Atlas of Contrast Enhanced Angiography

An Atlas of CONTRAST-ENHANCED
ANGIOGRAPHY
THE ENCYCLOPEDIA OF VISUAL MEDICINE SERIES
An Atlas of CONTRAST-
ENHANCED 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
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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
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First published in 2003

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Composition by The Parthenon Publishing Group
Contents
Foreword ix
Preface xi
Acknowledgements xii
1 Introduction and methods 1

2 Principles of magnetic resonance angiography 10
3 Magentic resonance of the aorta 18
4 Carotid artery disease 39
5 Magnetic resonance angiography of the pulmonary vessels 46
6 Magnetic resonance angiography of the coronary arteries 62
7 Magnetic resonance angiography of the renal vessels 79
8 Magnetic resonance angiography of the peripheral vessels 91
Conclusion 102
Index 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 anti-
parallel 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
Cerebrospinal fluid >4000 >2000
Blood 1200 300
Myocardium 850 60
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 read-
out 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 pre-
pulses can be used with both SE and GRE sequences to produce an image that is more
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
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
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 (frequency-
encoding 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 signal-
to-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 ‘first-
pass’ 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
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-
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.
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 k-
space2. 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).
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
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 three-
dimensional 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.
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 un-
enhanced 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.
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
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
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 non-
enhanced 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, Ehlers-
Danlos 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
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
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
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
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
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
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.
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))
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
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.
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
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
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
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 late-
phase 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))
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
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
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)
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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 gadolinium-
enhanced 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
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;
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9. Marsalese DL, Moodie DS, Lytle BW, et al. Cystic medial necrosis of the aorta in
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Coll Cardiol 1990; 16:68–73
10. Coselli JS, Buket S, Djukanovic B. Aortic arch operation: current treatment and
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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.
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 41
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 contrast-
enhancement 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
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
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.
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.
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308:81–106
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7
18. Gagne PJ, Matchett J, MacFarland D, et al. Can the NASCET technique for
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select candidates with recently symptomatic carotid stenosis for surgery: systematic
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distribution of an asymptomatic carotid artery. Lancet 1995; 345:209–12
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effect of carotid endarterectomy in symptomatic patients with high-grade carotid
stenosis. N Engl J Med 1991; 325:445–53
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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 47
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
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
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 three-
dimensional 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
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 life-
saving anticoagulation and possible thrombolysis.
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
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
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)
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
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
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
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.
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.
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6
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 63
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 three-
dimensional 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 breath-
hold 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
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
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 slit-
like 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.
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.
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.
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 X-
ray 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 coro-
nary 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
With navigator-gated sequences, it has become possible to obtain large-volume high-

resolution 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
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
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 non-
vascular 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 CE-
MRCA. 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
Figure 6.9 The same patient as in Figures 6.7 and 6.8 in transverse section
operation in 1994, presented with chest pain. Magnetic resonance
angiography demonstrates that the proximal part of the left internal
mammary artery graft is patent
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
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)
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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14. Brenner P, Wintersperger B, Von Smekal A, et al. detection of coronary artery bypass
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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.
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 T2-
weighted 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.
Magnetic resonance angiography of the renal vessels 81
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
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
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
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
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.
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.
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
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
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
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-
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 CE-
MRA, 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,
Magnetic resonance angiography of the peripheral vessels 93
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.
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
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 in-
patients over 65 years old. The natural history of the disease is that two-thirds to three-
quarters 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 non-
invasive 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 blood-
pressure control. If patients are stage III or stage IV, then angioplasty or surgery may be
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
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
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)
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
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
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 gadolinium-
enhanced 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
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
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-in-
progress. 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 short-
term 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 105
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

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 109
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
Index 110
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
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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Atlas of Contrast Enhanced Angiography

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An Atlas of CONTRAST-ENHANCED

Professor Sir Magdi Yacoub

The Parthenon Publishing Group

ISBN 0-203-00891-X Master e-book ISBN

ISBN - (Adobe e-Reader Format)

First published in 2003

1 Introduction and methods 1

Decision-making in surgery of the aorta and peripheral vessels is almost totally

Magnetic resonance of the cardiovascular system is a rapidly developing technique that

STATIC MAGNETIC FIELD

energy during collisions. The return of Mz to normal occurs in an exponential manner,

substance is a solid or a liquid and the presence of macromolecules. Although T2 is

To obtain a magnetic resonance image, it is necessary to spatially encode a signal to

location of nuclei in a structure. Two processes occur—slice selection and spatial

MAGNETIC RESONANCE CONTRAST AGENTS

The contrast agents used in magnetic resonance are either paramagnetic or

Figure 1.7 In order to obtain a magnetic resonance image, it is necessary to

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

1. Prince MR. Gadolinium-enhanced MR aortography. Radiology1994; 191:155–64

PRACTICAL MAGNETIC RESONANCE ANGIOGRAPHY

Optimal enhancement of the vascular structure

Figure 2.2 To enable subsequent image reconstruction and three-dimensional

Time to vascular enhancement

The adverse effects of MRA

Figure 2.5 Because of the high temporal resolution of the gradient-echo

can be diagnosed and followed up by ultrasound, but, if surgical intervention is planned,

Aortic dissection is an uncommon but potentially fatal condition4, predominantly

Table 3.1 Commonly used classification systems to describe aortic dissection

Figure 3.1 Graphical representation of the classification systems used to

Figure 3.3 A 50-year-old man had a surgical repair of an aortic coarctation in

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

Figure 3.5 A 68-year-old man had a surgical repair of an aortic coarctation in

vessel or hemodynamic collapse with pericardial tamponade. Suggestive clinical signs in

Aortic coarctation is a congenital abnormality of the aorta that usually presents in

Figure 3.7 A 74-year-old woman with a history of hypertension presented with

Figure 3.16 Surface-rendered three-dimensional contrast-enhanced MRA in the

artery disease is uncertain.

IMAGING OF CAROTID ARTERY STENOSIS

Figure 4.2 A 72-year-old woman with coronary artery disease, awaiting

SURGICAL INTERVENTION FOR CAROTID ARTERY STENOSIS

artery stenosis. The Asymptomatic Carotid Atherosclerosis Study (ACAS) assessed

1. MacMahon S, Rodgers A. Blood pressure, antihypertensive treatment and stroke risk. J

Figure 5.1 A 77-year-old woman presented with swollen ankles and

Figure 5.2 A 60-year-old man was investigated for hypertension. Transthoracic

echocardiography or right ventricular angiography. MRA demonstrates dilated

History and clinical symptoms

lingula. The left upper pulmonary vein was not seen

evidence for an alternative diagnosis such as an acute myocardial infarction or a

demonstrates the occlusions

Figure 5.7 A 33-year-old woman was referred with a history of Takayasu’s

demonstrates dilatation of the central pulmonary arteries. The right lower

Figure 5.9 A 38-year-old woman with scleroderma and increasing

Figure 5.10 A 47-year-old man had a rhabdomyosarcoma removed from the

a local recurrence. On spin-echo imaging (b), there is a pedunculated mass

Initial treatment in patients with suspected or confirmed pulmonary embolism is

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

Magnetic resonance coronary angiography (MRCA) has been developed to overcome

either prospectively or retrospectively to limit data acquisition to periods with limited

ANOMALOUS CORONARY ARTERIES

arteries17,18. The importance of anomalous coronary arteries is due to their association

CORONARY ARTERY DISEASE

With navigator-gated sequences, it has become possible to obtain large-volume high-

CORONARY ARTERY BYPASS GRAFTS

tortuous aortic and subclavian arteries can be difficult.