prince M, Londy F, Chenevert T. The effects of time varying intravascular signal intensity and k-space acquisition order on three-dimensional MR angiography image quality. J Magn Reson Imag 1996; 6:642–51 3. Wilman A, Riederer S, King B, et al. Fluoroscopically triggered contrast-enhanced three-dimensional MR angiography with elliptical centric view order: application to the renal arteries. Radiology 1997; 205:137–46 4. Ho V, Foo T. Optimization of gadolinium-enhanced magnetic resonance angiography using an automated bolus-detection algorithm (MR SmartPrep). Invest Radiol 1998; 33:515–23 5. Prince MR, Chenevert TL, Foo TK, et al. Contrast-enhanced abdominal MR angiography: optimization of imaging delay time by automating the detection of contrast material arrival in the aorta. Radiology 1997; 203:109–14 6. Earls J, Rofsky N, DeCorato D, Krinsky G, Weinreb J. Breath-hold single dose gadolinium-enhanced MR aortography: usefulness of a timing examination and a power injector. Radiology 1996; 201:705–10 7. Prince MR. Gadolinium-enhanced MR aortography. Radiology 1994; 191:155–64 8. Hany TF, Schmidt M, Hilfiker PR, et al. Optimization of contrast dosage for gadolinium-enhanced 3D MRA of the pulmonary and renal arteries. Magn Reson Imag 1998; 16:901–16 9. Ruehm SG, Nanz D, Baumann A, Schmid M, Debatin JF. 3D contrast-enhanced MR


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angiography of the run-off vessels: value of image subtraction. J Magn Reson Imag 2001; 13:402–11 10. Weiss KL. Severe anaphylactoid reaction after i.v. Gd-DTPA. Magn Reson Imag 1990; 8:817–18 11. Tardy B, Guy C, Barral G, Page Y, Ollagnier M, Bertrand JC. Anaphylactic shock induced by intravenous gadopentetate dimeglumine. Lancet 1992; 339:494 12. Meuli RA, Maeder P. Life-threatening anaphylactoid reaction after iv injection of gadoterate meglumine. Am J Roentgenol 1996; 166:729 13. Garcia N, Ramon E, Gonzalez del Valle L, Ruano M, Jimenez E. Importance of a previous allergy to an iodinated contrast agent in the administration of gadopentetate dimeglumine. Ann Pharmacother 1997; 31:374

3 Magnetic resonance of the aorta

INTRODUCTION Magnetic resonance can assess the anatomy of the aorta in three dimensions using nonenhanced spinecho and turbo-spin-echo sequences that can be used to diagnose aortic aneurysms or coarctation, and can detect an intimal flap in aortic dissections. However; to obtain angiographic projection images of the aorta and branches; it is necessary to use contrast-enhanced magnetic resonance angiography (MRA). Abdominal aortic aneurysms

Magnetic resonance of the aorta

19

can be diagnosed and followed up by ultrasound, but, if surgical intervention is planned, then X-ray angiography may be required. Contrast-enhanced MRA (CE-MRA) provides an accurate alternative that cannot only define the size and extent of the aneurysm (above and below the renal vessels) but also demonstrate the presence of significant thrombus around the effective lumen. In addition, CE-MRA can be used to identify associated renal artery stenosis and disease of the iliac vessels, and for the planning for arterial cross-clamping1,2. CE-MRA can also be used in patients with thoracic aortic disssections to demonstrate true and false lumens and to identify the presence of branch vessel stenoses3.

AORTIC DISSECTION Aortic dissection is an uncommon but potentially fatal condition4, predominantly affecting patients in the sixth and seventh decades of life5. It is twice as common in males and is associated with hypertension and the presence of a bicuspid aortic valve. In patients with inherited defects of connective tissue (e.g. Marfan syndrome5,6, EhlersDanlos syndrome), it can occur at a younger age, and is sometimes seen during pregnancy 7,8. In pathologic specimens, cystic medial necrosis of the aortic wall can be identified 9,10, and it is believed that either a primary tear in the intima allows the entry of blood into the media or that medial hemorrhage is the precipitating event with subsequent rupture of the intima11. In both cases, there can be prograde or retrograde extension of the tear to produce an aortic dissection

Table 3.1 Commonly used classification systems to describe aortic dissection

Classification Description DeBakey12 Type I

The dissection arises in the ascending aorta then extends to the aortic arch and usually more distally

Type II

The dissection arises and is confined to the ascending aorta

Type III

The dissection arises in the descending aorta distal to the left subclavian artery origin

Stanford13 Type A

All dissections that involve the ascending aorta

Type B

All dissections that do not involve the ascending aorta or aortic arch

Descriptive Proximal

Includes DeBakey types I and II or Stanford type A

Distal

DeBakey type III, Stanford type B


20

Figure 3.1 Graphical representation of the classification systems used to describe aortic dissections. For full description, see Table 3.1

flap, occlusion of arterial branches or dissection of the coronary arteries and valvular incompetence. In both the Debakey12 and Stanford13 classification systems (see Table 3.1), a separation into dissections that involve the ascending aorta and arch, from those of the distal thoracic aorta (distal to the left subclavian artery) can be helpful to determine management decisions (surgical, stenting or medical therapy). The most common clinical presentation is with a sudden onset of severe chest pain, sometimes described as an interscapular tearing sensation5,14. Less common features include acute pulmonary edema with valvular incompetence, acute myocardial infarction with coronary artery dissection; a cerebrovascular event with dissection of a carotid


21

Figure 3.2 A 21-year-old woman was admitted with acute chest and interscapular pain. She had previously received aortic root homografts in 1991 and 1998 for aortic root dilatation. Her admission chest X-ray demonstrated a widened mediastinum. MRA demonstrates a dilated aortic root measuring 56 mm in diameter. There is a type A aortic dissection from the ascending aorta, extending to the abdominal aorta beyond the level of the renal arteries


22

Figure 3.3 A 50-year-old man had a surgical repair of an aortic coarctation in 1977. Because of severe resistant hypertension (blood pressure 212/121 mmHg) he was referred for exclusion of re-coarctation of the aorta and concomitant renal artery stenosis. MRA demonstrates a circular aneurysm measuring 3.0×3.5×4.5 cm at the site of previous coarctation repair ((a) and (b) anterior view; (c) sagittal view). There


23

is no significant aortic re-coarctation. In addition, there was no evidence of renal artery stenosis

Figure 3.4 A 29-year-old woman with coarctation of the aorta and previous aortic interposition graft was referred for follow-up assessment of the graft. MRA demonstrates a patent interposition graft measuring 20 mm in diameter. The graft is slightly tortuous and slightly narrowed at its insertion. The aortic root appears normal. The residual hypoplastic distal aortic arch and descending thoracic aorta (responsible for the coarctation) can be identified

Figure 3.5 A 68-year-old man had a surgical repair of an aortic coarctation in 1962. He presented with resistant hypertension and was referred for assessment. MRA demonstrates a discrete severe stenosis at the site of previous coarctation repair. The proximal branches of the aortic arch (innominate artery, left common carotid artery and left subclavian artery) are dilated


24

Figure 3.6 A 13-year-old boy had a surgical repair of an aortic coarctation aged 2 years old. He was referred for follow-up assessment of the repair. MRA demonstrates a narrowed and tortuous aortic arch and descending aorta consistent with a significant re-coarctation (Oblique sagittal images viewed from the right (a) and left (c)). The proximal left subclavian artery is not demonstrated and therefore may have been used for the original repair. Sagittal multi-slice spin-echo images ((d)-(f)) demonstrate the arterial narrowing but it is only with MRA that the tortuous narrowing can be accurately imaged

vessel or hemodynamic collapse with pericardial tamponade. Suggestive clinical signs in a patient with chest pain include a diastolic murmur with aortic incompetence and a difference in blood pressures between the right and left arms. Magnetic resonance can


25

accurately identify the true and false lumens, detect intramural hematoma or ulceration, and determine vascular occlusion or insufficiency due to vascular origin from a false lumen15–17.

AORTIC COARCTATION Aortic coarctation is a congenital abnormality of the aorta that usually presents in childhood with cardiac failure or in young adults with resistant hypertension18. Many patients have an additional bicuspid aortic valve19,20, and some have aneurysm of the circle of Willis21. Clinical signs may include radio-femoral delay or upper limb hypertension, and a continuous interscapular or anterior chest murmur20. Three subgroups can be identified with MRA: a localized juxtaductal stenosis occurs opposite the site of the ductus arteriosus; hypoplastic arch produces a tubular narrowing of the arch aorta; and aortic arch interruption is usually fatal. MRA can be used to diagnose and for follow-up of native coarctations. In addition, in patients with prior surgery, which may have included end-end repair, subclavian flap aortoplasty or Dacron patch insertion, MRA can detect restenosis or aneurysm formation22–25.

TAKAYASU ARTERITIS This chronic inflammatory disease of unknown etiology is more common in Asia and Africa, and typically affects young women 26,27. Pathologic specimens reveal an early inflammatory granulomatous arteritis phase followed by a chronic proliferative phase with obliteration of the lumens of the aorta and its branches. The aortic arch and its branches are most commonly involved, but the disease may also affect the pulmonary arteries28. During the acute systemic phase, there is usually an elevated erythrocyte sedimentation rate, white cell count, mild anemia and raised immunoglobulins29. The late phase produces arterial stenoses and occlusion, with hypertension from renal artery stenosis and coarctation30. Giant cell arteritis can also produce an aortitis particularly affecting the head and neck vessels, although the affected individuals are usually over 50 years old.


26


27

Figure 3.7 A 74-year-old woman with a history of hypertension presented with severe back pain. MRA demonstrates an aortic lumen with an area of indentation that corresponds to the surrounding cuff of mural thrombus or hematoma seen on the spin-echo images ((b) and (c))


28

Figure 3.8 A 57-year-old man with previous aortic root and aortic valve replacement due to aortic dissection in 1989 was admitted with recurrent chest pain. MRA demonstrates extensive aortic dissection


29

involving the arch and descending thoracic aorta. The dissection extends back to the distal suture line of the ascending aortic graft and into the right brachiocephalic artery. There is a large posterior thrombosed false lumen (64 mm)

AORTIC ANEURYSM An aortic aneurysm is a pathologic dilatation of the aortic lumen that may be localized or diffuse; saccular or fusiform. A fusiform aneurysm occurs as a uniform dilatation of the aortic wall, whereas a saccular aneurysm is an outpouching from one side of the aorta. A false or pseudoaneurysm may follow aortic rupture and is formed from blood and connective tissue outside the real aortic wall. The incidence of aneurysms increases with age and the presence of atherosclerosis and hypertension, and is more common in men31,32. The most commonly affected site is the infrarenal aorta, although the ascending aorta and root may be affected in Marfan syndrome, syphilis or infective aortitis. Clinical manifestations are usually absent33, and the diagnosis is made during routine surveillance or following rupture. Abdominal aortic rupture may produce severe back and lower abdominal pain34. Clinical examination may reveal a pulsatile abdominal mass and the presence of hypotension35. Thoracic aneurysms may produce aortic regurgitation and congestive cardiac failure, or compression of adjacent structures leading to supe-rior vena cava syndrome, dysphagia, hoarseness, wheezing or chest pain. MRA can accurately size the aneurysm in three dimensions (important when considering intravascular stenting) and identify associated stenoses in the renal and peripheral vascular beds36,37.


30

Figure 3.9 A 50-year-old man was admitted with chest pain. In 1997, he suffered a type A aortic dissection that was repaired with an aortic root homograft. In 1998, he had an aortic valve replacement for aortic


31

regurgitation. Early (b) and late-phase (c) MRA demonstrate a false aortic aneurysm anterior and to the right of the repaired ascending aorta. The communication point is probably at the site of the proximal suture line. Both the MRA ((b) and (c)) and spin-echo ((a) and (e)) images also show aortic dissection with the intimal flap extending from the proximal aortic arch into the thoracic aorta to the level of just above the aortic hiatus


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Figure 3.10 A 52-year-old man was admitted with sudden onset of severe chest and back pain. Chest X-ray showed a widened mediastinum. MRA demonstrates a type B aortic dissection that arises distal to the left subclavian artery and descends to below the diaphragm

Figure 3.11 A 59-year-old man with a known chronic type B aortic dissection was referred with a recurrence of chest and back pain. MRA demonstrates a type B dissection, arising just distal to the left subclavian artery and descending below the diaphragm. There is a visible flap that separates the anterior true lumen from the posterior false lumen, and an entry site is clearly seen


33

Figure 3.12 A 33-year-old woman with Takayasu arteritis was referred with left biceps claudication. MRA demonstrates occlusion of the left subclavian artery with multiple collateral vessels. There is also mild narrowing of the left common carotid artery. The early- and latephase MRA raw data show that the thoracic aortic wall is circumferentially thickened and enhances following gadolinium administration that is consistent with active inflammation ((c) and (d))


34

Figure 3.13 A 26-year-old woman was referred with left arm pain, reduced left brachial and radial arterial pulsation and blood pressure. MRA demonstrates a long diffuse stenosis in the proximal left subclavian artery. The distal vessel reconstitutes

Figure 3.14 A 32-year-old woman was admitted with right arm discomfort


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with exercise. MRA demonstrates a long severe stenosis of the right subclavian artery

Figure 3.15 A 63-year-old man with previous coronary artery bypass surgery had repeat coronary angiography which confirmed three patent vein grafts. Because of an occluded left subclavian artery, it was not possible to identify the left internal mammary graft so the patient was referred for CE-MRA. This confirmed the occluded left subclavian artery (a, arrow]. Phase-velocity mapping (b) was performed during hand-grasp exercise to determine if there was significant vertebral steal syndrome. This demonstrated caudal flow in the left vertebral artery during systole, with cranial flow in the right vessels and left


36

carotid artery. Mean velocity (c) during the cardiac cycle confirmed the caudal flow in the left vertebral artery

Figure 3.16 Surface-rendered three-dimensional contrast-enhanced MRA in the left lateral view acquired in a patient with aortic coarctation repaired 20 years earlier using Dacron patch, and presented with hemoptesis (a) The initial study showed a false aneurysm caused by rupture of the distal sutures of the Dacron patch (arrow); (b) following resection of the false aneurysm and insertion of a Dacron tube (arrow)

REFERENCES 1. Kaufman JA, Geller SC, Petersen MJ, Cambria RP, Prince MR, Waltman AC. MR imaging (including MR angiography) of abdominal aortic aneurysms: comparison with conventional angiography. Am J Roentgenol 1994; 163:203–10 2. Petersen MJ, Cambria RP, Kaufman JA, et al. Magnetic resonance angiography in the preoperative evaluation of abdominal aortic aneurysms. J Vasc Surg 1995; 21:891–8 3. Prince MR, Narasimham DL, Jacoby WT, et al. Three-dimensional gadoliniumenhanced MR angiography of the thoracic aorta. Am J Roentgenol 1996; 166:1387–97 4. Hirst AE, Johns VJ Jr, Kime SW Jr. Dissection aneurysm of the aorta: a review of 505 cases. Medicine 1958; 37:217 5. Spittell PC, Spittell JA, Joyce JW, et al. Clinical features and differential diagnosis of aortic dissection: experience with 236 cases (1980 through 1990). Mayo Clin Proc 1993; 68:642–51 6. Larson EW, Edwards WD. Risk factors for aortic dissection: a necropsy study of 161 patients. Am J Cardiol 1984; 53:849–55


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7. Williams GM, Gott VL, Brawley RK, et al. Aortic disease associated with pregnancy. J Vasc Surg 1988; 8:470–5 8. Pumphrey CW, Fay T, Weir I. Aortic dissection during pregnancy. Br Heart J 1986; 55:106–8 9. 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 1990; 16:68–73 10. Coselli JS, Buket S, Djukanovic B. Aortic arch operation: current treatment and results. Ann Thorac Surg 1995; 59:19–26 11. Wilson SK, Hutchins GM. Aortic dissecting aneurysms: causative factors in 204 subjects. Arch Pathol Lab Med 1982; 106:175–80 12. Debakey ME, McCollum CH, Crawford ES, et al.Dissection and dissecting aneurysms of the aorta: twenty-year follow-up of five hundred twenty-seven patients treated surgically. Surgery 1982; 92:1118–34 13. Daily PO, Trueblood HW, Stinson EB, Wuerflein RD, Shumway NE. Management of acute aortic dissections. Ann Thorac Surg 1970; 20:237–47 14. Slater EE, DeSanctis RW. The clinical recognition of dissecting aortic aneurysm. Am J Med 1976; 60:625–33 15. Nienaber CA, Spielmann RP, von Kodolitsch Y, et al. Diagnosis of thoracic aortic dissection. Magnetic resonance imaging versus transesophageal echocardiography. Circulation 1992; 85:434–7 16. Nienaber CA, von Kodolitsch Y, Nicolas V, et al. The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. N Engl J Med 1993; 328:1–9 17. Masani ND, Banning AP, Jones RA, Ruttley MST, Fraser AG. Follow up of chronic thoracic aortic dissection: comparison of transesophageal echocardiography and magnetic resonance imaging. Am Heart J 1996; 131:1156–63 18. Campbell M. Natural history of coarctation of the aorta. Br Heart J 1970; 32:633–40 19. Steiner RM, Gross G, Flicker S, et al. Congenital heart disease in the adult patient: the value of plain film chest radiology.J Thorac Imag 1995; 10:1–25 20. Perloff JK. The Clinical Recognition of Congenital Heart Disease, 4th ed. Philadelphia: WB Saunders, 1994 21. Hodes HL, Steinfeld L, Blumenthal S. Congenital cerebral aneurysms and coarctation of the aorta. Arch Pediatr l959; 76:28 22. Hirsch R, Kilner PJ, Connelly MS, et al. Diagnosis in adolescents and adults with congenital heart disease. Prospective assessment of individual and combined roles of magnetic resonance imaging and trans-esophageal echocardiography. Circulation 1994; 90:2937–51 23. Creenberg B, Balsara RK, Faerber EN. Coarctation of the aorta: diagnostic imaging after corrective surgery. J Thorac Imag 1995; 10:36 24. Gomes AS. MR imaging of congenital anomalies of the thoracic aorta and pulmonary arteries. Radiol Clin N Am 1989; 27:1171–81 25. Wexler L, Higgins CB, Herfkens RJ. Magnetic resonance imaging in adult congenital heart disease. J Thorac Imag 1994;9:219–29 26. Procter CD, Hollier LH. Takayasu’s arteritis and temporal arteritis. Ann Vasc Surg 1992; 6:195–8 27. Ishikawa K. Diagnostic approach and proposed criteria for the clinical diagnosis of Takayasu’s arteriopathy. J Am Coll Cardiol 1988; 12:964–72 28. Lupi-Herrera E, Sanchez-Torres G, Marcushamer J, et al. Takayasu’s arteritis. Clinical study of 107 cases. Am Heart J 1977; 93:94–103


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29. Shelhamer JH, Volkman DJ, Parillo JE, et al. Takayasu’s arteritis and its therapy. Ann Intern Med 1985; 103:121 30. Ishikawa K, Maetani S. Long term outcome for 120 Japanese patients with Takaysu’s disease. Circulation 1994; 90:1855 31. Bengtsson H, Bergqusit D, Sternby NH. Increasing prevalence of aortic aneurysms: a necropsy study. Eur J Surg 1992; 158:19 32. Anidjar S, Kieffer E. Pathogenesis of acquired aneurysms of the abdominal aorta. Ann Vasc Surg 1992;6:298 33. Bickerstaff LK, Hollier LH, Van Peenan HJ, et al. Abdominal aortic aneurysms: the changing natural history. J Vasc Surg 1984; 1:64 34. Kiell CS, Ernst CB. Advances in the management of abdominal aortic aneurysm. Adv Surg 1993; 26:73 35. Crew JR, Bashour TT, Ellertson D, et al. Ruptured abdominal aortic aneurysms: Experience with 70 cases. Clin Cardiol 1985; 8:433 36. Petersen MJ, Cambria RP, Kaufman JA, et al. Magnetic resonance angiography in the preoperative evaluation of abdominal aortic aneurysms. J Vasc Surg l995; 21:891 37. Edelman RR. MR angiography: Present and future. Am J Roentgenol 1993; 161:1

4 Carotid artery disease

INTRODUCTION Atheromatous disease affecting the carotid arteries may result in vessel narrowing; leading to symptoms of cerebral ischemia that may vary from temporary blindness (transient retinal ischemia) to complete limb paralysis (hemiparesis). Management of carotid artery disease includes risk factor modification; identification of carotid artery stenosis, and subsequent surgical or medical management.


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Figure 4.1 A 70-year-old man was admitted with headache and a right-sided weakness. Initial examination confirmed a right hemiplegia and a left carotid bruit was heard. A cranial CT scan confirmed a right cerebral infarct. MRA demonstrates a tight stenosis at the origin of the left internal carotid artery. The patient was referred for carotid endarterectomy

RISK FACTORS Hypertension is one of the most important risk factors for carotid artery disease and subsequent stroke1. Both systolic and diastolic blood pressures are important, and reduction in both can significantly reduce the risk of subsequent strokes. An average reduction in diastolic blood pressure of 6 mmHg can produce a 42% reduction in the risk of stroke2. Treatment of elevated systolic blood pressure in people over 60 years of age can reduce the incidence of stroke by 36%3. Cigarette smoking is associated with a relative risk of stroke of between 1.5 and 2.2 compared to non-smoking patients4–6. However; stopping smoking rapidly reduces the risks of stroke and so should be encouraged in all patients4,5,7. Hyperlipidemia is a risk factor for stroke. This was demonstrated in the Scandinavian Simvastatin Survival Study, where 4444 patients with stable angina or previous myocardial infarction were randomized to receive simvastatin or placebo8. In the patients allocated to simvastatin, there was a 30% reduction in the rate of fatal and non-fatal strokes, in addition to the reduction of coronary events. Statin drugs have also been shown to slow the progression of carotid atherosclerosis, as documented with carotid ultrasound9,10. Heavy alcohol intake can increase the risk of stroke; but moderate alcohol intake may be neutral or reduce the risk of stroke11–13. The role of hormone replacement therapy in the etiology and prevention of carotid

Carotid artery disease

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artery disease is uncertain. Antiplatelet therapy has been shown to be beneficial in patients at high risk of cerebrovascular accidents. The Antiplatelet Trialists’ Collaboration overview found that antiplatelet drugs such as aspirin reduced the rate of non-fatal strokes by 23% in patients with a previous transient ischemic attack or stroke14. The optimal dose of aspirin recommended by the American Heart Association for patients with transient ischemic attacks is 325 mg/day15.

IMAGING OF CAROTID ARTERY STENOSIS The accurate detection and quantification of carotid artery stenosis are important when considering whether a patient should receive optimal medical management or be referred for surgical endarterectomy. X-ray angiography is considered the standard of reference for patients requiring surgical intervention and has been used in multicenter studies to demonstrate the effectiveness of surgical intervention in patients with severe carotid artery stenosis. However, it carries a quantifiable risk of precipitating a stroke of between 0.5 and 2.0%16 and exposes the patient to the risks of ionizing radiation and iodinated contrast agents. Because it is a two-dimensional technique and can therefore underestimate the severity of elliptical stenoses, the reproducibility of X-ray carotid angiography is approximately 94%17–19 Doppler ultrasound carries no risk to the patient during the examination and can be used for routine screening of both asymptomatic and symptomatic patients. However, unlike X-ray angiography and contrast-enhance magnetic resonance angiography (MRA), it does not provide an anatomic representation of the vascular tree. Magnetic resonance has several techniques that have been extensively used to study carotid arterial disease. Two-dimensional ‘time-of-flight’ (TOF) imaging20 relies on the inflow of fresh blood within the imaging plane to produce a bright blood pool signal from vascular structures. It is flow-sensitive and can be useful in cases where the arterial velocity is low, such as differentiating between near and complete arterial occlusion. However, it can be affected by blood turbulence that results in an over-estimate of the severity of a stenosis. Three-dimensional TOF imaging provides superior resolution but is less flow-sensitive. Contrast-enhanced (CE) MRA is a newer technique that is rapid to acquire and can be performed within a single breath-hold21. It is less susceptible to artifacts related to slow flow, but does require accurate coordination of contrastenhancement and sequence acquisition, and requires modern magnetic hardware. In a systematic review of the published trials in patients with severe (70–99%) carotid artery stenosis, CE-MRA appeared very effective, although the numbers of patients studied were low22. Comparisons of MRA and X-ray angiography are good for high-grade stenoses, with a median sensitivity of 93% and a median specificity of 88%. In fact, comparisons with pathologic specimens show a better agreement with magnetic resonance and Doppler ultrasound than with X-ray angiography23. When applying cost-effectiveness criteria to various imaging strategies, it appears that the optimal approach is to perform Doppler ultrasound and MRA, then X-ray angiography if there is a disagreement between the


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Doppler ultrasound and MRA24. When investigating asymptomatic patients, it was found that using X-ray angiography alone gave the highest risk of stroke (7.12%), when compared to a more selective approach of Doppler ultrasound and MRA, then X-ray angiography if required (stroke rate 6.34%)25.

Figure 4.2 A 72-year-old woman with coronary artery disease, awaiting coronary angioplasty, was noted to have a carotid bruit. She had no previous history of cerebrovascular events. MRA demonstrates mild narrowings at the origins of the right and left internal carotid arteries. There are severe stenoses near the origins of the left and right external carotid arteries. She was referred for a neurological opinion prior to coronary intervention

SURGICAL INTERVENTION FOR CAROTID ARTERY STENOSIS Asymptomatic patients Several trials have investigated the role of surgical intervention in patients with carotid


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artery stenosis. The Asymptomatic Carotid Atherosclerosis Study (ACAS) assessed whether the addition of carotid endarterectomy to aggressive medical management reduced the incidence of stroke in patients with asymptomatic carotid artery stenosis26. Forty-two thousand patients were screened between 1987 and 1993 from 39 North American centers, resulting in 1662 patients. Inclusion criteria were age between 40 and 79 years; with a carotid artery stenosis of more than 60% diagnosed by X-ray angiography or Doppler ultrasound. Exclusion criteria were an ipsilateral stroke, vertebrobasilar events, or a contralateral stroke within 45 days of inclusion. Patients were randomized to best medical care including aspirin 325 mg/day, or the addition of carotid endarterectomy. All patients referred for surgery and one-third of the medical patients underwent X-ray angiography. In the surgical group, there was a 2.3% risk of stroke in the perioperative period that included eight out of 19 patients before operation. At 5 years, the risk of ipsilateral stroke in the surgical group was 5.1% compared to 11% in the medical group. Presurgical X-ray angiography caused a stroke in 1.2% of patients, which included all patients with a carotid stenosis of 60–99%. The European Carotid Surgery Trialists Collaborative Group was a multicenter trial of carotid endarterectomy for patients who, after a carotid territory non-disabling ischemic stroke, transient ischemic attack or retinal infarct, were found to have a stenosis in the relevant (ipsilateral) carotid artery27. The study included 2295 patients. The overall risk of stroke at 3 years was 2.1%, but increased markedly when the severity of the stenosis increased from 80 to 89% (risk 9.8%) and to 90–99% (risk 14.4%). Surgical intervention can therefore be recommended if there is a carotid artery stenosis of greater than 60% and if the patient (and surgeon) has a low surgical risk, and possibly for patients with a stenosis of more than 75% if the surgical risk is moderate. Symptomatic patients Surgical intervention improves patient outcome for symptomatic patients with severe stenoses. The North American Symptomatic Carotid Endarterectomy Trial Collaborators’ study28 investigated 50 surgical centers in the USA and Canada where the surgical risk (less than 6% mortality or stroke) was low. Patients were included if they were under 79 years old with a cerebral or retinal transient ischemic attack or non-disabling stroke within 120 days, and had a severe carotid stenosis of 70–99%. Six hundred and fifty-nine patients were assessed and 328 were referred for surgery. The 30-day combined mortality and stroke rate for patients undergoing surgery was 5.8%. At 2 years, the risk of ipsilateral stroke was 9% in the surgical group and 26% in the medical group. The Carotid Endarterectomy and Prevention of Cerebral Ischemia in Symptomatic Carotid Stenosis study29 investigated patients with a greater than 50% stenosis of the internal carotid artery and a previous cerebral event. Sixteen Veterans Affairs medical centers with a low surgical morbidity and mortality rate recruited 193 patients, of whom 92 had surgery. All received aspirin 325 mg/day. However, the study was terminated early following the publication of NASCET and ESCT trials, but they did manage to identify that, in patients with a carotid artery stenosis of more than 70%, there was a risk of stroke of 7.9% in the surgical group and 25.6% in the medical group.


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CONCLUSION Carotid artery disease is a common condition that can lead to significant morbidity and mortality. Identification and management of risk factors can reduce the stroke event rate. Non-invasive assessment by combined Doppler ultrasound and MRA followed by X-ray angiography for selected cases appears to be the safest and most effective method for identifying those patients that require surgery. Surgery is now beneficial in symptomatic and asymptomatic patients with severe stenoses.

REFERENCES 1. MacMahon S, Rodgers A. Blood pressure, antihypertensive treatment and stroke risk. J Hypertens 1994; 2(suppl):s5–14 2. Collins R, Peto R, MacMahon S, Hebert P, Fiebach NH, Eberlein KA, Godwin J, Qizilbash N, Taylor JO, Hennekens CH. Blood pressure, stroke, and coronary heart disease, part 2: short-term reductions in blood pressure. Overview of randomised drug trials in their epidemiological context. Lancet 1990; 335:827–38 3. SHEP Cooperative Research Group. Prevention of stroke by antihypertensive drug treatment in older persons with isolated systolic hypertension. Final results of the Systolic Hypertension in the Elderly Program (SHEP). JAMA 1991; 265:3255–64 4. Abbott RD, Yin Y, Reed DM, Yano K. Risk of stroke in male cigarette smokers. N Engl J Med 1986; 315:717–20 5. Colditz GA, Bonita R, Stampfer MJ, et al. Cigarette smoking and risk of stroke in middle-aged women. N Engl J Med 1988; 318:937–41 6. Shinton R, Beevers G. Meta-analysis of relation between cigarette smoking and stroke. Br Med J 1989; 298:789–94 7. Wolf PA, D’Agostino RB, Kannel WB, Bonita R, Belanger AJ. Cigarette smoking as a risk factor for stroke: the Framingham Study. JAMA 1988; 259:1025–9 8. Randomised trial of cholesterol lowering in 4444 patients with coronary heart disease: the Scandinavian Simvastatin Survival Study (4S). Lancet 1994:344:1383–9 9. Furberg CD, Adams HP Jr, Applegate WB, et al, for the Asymptomatic Carotid Artery Progression Study (ACAPS) Research Group. Effect of lovastatin on early carotid atherosclerosisand cardiovascular events. Circulation 1994; 90:1679–87 10. Crouse JR III, Byington RP, Bond MG, et al. Pravastatin, Lipids, and Atherosclerosis in the Carotid Arteries (PLAC-II). Am J Cardiol 1995; 75:455–9 11. Gorelick PB. The status of alcohol as a risk factor for stroke [Review]. Stroke 1989; 20:1607–10 12. Camargo CA Jr. Moderate alcohol consumption and stroke: the epidemiologic evidence [Review]. Stroke 1989; 20:1611–26 13. Palomaki H, Kaste M. Regular light-to-moderate intake of alcohol and the risk of ischemic stroke: is there a beneficial effect? Stroke 1993; 24:1828–32 14. Antiplatelet Trialists’ Collaboration. Collaborative overview of randomised trials of antiplatelet therapy, I: prevention of death; myocardial infarction, and stroke by prolonged antiplatelet therapy in various categories of patients. Br Med J 1994; 308:81–106


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15. Guidelines for the management of transient ischemic attacks. From the Ad Hoc Committee on Guidelines for the Management of Transient Ischemic Attacks of the Stroke Council of the American Heart Association. Stroke 1994; 25:1320–35 16. Davies KN, Humphrey PR. Complications of cerebral angiography in patients with symptomatic carotid territory ischaemia screened by carotid ultrasound. J Neurol Neurosurg Psychiatry 1993; 56:967–72 17. Young GR, Sandercock PA, Slattery J, Humphrey PR, Smith ET, Brock L. Observer variation in the interpretation of intra-arterial angiograms and the risk of inappropriate decisions about carotid endarterectomy. J Neurol Neurosurg Psychiatry 1996; 60:152– 7 18. Gagne PJ, Matchett J, MacFarland D, et al. Can the NASCET technique for measuring carotid stenosis be reliably applied outside the trial? J Vasc Surg 1996; 24:449–6 19. Eliasziw M, Fox AJ, Sharpe BL, Barnett HJ. Carotid artery stenosis: external validity of the North American Symptomatic Carotid Endarterectomy Trial measurement method. Radiology 1997; 204:229–33 20. Keller PJ, Drayer BP, Fram EK, Williams KD, Dumoulin CL, Souza SP. MR angiography with two-dimensional acquisition and three dimensional display: work in progress. Radiology 1989; 173:527–32 21. Cloft HJ, Murphy KJ, Prince MR, Brunberg JA. 3D gadoliniumenhanced MR angiography of the carotid arteries. Magn Reson Imaging 1996; 14:593–600 22. Westwood ME, Kelly S, Berry E, et al. Use of magnetic resonance angiography to select candidates with recently symptomatic carotid stenosis for surgery: systematic review. Br Med J 2002; 324:198 23. Pan XM, Saloner D, Reilly LM, et al. Assessment of carotid artery stenosis by ultrasonography conventional angiography, and magnetic resonance angiography: correlation with ex vivo measurement of plaque stenosis. J Vasc Surg 1995; 21:82–8 24. Kent KC, Kuntz KM, Patel MR, et al. Perioperative imaging strategies for carotid endarterectomy: an analysis of morbidity and cost-effectiveness in symptomatic patients. JAMA 1995; 274:888–93 25. Kuntz KM, Skillman JJ, Whittemore AD, Kent KC. Carotid endarterectomy in asymptomatic patients: is contrast angiography necessary? A morbidity analysis. J Vasc Surg 1995; 22:706–14 26. Executive Committee for the Asymptomatic Carotid Atherosclerosis Study. Endarterectomy for asymptomatic carotid artery stenosis. JAMA 1995; 273:1421–8 27. The European Carotid Surgery Trialists Collaborative Group. Risk of stroke in the distribution of an asymptomatic carotid artery. Lancet 1995; 345:209–12 28. 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 29. Mayberg MR, Wilson SE, Yatsu F, et al., for the Veterans Affairs Cooperative Studies Program 309 Trialist Group. Carotid endarterectomy and prevention of cerebral ischemia in symptomatic carotid stenosis. JAMA 1991; 266:3289–94

5 Magnetic resonance angiography of the pulmonary vessels

INTRODUCTION Both pulmonary arteries and veins can be assessed by pulmonary magnetic resonance angiography (MRA). With the advent of gadolinium-enhanced sequences, it is now possible to obtain high-resolution images of the pulmonary vessels, and pulmonary MRA is now considered a desirable alternative to X-ray angiography, transthoracic and transesophageal echocardiography, computed tomography and scintigraphic imaging for the assessment of patients with pulmonary vascular diseases.

Magnetic resonance angiography of the pulmonary vessels

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However, successful imaging of the pulmonary vessels with magnetic resonance places certain requirements on the scanner and sequence employed. The air-tissue interface within the lungs can result in susceptibility artifacts if the echo time used is not sufficiently short. In addition, cardiorespiratory motion produces blurring of the vascular structures if respiratory suppression techniques are

Figure 5.1 A 77-year-old woman presented with swollen ankles and breathlessness on exertion. On examination; the patient was cyanosed, with an elevated jugular venous pressure, pulsatile hepatomegaly and gross peripheral edema. She was referred for magnetic resonance (MR) to assess bi-ventricular function and for pulmonary angiography. Cine MR demonstrated a dilated and hypertrophied right ventricle. TrueFISP (a, b) and HASTE (c) anatomical imaging demonstrate two thrombi within the apex of the right ventricle. With MRA (d) there is reduced opacification of the left upper lobe pulmonary arteries and, to a lesser extent, the right upper lobe arteries, which is suggestive for pulmonary embolic disease. The patient was treated with diuretics and anticoagulation


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Figure 5.2 A 60-year-old man was investigated for hypertension. Transthoracic echocardiography showed a dilated and hypertrophied right ventricle. No atrial-septal defect was identified with transesophageal


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echocardiography or right ventricular angiography. MRA demonstrates dilated pulmonary arteries but without peripheral pruning (a), and anomalous drainage of the right upper and lower pulmonary veins into the inferior vena cava via a large common vein (b). The pulmonary arteries are dilated without peripheral pruning. The patient was referred for consideration of surgical reconstruction

Figure 5.3 A 17-year-old patient with thalassemia and previous iron overload developed increasing pulmonary hypertension. She was referred for pulmonary angiography. MRA demonstrates proximal narrowing of the right upper lobe branches with occlusion of the right lower lobe arteries. The left apical branch and left lateral basal arteries have proximal stenoses and a patent interposition graft measuring 20 mm in diameter. The differential diagnoses include multiple pulmonary emboli or a congenital abnormality

not used. The volume of lung tissue required for imaging necessitates that a large field of view is used; which may affect the resolution required or significantly prolong the scan acquisition time. With the advent of gadolinium contrast-enhanced sequences, some of these difficulties are addressed1,2. The T1 shortening effects of the paramagnetic contrast agents increase the signal-to-noise ratio; enabling the acquisition of a large-volume threedimensional slab within a single breath-hold using ultra-fast sequences with short TE/TR. These short echo-time sequences eliminate the problems with air-tissue interface; and reduce the scan-time acquisition. The field of view is an important consideration when performing pulmonary MRA, as the three-dimensional slab can be acquired in either a single coronal plane or as two slabs


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in the sagittal plane. Coronal acquisition requires a large field of view to encompass all the pulmonary vessels, and wrap must be avoided by ensuring the patient extends their arms above their head or across the front of their chest. Imaging in the coronal plane can be performed using a single injection of contrast agent repeated several times3, but resolution is limited because of the large field of view. For sagittal acquisition, the patient’s arms should be by their sides; and two separate acquistions are performed, one of the right chest and one of the left; using two separate contrast agent injections. This also enables an asymmetric field of view to be used; which can provide reduced scan times or improved resolution. A small disadvantage of the sagittal acquisition is the lack of central pulmonary artery coverage, although isolated central pulmonary emboli are rarely seen. Pulmonary MRA can be used to investigate pulmonary embolic disease, but has also been used to investigate pulmonary hypertension, pulmonary arterial and venous anomalies, and in patients with congenital heart disease.

PULMONARY EMBOLISM History and clinical symptoms Pulmonary embolism is a life-threatening condition that annually affects over 600 000 people in the USA, causing death in up to 60000 cases4–6. Risk factors for pulmonary embolism include immobility (often affecting debilitated hospitalized patients), surgery; malignancy and pregnancy7. In some patients with thrombophilia, there is an increased tendency to thrombosis, which may be inherited (antithrombin III deficiency, protein C and protein S deficiencies, dysfibrinogenemia, and activated protein C resistance)8–17 or acquired (anticardiolipin antibody or lupus anticoagulant18, malignancy or chemotherapy19,20, paroxysmal nocturnal hemoglobinuria, myeloproliferative disorders; nephrotic syndrome and hormonal treatment for infertility). The clinical diagnosis of a pulmonary embolism can be difficult because the symptoms and signs may be simulated by other cardiorespiratory or musculoskeletal diseases21–28. Features of a minor pulmonary embolism include breathlessness, sharp chest pain made worse with inspiration and hemoptysis, but several of these symptoms can occur with a respiratory tract infection; bronchiectasis, pneumonia or atelectasis. Patients with a major or massive pulmonary embolism usually complain of severe breathlessness, chest pain and may have evidence of right-heart failure or circulatory collapse. However, these symptoms can also occur with an acute myocardial infarction, severe pneumonia, thoracic aorta dissection or pericardial tamponade. Therefore, accurate investigations are essential to diagnose correctly those patients with a pulmonary embolus who require lifesaving anticoagulation and possible thrombolysis.


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Figure 5.4 A 48-year-old woman with a large cell carcinoma of the left upper lobe was referred for a preoperative assessment, in particular to determine the relationship between the tumor and the thoracic blood vessels. On the anatomical spin-echo images (c, d, e), the large tumor can be seen in the left upper lobe. MRA (a, b) demonstrates abrupt interruption of the arterial branches supplying the left upper lobe and


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lingula. The left upper pulmonary vein was not seen

Figure 5.5 A 27-year-old woman with known Takayasu arteritis presented with breathlessness. A ventilation-perfusion scan had shown reduced perfusion to the right upper lobe, but normal ventilation. With MRA, the right pulmonary artery is small with severe stenosis of its main branches. There is poor enhancement of the right lung parenchyma. There is a moderate stenosis in the proximal part of the left lower pulmonary artery

INVESTIGATIONS A 12-lead ECG with evidence of right heart strain provides supportive evidence of a pulmonary embolism, as does a chest X-ray that demonstrates a Hampton lump, pleural effusion, subsegmental atelectasis, pulmonary in filtrates, raised hemidiaphragm, regional oligemia or a prominent pulmonary vascular shadow at the hilum. However, all of these features are non-specific and can be present in other cardiorespiratory disease. In many cases, the ECG and chest X-ray are both normal29−31. However, both tests may provide


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evidence for an alternative diagnosis such as an acute myocardial infarction or a pneumothorax. Arterial blood gases with hypoxemia and hypocarbia may occur, but are also non-specific29. A more useful clinical investigation to detect pulmonary embolism is the radionuclide ventilation-perfusion scan that can be performed non-invasively in almost all patients. Pulmonary perfusion is assessed by intravenously injecting radioactively labeled human macroaggregates of albumin which become trapped in the pulmonary capillary bed.

Figure 5.6 A 22-year-old man with antithrombin III deficiency and recurrent episodes of dyspnea and chest pain was referred for assessment. MRA (a, b) demonstrates multiple segmental occlusions of the left and right pulmonary arteries. There is also moderate enlargement of both left and right main pulmonary arteries. Surface rendering (c)


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demonstrates the occlusions

Figure 5.7 A 33-year-old woman was referred with a history of Takayasu’s arteritis and increasing dyspnea. Viewed from behind (a), the MRA


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demonstrates dilatation of the central pulmonary arteries. The right lower segmental pulmonary artery branches are poorly visualized; which is compatible with pulmonary Takayasu’s arteritis. Surface rendering (b) confirms the reduction in the right lower segmental pulmonary artery branches

These can then be assessed with a photoscanner. Normal pulmonary perfusion virtually excludes a pulmonary embolism27,28,32. A ventilation scan is performed using the inhalation of radioactive aerosols and by assessing alveolar ventilation with a gamma camera. However, abnormal ventilation can occur in a myriad of respiratory conditions33,34, and so the perfusion and ventilation scans and clinical history are usually combined to determine the probability of a pulmonary embolism35,36. Patients with large perfusion defects and perfusion/ventilation mismatches are most likely to have a pulmonary embolism. The combination of a high probability nuclear scan with a high clinical probability is associated with a pulmonary embolism in 96% of patients. This figure is reduced to 80–88% of patients if the clinical probability is moderate24,37. In these cases, which may occur in up to one-third of patients, the patient should then be treated for a pulmonary

Figure 5.8 A 17-year-old girl with pulmonary hypertension was referred for assessment. MRA demonstrates dilated proximal pulmonary vessels with marked pruning of the distal vasculature, consistent with primary pulmonary hypertension


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Figure 5.9 A 38-year-old woman with scleroderma and increasing breathlessness on exertion was referred for pulmonary angiography. MRA demonstrates dilatation of the central pulmonary arteries with peripheral pruning of the distal vasculature. The appearances are compatible with pulmonary hypertension

Figure 5.10 A 47-year-old man had a rhabdomyosarcoma removed from the left atrium. Subsequent transesophageal echocardiography suggested


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a local recurrence. On spin-echo imaging (b), there is a pedunculated mass attatched to the lower wall of the right upper pulmonary vein. There is an additional mass attached to the posterolateral wall of the left atrium. With MRA the right-sided mass can be seen to partially obstruct the vessel lumen

embolism. Conversely, if both clinical history and nuclear scan have a low probability (occurring in 15% of patients), then a pulmonary embolus is unlikely and the patient can be treated accordingly. For those patients with a clinically suspected pulmonary embolism and an indeterminate nuclear scan, further diagnostic tests are required. Traditionally, the gold-standard investigation has been the X-ray angiogram because a normal angiogram virtually excludes the diagnosis, whereas an intraluminal-filling defect in a pulmonary artery or branch confirms the diagnosis38–42. However, pulmonary angiography requires iodinated contrast agents and exposes the patient to the hazards of cardiac catheterization and ionizing radiation. More recently computed tomography (CT) and pulmonary MRA have been investigated as non-invasive methods of confirming or excluding pulmonary embolism. Spiral CT has been used to diagnose pulmonary embolism. Mayo and colleagues compared spiral CT with nuclear scintigraphy for the detection of pulmonary emboli in 139 patients43. Both methods agreed in 29 patients with embolism and 74 without. In 20 patients with an indeterminate probability on nuclear scintigraphy and who had X-ray angiography, six had a pulmonary embolism while the remaining 14 did not; spiral CT was correct in 16 of these cases. In the 12 patients with discordant spiral CT and nuclear scintigraphy, the latter was correct in only one case. The sensitivity and specificity for spiral CT were 87% and 95%, respectively, and for nuclear scintigraphy were 65% and 94%. Meaney and associates compared gadoliniumenhanced pulmonary MRA with X-ray angiography in 30 consecutive patients with suspected pulmonary embolism1. Pulmonary embolism was detected in eight patients with X-ray pulmonary angiography and all five lobar emboli with pulmonary MRA. Sixteen of the 17 segmental emboli were detected with pulmonary MRA. For three separate MRA observers; the sensitivities for pulmonary MRA were 100%, 87% and 75%, with specificities of 95%, 100% and 95%. In a second study, Oudkerk and colleagues investigated the diagnostic accuracy of pulmonary MRA for the detection of pulmonary embolism compared to X-ray angiography as the gold standard44. They recruited 141 patients with a suspected pulmonary embolism and an abnormal nuclear scan. Pulmonary MRA was contraindicated in 13 patients, and images were not interpretable in eight patients. Two patients were not suitable for X-ray pulmonary angiography. In the remaining 118 patients, the sensitivities of pulmonary MRA for central, segmental or subsegmental pulmonary embolism were 100%, 84% and 40%, respectively. However, even with X-ray angiography, there is considerable interobserver variability in the diagnosis of subsegmental pulmonary emboli, with agreement in only two of 15 cases in a study by Quinn and co-workers45. Both pulmonary MRA and spiral CT can be considered to be accurate investigations for pulmonary embolism, with local availability determining which test is used.


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TREATMENT Initial treatment in patients with suspected or confirmed pulmonary embolism is anticoagulation with unfractionated or low-molecular weight heparin46, given either intravenously or subcutaneously47,48, followed by oral warfar in49–51to maintain an International Normalized Ratio of 2–3 for 3–6 months52,53. In some patients with a massive pulmonary embolism and circulatory collapse, thrombolysis is indicated54,55.

REFERENCES 1. Meaney JF, Weg JG, Chenevert TL, Stafford-Johnson D, Hamilton BH, Prince MR. Diagnosis of pulmonary embolism with magnetic resonance angiography. N Engl J Med 1997; 336:1449–51 2. Gupta A; Frazer CK, Ferguson JM, et al. Acute pulmonary embolism: diagnosis with MR angiography. Radiology 1999; 210:353–9 3. Goyen MG, Laub G, Ladd ME, et al. Dynamic 3D MR angiography of the pulmonary arteries in under four seconds. J Magn Reson Imag 2001; 13:372–7 4. Rubinstein I, Murray D, Hoffstein V. Fatal pulmonary emboli in hospitalized patients: an autopsy study. Arch Intern Med 1988; 148:1425–6 5. Dalen JE, Alpert JS. Natural history of pulmonary embolism. Prog Cardiovasc Dis 1975; 17:259–70 6. Bell WR, Simon TL. Current status of pulmonary thromboembolic disease: pathophysiology, diagnosis, prevention, and treatment. Am Heart J 1982; 103:239–62 7. Kaunitz AM, Hughes JM, Grimes DA, Smith JC, Rochat RW, Kafrissen ME. Causes of maternal mortality in the United States. Obstet Gynecol 1985; 65:605–12 8. Egeberg O. Inherited antithrombin deficiency causing thrombophilia. Thromb Diath Haemorrh 1965; 13:516–30 9. Gladson CL, Scharrer I, Hach V, Beck KH, Griffin JH. The frequency of type I heterozygous protein S and protein C deficiency in 141 unrelated young patients with venous thrombosis. Thromb Haemost 1988; 59:18–22 10. Heijboer H, Brandjes DP, Buller HR, Sturk A, ten Cate JW. Deficiencies of coagulation-inhibiting and fibrinolytic proteins in outpatients with deep-vein thrombosis. N Engl J Med 1990; 323:1512–16 11. Coller BS, Owen J, Jesty J, et al. Deficiency of plasma protein S, protein C, or antithrombin III and arterial thrombosis. Arteriosclerosis 1987; 7:456–62 12. Allaart CF, Aronson DC, Ruys T, et al. Hereditary protein S deficiency in young adults with arterial occlusive disease. Thromb Haemost 1990; 64:206–10 13. Bovill EG, Bauer KA, Dickerman JD, Callas P, West B. The clinical spectrum of heterozygous protein C deficiency in a large New England kindred. Blood 1989; 73:712–17 14. Mannucci PM, Tripodi A, Bertina RM. Protein S deficiency associated with juvenile arterial and venous thromboses [Letter]. Thromb Haemost 1986; 55:440 15. Broekmans AW, Veltkamp JJ, Bertina RM. Congenital protein C deficiency and venous thromboembolism: a study in three Dutch families. N Engl J Med 1983; 309:340–4


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16. Horellou MH, Conard J, Bertina RM, Samama M. Congenital protein C deficiency and thrombotic disease in nine French families. Br Med J 1984; 289:1285–7 17. Rodgers GM. Activated protein C resistance and inherited thrombosis. Am J Clin Pathol 1995; 103:261–2 18. Triplett DA, Brandt JT. Lupus anticoagulants: misnomer, paradox, riddle, epiphenomenon. Hematol Pathol 1988; 2:121–43 19. Levine MN, Gent M, Hirsh J, et al. The thrombogenic effect of anticancer drug therapy in women with stage II breast cancer. N Engl J Med 1988; 318:404–7 20. Clarke CS, Otridge BW, Carney DN. Thromboembolism: a complication of weekly chemotherapy in the treatment of non-Hodgkin’s lymphoma. Cancer 1990; 66:2027– 30 21. Hull RD, Raskob GE, Carter CJ, et al. Pulmonary embolism in outpatients with pleuritic chest pain. Arch Intern Med 1988; 148:838–4 22. The urokinase pulmonary embolism trial: a national cooperative study. Circulation 1973; 47 (suppl 2):1–108 23. Bell WR, Simon TL, DeMets DL. The clinical features of submassive and massive pulmonary emboli. Am J Med 1977; 62:355–60 24. Hull RD, Hirsh J, Carter CJ, et al. Diagnostic value of ventilation-perfusion lung scanning in patients with suspected pulmonary embolism. Chest 1985; 88:819–28 25. Stein PD, Willis PW III, DeMets DL. History and physical examination in acute pulmonary embolism in patients without preexisting cardiac or pulmonary disease. Am J Cardiol 1981; 47:218–23 26. Dalen JE, Grossman W. Profiles in pulmonary embolism. In Grossman W, ed. Cardiac Catheterization and Angiography. Philadelphia: Lea & Febiger, 1980:336–45 27. Bell WR, Simon TL. A comparative analysis of pulmonary perfusion scans with pulmonary angiograms. Am Heart J 1976; 92:700–6 28. The 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 29. Szucs MM Jr, Brooks HL, Grossman W, et al. Diagnostic sensitivity of laboratory findings in acute pulmonary embolism. Ann Intern Med 1971; 74:161–6 30. Weber DM, Phillips JH Jr. A re-evaluation of electrocardiographic changes accompanying acute pulmonary embolism. Am J Med Sci 1966; 251:381–98 31. Hull RD, Raskob GE, Carter CJ, et al. Pulmonary embolism in outpatients with pleuritic chest pain. Arch Intern Med 1988; 148:838–44 32. Kipper MS, Moser KM, Kortman KE, Ashburn WL. Longterm follow-up of patients with suspected pulmonary embolism and a normal lung scan: perfusion scans in embolic suspects. Chest 1982; 82:411–15 33. McNeil BJ. Ventilation-perfusion studies and the diagnosis of pulmonary embolism: concise communication. J Nucl Med 1980; 21:319–23 34. Biello DR, Mattar AG, McKnight RC, Siegel BA. Ventilation-perfusion studies in suspected pulmonary embolism. Am J Roentgenol 1979; 133:1033–7 35. Alderson PO, Rujanavech N, Sicker-Walker RH, McKnight RC. The role of 133Xe ventilation studies in the scintigraphic detection of pulmonary embolism. Radiology 1976; 120:633–40 36. Cheely R, McCartney WH, Perry JR, et al. The role of noninvasive tests versus pulmonary angiography in the diagnosis of pulmonary embolism. Am J Med 1981; 70:17–22 37. Hull RD, Hirsh J, Carter CJ, et al. Pulmonary angiography, ventilation lung scanning,


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and venography for clinically suspected pulmonary embolism with abnormal perfusion lung scan. Ann Intern Med 1983; 98:891–9 38. Bookstein JJ, Silver TM. The angiographic differential diagnosis of acute pulmonary embolism. Radiology 1974; 110:25–33 39. Novelline RA, Baltarowich OH, Athanasoulis CA, Waltman AC, Greenfield AJ, McKusick KA. The clinical course of patients with suspected pulmonary embolism and a negative pulmonary arteriogram. Radiology 1978; 126:561–7 40. Bookstein JJ. Segmental arteriography by pulmonary embolism. Radiology 1969; 93:1007–12 41. Grollman JH Jr, Gyepes MT, Helmer E. Transfemoral selective bilateral pulmonary arteriography with a pulmonary-artery-seeking catheter. Radiology 1970; 96:202–4 42. Meyerovitz MF, Levin DC, Harrington DP, et al. Evaluation of optimized biplane pulmonary cineangiography. Invest Radiol 1985; 20:945–9 43. Mayo JR, Remy-Jardin M, Muller NL, et al. Pulmonary embolism: prospective comparison of spiral CT with ventilation-perfusion scintigraphy. Radiology 1997; 205:447–52 44. Oudkerk M, van Beek EJ, Wielopolski P, et al. Comparison of contrast-enhanced magnetic resonance angiography and conventional pulmonary angiography for the diagnosis of pulmonary embolism: a prospective study. Lancet 2002; 359:1643–7 45. Quinn MF, Lundell CJ, Klotz TA, et al. Reliability of selective pulmonary arteriography in the diagnosis of pulmonary embolism. Am J Roentgenol 1987; 149:469–71 46. Monreal M, Lafoz E, Olive A, del Rio L, Vedia C. Comparison of subcutaneous unfractionated heparin with a low molecular weight heparin (Fragmin) in patients with venous thromboembolism and contraindications to coumarin. Thromb Haemost 1994; 71:7–11 47. Raschke RA, Reilly BM, Guidry JR, Fontana JR, Srinivas S. The weight-based heparin dosing nomogram compared with a standard care nomogram: a randomized controlled trial. Ann Intern Med 1993; 19:874–81 48. Pini M, Pattachini C, Quintavalla R, et al. Subcutaneous vs intravenous heparin in the treatment of deep venous thrombosis: a randomized clinical trial. Thromb Haemost 1990;64:222–6 49. Hull R, Delmore T, Genton E, et al. Warfarin sodium versus low-dose heparin in the long-term treatment of venous thrombosis. N Engl J Med 1979; 301:855–8 50. Brandjes DPM, Heijboer H, Buller HR, de Rijk M, Jagt H, ten Cate JW. Acenocoumarol and heparin compared with acenocoumarol alone in the initial treatment of proximal-vein thrombosis. N Engl J Med 1992; 327:1485–9 51. Gallus A, Jackaman J, Tillett J, Mills W, Wycherley A. Safety and efficacy of warfarin started early after submassive venous thrombosis or pulmonary embolism. Lancet 1986; 2:1293–6 52. Hull R, Hirsh J, Jay RM, et al. Different intensities of oral anticoagulant therapy in the treatment of proximal-vein thrombosis. N Engl J Med 1982; 307:1676–81 53. Lagerstedt CI, Olsson CG, Fagher BO, Oqvist BW, Albrechtsson U. Need for longterm anticoagulant treatment in symptomatic calf-vein thrombosis. Lancet 1985; 2:515–18 54. Miller GAH, Sutton GC, Kerr IH, Gibson RV, Honey M. Comparison of streptokinase and heparin in the treatment of isolated acute massive pulmonary embolism. Br Med J 1971; 2:681–4 55. Anderson DR, Levine MN. Thrombolytic therapy for the treatment of acute


pulmonary embolism. Can Med Assoc J 1992; 146:1317–24

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6 Magnetic resonance angiography of the coronary arteries

INTRODUCTION Magnetic resonance coronary angiography (MRCA) has been developed to overcome specific anatomic and physiologic properties of the coronary arteries. In the normal adult, the coronary arteries are extremely small (measuring 3–6 mm)1 and tortuous as they descend from the sinuses of Valsalva to the apex of the heart. Imaging of complete coronary arteries requires the acquisition of multiple thin two-dimensional slices (3–5 mm)2–4 or several three-dimensional volume slabs (20–30 mm)5,6.

Magnetic resonance angiography of the coronary arteries

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The proximal coronary arteries are surrounded by perivascular fat and, to improve vessel contrast; it is necessary to apply a selective fat-suppression pulse to null the signal from this fat6,7. During the cardiac cycle (systole and diastole), there is significant threedimensional motion of the coronary arteries8 which can produce significant blurring of the narrow vessels. In order to reduce the blurring, it is important to acquire the data in diastole when there is relative cardiac stasis and to use rapid sequences with temporal resolution less than 100 ms. This can be performed by segmenting data acquisition between successive heart beats. Movement during respiration is a significant cause of artifacts during MRCA, producing both vessel blurring and linear chest wall artifacts in the

Figure 6.1 Schematic representation of the orientation of the major vessels. ao, aorta; la, left atrium; lad, left anterior descending; lcx, left cross; ra, right atrium; rca, right coronary artery, rvot, right ventricular outflow tract

phase-encoding direction. The simplest strategy is to acquire the scan during a breathhold that can be effective for a single slice acquisition; but can limit the resolution of the image. In addition; many patients find breath-holding difficult9, particularly when multiple breath-holds in the same position are required to cover a whole coronary artery without slice misregistration. Rapid acquisition with modern scanners can make it possible to obtain an ECG-gated three-dimensional volume slab in a single breath-hold, but contrast agents may be required to increase signal-to-noise. An alternative strategy is to use respiratory-navigators to limit data acquisition to periods of respiration with minimal motion. Studies have shown that motion of the diaphragm is related to the displacement of the heart and coronary arteries10,11. Positioning a navigator pulse through the right hemidiaphragm can monitor the diaphragmatic motion; which can then be used


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either prospectively or retrospectively to limit data acquisition to periods with limited respiratory displacement12. Contrast-to-noise ratio within the coronary arteries can be improved using extra- and intravascular contrast

Figure 6.2 A 63-year-old man, who received a coronary artery bypass graft operation in 1995, was admitted with a lower respiratory tract infection. Routine chest X-ray and subsequent computed tomography scan identified a large calcified anterior mediastinal mass measuring 10 ¥ 10 cm. Magnetic resonance angiography demonstrates a large ellipsoid mass that compresses the right ventricular outflow tract and main pulmonary artery. The mass represents a thrombosed saphenous vein graft aneurysm but with no distal flow. A patent left internal mammary artery and saphenous vein graft to the first marginal branch of the circumflex artery can be seen

agents. Because extravascular agents, such as gadolinium salts, are rapidly transferred from the vascular lumen to the extravascular space, most contrast-enhanced MRCA is performed during a breath-hold13,14. However, with newer intravascular contrast agents, it is possible to acquire the scans during multiple breath-holds or during free-breathing acquisition15,16.

ANOMALOUS CORONARY ARTERIES Coronary arteries are described as anomalous when they originate from an unusual coronary sinus (e.g. the right coronary artery from the left coronary sinus, or the circumflex coronary artery from the right coronary sinus) or from the pulmonary


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arteries17,18. The importance of anomalous coronary arteries is due to their association with sudden cardiac death in young adults, typically during heavy exertion, when the anomalous vessel runs between the aorta and right ventricular outflow tract (see Figure 6.1)19–21. The mechanism of sudden death or myocardial ischemia is thought to be related to three mechanisms: acute angulation of the anomalous vessel from the aortic root; a slitlike ostium of the aberrant vessel; and compression of the anomalous vessel lumen by aortic expansion during strenuous exercise, possibly against the pulmonary trunk. X-ray cardiac catheterization is typically the initial diagnostic investigation that identifies the coronary artery anomaly (although it can sometimes be difficult to cannulate the anomalous vessel selectively), but identification of the proximal course can be difficult, even with experienced operators.

Figure 6.3 A 72-year-old man, who received a coronary artery bypass graft operation in 1990; presented with chest pain. Routine chest X-ray and transthoracic echocardiography identified an anterior mediastinal mass. As a 50-year-old man, the patient had a surgical repair of an aortic coarctation in 1977. Magnetic resonance angiography demonstrates a large aneurysm of the saphenous vein graft to the left anterior descending artery with a patent distal vessel

MRCA is ideally suited to identify the anomalous vessels because it can be acquired and reformatted in multiple planes and accurately displays the aorta and right ventricular outflow tract. Multiple two-dimensional MRCA has been used with good accuracy for the diagnosis of anomalous coronary arteries22–24, and this approach has also been used in patients with adult congenital heart disease25 in whom there is a significant risk of vascular injury during reconstructive vascular surgery.


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Figure 6.4 A 52-year-old man, who had received a coronary artery bypass graft operation 4 months previously presented with a recurrence of his angina. Magnetic resonance angiography was requested to confirm patency of the grafts. Maximum intensity projection (a) demonstrates a patent saphenous vein graft to the posterior descending artery. The surface rendered image (b, c) shows this graft but also the origins of the grafts to the first diagonal and marginal arteries

CORONARY ARTERY DISEASE Atheromatous coronary artery disease causes significant mortality and morbidity in the USA, with 500 000 deaths reported in 1996. The current ‘standard of reference’ diagnostic investigation for a patient’s chest pain is an X-ray coronary angiogram.


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However; this can be expensive and exposes the patient to the hazards of ionizing radiation and iodinated contrast agents. In routine cases, ithas a risk of mortality and morbidity to the patient of 0.1–1%. MRCA is a safe non-invasive method of diagnosing coronary artery disease and; with continuing improvements in technology, may soon be a clinically useful alternative to Xray angiography. Preliminary studies have used single-slice two-dimensional MRCA for the assessment of coronary artery stenoses26,27. With multiple breath-hold acquisitions, it is possible to identify proximal coronary artery stenoses in patients with coronary artery disease with a high sensitivity and specificity. The accuracy in most of the published series was greatest for the left main stem, proximal right and left coronary arteries and worst for the circumflex artery. The latter vessel is located most posteriorly and so can be difficult to image with MRCA. Both operator and interpreter require a significant amount of experience to obtain multiple overlapping slices and not to interpret a misalignment of slices as a significant coronary artery stenosis.

Figure 6.5 A 59-year-old man with angina had an abnormal exercise tolerance test with ST-segment changes in the anterior chest leads V2-V4. Magnetic resonance angiography demonstrates patency of the proximal right coronary artery from the right sinus of Valsalva to the base of the heart


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With navigator-gated sequences, it has become possible to obtain large-volume highresolution images of coronary artery vessels and stenoses. Interestingly; sensitivity and specificity remain similar to those with the two-dimensional scans, probably due to residual blurring from respiration and patient motion28,29. With modern scanners that are capable of acquiring a three-dimensional volume set in a single breath-hold, and with novel intravascular contrast agents, it may soon be possible to produce angiographic quality images similar to those with cardiac catheterization. Intravascular coronary stents can cause considerable artifact in MRCA images, but it is important to note that MRCA is not hazardous to any patient with a coronary stent in situ30,31.

Figure 6.6 A 43-year-old man with chest pain had received X-ray coronary angiography that identified an anomalous left coronary artery arising from the right sinus of Valsalva. He was referred for magnetic resonance angiography (MRA) to determine the proximal course of the anomalous vessel. MRA demonstrates the right coronary artery arising from the right sinus of Valsalva and descending to the margin


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of the heart. The anomalous left coronary artery arises from the right sinus of Valsalva and passes anteriorly and superiorly across the right ventricular outflow tract to enter the interventricular sulcus

Figure 6.7 A 24-year-old woman with chest pain had received X-ray coronary angiography which identified an anomalous left coronary artery arising from the right sinus of Valsalva. She was referred for magnetic resonance angiography (MRA) to determine the proximal course of the anomalous vessel. MRA demonstrates the anomalous vessel arising from the right sinus of Valsalva and passing between the aorta and right ventricular outflow tract

CORONARY ARTERY BYPASS GRAFTS Coronary artery bypass grafting is an increasingly common operation for patients with coronary artery disease. It relieves angina, can improve heart failure and, in some patients, improves prognosis. However, the long-term patency of venous and arterial conduits is progressively reduced by early vascular occlusion and progressive intimal hyperplasia and recurrence of atheromatous disease. By 10 years postoperatively, up to 50% of venous grafts and 10% of arterial grafts may be occluded. The gold standard for the diagnosis of graft patency is X-ray cardiac catheterization, but in this population there is an increased exposure to radiation and nephrotoxic contrast agents, and negotiating


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tortuous aortic and subclavian arteries can be difficult. Preliminary studies were performed with ‘black blood’ spin-echo sequences that demonstrated vessel patency showing black blood. But diagnostic accuracy can be reduced as it can be difficult to distinguish a patent graft from adjacent vascular and nonvascular structures, and limited information can be obtained about graft stenosis or dysfunction32–34. With ‘white blood’ gradient-echo sequences, graft patency is demonstrated with a white blood structure; although similarly no information about dysfunction is obtained35,36. Using phase-shift velocity-mapping, it can be possible to identify graft patency, graft flow and to gain information regarding graft dysfunction. As a non-invasive technique; contrast-enhanced (CE) MRCA is being increasingly used to demonstrate graft patency. Because there is less motion of the aorta and attached grafts, good results have been obtained for proximal anastamoses, using ungated CEMRCA. This enables the acquisition of submillimeter resolution images within a reasonable breath-hold (20–40 s). Cardiac-gating of the acquisition—so that data are only acquired during the short periods of cardiac stasis—is required for imaging of the distal insertion of the grafts. However, this increases the duration of the scan so that a lower spatial resolution must be used to allow for the patient’s breath-holding capabilities. A wide three-dimensional volume slab, positioned in either a coronal or sagittal orientation, will include the majority of aortic grafts.

Figure 6.8 The same patient as in Figure 6.7 in oblique sagittal section


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Figure 6.9 The same patient as in Figures 6.7 and 6.8 in transverse section


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Figure 6.10 A 74-year-old man, who received a coronary artery bypass graft operation in 1994, presented with chest pain. Magnetic resonance angiography demonstrates that the proximal part of the left internal mammary artery graft is patent


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Figure 6.11 Signal void in the proximal left anterior descending artery is demonstrated corresponding to a severe luminal stenosis on conventional X-ray coronary angiography


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Figure 6.12 A 79-year-old man, who received a coronary artery bypass graft operation in 1985, presented with chest pain. Surface-rendered magnetic resonance angiography (a) demonstrates a patent saphenous vein graft to the circumflex artery. The patient was also scanned using a maximum-intensity projection image (b)

Figure 6.13 A 69-year-old man, who received a coronary artery bypass graft operation in 1992, presented with chest pain. With magnetic resonance angiography, two stumps are seen on maximum-intensity projection (a). Surface-rendered images of the patient (b) show a patent saphenous vein graft to the circumflex artery


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REFERENCES 1. Dodge JT Jr, Brown G, Bolson EL, Dodge HT. Lumen diameter of normal human coronary arteries. Influence of age, sex, anatomic variation and left ventricular hypertrophy or dilation. Circulation 1992; 86:232–46 2. Edelman RR, Manning WJ, Burstein D, Paulin S. Coronary arteries: breath-hold MR angiography. Radiology 1991; 181:641–3 3. Pennell DJ, Keegan J, Firmin DN, Gatehouse PD, Underwood SR, Longmore DB. Magnetic resonance imaging of coronaries: technique and preliminary results. Br Heart J 1993; 70:315–26 4. Post JC, van Rossum AC, Hofman MBM, de Cock CC, Valk J, Visser CA. Clinical utility of two-dimensional magnetic resonance angiography in detecting coronary artery disease. Eur Heart J 1997; 18:426–33 5. Jhooti P, Keegan J, Gatehouse PD, et al. 3D coronary artery imaging with phase reordering for improved scan efficiency. Magn Reson Med 1999; 41:555–62 6. Li D, Paschal CB, Haacke EM, Adler LP. Coronary arteries: Three-dimensional MR imaging with fat saturation and magnetization transfer contrast. Radiology 1993; 187:401–6 7. Muller MF, Fleisch M, Kroeker R, Chatterjee T, Meier B, Vock P. Proximal coronary artery stenosis: three-dimensional MRI with fat saturation and navigator echo. J Magn Reson Imaging 1997; 7:644–51 8. Hoffman MBM, Wickline SA, Lorenz C. Quantification of in-plane motion of the coronary arteries during the cardiac cycle: implications for acquisition window duration for MR flow quantification.J Magn Reson Imaging 1998; 8:568–76 9. Taylor AM, Keegan J, Jhooti P, Gatehouse PD, Firmin DN, Pennell DJ. Differences between normal subjects and patients with coronary artery disease for three different MR coronary angiography respiratory suppression techniques.J Magn Reson Imaging 1999; 9:786–93 10. Wang Y, Riederer SJ, Ehman RL. Respiratory motion of the heart: kinematics and the implications for the spatial resolution in coronary imaging. Magn Reson Med 1995; 33:713–19 11. Taylor AM, Keegan J, Jhooti P, Firmin DN, Pennell DJ. Calculation of a subject specific adaptive motion correction factor for improved real-time navigator echo gated MR coronary angiography. J Cardiovascular Magn Reson 1999; 1:131–8 12. Liu YL, Riedere SJ, Rossman PJ, Grimm RC, Debbins JP, Ehman RL. A monitoring, feedback and triggering system for reproducible breath-hold MR imaging. Magn Reson Med 1993; 30:507–11 13. Wintersperger BJ, Engelmann MG, von Smekal A, et al. Patency of coronary bypass grafts: assessment with breath-hold contrast-enhanced MR angiographyvalue of a nonelectrocardiographically triggered technique. Radiology 1998; 208:345–51 14. Brenner P, Wintersperger B, Von Smekal A, et al. detection of coronary artery bypass graft patency by contrast enhanced magnetic resonance angiography. Eur J Cardiothorac Surg 1999; 15:389–93 15. Taylor AM, Panting JR, Keegan J, et al. Safety and preliminary findings with the new intravascular contrast agent, NC100150 injection, for MR coronary angiography. J Magn Reson Imaging 1999; 9:220–7 16. Li D, Dolan RP, Walovitch RC, Lauffer RB. Three dimensional MRI of coronary


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arteries using an intravascular contrast agent. Magn Reson Med 1998; 39:1014–18 17. Garg N, Tewari S, Kapoor A, Gupta DK, Sinha N. Primary congenital anomalies of the coronary arteries: a coronary arteriographic study. Int J Cardiol 2000; 74:39–46 18. Desmet W, Vanhaecke J, Vrolix M, et al. Isolated single coronary artery: a review of 50,000 consecutive coronary angiographies. Eur Heart J 1992; 13:1637–40 19. Cheitlin MD, De Castro CM, McAllister HA. Sudden death as a complication of anomalous left coronary origin from the anterior sinus of valsalva. Circulation 1974; 50:780–7 20. Liberthson RR, Dinsmore RE, Bharati S, et al. Aberrant coronary artery origin from the aorta: diagnosis and clinical significance. Circulation 1974; 50:774–9 21. Cox ID, Bunce N, Fluck DS. Failed sudden cardiac death in a patient with an anomalous origin of the right coronary artery. Circulation 2000; 102:1461–2 22. Post JC, van Rossum AC, Bronzwaer JG, de Cock CC, Hofman MB, Visser VJ. Magnetic resonance angiography of anomalous coronary arteries. A new gold standard for delineating the proximal course. Circulation 1995; 92:3163–71 23. McConnell MV, Ganz P, Selwyn AP, Li W, Edelman RR, Manning WJ. Identification of anomalous coronary arteries and their anatomic course by magnetic resonance coronary angiography. Circulation 1995; 92:3158–62 24. Bekedam MA, Vliegen HW, Doornbos J, Jukema JW, de Roos A, van der Wall EE. Diagnosis and management of anomalous origin of the right coronary artery from the left coronary sinus. Int J Card Imaging 1999; 15:253–8 25. Taylor AM, Thorne SA, Rubens MB, et al. Coronary artery imaging in grown up congenital heart disease: complementary role of magnetic resonance and x-ray coronary angiography. Circulation 2000; 101:1670–8 26. Pennell DJ, Bogren HG, Keegan J, Firmin DN, Underwood SR. Assessment of coronary artery stenosis by magnetic resonance imaging. Heart 1996; 75:127–33 27. Post JC, van Rossum AC, Hoffman MBM, deCock CC, Valk J, Visser CA. Clinical utility of two-dimensional magnetic resonance angiography in detecting coronary artery disease. Eur Heart J 1997; 18:426–33 28. Muller MF, Fleisch M, Kroeker R, Chatterjee T, Meier B, Vock P. Proximal coronary artery stenosis: three-dimensional MRI with fat saturation and navigator echo. J Magn Reson Imaging 1997; 7:644–51 29. Post JC, van Rossum AC, Hoffman MBM, Valk J, Visser CA. Three dimensional respiratory gated MR angiography of coronary arteries: comparison with conventional coronary angiography. Am J Roentgenol 1996; 166:1399–404 30. Strohm O, Kivelitz D, Gross W, et al. Safety of implantable coronary stents during H1 magnetic resonance imaging at 1.0 and 1.5 T.J Cardiovasc Magn Reson 1999; 1:239–45 31. Scott NA, Pettigrew RI. Absence of movement of coronary stents after placement in a magnetic resonance imaging field. Am J Cardiol 1994; 73:900–1 32. White RD, Caputo GR, Mark AS, Modin GW, Higgins CB. Coronary artery bypass graft patency: non-invasive evaluation with MR imaging. Radiology 1987; 164:681–6 33. Rubinstein RI, Askenase AD, Thickman D, Feldman MS, Agarwal JB, Helfant RH. Magnetic resonance imaging to evaluate patency of aortocoronary bypass grafts. Circulation 1987; 76:786–91 34. Galjee MA, van Rossum AC, Doesburg T, van Eenige MJ, Visser CA. Value of magnetic resonance imaging in assessing patency and function of coronary artery bypass grafts. Circulation 1996; 93:660–6 35. Wintersperger BJ, Engelmann MG, Von Smekal A, et al. Patency of coronary bypass


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grafts: assessment with breath-hold contrast-enhanced MR angiography—value of a nonelectrocardiographically triggered technique. Radiology 1998; 208:345–51 36. Hoogendoorn LI, Pattynama PMT, Buis B, van der Geest RJ, van der Wall EE, de Roos A. Non-invasive evaluation of aortocoronary bypass grafts with magnetic resonance flow mapping. Am J Cardiol 1995; 75:845–8

7 Magnetic resonance angiography of the renal vessels

INTRODUCTION Magnetic resonance can be performed to assess the anatomical structure of the kidney (e.g. single kidney, horseshoe kidney, transplant kidney) and for the presence of any mass (e.g. renal neoplasm, adrenal adenoma). With gadolinium-enhanced magnetic resonance angiography (MRA), it is now possible to accurately image the renal arteries and renal veins. In addition, renal artery stenosis can be confirmed with the use of phase-contrast velocity mapping perpendicular to the artery, before and after the stenosis.


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Figure 7.1 An 81-year-old man with resistant hypertension and a low creatinine clearance was referred for exclusion of renal artery stenosis. Magnetic resonance angiography demonstrates normal-sized kidneys. Both renal arteries are patent with no significant stenosis

A typical MRA protocol of the renal arteries would begin with either a T1- or T2weighted unenhanced sequence to provide anatomical information about the kidneys and to locate the origin of the renal arteries from the abdominal aorta. These pilot scans can be repeated in coronal, transverse and sagittal planes for accurate localization of the three-dimensional MRA slab. To include both the left and right renal arteries, MRA is typically performed in the coronal plane. To reduce movement artifacts, the acquisition is performed during breath holding. A baseline precontrast acquisition is performed to allow for subsequent image subtraction. Then a timing scan is performed using an injection of a low dose of contrast at a set injection rate (e.g. 2 ml contrast at 3 ml/s). One image of the abdominal aorta is acquired every second to determine the transit time. This will vary for each patient according to the injection site and cardiac output. Using a larger dose of contrast, the three-dimensional coronal acquisition is then repeated either as one or two high-resolution slabs coordinated with renal arterial and renal vein enhancement; or as multiple lower resolution slabs to provide a dynamic series. Subsequent analysis of the MRA data is performed by reviewing the raw data and also after maximumintensity projection of the data and three-dimensional volume rendering. Renal MRA can be used to investigate patients with hypertension to identify renal artery stenosis, renal thrombosis; transplant kidneys and pulmonary embolic disease, but has also been used to investigate pulmonary hypertension and renal tumors.

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RENAL ARTERY STENOSIS History and clinical symptoms Reduction in the blood supply to one or both kidneys due to renal artery stenosis may lead to drugresistant hypertension, deterioration in renal function and ‘flash’ pulmonary edema in the absence of significant cardiac disease. Renal artery stenosis can be divided into fibromuscular arterial stenosis (more common in younger people and in women) and atherosclerotic arterial stenosis (more common in older people and in men, and often associated with coronary and cerebrovascular disease). Diagnostic features of renal artery stenosis include early-onset

Figure 7.2 A 27-year-old man with resistant hypertension was referred to exclude renal artery stenosis and adrenal tumors. Magnetic resonance angiography demonstrates normal-sized kidneys with no adrenal mass identified. There is an accessory right renal artery. No evidence for renal artery stenosis


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Figure 7.3 A 59-year-old man with hypertension and a left renal bruit was referred for assessment. Magnetic resonance angiography demonstrates normal-sized kidneys. There is a severe stenosis in the origin of the left renal artery. The patient’s blood pressure control improved following renal angioplasty

hypertension, hypertension that is rapidly accelerating or difficult to control; the presence of an abdominal bruit and deterioration in renal function after commencement of an angiotensin-converting enzyme (ACE) inhibitor. Clinical examination may be unhelpful in a patient with renal artery stenosis. Neither kidney will be enlarged and a small kidney will not be palpable. There may be a renal bruit, and this is an important sign to identify patients with hypertension. The presence of co-existing peripheral, cranial or cardiovascular disease should be sought; and other secondary causes of hypertension should be excluded (e.g. a patient with polycystic kidney disease). Investigations Mann and Pickering1 have classified patients into low, moderate and high clinical index of suspicion of


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Figure 7.4 A 67-year-old woman with abnormal renal function and abnormally sized kidneys on renal ultrasound was referred for assessment. With magnetic resonance angiography, the left kidney is normal in size but has a moderate stenosis in the mid-part of the left renal artery. The right kidney is small and appears to be supplied by tortuous collaterals. There was delayed hyperenhancement of the renal cortex

Figure 7.5 A 66-year-old woman was admitted with flash pulmonary edema. She was known to suffer with hypertension and had a history of cerebrovascular disease. With magnetic resonance angiography, both kidneys appear normal in size. The left kidney is supplied by a small


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single left renal artery. The right renal artery has a severe stenosis at its origin

renovascular hypertension, in an attempt to determine which patients should be investigated by either non-invasive or invasive testing. Patients at moderate risk who would be considered for non-invasive imaging include those with severe hypertension (diastolic blood pressure of greater than 120 mmHg, refractory hypertension, abrupt onset moderate-severe hypertension in those under 20 and over 50 years of age, hypertension with an abdominal bruit, moderate hypertension (diastolic blood pressure of greater than 105 mmHg, in a patient with co-existent vascular disease or with an unexplained elevated creatinine, or normalization of blood pressure with an ACE inhibitor in a patient with moderate to

Figure 7.6 Magnetic resonance angiography demonstrates normal renal arteries and a normal abdominal aorta in a 28-yearold woman with hypertension

severe hypertension). Those at high risk would be considered directly for X-ray angiography (although these comments precede the advent of computed tomography angiography and MRA), and would include patients with severe hypertension resistant to therapy or with a raised creatinine, especially in a smoker, patients with malignant or accelerated hypertension; patients with hypertension and ACE inhibitor-induced elevation of serum creatinine, and severe hypertension with asymmetric kidneys. Isotopic renography and plasma renin measurements after an oral captopril challenge are one method of detecting renal artery stenosis, as captopril (an ACE inhibitor) may induce renal ischemia in a kidney supplied by an stenosed artery2,3. The captopril abruptly reduces the levels of circulating angiotensin II that are required to maintain perfusion to a kidney supplied by a stenosed renal artery. The ischemic kidney then releases renin and suffers a reduction in blood flow and glomerular filtration rate, which can then be quantified. The test is best performed on a normal sodium intake, with the patient off diuretics and antihypertensive drugs. Measuring increases in plasma renin


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activity can produce a sensitivity and specificity of 73–100% and 73–95%; respectively3. Isotope renography—using hippurate for renal blood flow, or diethylenetriaminepentaacetic acid (DTPA) or mercaptoacetyltriglycine (MAG3) for glomerular filtration rate– performed 1 h after a 50 mg captopril challenge may be more accurate4.

Figure 7.7 Surface-rendered three-dimensional contrast-enhanced MRA of the renal arteries and abdominal aorta in a patient with hypertension and suspected renal artery stenosis. Arterial phase (a) and venous phase (b) images in the anterior-posterior view. There is single renal artery on both sides with no evidence of renal artery stenosis. Localized aneurysm of the distal abdominal aorta immediately above the aortic bifurcation was noticed (arrow)

Abdominal ultrasound may be normal; although some patients with chronic severe renal artery stenosis or occlusion may have a small shrunken kidney. Renal artery Doppler scanning may be able to detect renal artery stenosis in thin patients. In a study of 56 patients with suspected renal artery stenosis by Halpern and colleagues5, Doppler ultrasound was compared with CT angiography (CTA) and X-ray angiography as the gold standard. In this patient group, there were 27 renal artery stenoses in 20 patients. Doppler ultrasound had a sensitivity of only 63% as compared to 96% for CTA for diagnosing a significant stenosis, although the specificities of both techniques were high at 89% and 88%, respectively.


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CTA is an accurate method of diagnosing renal artery stenosis. Johnson and associates6 studied helical CTA versus X-ray angiography for the diagnosis of renal arterial disease. They assessed 25 patients (14 men, 11 women, age range 24–73 years) using a timing bolus of 20 ml non-ionic contrast medium; then 120 ml of contrast for the CTA acquisition. In this group, there were 50 main renal arteries and 11 accessory renal arteries, with three severe, five moderate and 13 mild renal artery stenoses. The sensitivity was 89–94% (depending on whether maximum-intensity projection or volume rendered images were assessed), with a specificity of 99–87%. However, CTA did overestimate the severity of stenosis in the small accessory renal arteries; and could be adversely affected by the presence of calcification leading to an error in the quantification of a stenosis. Similar results have been reported from many centers with sensitivities of 94–100% and specificities of 97–98%7,8. Computed tomography also has the advantage of being available in most hospitals, unlike magnetic resonance that is still a limited resource. However, computed tomography does expose the patient to the hazards of ionizing radiation and the problems with contrast medium. In a study by Lufft and colleagues9, the authors studied 80 patients who were randomized to either CTA (where a large dose of contrast medium is injected into a peripheral vein) or digital subtraction angiography (DSA, where a smaller dose of contrast medium is injected into the renal artery). They measured serum creatinine, inulin clearance, and beta N-acetyl glucoseaminidase level (a marker of tubular toxicity). CTA involved a dose of 163±13 ml contrast, as opposed to DSA of 104±56 ml, and both increased serum creatinine by a small amount, but in three of the 33 CTA and two of the 31 DSA patients there was contrast medium nephropathy that persisted for up to 7 days.


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Figure 7.8 A 75-year-old man had been treated for hypertension. Because of a deterioration of renal function after starting ACE inhibitors, the patient was referred for CE-MRA. This demonstrated a severe stenosis in the proximal left renal artery. The patient has been referred for consideration of revascularization

MRA dose not expose the patient to a nephrotoxic contrast agent and does not involve ionizing radiation. Shetty and associates10 assessed 51 patients with three-dimensional breath-hold MRA versus X-ray angiography. They evaluated both MRA and X-ray angiography using a six-point scale, where 0 represented the normal, 1 was mild (< 50% stenosis), 2 was moderate (50–75% stenosis), 3 was severe (> 75% stenosis), 4 represented occluded and 5 was aneurysmal. They identified 115 renal arteries, including 11 accessory renal arteries and three stents. The results were concordant in 42 of the patients; in three patients the X-ray angiography overcalled the severity of the stenosis, and in two patients the disease severity had progressed between the two tests. Overall sensitivity and specificity were 96% and 92%, respectively. In a meta-analysis of the diagnostic tests used in patients with renovascular hypertension, Vasbinder and colleagues11 evaluated trials of CTA, MRA, Doppler ultrasound, captopril renal scintigraphy, and the captopril test, that used X-ray angiography as the gold standard for the diagnosis of renal artery stenosis. They found that three-dimensional MRA and CTA performed best. In a recent study by Schoenberg and co-workers12, the authors produced a rapid protocol that could acquire anatomical, functional and angiographic data in five breath-holds. This included T1 FLASH and T2 Turbo spin-echo images for renal morphology, then multiphase three-dimensional gadolinium-enhanced MRA and finally


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segmented EPI cine phase-contrast imaging for renal arterial blood flow, providing a complete assessment of the renal system in a time-efficient manner. Treatment Treatment of the hypertension may be better and safer with calcium channel blockers rather than with ACE inhibitors13. In most patients, blood pressure control should be obtained gradually to maintain renal perfusion, unless the patient is systemically unwell. Renal angioplasty and renal stenting can improve the majority of patients with the best results obtainable in patients with fibromuscular dysplasia14,15. Renal angioplasty can also be performed in patients with contraindications to vascular surgery. Surgical repair can also be successful in renovascular hypertension16,17.

RENAL MRA Renal MRA may also be used in patients with transplant kidneys to determine if there is any stenosis of the supplying artery. In addition, renal MRA and unenhanced magnetic resonance imaging may be useful to provide accurate anatomic information prior to surgical intervention for neoplasia.

REFERENCES 1. Mann SJ, Pickering TG. Detection of Renovascular Hypertension. State of the art. Ann Intern Med 1992; 117:845. 2. Canzanello VJ, Textor SC. Noninvasive diagnosis of renovascular disease. Mayo Clin. Proc 1994; 69:1172 3. Derkx FHM, Schalekamp MADH. Renal artery stenosis and hypertension. Lancet 1994; 344:237 4. Elliot WJ, Martin WB, Murphy MB. Comparison of two noninvasive screening tests for renovascular hypertension. Arch Intern Med 1993; 153:755 5. Halpern EJ, Rutter CM, Gardiner GA Jr, et al. Comparison of Doppler US and CT angiography for evaluation of renal artery stenosis. Acad Radiol 1998:5:524–32 6. Johnson PT, Halpern EJ, Kuszyk BS, et al. Renal artery stenosis: CT angiography— comparison of real-time volume-rendering and maximum intensity projection algorithms. Radiology 1999; 211:337–43 7. Wittenberg G, Kenn W, Tschammler A, Sandstede J, Hahn D. Spiral CT angiography of renal arteries: comparison with angiography. Eur Radiol 1999; 9:546–51 8. Kim TS, Chung JW, ParkJ H, Kim SH, Yeon KM, Han MC. Renal artery evaluation: comparison of spiral CT angiography to intra-arterial DSA. J Vasc Interv Radiol 1998; 9:553–9 9. Lufft V, Hoogestraat-Lufft L, Fels LM, et al. Contrast media nephropathy: intravenous CT angiography versus intra arterial digital subtraction angiography in renal artery stenosis: a prospective randomized trial. Am J Kidney Dis 2002; 40:236–42 10. Shetty AN, Bis KG, Kirsch M, Weintraub J, Laub G. Contrast-enhanced breath-hold


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three-dimensional magnetic resonance angiography in the evaluation of renal arteries: optimization of technique and pitfalls. J Magn Reson Imag 2000; 12:912–23 11. Vasbinder GB, Nelemans PJ, Kessels AG, Kroon AA, de Leeuw PW, van Engelshoven JM. Diagnostic tests for renal artery stenosis in patients suspected of having renovascular hypertension: a meta-analysis. Ann Intern Med 2001; 135:401–11 12. Schoenberg SO, Essig M, Bock M, Hawighorst H, Sharafuddin M, Knopp MV. Comprehensive MR Evaluation of Renovascular Disease in Five Breath Holds. J Magn Reson Imag 1999; 10:347–356 13. Mimram A. Renal affects of antihypertensive drugs in parenchymal renal disease and renovascular hypertension. J Cardiovasc Pharmacol 1992; 19 (suppl 6):45 14. Losinno F, Zuccala A, Busato F, Zucchelli P. Renal artery angioplasty for renovascular hypertension and preservation of renal function: Long-term angio-graphic and clinical follow-up. Am J Roentgenol 1994; 162:853 15. Tykarski A, Edward E, Dominiczak AF, Reid JL. Percutaneous transluminal renal angioplasty in the management of hypertension and renal failure in patients with renal artery stenosis. J Hum Hypertens 1993; 7:491 16. Bedoya L, Ziegelbaum M, Vidt DG, et al. Baseline renal function and surgical revascularization in atherosclerotic renal arterial disease in the elderly. Cleveland Clin J Med 1989; 56:415 17. Libertino JA, Bosco PJ, Ying CY, et al. Renal revascularisation to preserve and restore renal function. J Urol 1992:147:1485

8 Magnetic resonance angiography of the peripheral vessels

MRA OF THE PERIPHERAL VESSELS Magnetic resonance can provide a high-resolution ‘road-map’ of the peripheral vascular system. Initial sequences were two-dimensional ‘time-of-flight’ (TOF) examinations that relied upon flowing blood to provide vessel contrast. For the assessment of peripheral vascular disease, Mulligan and colleagues found a good agreement with X-ray angiography1. When applied to the tibial vessels by Owen and co-workers, magnetic resonance could provide more information than X-ray angiography regarding distal run-


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off vessels, sufficient to alter surgical management plans2. However, when applied to the infrainguinal vessels, there was significant variation in the accuracy of the technique, varying from 52% by Snidow and associates3 to 87% by Carpenter and colleagues4. A major disadvantage was the amount of scanning time required (>2 h) to product satisfactory assessment of iliac to tibial vessels.

Figure 8.1 A 77-year-old male smoker with hyperlipidemia and hypertension was referred with leg claudication. With magnetic resonance angiography, the abdominal aorta is diffusely irregular, consistent with atherosclerosis. There is a tight stenosis of the right common iliac artery above its bifurcation with a moderate stenosis of the left common iliac artery. There was no evidence of renal artery stenosis

With the development of contrast-enhanced magnetic resonance angiography (MRA), it became possible to rapidly produce high-resolution images of the whole distal vasculature. Prince and associates5 used three-dimensional contrast-enhanced (CE)-MRA of the abdominal aorta, renal vessels and iliac arteries in 16 patients and were able to provide good-quality images with minimal venous enhancement and no flow-related artifacts. More recent studies have confirmed the usefulness of CE-MRA as a real alternative to X-ray angiography for the diagnosis of peripheral vascular disease. Initial protocols were limited to displaying a field of view of 40–48 cm and requiring several injections of contrast agent to image from iliac to tibial vessels. However, with the development of ‘bolus-chase’ techniques6,7, it has become possible to perform the complete study with a single dose of contrast agent. Using a slow injection of gadolinium contrast agent during a long breath-hold, two or three-dimensional datasets can be acquired using a 10–s pause between datasets to allow for movement of the examination table (either manual or automated). Optimal timing of the acquisition with peak arterial enhancement is important and this can be aided by the use of automation software that detects vascular enhancement. It may be helpful to perform unenhanced precontrast three-dimensional datasets, to allow for image subtraction. Using three-dimensional CEMRA, Ruehm and colleagues8 studied 23 patients (13 men, 10 women, age range 46–85 years) undergoing digital subtraction angiography (DSA). Using non-subtracted datasets, the authors demonstrated sensitivity and specificity of 90.2% and 95.1%, respectively for the detection of a severe stenosis or vascular occlusion. Using subtracted data, the values were 90.3% and 95.6%, respectively, but there is a time penalty with this method,

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increasing a study from 15 to 25 min in duration. In a similar study to

Figure 8.2 A 63-year-old man with uncontrolled hypertension presented with chest pain. On physical examination, there was marked radiofemoral delay and a loud abdominal bruit was heard. Magnetic resonance angiography demonstrates severe peripheral aortic stenosis at the level of the aortic hiatus. The stenotic segment is 7 mm in diameter and 40 mm in length. Distal to this, the upper abdominal aorta dilates. The left and right renal arteries are of normal caliber

determine the value of image subtraction versus non-subtracted or fat-suppressed images; Leiner and associates9 studied ten patients (seven men, three women, mean age 63 years) with peripheral vascular disease. They found that, although subtracted data required more time for acquisition, interpretability and suppression of venous enhancement were best for the subtracted technique. Overall; in several studies, CE-MRA has produced sensitivities and specificities in the 90–100% range6, 7, 10–12.


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Figure 8.3 An 80-year-old woman presented with hypertension. Magnetic resonance angiography demonstrates a tortuous abdominal aorta, with an acute bend to the right at the level of the renal arteries. The left


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renal artery is stretched and displaced by the tortuous aorta

PERIPHERAL VASCULAR DISEASE Peripheral vascular disease is a manifestation of widespread atherosclerosis. In the Framingham study13, which defined the presence of peripheral vascular disease by the presence of claudication, the incidence of the disease was more common in men and increased with age. Between 30 and 44 years of age, the annual incidence per 10 000 patients was six for men and three for women; by 45–54 years it was 19 and seven, respectively; by 55–64 years it was 53 and 18; respectively; and by 65–74 years it was 61 and 54, respectively. In the USA, some 229 000 men and 184 000 women annually will have a diagnosis of chronic peripheral vascular disease, with the majority occurring inpatients over 65 years old. The natural history of the disease is that two-thirds to threequarters will remain stable, but between one-third and one-quarter will progress or deteriorate, so that 1–5% will require amputation of an affected limb. Diagnosis of the condition is based upon a good history, clinical examination and noninvasive tests. Fontaine provided a classification of the symptoms of claudication. Stage I were asymptomatic, stage IIa were pain-free at rest but had intermittent claudication (pain in the leg muscles on exertion) walking over 200 m, stage IIb were pain-free at rest but developed claudication when walking less than 200 m, stage III had rest and nocturnal pain, and stage IV had evidence of limb ischemia with necrosis or gangrene. Examination of the limbs would include inspection for skin color (as an ischemic limb may be pale or white); skin temperature (as an ischemic limb will be cooler unless there is super- added infection); capillary filling time (prolonged in patients with severe ischemia); and for ulceration, necrosis or gangrene. Palpation of the peripheral pulses may identify an absent pulse with a severe stenosis or auscultation for the presence of an arterial bruit due to turbulence at the site of vessel narrowing. Non-invasive assessment would include measurement of the ankle/brachial systolic blood pressure index; using multiple cuffs for different segments of a limb. This can be used to determine the site of a significant arterial stenosis. If the resting ankle/brachial systolic blood pressure index is normal but the patient is symptomatic, then the test can be repeated after a simple treadmill test (5 min at 2 mph on a 12% incline). Plethysmography and Doppler ultrasound can also be used to determine significant limb ischemia and to limit the number of patients requiring X-ray angiography. In expert centers, CE-MRA is now the preferred diagnostic examination in preference to X-ray angiography. Treatment of peripheral vascular disease consists of medical therapy, angioplasty/stenting, or surgery. Medical therapy would be appropriate for patients in stage I or II, and consists of smoking cessation, as up to 85% of patients can increase their exercise tolerance by 200–300% with this intervention14–17. Physician-guided exercise programs can also increase claudication distance18–21. The most effective drug therapies may be for treating the co-existing cardio-vascular and cerebrovascular disease; and diabetes, including statin drugs for hyperlipidemia, anti-platelet agents (such as aspirin or clopidogrel), insulin therapy in poorly controlled diabetics and good bloodpressure control. If patients are stage III or stage IV, then angioplasty or surgery may be


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indicated. Angioplasty has been shown to be effective in iliac vessels where stenoses tend to be discrete and focal. Becker and co-workers reviewed 2697 procedures from the published literature, and reported a 92% initial success rate, with 2-year and 5-year patencies of 81% and 75%, respectively22. For the femoral vessels, where there may be more occlusive lesions and particularly long segments, the results are still good with patencies of 81%, 61% and 58% at 1-, 3- and 5-year follow-up, even in relatively older studies23. For the tibial vessels, a primary success of 97% with 2-year limb salvage of 83% was reported by Schwarten and Cutcliff24. Surgical therapy may be required in certain patients.

Figure 8.4 A 71 -year-old man with suspected coronary artery disease was referred for X-ray coronary angiography. The procedure was terminated due to difficult vascular access. Magnetic resonance angiography demonstrates diffuse atherosclerosis of the aorta. There is a mild-moderate stenosis of the left renal artery and near complete occlusion of the right common iliac artery with distal reconstitution of the femoral artery by collateral vessels. The left iliac artery has a moderate focal stenosis near its origin


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Figure 8.5 A 72-year-old hypertensive man was referred for renal magnetic resonance angiography (MRA). MRA demonstrates that both kidneys and renal arteries are normal in size with no evidence of stenoses. There is a fusiform aneurysm of the suprarenal aorta


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Figure 8.6 A 75-year-old hypertensive man was referred for assessment of a pulsatile abdominal mass. Magnetic resonance angiography demonstrates an infrarenal aortic aneurysm that measures 50 mm in maximal cross-sectional diameter (see also Figure 8.7)


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Figure 8.7 A 68-year-old man was admitted with severe abdominal pain that radiated through to the back. On clinical examination, there was reduced pulsation of the left femoral artery. Magnetic resonance angiography demonstrates an abdominal aortic dissection that extends from the infrarenal aorta into the left iliac artery


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Figure 8.8 In the same patient as in Figure 8.7, the left iliac artery now arises from the false lumen

REFERENCES 1. Mulligan SA, Matsuda T, Lanzer P, et al. Peripheral arterial occlusive disease: prospective comparison of MR angiography and color duplex US with conventional angiography. Radiology 1991; 178:695–700 2. Owen RS, Carpenter JP, Baum RA, Perloff LJ, Cope C. Magnetic resonance imaging of angiographically occult runoff vessels in peripheral arterial occlusive disease. N Engl J Med 1992; 326:1577–81 3. Snidow JJ, Harris VJ, Johnson MS, et al. Iliac artery evaluation with two-dimensional time-offlight MR angiography: update. J Vasc Interv Radiol 1996; 7:213–20 4. Carpenter JP, Owen RS, Holland GA, Baum RA, Barker CF, Perloff LJ, Golden MA, Cope C. Magnetic resonance angiography of the aorta, iliac, and femoral arteries. Surgery 1994; 116:17–23 5. Prince MR, Yucel EK, Kaufman JA, Harrison DC, Geller SC. Dynamic gadoliniumenhanced three-dimensional abdominal MR arteriography. J Magn Reson Imag 1993; 3:877–81 6. Ho KY, Leiner T, de Haan MW, Kessels AG, Kitslaar PJ, van Engelshoven JM. Peripheral vascular tree stenoses: evaluation with moving-bed infusion-tracking MR angiography. Radiology 1998; 206:683–92 7. Meaney JF, Ridgway JP, Chakraverty S, et al. Stepping-table gadolinium-enhanced digital subtraction MR angiography of the aorta and lower extremity arteries: preliminary experience. Radiology 1999; 211:59–67 8. Ruehm SG, Nanz D, Baumann A, Schmid M, Debatin JF. 3D Contrast-enhanced MR angiography of the run-off vessels: value of image subtraction. J Magn Reson Imag 2001; 13:402–11 9. Leiner T, de Weert TT, Nijenhuis RJ, et al. Need for background suppression in contrast-enhanced peripheral magnetic resonance angiography. J Magn Reson Imag 2001; 14:724–33 10. Busch HP, Hoffmann HG, Metzner C, Oettinger W. MR angiography of the lower


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extremities with an automatic table translation (Mobitrak) compared to i.a. DSA. Rofo Fortschr Geb Rontgenstr Neuen Bildgeb Verfahr 1999; 170:275–83 11. Ho VB, Choyke PL, FooTK, et al. Automated bolus chase peripheral MR angiography: initial practical experiences and future directions of this work-inprogress. J Magn Reson Imaging 1999; 10:376–388 12. Ruehm SG, Hany TF, Pfammatter T, Schneider E, Ladd M, Debatin JF. Pelvic and lower extremity arterial imaging: diagnostic performance of three-dimensional contrast-enhanced MR angiography. Am J Roentgenol 2000; 174:1127–35 13. Kannel WB, Skinner JJ Jr, Schwartz MJ, Shurtleff D. Intermittent claudication: incidence in the Framingham Study. Circulation 1970; 41:875–83 14. Cronenwett JL, Warner KG, Zelenock GB, et al. Intermittent claudication: current results of nonoperative management. Arch Surg 1984; 119:430–6 15. Couch NP. On the arterial consequences of smoking. J Vasc Surg 1986; 3:807–12 16. Krupski WC, Rapp JH. Smoking and atherosclerosis. Perspect Vasc Surg 1989; 1:103–34 17. Quick CR, Cotton LT. The measured effect of stopping smoking on intermittent claudication. Br J Surg 1982; 69 (suppl):s24–6 18. Hiatt WR, Regensteiner JG, Hargarten ME, Wolfel EE, Brass EP. Benefit of exercise conditioning for patients with peripheral arterial disease. Circulation 1990; 81:602–9 19. Lundgren F, Dahllöf AG, Lundholm K, Scherstén T, Volkmann R. Intermittent claudication—surgical reconstruction or physical training? A prospective randomized trial of treatment efficiency. Ann Surg 1989; 209:346–55 20. Clifford PC, Davies PW, Hayne JA, Baird RN. Intermittent claudication: is a supervised exercise class worth while? Br Med J 1980; 280:1503–5 21. Carter SA, Hamel ER, Paterson JM, Snow CJ, Mymin D. Walking ability and ankle systolic pressures: observations in patients with intermittent claudication in a shortterm walking exercise program. J Vasc Surg 1989; 10:642–9 22. Becker GJ, Katzen BT, Dake MD. Noncoronary angioplasty. Radiology 1989; 170:921–40 23. Capek P, McLean GK, Berkowitz HD. Femoropopliteal angioplasty: factors influencing long-term success. Circulation 1991; 83 (suppl I):170–80 24. Schwarten DE, Cutcliff WB. Arterial occlusive disease below the knee: treatment with percutaneous transluminal angioplasty performed with low-profile catheters and steerable guide wires. Radiology 1988; 169:71–4

Conclusion Contrast-enhanced magnetic resonance angiography is emerging as an effective and desirable technique for the assessment of the cardiovascular system. With the recent improvements in scanner technology, it has become possible to acquire high-resolution images of arterial and venous structures within a single breath-hold. Additional benefits over traditional X-ray angiography include the lack of ionizing radiation and a necessity for only peripheral administration of a very safe contrast agent. In many disciplines, contrast-enhanced magnetic resonance angiography can now be considered the optimal diagnostic investigation for patients with disorders of the cardiovascular system. Increasing physician familiarity with the technique and the increased availability of magnetic resonance scanners will contribute to the acceptance of contrast-enhanced magnetic resonance angiography in routine clinical practice.

Index

abdominal aorta 94, 103 aneurysm 96–7 coarctation 106 dilation 104 dissection 19 tortuous 108 abdominal bruit 92, 104 adult congenital heart disease 72 air-tissue interface 53, 56 alcohol intake 45 alveolar ventilation 60 aneurysms aortic 18, 21, 40–1,96–7,110 in coronary artery bypass graft 70, 72 false or pseudoaneurysm 40 fusiform 41, 109 saccular 41 angiography see X-ray angiography angioplasty 99, 112 angiotensin-converting (ACE) inhibitors 92, 94, 97, 98 ankle/brachial systolic blood pressure index 109 anomalous vessels coronary arteries 72, 77, 79 pulmonary veins 54 antiplatelet therapy 45–6,112 anticoagulation therapy 67 antithrombin III deficiency 57, 61 aorta 17–41, 79 ascending 17, 20 atherosclerosis 108 descending 17, 20 dissection 14, 18, 19, 24, 31–5,111 infrarenal 110 stenosis 104 suprarenal 109 see also abdominal aorta; aortic arch aortic aneurysms 18, 21, 40–1,110 false 31–3 fusiform 41, 109

Index saccular 41 aortic arch 102 anomalies in aortic coarctation 36 dissection 19, 31–3 hypoplastic 23, 37 proximal 33 aortic coarctation 18, 23, 24–6,36 recurrence 24–6 repair site 23, 24, 73 aortic conduit graft 23 aortic hiatus, stenosis 104 aortic lumen, true and false 14, 35 aortic root 12 dilated 21 true lumen 14 aortic valve, bicuspid 19, 24 arterial bruit 109 arterial stenosis 19, 23, 37 carotid arteries 46–9 coronary arteries 72–6 fibromuscular 90, 99 renal arteries 89–98 see also aortic coarctation aspirin (anti-platelet agent) for carotid artery disease 44–6,48 for peripheral vascular disease 112 atherosclerosis coronary heart disease 72–6 peripheral vessels 102, 105, 108, 112 renal arteries 89 atomic nuclei in magnetic field xii–1, 2 axillary artery 102 baseline acquisition 9, 10 black blood spin-echo sequences 77 blood, interaction with contrast agents 5 blood gases, arterial, pulmonary embolism 59 blood pressure aortic dissection and 19, 24 peripheral vascular disease and 112 see also hypertension body tissues interaction with contrast agents 5 T1 and T2 values 1 ‘bolus chase’ techniques 11, 89, 95, 103 brachiocephalic vessels 17, 31 calcium channel blockers 98

105

Index

106

captopril challenge 94 see also angiotensin-converting (ACE) inhibitors cardiac motion, in imaging 53 carotid arteries 44 carotid artery disease 44–9 stenosis 45, 46–9 CE-MRA see contrast-enhanced magnetic resonance angiography (CE-MRA) circle of Willis, aneurysm 26 circumflex artery 70, 76 vein graft to 75, 82, 84 claudication 104, 108, 112 coeliac artery 102 common carotid arteries 17, 102 left 24, 36 computed tomography angiography (CTA), renal arteries 94–7 computed tomography (CT), pulmonary embolism 66 contrast agents 5–7 adverse reactions 13 extravascular 5–7, 70–3 intravascular 7, 72 iodinated 66, 74 nephrotoxicity 76, 95 pulmonary imaging 52, 56 renal imaging 89, 95 contrast-enhanced magnetic resonance angiography (CE-MRA) 9–14 carotid arteries 46–8,49 coronary arteries 70–2,77 peripheral vessels 102–5,108 pulmonary vessels 56, 66 renal vessels 89, 97 coronal plane, pulmonary imaging 56 coronary angiography 7, 72 coronary arteries 4–6, 17, 70–84 anomalous 73, 78, 79 anterior/posterior descending 75, 83 diagonal 75 left 78, 79, 82 marginal 75 right 76, 78 stenosis 72–6,83 coronary artery bypass grafts 72, 74, 79, 82, 84 aneurysms 70, 72 imaging 76–9 thrombosis 70 creatinine serum levels 94,95 CTA see computed tomography angiography (CTA) diabetes, peripheral vascular disease and 112

Index

107

diethylenetriaminepentaacetic acid (DPTA) 95 digital subtraction angiography (DSA) 95, 102–4 dissection, aortic 14, 18, 19, 24, 31–5,110 Doppler ultrasound benefits and weaknesses 46, 49 peripheral vascular disease 108 renal arteries 94 ECG, pulmonary embolism 59 Ehlers-Danlos syndrome 20 excitation of nuclei xii–1 exercise claudication therapy 112 sudden death in 73 fat, perivascular 71, 105 femoral vessels 108, 111, 112 field of view 4, 9, 56 ‘flash’ pulmonary edema 90, 93 free induction decay (FID) signal 1 gadolinium contrast agents 5–7, 66, 90 adverse reactions 13 glomerular filtration rate 94 gradient-echo (SE) pulse sequence 2, 77 hand-grasp exercise, phase-velocity mapping 38 heart, apex 71, 76 helical CTA 95 hematoma, intramural 26, 28 hippurate, in isotope renography 94 hyperlipidemia 112 carotid artery disease 44 peripheral vascular disease 102, 112 hypertension carotid artery disease 44 peripheral vascular disease 102, 105, 106, 109, 112 renal artery stenosis 89–98 iliac vessels arteries 102 left 108, 111 right common, occlusion 108 stenosis 103, 108, 112 image formation 2–5 postprocessing 13, 15

Index

108

quality 5 image subtraction see digital subtraction angiography (DSA) imaging time, pulse sequences and 2 inflammatory disease, Takayasu arteritis 36, 40 infrainguinal vessels 102 innominate artery, dilated 23 instrumentation in MRI 7 interventricular sulcus 78 intimal damage 18, 19, 33 intravenous access for CE-MRA 9 isotope renography 94 jugular veins 17 juxtaductal stenosis 37 kidneys 90, 91, 92, 109 Larmor frequency xii limb ischemia 106, 108, 112 longitudinal-relaxation (spin-lattice/T1) xii, 4 lumens 26, 27 false 31, 112 thrombosed 27, 31 magnet types 7 magnetic field gradients 4, 6, 7 induction xii, 2 magnetic moment xii, 2 magnetic resonance angiography (MRA) 9–14 coronary arteries 70–84 peripheral vessels 102–12 pulmonary vessels 52–66 renal vessels 89–98 magnetic resonance imaging xii–4 magnetic resonance techniques aortic imaging 17–41 cardiac imaging 5 carotid artery imaging 46–8 magnetic spin xii malignancy, pulmonary 57, 59, 64 mammary arteries, internal 70, 82 Marfan syndrome 20 mercaptoacetyltriglycerine (MAG3) 94 mesenteric arteries 102 myocardial perfusion imaging 5, 7

Index navigator-gated sequences 71, 77 nephrotoxic contrast agents 77, 96 net magnetization xii, 2 nuclear scintigraphy, pulmonary embolism 66 peripheral vessels, MRA of 102–12 phase-contrast velocity mapping 39, 90 pilot scans 9, 10, 90 plethysmography 109 pulmonary arteries 52–66 dilatation 54, 64 enlargement 61 graft 56 occlusions 61 right 70 stenosis 56 Takayasu arteritis 59, 64 pulmonary edema, ‘flash’ 90, 93 pulmonary embolism 52, 56, 59 imaging 56, 59–60,66 pulmonary hypertension investigation 56 pulmonary vessel dilatation 64 thalassemia 56 pulmonary malignancy 57, 59, 64 pulmonary perfusion investigations 59–60 pulmonary veins 52–66 dilatation 64 pulmonary vessels, MRA of 52–66 pulse sequences, magnetic resonance signals 2 radiofrequency coils 7 radiofrequency pulse xii, 4, 7 radionuclide ventilation-perfusion scan 59–60 relaxation of nuclei xii–1 renal blood flow, isotope renography 94 renal bruit 91 renal function ACE inhibitors and 92, 98 renal artery stenosis and 89 renal ischemia 94 renal transplant, MRA monitoring 98 renal vessels 89–98 arteries 89, 90, 91, 94, 102, 103, 105, 109 displacement 106 left, stenosis 91, 92, 98, 108 right 92 stenosis 92

109

Index stenosis 90–8 renin, plasma measurements 94 respiratory motion, in imaging 53, 71, 77 right ventricle, dilated and hypertrophied 53, 54 sagittal plane, pulmonary imaging 56 saphenous vein grafts 72, 75, 84 scanning time 4, 56, 103 scleroderma, pulmonary vessels 64 shielding, in magnetization 8 sinus of Valsalva 71, 76, 78, 79 slice selection, image formation 4, 5 smoking carotid artery disease and 44 hypertension and 94 peripheral vascular disease and 102, 112 spatial encoding, image formation 4 spatial resolution (voxel size) 4, 9 spin-echo (SE) pulse sequence 2, 77 spin-lattice (longitudinal-relaxation/Tl) xii, 4 spin-spin (transverse-relaxation/T2) xii–1 spiral CT, pulmonary embolism 66 static magnetic field xii, 1, 2 stents 77, 97, 98 stroke risk factors 45–9 subclavian vessels 17 arteries left 35 dilated 24 occluded 36, 39 right, stenosis 37 sudden death, in exercise 73 T1 longitudinal relaxation time xii, 4–5 T2 transverse relaxation time xii–1, 4–5 Takayasu arteritis 36, 40 pulmonary 59, 62 thalassemia, pulmonary hypertension 56 thoracic aorta 9–15, 17 descending 23, 31 dissection 31–3 false lumen 14 proximal 33 thoracic artery, internal 102 three-dimensional image formation 5, 7 three-dimensional MRA, renal arteries 97 thrombus in coronary artery bypass graft 70 in lumen 28, 31

110

Index

111

in right ventricle 54 see also pulmonary embolism tibial vessels 102, 112 ‘time-of-flight’ (TOF) imaging 46, 103 timing scans see ‘bolus chase’ techniques transverse-relaxation (spin-spin/T2) xii–1 two-dimensional images 4, 46, 103 two-dimensional MRA 72, 74 ultrasmall superparamagnetic iron oxide particles 7 Valsalva, sinus of 71, 76, 78, 79 vascular enhancement, time of 9, 11 vascular occlusion, peripheral vessels 102 vascular stenosis, peripheral vessels 102, 104, 108, 112 ventilation-perfusion scan 59–60 ventricular outflow tract 80 vertebral artery 102 vertebral steal syndrome 40 voxel size (spatial resolution) 4 white blood gradient-echo sequences 77 X-ray, chest, pulmonary embolism 59 X-ray angiography benefits and risks 46, 48, 49, 72 coronary 72 peripheral vessels 102, 108 pulmonary embolism 66 renal vessels 94, 97 X-ray cardiac catheterization 76

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