coronary heart disease - clin., pathol., imaging, molec. profiles - z. vlodaver, et. al., (springer, 2012)

Coronary Heart Disease



Zeev Vlodaver    Robert F. Wilson    Daniel J. Garry
●

●

Editors

Coronary Heart Disease
Clinical, Pathological, Imaging, and Molecular Profiles


Editors
Zeev Vlodaver
Division of Cardiovascular Medicine
University of Minnesota
Minneapolis, MN, USA


Robert F. Wilson
Division of Cardiovascular Medicine
University of Minnesota
Minneapolis, MN, USA


Daniel J. Garry
Division of Cardiovascular Medicine

University of Minnesota
Minneapolis, MN, USA


ISBN 978-1-4614-1474-2
e-ISBN 978-1-4614-1475-9
DOI 10.1007/978-1-4614-1475-9
Springer New York Dordrecht Heidelberg London
Library of Congress Control Number: 2011943085
© Springer Science+Business Media, LLC 2012
All rights reserved. This work may not be translated or copied in whole or in part without the written permission of the publisher (Springer Science+Business
Media, LLC, 233 Spring Street, New York, NY 10013, USA), except for brief excerpts in connection with reviews or scholarly analysis. Use in connection
with any form of information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter
developed is forbidden.
The use in this publication of trade names, trademarks, service marks, and similar terms, even if they are not identified as such, is not to be taken as an
expression of opinion as to whether or not they are subject to proprietary rights.
While the advice and information in this book are believed to be true and accurate at the date of going to press, neither the authors nor the editors nor the
publisher can accept any legal responsibility for any errors or omissions that may be made. The publisher makes no warranty, express or implied, with
respect to the material contained herein.
Printed on acid-free paper
Springer is part of Springer Science+Business Media (www.springer.com)


This book is dedicated to our wives
Dalia P. Viodaver
Betsy Wilson
Mary G. Garry
For their encouragement, devotion and support.

Preface

Coronary Heart Disease
Clinical, Pathological, Imaging, and Molecular Profiles
This book will present a comprehensive picture of ischemic heart disease to those who, either as practitioners, students or
investigators, deal with the varied facets of this complex subject. It has meaning to the fields of clinical cardiology, thoracic
surgery, pathology, and cardiovascular molecular research.
After introductory chapters on the anatomy of the coronary blood vessels and cardiac development, several chapters
will consider stress echo and nuclear diagnostics tests, noninvasive imaging and coronary angiography in ischemic heart
disease, with techniques, indications, and examples of normal and abnormal patterns. In most instances, angiograms are
paired with labeled line drawings, which help the initiated in the reading of films. Specific chapters will deal with congenital anomalies of the coronary arteries, which may engender states of ischemic heart disease.
The principal thrust of the work concerns the main arena of ischemic heart disease, namely, coronary atherosclerosis.
The pathology of coronary atherosclerosis will be presented in conjunction with the results of anatomic, noninvasive imaging and angiographic studies. Related chapters on atherogenesis will present new insights into the pathophysiology of the
vulnerable plaque, role of progenitor cells in vascular injury, inflammation and atherogenesis, and genomics of vascular
remodeling.
Major chapters will discuss the subject of angina pectoris, acute coronary syndromes, healed myocardial infarction and
congestive heart failure, catheter-based and surgical revascularization, and surgical treatment of myocardial infarction and
its sequelae. Final chapters will present therapies for refractory angina; metabolic syndromes and coronary heart disease;
coronary heart disease in women; and prevention and regression of atherosclerosis.
What is unique in this book is that many of the chapters will be case material from which profiles of the various manifestations are obtained through correlation of clinical, imaging, and pathological studies. The quality of the authors’ contribution to this book will provide an immense depth to the book as they have hands on experience and are national leaders
in their field of cardiac pathology, clinical cardiology, and cardiovascular molecular research. This book will present a
comprehensive and real picture of the complexities of ischemic heart disease, both to the practitioners, who deal with it in
day-to-day practice with its problems, and to the students, residents, and investigators who try to develop firm concepts
regarding the varied states observed in this common condition and preparing them to the future advances in coronary heart
disease.
Minneapolis, MN, USA
Minneapolis, MN, USA
Minneapolis, MN, USA

Zeev Vlodaver, M.D.
Robert F. Wilson, M.D.
Daniel J. Garry, M.D., Ph.D.

vii



Acknowledgments

We wish to recognize four pillars of medical science whose important contributions to cardiovascular medicine are
reflected in our book.
To Jesse E. Edwards, MD, a world-renowned, pioneering, and leading cardiac pathologist who had an extraordinary
passion for teaching. He was professor of pathology at the Mayo Clinic in Rochester, Minn., and at the University of
Minnesota, Minneapolis. He taught many medical students, pathologists, cardiologists, cardiac surgeons, and visiting
medical experts from around the world. Dr. Edwards housed an enormous collection of autopsied hearts at United Hospital,
81. Paul, Minn., known as the Dr. Edwards' Cardiovascular Registry that became a principal resource for his illustrated
reference books: "An Atlas of Acquired Diseases of the Heart and Great Vessels" (1961), and "Congenital Heart Disease"
(1965). He also co-authored nearly 800 journal articles and 14 books. Dr. Vlodaver pays special acknowledgment to Dr.
Edwards who was his teacher, mentor and "inspirational force in his medical life." He died in 2008 at the age of 96.
C. Walton Lillehei, MD, world-renowned as the "Father of Open-Heart Surgery," was professor of surgery at the
University of Minnesota. In 1952, he participated in the world's first successful open-heart operation using hypothermia,
performed at the University of Minnesota, and in1954, he performed the world's first open-heart surgery using cross-circulation. In 1958, Dr. Lillehei was responsible for the world's first use of a small, portable, battery-powered pacemaker;
he also developed and implanted the world's first prosthetic valve in1966. Thousands of cardiac surgeons over the world
are indebted to Dr. Lillehei for his monumental contributions. Dr. Lillehei died in 1999 at the age of 80.
Kurt Amplatz, MD, professor of radiology for more than 40 years at the University of Minnesota, retired in 1999.
A  pioneer in cardiovascular interventional radiology, he is well known for his many inventions which bridged medical
disciplines and included devices such as high-resolution x-ray equipment, heparin-coated wires, specially shaped cardiac
catheters, and vascular occlusive devices. Although retired, he continues to improve patients' lives through the development
of new technologies.

Howard B. Burchell, MD, cardiologist, professor of medicine at the Mayo Clinic in Rochester and chief of cardiology
at the University of Minnesota. He was editor-in-chief of the journal Circulation from 1965-1970, a tenure marked by rapid
advances in cardiac pacing and electrophysiology. Teaching and writing with a central theme of sound scientific evidence
were hallmarks of Dr. Burchell's career. He passed We also extendour gratitude to the manyspecialists who have contributed generously to this bookwith considerable experience in their specialty areas.
We acknowledge and thankJane Hutchins-Peterson, Stephanie Esperson and Andrea Silverman for their outstanding
help and for handling the flow of material from the writers to the publisher.
We recognize with deepappreciation Barb Umbergerfor her dedication in the editing of the manuscript in the minutestdetail to ensurethe high quality of this project.
Our sincere thanks to Howard Gillbert for his invaluable illustrations and other artwork.
Our gratitude to Michael Griffin, developmental editor, Springer Publishing, for his tireless and utmost attention to all
details needed for the production of the book.
We wish to acknowledge the supportof and encouragement by Andrew Moyer, Senior Editor of Clinical Medicine, at
Springer, and his predecessors Melissa Ramondetta and Frances Louie, for their enthusiasm for this projectin bringing it
to reality.
Minneapolis, MN, USA
Minneapolis, MN, USA
Minneapolis, MN, USA

Zeev Vlodaver, M.D.
Robert F. Wilson, M.D.
Daniel J. Garry, M.D., Ph.D

ix



Contents

  1  Anatomy of Coronary Vessels...............................................................................................................................
Zeev Vlodaver and John R. Lesser

1

  2  Cardiac Development and Congenital Heart Disease........................................................................................
.
Jamie L. Lohr, Cindy M. Martin, and Daniel J. Garry

19

  3  Echocardiographic Evaluation of Ischemic Heart Disease................................................................................
Richard W. Asinger, Fouad A. Bachour, and Gautam R. Shroff

43

  4  Nuclear Imaging in Ischemic Heart Disease. ......................................................................................................
.
Sharmila Dorbala and Marcelo F. Di Carli

63

  5  Noninvasive Coronary Artery Imaging with CT and MRI................................................................................
Marc C. Newell, Robert S. Schwartz, and John R. Lesser

83

  6  Catheter-Based Coronary Angiography..............................................................................................................
Robert F. Wilson and Zeev Vlodaver

97

  7  Coronary Artery Anomalies................................................................................................................................. 125

Thomas Knickelbine, Michael Bolooki, and Zeev Vlodaver
  8  Pathology of Chronic Obstructive Coronary Disease......................................................................................... 159
Zeev Vlodaver
  9  Vulnerable Plaque.................................................................................................................................................. 187
Masataka Nakano, Frank D. Kolodgie, Fumiyuki Otsuka, Saami K. Yazdani,
Elena R. Ladich, and Renu Virmani
10  Genetics and Coronary Heart Disease................................................................................................................. 199
Jennifer L. Hall, Ryan J. Palacio, and Eric M. Meslin
11  Endothelium Biology............................................................................................................................................. 219
Michael Sean McMurtry and Evangelos D. Michelakis
12  Stem Cells and Atherosclerosis............................................................................................................................. 239
Jay H. Traverse
13  Induced Pluripotential Stem Cells and the Prospects for Cardiac Cell Therapy............................................ 249
Jonathan M.W. Slack and James R. Dutton
14  Regulation of Vasculogenesis and Angiogenesis. ................................................................................................ 261
.
Rita C.R. Perlingeiro
15  Chronic Stable Angina.......................................................................................................................................... 271
Santiago Garcia and Edward O. McFalls

xi


xii

Contents

16  Pathology of Sudden Death in Coronary Arterial Diseases................................................................................. 291
Shannon M. Mackey-Bojack, Emily R. Duncanson, and Susan J. Roe
17  Acute Coronary Syndromes.................................................................................................................................... 307

Robert F. Wilson
18  Complications of Acute Myocardial Infarction.................................................................................................... 321
.
Zeev Vlodaver and Robert F. Wilson
19  Healed Myocardial Infarction................................................................................................................................ 349
.
Gary S. Francis and Daniel J. Garry
20  Nonatherosclerotic Ischemic Heart Disease.......................................................................................................... 365
Uma S. Valeti, Robert F. Wilson, and Zeev Vlodaver
21  Transcatheter Treatment of Coronary Artery Disease........................................................................................ 389
.
Robert F. Wilson
22  Surgical Treatment of Coronary Artery Disease.................................................................................................. 405
Kenneth Liao
23  Noncoronary Surgical Therapy for Ischemic Heart Disease............................................................................... 423
Christopher B. Komanapalli, Balaji Krishnan, and Ranjit John
24  Refractory Angina................................................................................................................................................... 431
Mohammad Sarraf, Daniel J. Hellrung, and Timothy D. Henry
25  Acute Catheter-Based Mechanical Circulatory Support..................................................................................... 445
Gladwin S. Das, Ganesh Raveendran, and Jason C. Schultz
26  Surgical Mechanical Circulatory Support............................................................................................................ 455
.
Forum Kamdar and Ranjit John
27  Diabetes and Coronary Heart Disease................................................................................................................... 471
Graham T. McMahon
28  Cardiovascular Disease in Women......................................................................................................................... 485
Margo Tolins-Mejia
29  Prevention of Coronary Artery Disease................................................................................................................. 497
Daniel Duprez
30  Innovations in Twenty-First Century Cardiovascular Medicine........................................................................ 509

.
Mary G. Garry, Joseph M. Metzger, Xiaozhong Shi, and Daniel J. Garry
Index.................................................................................................................................................................................. 525


Contributors

Richard W. Asinger, MD  Department of Medicine, Hennepin County Medical Center, Minneapolis, MN, USA
Fouad A. Bachour, MD, FSCA1  Department of Medicine, Hennepin County Medical Center,
Minneapolis, MN, USA
Michael Bolooki, MD  University of Minnesota, Minneapolis, MN, USA
Marcelo F. Di Carli, MD,FACC  Chief, Division of Nuclear Medicine and Molecular Imaging,
Department of Radiology and Medicine, Brigham and Women’s Hospital, Boston, MA, USA
Gladwin S. Das, MD  Cardiovascular Division, University of Minnesota, Minneapolis, MN, USA
Sharmila Dorbala, MD, MPH  Division of Nuclear Medicine and Molecular Imaging, Department of Radiology,
Brigham and Women’s Hospital, Boston, MA, USA
Emily R. Duncanson, MD  Department of Jesse E. Edwards Registry of Cardiovascular Disease, United Hospital,
St. Paul, MN, USA
Daniel Duprez, MD, PhD  Cardiovascular Division, University of Minnesota, Minneapolis, MN, USA
James R. Dutton, BSc, PhD  Stem Cell Institute, University of Minnesota, Minneapolis, MN, USA
Gary S. Francis, MD  Division of Cardiovascular Medicine, University of Minnesota, Minneapolis, MN, USA
Santiago Garcia, MD  Department of Cardiology, University of Minnesota, Minneapolis VA Medical Center,
Minneapolis, MN, USA
Daniel J. Garry, MD, PhD  Division of Cardiovascular Medicine, University of Minnesota, Minneapolis, MN, USA
Mary G. Garry, PhD  Lillehei Heart Institute, University of Minnesota, Minneapolis, MN, USA
Daniel J. Hellrung, DO, PhD  Mercy Hospital, Department of Internal Medicine, Coon Rapids, MN, USA
Timothy D. Henry, MD  Minneapolis Heart Institute Foundation, Minneapolis, MN, USA
Jamie L. Lohr, MD  Division of Pediatric Cardiology, University of Minnesota Amplatz Children’s Hospital,
Minneapolis, MN, USA
Joseph M. Metzger, PhD  Department of Integrative Biology and Physiology, University of Minnesota,

Minneapolis, MN, USA
Xiaozhong Shi, PhD  Lillehei Heart Institute, University of Minnesota, Minneapolis, MN, USA
Jennifer L. Hall, PhD  Department of Medicine, Lillehei Heart Institute, University of Minnesota,
Minneapolis, MN, USA
Ranjit John, MD  Division of Cardiothoracic Surgery, University of Minnesota Medical Center–Fairview,
Minneapolis, MN, USA
Forum Kamdar, MD  Cardiology Fellow, University of Minnesota, MN, USA

xiii


xiv

Contributors

Thomas Knickelbine, MD, FACC, FSCAI  Minneapolis Heart Institute, Minneapolis, MN, USA
Frank D. Kolodgie, PhD  CVPath Institute, Gaithersburg, MD, USA
Christopher B. Komanapalli, MD  Surgery, Division of Cardiovascular and Thoracic Surgery,
University of Minnesota Medical Center–Fairview, Minneapolis, MN, USA
Balaji Krishnan, MD, MS  Department of Medicine, Division of Cardiovascular Medicine, University of Minnesota
Medical Center–Fairview, Minneapolis, MN, USA
Elena R. Ladich, MD  CVPath Institute, Gaithersburg, MD, USA
John R. Lesser, MD  Department of Cardiology, Minneapolis Heart Institute, Abbott Northwestern Hospital,
Minneapolis, MN, USA
Department of Cardiology, Minneapolis, MN, USA
Kenneth Liao, MD, PhD  University of Minnesota, Minneapolis, MN, USA
Shannon M. Mackey-Bojack, MD  Department of Jesse E. Edwards Registry of Cardiovascular
Disease, United Hospital, St. Paul, MN, USA
Cindy M. Martin, MD  Division of Cardiovascular Medicine, University of Minnesota,
Minneapolis, MN, USA

Edward O. McFalls, MD, PhD  Department of Cardiology, University of Minnesota, Minneapolis, VA Medical Center,
Professor of Medicine, Minneapolis, MN, USA
Graham T. McMahon, MD, MMSc  Division of Endocrinology, Harvard Medical School,
Diabetes and Hypertension, Brigham and Women’s Hospital, Boston, MA, USA
Michael Sean McMurtry, BASc, MD, PhD  Department of Medicine, University of Alberta Hospital,
Edmonton, AB, Canada
Eric M. Meslin, PhD  Indiana University School of Medicine, Indianapolis, IN, USA
Evangelos D. Michelakis, MD, PhD  Department of Medicine, University of Alberta, Edmonton, AB, Canada
Masataka Nakano, MD  CVPath Institute, Gaithersburg, MD, USA
Marc C. Newell, MD  Minneapolis Heart Institute, Abbott Northwestern Hospital, MHI Cardiology,
Minneapolis, MN, USA
Fumiyuki Otsuka, MD  CVPath Institute, Gaithersburg, MD, USA
Ryan J. Palacio, BA  Department of Anesthesiology, University of Minnesota Medical School, Minneapolis, MN, USA
Rita C.R. Perlingeiro, PhD, MSc, BSc  Lillehei Heart Institute, Department of Medicine, University of Minnesota,
Minneapolis, MN, USA
Ganesh Raveendran, MD  Cardiovascular Division, University of Minnesota, Minneapolis, MN, USA
Susan J. Roe, MD  Department of Jesse E. Edwards Registry of Cardiovascular Disease, United Hospital,
St. Paul, MN, USA
Mohammad Sarraf, MD  Cardiovascular Division, University of Minnesota Hospital, Minneapolis, MN, USA
Jason C. Schultz, MD  University of Minnesota Medical Center-Fairview and Minnesota
Cardiovascular Division, Minneapolis, MN, USA
Robert S. Schwartz, MD  Minneapolis Heart Institute, Minneapolis, MN, USA
Gautam R. Shroff, MBBS  Department of Medicine, Hennepin County Medical Center, Minneapolis, MN, USA
Jonathan M.W. Slack, MA, PhD  Stem Cell Institute, University of Minnesota, Minneapolis, MN, USA
Margo Tolins-Mejia, MD, FACC  Department of Cardiology, Mercy/Unity Medical Centers, Minneapolis, MN, USA


Contributors

xv

Jay H. Traverse, MD  Department of Cardiology, University of Minnesota Medical School, Minneapolis Heart Institute at
Abbott Northwestern Hospital, Minneapolis, MN, USA
Uma S. Valeti, MD, FACC  Cardiovascular Division, Department of Medicine, University of Minnesota,
Minneapolis, MN, USA
Renu Virmani, MD  CVPath Institute, Gaithersburg, MD, USA
Zeev Vlodaver, MD  Division of Cardiovascular Medicine, University of Minnesota, Minneapolis, MN, USA
Robert F. Wilson, MD  Division of Cardiovascular Medicine, University of Minnesota,
Minneapolis, MN, USA
Saami K. Yazdani, PhD  CVPath Institute, Gaithersburg, MD, USA



Chapter 1

Anatomy of Coronary Vessels
Zeev Vlodaver and John R. Lesser

Anatomy of the Coronary Vessels
In the normal heart, oxygenated blood is supplied by two coronary arteries that form the first branches of the aorta. The
origin of the left and right coronary arteries from the aorta is through their ostia positioned in the left and right aortic
sinuses of Valsalva, located just distal to the right and left aortic cusps, respectively, of the aortic valve.
In about half of the population, a third artery, the conus artery (CA), also originates from the aorta. Diagrams of the
main coronary arteries and their important branches are shown in Fig. 1.1.
In addition, there are two types of cardiac veins: (1) the large veins, which run in the epicardium and terminate in the
coronary sinus (CS), and (2) the thebesian veins, small “tributary veins” which terminate directly in either the left atrium
(LA) or right atrium (RA).

Left Coronary Arterial System
Left Main Coronary Artery

The left main coronary artery (LM) branches from the upper part of the aortic sinus and runs toward the left, under the LA
appendage. After a short course, the LM branches into two vessels: the left anterior descending coronary artery (LAD) and
the left circumflex artery (CX) (Figs. 1.2 and 1.3).
The LM is most often 0.5–1.5 cm long; when it is less than 0.5 mm long, it is considered to be short. Angiographic
measurements of coronary length are probably less accurate than postmortem pathologic studies, due to underestimation
of the effects of rotation, angulation, and foreshortening.
In some hearts, the LM exhibits a trifurcation at its origin instead of the usual bifurcation. This third artery, termed
ramus intermedius (RI) or ramus diagonalis, acts functionally as a circumflex artery, supplying a portion of the obtuse
margin of the heart (Figs. 1.4 and 1.5).

Anterior Descending Coronary Artery
The LAD runs in the anterior interventricular sulcus, usually as a direct continuation of the LM, and extends toward the
apex, terminating in the apical part of the crux (Figs. 1.6 and 1.7).

Z. Vlodaver, MD ( )
Division of Cardiovascular Medicine, University of Minnesota, Minneapolis, MN, USA
e-mail:
J.R. Lesser
Department of Cardiology, Minneapolis Heart Institute, Abbott Northwestern Hospital, Minneapolis, MN, USA
Z. Vlodaver et al. (eds.), Coronary Heart Disease: Clinical, Pathological, Imaging, and Molecular Profiles,
DOI 10.1007/978-1-4614-1475-9_1, © Springer Science+Business Media, LLC 2012

1


2
Fig. 1.1 Diagrams of the
main coronary arteries and
their branches as seen from
the anterior (a) and posterior

(b) aspects of the heart. This
illustration shows the
common phenomenon in
which the right posterior
descending artery (RPDA)
arises from the terminal
branch of the right coronary
artery (RCA)

Fig. 1.2 Volume-rendered
image shows the left main
coronary artery (LM) arising
from the aorta and bifurcating
into the left anterior
descending (LAD) and
circumflex (CX) arteries
and their branches

Fig. 1.3 LC arteriogram
in the right anterior oblique
(RAO) view showing the
classic distribution of the left
coronary arterial system

Z. Vlodaver and J.R. Lesser


1

Anatomy of Coronary Vessels

Fig. 1.4 Gross specimen of
a portion of the aortic wall,
the left main coronary artery
(LM) proceeding from it, and
branches of the LM. The LM
measured 1.6 cm, which is
normal. The branching is
unusual because there is
trifurcation of the LM into
the left anterior descending
artery (LAD), circumflex
artery (CX), and a large
branch ramus intermedius.
The branch from the upper
aspect of the CX is an atrial
branch. The lower two
branches of the CX are
obtuse marginal branches
(OMs)

Fig. 1.5 Volume-rendered
image shows the ramus
intermediate branch arising
between the left anterior
descending artery (LAD)
and circumflex artery (CX),
resulting in trifurcation
of the LM

Fig. 1.6 Volume-rendered
image illustrating the left
anterior descending artery
(LAD) and two diagonal
branches arising from the left
aspect of the artery and
coursing over the left anterior
aspect of the left ventricle

3


4

Z. Vlodaver and J.R. Lesser

Fig. 1.7 Multidetector
computed tomography
angiography, long axis view,
illustrating a septal branch
of the left anterior descending
artery (LAD) which
penetrates the basal aspect
of the ventricular septum
anteriorly

The common branches of the LAD, proximally to distally, are (1) the septal branch (SB), which penetrates the basal
aspect of the ventricular septum anteriorly (Fig. 1.7), and (2) one or more diagonal branches (Diag Bs), one proximal to the
other, which arise from the left aspect of the LAD and course over the left anterior aspect of the LV. If two Diag Bs are
present, the larger is usually first. In some cases, the width of the first Diag B may be equal to or exceed that of the LAD.

Left Circumflex Coronary Artery
The CX is one of the LM’s two terminal branches. It arises at a sharp angle from the left side of the LM and courses forward
under the LA appendage to enter the left atrioventricular (AV) sulcus, a position corresponding to the base of the mitral
valve (Fig. 1.2).
Considerable variations occur in the course of the CX. In some instances, the artery terminates at the obtuse marginal
branch (OM), which runs from the AV sulcus toward the apex along the lateral wall of the left ventricle (LV).
In other instances, the CX, after giving off the OM, continues in the left atrioventricular sulcus and terminates near the
base of the crux, given off atrial branches and, occasionally, the sino-atrial branch.
Unusually Long Left Main Coronary Artery
According to Lewis et al., the length of the LM in 25 patients selected at random from a series of 354 arteriograms ranged
from 7.5 to 20.5 mm (M = 12.8 mm) [1]. These findings are similar to those reported from the pathological studies of Baroldi
and Scomazzoni [2].
Figure 1.8 depicts the features of an unusually long LM.
Short Left Main Coronary Artery
The practical significance of a short LM is that it may complicate perfusion of the left coronary arterial system during operative procedures, as in aortic valve replacement. Especially with a short LM and despite apparent optimal placement, the
cannula may perfuse either the LAD or the CX, but not both, causing myocardial ischemia with resulting ventricular
arrhythmias, myocardial infarct, or both.
Furlong et al. [3] observed that the angle of bifurcation of the LM is increased when LVH is present, as a result of upward
displacement of the CX. This process may accentuate the problem of cannulating the left system when the main artery is
short [3]. Figure 1.9 illustrates coronary angiographic features of a short LM.
A coronary artery is considered “short” when its intrinsic structure is uniformly narrow and it has a shorter course than
usual. When a short artery is present, the region of the heart usually supplied by this artery is perfused through branches from
the other coronary arteries. As a rule, only one of the coronary arteries is short – either the right or a branch of the left.
In the absence of other disease, a short artery is functionally insignificant.


1

Anatomy of Coronary Vessels

5

Fig. 1.8 LC arteriogram in the anterior posterior (AP) view showing a long LM, measuring approximately 30 mm

Fig. 1.9 LC arteriogram in RAO view showing a short LM

It should be recognized, however, that during both arteriography and surgery, it has been difficult to determine whether
a narrow artery harbors disease or is congenital.

Short Left Anterior Descending Artery
Figure 1.10 shows a coronary arteriogram for a 44-year-old man with hypercholesterolemia. The arteriogram showed a large
CX, while the LAD was short and terminated in small branches.

Short Circumflex Artery
Figures 1.11 and 1.12 pertain to a 10-year-old asymptomatic girl with familial hyperlipidemia. The ECG was normal.
Coronary arteriography showed no lesions, and only two indistinct short vessels were noted in the anticipated location of
the CX.


6

Z. Vlodaver and J.R. Lesser

Fig. 1.10 Arteriogram in a lateral view showing a left coronary artery with a short left anterior descending artery (LAD)

Fig. 1.11 RAO view of LC arteriogram shows a short circumflex artery (CX) leaving the left AV groove shortly after its origin and dividing into
two obtuse marginal branches (OMs)

Fig. 1.12 Left anterior oblique (LAO) view of RC arteriogram shows unusual preponderance of the RCA. This artery continues in the atrioventricular (AV) groove toward the left ventricle (LV)

1

Anatomy of Coronary Vessels

7

Right Coronary Arterial System
The right coronary artery (RCA) arises from the upper part of the right aortic sinus; as it leaves the aorta, it points somewhat
anteriorly and proceeds toward the right, between the pulmonary artery to its left and the right atrium to its right, to enter
the right AV sulcus. It then passes along the right AV sulcus past the acute margin of the heart to the base of the posterior
(post) interventricular sulcus (the “crux”).
The RV terminates at the crux about 10% of the time [4], but it is far more common for the artery to form a sharp
U-shaped turn, and continue in the crux toward the cardiac apex as the right posterior descending artery (RPDA).
Several branches of the RCA have been given names. The conus artery (CA), when it does not begin from the aorta,
appears as the first branch of the RCA and supplies the right ventricular infundibulum. Usually (about 55% of the time), the
next major branch arising from the RCA is the sinus node artery (SA), which runs posterior to the RA appendage and proceeds upward toward the junction of the superior vena cava (SVC) and the RA [5]. In its course, the sinus node artery supplies branches to the RA. Past the origin of the SA, another right atria branch usually arises, often called the mid-right atrial
branch (MRAB).
The RCA also gives off two or more branches to the free wall of the right ventricle (RV), the muscular branches (MuBs).
The largest branch of the RCA runs along the acute margin of the RV. Called the acute marginal branch (AC Marg), it supplies the anterior and diaphragmatic wall of the RV.
In many hearts, the RCA terminates as the RPDA. However, it is also common for the RCA to terminate by dividing into
two branches: the RPDA and a right posterior atrioventricular branch (RPAV). The latter courses in the left AV sulcus for varying
distances and then proceeds over the lateral wall of the LV, where it terminates. In some cases, an accessory posterior descending
artery (LPDA) originates from the RPAV and courses over the diaphragmatic surface of the LV from its base toward the apex.
The artery of the AV node, the so-called nodal artery (NA), usually arises from the RCA just proximal to the origin of
the PDA. It proceeds upward to penetrate the atrial septum for supplying the AV node.
All of the classic branches of the RCA are illustrated in Figs. 1.13–1.15.

Short Nondominant Right Coronary Artery

The term “short nondominant RCA” characterizes an unusually short course of this artery: one that’s only a few millimeters
in length and does not reach the region of the crux. Figure 1.16 shows a diagram of a short nondominant RCA. Figure 1.17a,
b pertains to a woman who died of obstructive biliary tract disease. The RCA was small and did not reach the right cardiac
margin. Figure 1.18 shows a short nondominant RCA as seen in volume-rendering techniques with cardiac computed
tomography angiography (VRT–CCTA). Images in Figs. 1.19 and 1.20 are from a 58-year-old woman with atypical chest
pain. Coronary arteriography showed a short and narrow RCA, but no obstructive lesions.

Fig. 1.13 Volume-rendered
image in RAO orientation
portrays all classical branches
of the right coronary artery
(RCA)


Fig. 1.14 RC arteriogram in RAO, which branches as indicated. Beyond the origin of the posterior descending artery (PDA) is a prominent right
posterolateral (RPL) branch extending to the lateral wall. In this example, the conus artery (CA) arises from the right coronary artery (RCA)

Fig. 1.15 Volume-rendered image, lateral wall of the RV, showing the RCA and its branches

Fig. 1.16 Diagram of a short nondominant right coronary artery (RCA)