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List of Contributors
STUDENT CONTRIBUTORS Patricia Challender Come, MD
Associate Professor of Medicine
Andrey V. Dolinko (MD 2016) Harvard Medical School
Joshua Drago (MD 2015) Cardiologist, Harvard Vanguard Medical
David B. Fischer (MD 2016) Associates
Boston, Massachusetts
P. Connor Johnson (MD 2015)
Zena L. Knight (MD 2015)
Mark A. Creager, MD
Michael T. Kuntz (MD 2015) Professor of Medicine
Jacob E. Lemieux, D.Phil. (MD 2015) Geisel School of Medicine at
Dartmouth
Diana M. López (MD 2016)
Director, Heart and Vascular Center
David Miranda (MD 2016)
Dartmouth-Hitchcock Medical Center
Morgan J. Prust (MD 2015) Lebanon, New Hampshire
Sruthi Renati (MD 2015)
Elizabeth Ryznar, MSc (MD 2015) G. William Dec, MD
Roman W. DeSanctis Professor of
Sarrah Shahawy (MD 2016)
Medicine
Jayme Wilder (MD 2015) Harvard Medical School
Chief (Emeritus), Cardiology Division
Massachusetts General Hospital
FACULTY CONTRIBUTORS Boston, Massachusetts
Elliott M. Antman, MD
Professor of Medicine Elazer R. Edelman, MD, PhD
Harvard Medical School Thomas D. and Virginia W. Cabot
Professor of Health Sciences and
Cardiovascular Division
Technology
Brigham and Women’s Hospital
Massachusetts Institute of Technology
Boston, Massachusetts
Director, Harvard–MIT Biomedical
Eugene Braunwald, MD (Foreword) Engineering Center
Distinguished Hersey Professor of Professor of Medicine
Medicine Harvard Medical School
Harvard Medical School Boston, Massachusetts
Founding Chairman, TIMI Study Group
Brigham and Women’s Hospital Michael A. Fifer, MD
Boston, Massachusetts Professor of Medicine
Harvard Medical School
David W. Brown, MD Director, Cardiac Catheterization
Associate Professor of Pediatrics Laboratory
Harvard Medical School Director, Hypertrophic Cardiomyopathy
Cardiology Division Program
Children’s Hospital Massachusetts General Hospital
Boston, Massachusetts Boston, Massachusetts
vi
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List of Contributors vii
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Foreword
It is axiomatic that when designing any product or service, the needs of the prospective
user must receive primary consideration. Regrettably, this is rarely the case with medical
textbooks, which play a vital role in the education of students, residents, fellows, practicing
physicians, and paramedical professionals. Most books are written for a wide audience so as
to attract as many readers (and buyers) as possible. Most medical textbooks are tomes written
either for the specialist or advanced trainee or they are technical “how to” manuals.
Medical educators appreciate that the needs of medical students exposed to a subject for
the first time differ importantly from those of practicing physicians who wish to review an
area learned previously or to be updated on new developments in a field with which they
already have some familiarity. The lack of textbooks designed specifically for students leads
faculty at schools around the country to spend countless hours preparing and duplicating
voluminous lecture notes, and providing students with custom-designed “camels” (a camel is
a cow created by a committee!).
Pathophysiology of Heart Disease: A Collaborative Project of Medical Students and Faculty
represents a refreshing and innovative departure in the preparation of a medical text.
Students—the intended user—dissatisfied with currently available textbooks on cardiology,
made their needs clear. They need to understand the pathophysiology of cardiovascular dis-
orders, and how the pathophysiology leads to key clinical and laboratory findings and to the
rationale for management. Fortunately, their pleas fell on receptive ears. Dr. Leonard Lilly, a
Professor of Medicine at Harvard Medical School, who is a brilliant teacher and a respected
cardiologist at the Brigham and Women’s and Faulkner Hospitals, has served as the senior
editor of this project. He has brought together a group of talented Harvard medical students
and faculty who have collaborated closely to produce this superb introductory text specifically
designed to meet the needs of medical students during their initial encounters with patients
with heart disease. Dr. Lilly, who was a co-author of most of the chapters made certain that
there were no repetitions or major gaps, as so often occurs with multi-authored texts. While
Pathophysiology of Heart Disease is not meant to be encyclopedic or all inclusive, it is remark-
ably thorough.
The first five editions of this fine book were received enthusiastically, and Pathophysiology
of Heart Disease is now a required or recommended text at many medical schools not only
in the United States and Canada, but in other countries as well. It has been translated into
several languages, has received two awards of excellence from the American Medical Writers
Association, and has inspired other student–faculty collaborative book projects at Harvard
and at other medical schools. This sixth edition is completely updated, as is required by a
field as dynamic as cardiology. The figures have been upgraded, are now in full color, and
they display complex concepts in uncomplicated ways. This edition will prove to be even
more valuable than its predecessors.
Dr. Lilly and his colleagues—both faculty and students—have made a significant and
unique contribution in preparing this important book. Future generations of medical educa-
tors and students, and ultimately the patients that they serve, will be indebted to them for
this important contribution.
Eugene Braunwald, MD
Distinguished Hersey Professor of Medicine
Harvard Medical School
Boston, Massachusetts
viii
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Preface
This textbook is a comprehensive introduction to diseases of the cardiovascular system.
Although excellent cardiology reference books are available, their encyclopedic content can
overwhelm the beginning student. Therefore, this text was created to serve as a simplified
bridge between courses in basic physiology and the care of patients in clinical settings. It
is intended to help medical students and physicians-in-training form a solid foundation of
knowledge of diseases of the heart and circulation and is designed to be read in its entirety
during standard courses in cardiovascular pathophysiology. Emphasis has been placed on the
basic mechanisms by which cardiac illnesses develop, in order to facilitate subsequent in-
depth study of clinical diagnosis and therapy.
The original motivation for writing this book was the need for such a text voiced by
our medical students, as well as their desire to participate in its creation and direction.
Consequently, the book’s development is unusual in that it represents a close collaboration
between Harvard medical students and cardiology faculty, who shared in the writing and edit-
ing of the manuscript. The goal of this pairing was to focus the subject matter on the needs of
the student, while providing the expertise of our faculty members. In this updated and rewrit-
ten sixth edition of Pathophysiology of Heart Disease, the collaborative effort has continued
between a new generation of medical students and our cardiovascular faculty.
The introductory chapters of the book review basic cardiac anatomy and physiology and
describe the tools needed for understanding clinical aspects of subsequently presented mate-
rial. The remainder of the text addresses the major groups of cardiovascular diseases. The
chapters are designed and edited to be read in sequence but are sufficiently cross-referenced
so that they can also be used out of order. The final chapter describes the major classes of
cardiovascular drugs and explains the physiologic rationale for their uses.
It has been a great privilege for me to collaborate with the 106 talented and creative medi-
cal students who have contributed to the six editions of this book. Their intelligence enthu-
siasm, energy, and dedication have made the production of each manuscript enjoyable and
intellectually stimulating. I particularly recognize David Fischer, who stepped forward as the
main student author liaison for this edition and was instrumental in facilitating organization
of this project.
I am indebted to my faculty colleague coauthors for their time, their expertise, and their
continued commitment to this book. I especially acknowledge Professor Gary Strichartz, who
has been an essential contributor to this project since 1996, and whose input into future edi-
tions I will greatly miss as he transitions to retirement and new pursuits.
I sincerely appreciate the thoughtful and constructive comments received from faculty and
students around the globe pertaining to previous editions of this book. These communica-
tions have been very helpful in directing the current revision, and the many warm remarks
and have been an important source of encouragement. I also acknowledge with gratitude
several individuals who provided material, detailed comments and reviews, or other sup-
port to this edition: Suhny Abbara, Lauren Bayer, Marcelo DiCarli, Sharmila Dorbala, Marie
Gerhard-Herman, Andetta Hunsaker, Raymond Kwong, Gillian Lieberman, Robert Padera,
Helmut Rennke, Frank Rybicki, Christian Sampson, Frederick Schoen, Pinak Shah, Benjamin
Smith, Michael Steigner, and Scott Streckenbach.
It has been a pleasure to work with the editorial and production staffs of our publisher,
Lippincott Williams & Wilkins. In particular, I thank Amy Weintraub, Crystal Taylor, Marian
Bellus, Holly McLaughlin, and Leslie Jebaraj for their skill and professionalism in bringing
this edition to completion.
ix
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x Preface
Finally, a project of this magnitude could not be undertaken without the support and
patience of my family, and for that, I am very grateful.
On behalf of the contributors, I hope that this book enhances your understanding of car-
diovascular diseases and provides a solid foundation for further learning and clinical care of
your patients.
Leonard S. Lilly, MD
Boston, Massachusetts
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Table of Contents
List of Contributors vi Chapter 10
Foreword viii The Cardiomyopathies 249
Preface ix P. Connor Johnson, G. William Dec,
and Leonard S. Lilly
Ch a p ter 1
Normal Cardiac Structure Chapter 11
and Function 1 Mechanisms of Cardiac
Jacob E. Lemieux, Elazer R. Edelman, Arrhythmias 268
Gary R. Strichartz, and Leonard S. Lilly Morgan J. Prust, William G. Stevenson,
Gary R. Strichartz, and Leonard S. Lilly
Ch a p ter 2
The Cardiac Cycle: Mechanisms Chapter 12
of Heart Sounds and Murmurs 26 Clinical Aspects of Cardiac
David B. Fischer and Leonard S. Lilly Arrhythmias 287
Morgan J. Prust, William G. Stevenson,
Ch a p ter 3 and Leonard S. Lilly
Cardiac Imaging
and Catheterization 43 Chapter 13
Diana M. López and Patricia Hypertension 310
Challender Come Joshua Drago, Gordon H. Williams,
and Leonard S. Lilly
Ch a p ter 4
The Electrocardiogram 74 Chapter 14
David B. Fischer and Leonard S. Lilly Diseases of the Pericardium 334
Leonard S. Lilly
Ch a p ter 5
Atherosclerosis 112 Chapter 15
Sarrah Shahawy and Peter Libby Diseases of the Peripheral
Vasculature 350
Ch a p ter 6 Sruthi Renati and Mark A. Creager
Ischemic Heart Disease 134
Jayme Wilder, Marc S. Sabatine, Chapter 16
and Leonard S. Lilly Congenital Heart Disease 373
Zena L. Knight and David W. Brown
Ch a p ter 7
Acute Coronary Syndromes 162 Chapter 17
Jayme Wilder, Marc S. Sabatine, Cardiovascular Drugs 400
and Leonard S. Lilly Andrey V. Dolinko, Michael T. Kuntz,
Elliott M. Antman, Gary R. Strichartz,
Ch a p ter 8 and Leonard S. Lilly
Valvular Heart Disease 192
Elizabeth Ryznar, Patrick T. O’Gara, Index 456
and Leonard S. Lilly
Ch a p ter 9
Heart Failure 220
David Miranda, Gregory D. Lewis,
and Michael A. Fifer
xi
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Normal Cardiac Structure
and Function
Jacob E. Lemieux
Elazer R. Edelman
1
Gary R. Strichartz
Leonard S. Lilly
Chapter Outline
Cardiac Anatomy and Histology
K nowledge of normal structure and function of the heart is
crucial to understanding diseases that afflict the cardiovas-
cular system. The purpose of this chapter is to describe the heart’s
Pericardium
basic anatomy, its electrical system, and the cellular and molecular
Surface Anatomy of the Heart
Internal Structure of the Heart mechanisms of contraction that allow the heart to serve its critical
Impulse-Conducting System functions.
Cardiac Innervation
Cardiac Vessels
Histology of Ventricular CARDIAC ANATOMY AND HISTOLOGY
Myocardial Cells Although the study of cardiac anatomy dates back to ancient
Basic Electrophysiology times, interest in this field has recently gained momentum.
Ion Movement and Channels The application of sophisticated cardiac imaging tech-
Resting Potential niques such as coronary angiography, echocardiography,
Action Potential computed tomography, and magnetic resonance imaging
Refractory Periods requires an intimate knowledge of the spatial relationships
Impulse Conduction of cardiac structures. Such information also proves help-
Normal Sequence of Cardiac ful in understanding the pathophysiology of heart disease.
Depolarization This section emphasizes the aspects of cardiac anatomy
Excitation–Contraction Coupling that are important to the clinician—that is, the “functional”
Contractile Proteins in the anatomy.
Myocyte
Calcium-Induced Calcium
Release and the Contractile Pericardium
Cycle The heart and roots of the great vessels are enclosed by a
Introduction to Cardiac Signaling fibroserous sac called the pericardium (Fig. 1-1). This struc-
Systems ture consists of two layers: a strong outer fibrous layer and
β-Adrenergic and Cholinergic an inner serosal layer. The inner serosal layer adheres to the
Signaling external wall of the heart and is called the visceral pericar-
dium. The visceral pericardium reflects back on itself and
lines the outer fibrous layer, forming the parietal pericar-
dium. The space between the visceral and parietal layers
contains a thin film of pericardial fluid that allows the heart
to beat in a minimal-friction environment.
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2 Chapter 1
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Normal Cardiac Structure and Function 3
Left common
Brachiocephalic artery carotid artery
Left subclavian
Superior vena cava artery
Ascending aorta
Left pulmonary
Right superior artery
pulmonary artery
Right inferior Left pulmonary
pulmonary artery veins
Right atrial
appendage Left ventricle
Right atrium
Left subclavian
artery Arch of aorta
Left pulmonary
artery
Superior vena cava
Left superior Right pulmonary
pulmonary vein artery
Right inferior
Left atrium pulmonary vein
Right atrium
Coronary Inferior vena
sulcus cava
Left Coronary
ventricle sinus
FIGURE 1-2. The heart and great vessels. A. The anterior view. B. The posterior aspect (or base), as viewed
from the back. (From Moore KL, Dalley AF, Agur AMR. Clinically Oriented Anatomy, 7th ed. Philadelphia, PA:
Lippincott Williams & Wilkins; 2014:137–138.)
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4 Chapter 1
Anterior
Pulmonic
valve
Aortic
valve
FIGURE 1-3. The four heart valves
Tricuspid viewed from above with atria removed.
valve The figure depicts the period of
Mitral ventricular filling (diastole) during which
valve the tricuspid and mitral valves are open
Annulus
and the semilunar valves (pulmonic and
fibrosus
aortic) are closed. Each annulus fibrosus
Annulus
surrounding the mitral and tricuspid
fibrosus
valves is thicker than those surrounding
the pulmonic and aortic valves; all four
contribute to the heart’s fibrous skeleton,
which is composed of dense connective
Posterior tissue.
cardiac muscle cells, the histology of which is described later in the chapter. External to the
myocardium is a layer of connective tissue and adipose tissue through which pass the larger
blood vessels and nerves that supply the heart muscle. The epicardium is the outermost
layer of the heart and is identical to, and just another term for, the visceral pericardium
previously described.
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Normal Cardiac Structure and Function 5
Pulmonary artery
Aorta
Pulmonic valve
Right atrium
Moderator
band
Trabeculae
carneae
Inferior vena cava
Coronary sinus
heart, distending the valve cusps toward one another. This action closes the pulmonic valve
and prevents regurgitation of blood back into the right ventricle.
Interventricular Septum
The interventricular septum is the thick wall between the left and right ventricles. It is com-
posed of a muscular and a membranous part (see Fig. 1-5B). The margins of this septum
can be traced on the surface of the heart by following the anterior and posterior interven-
tricular grooves. Owing to the greater hydrostatic pressure within the left ventricle, the large
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6 Chapter 1
Pulmonary veins
Left atrium
Left atrial
appendage
Fibrous ring of
left AV orifice
Chordae tendineae
Left ventricle
Papillary muscles
To aortic vestibule
Interventricular septum,
membranous part
Chordae tendineae
Interventricular
septum, muscular part Anterior cusp of mitral valve
Posterior
papillary muscle
Trabeculae carneae
B
FIGURE 1-5. Interior structures of the left atrium and left ventricle. A. The left atrium and left ventricular (LV) inflow
region. B. Interior structures of the LV cavity. (Modified from Moore KL, Dalley AF, Agur AMR. Clinically Oriented Anatomy,
7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2014:142–143.)
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Normal Cardiac Structure and Function 7
muscular portion of the septum bulges toward the right ventricle. The small, oval-shaped
membranous part of the septum is thin and located just inferior to the cusps of the aortic
valve.
To summarize the functional anatomic points presented in this section, the following is a
review of the path of blood flow: deoxygenated blood is delivered to the heart through the
inferior and superior venae cavae, which enter into the right atrium. Flow continues through
the tricuspid valve orifice into the right ventricle. Contraction of the right ventricle propels the
blood across the pulmonic valve to the pulmonary artery and lungs, where carbon dioxide is
released and oxygen is absorbed. The oxygen-rich blood returns to the heart through the pul-
monary veins to the left atrium and then passes across the mitral valve into the left ventricle.
Contraction of the left ventricle pumps the oxygenated blood across the aortic valve into the
aorta, from which it is distributed to all other tissues of the body.
Impulse-Conducting System
The impulse-conducting system (Fig. 1-6) consists of specialized cells that initiate the heart-
beat and electrically coordinate contractions of the heart chambers. The sinoatrial (SA) node
is a small mass of specialized cardiac muscle fibers in the wall of the right atrium. It is located
to the right of the superior vena cava entrance and normally initiates the electrical impulse
for contraction. The atrioventricular (AV) node lies beneath the endocardium in the infero-
posterior part of the interatrial septum.
Distal to the AV node is the bundle of His, which perforates the interventricular septum
posteriorly. Within the septum, the bundle of His bifurcates into a compact, cablelike struc-
ture on the right side, known as the right bundle branch, and a broad sheet of fibers that
continues over the left side of the septum, the left bundle branch.
The right bundle branch is thick and deeply buried in the muscle of the interventricular
septum and continues toward the apex. Near the junction of the interventricular septum
and the anterior wall of the right ventricle, the right bundle branch becomes subendocardial
Sinoatrial node
Mitral valve
Membranous part of
Coronary sinus IV septum
Bifurcation of bundle
of His
Atrioventricular node Muscular part of
IV septum
Bundle of His
Left bundle branch
FIGURE 1-6. Main components of the cardiac conduction system. This system includes the sinoatrial node,
atrioventricular node, bundle of His, right and left bundle branches, and the Purkinje fibers. The moderator
band carries a large portion of the right bundle. (IV, interventricular).
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8 Chapter 1
and bifurcates. One branch travels across the right ventricular cavity in the moderator band,
whereas the other continues toward the tip of the ventricle. These branches eventually arbo-
rize into a finely divided anastomosing plexus that travels throughout the right ventricle.
Functionally, the left bundle branch is divided into an anterior and a posterior fascicle and
a small branch to the septum. The anterior fascicle runs anteriorly toward the apex, forming a
subendocardial plexus in the area of the anterior papillary muscle. The posterior fascicle trav-
els to the area of the posterior papillary muscle; it then divides into a subendocardial plexus
and spreads to the rest of the left ventricle.
The subendocardial plexuses of both ventricles send distributing Purkinje fibers to the
ventricular muscle. Impulses within the His–Purkinje system are transmitted first to the papil-
lary muscles and then throughout the walls of the ventricles, allowing papillary muscle con-
traction to precede that of the ventricles. This coordination prevents regurgitation of blood
flow through the AV valves, as discussed earlier.
Cardiac Innervation
The heart is innervated by both parasympathetic and sympathetic afferent and efferent
nerves. Preganglionic sympathetic neurons, with cell bodies located within the upper five
to six thoracic levels of the spinal cord, synapse with second-order neurons in the cervical
sympathetic ganglia. Traveling within the cardiac nerves, these fibers terminate in the heart
and great vessels. Preganglionic parasympathetic fibers originate in the dorsal motor nucleus
of the medulla and pass as branches of the vagus nerve to the heart and great vessels. Here,
the fibers synapse with second-order neurons located in ganglia within these structures. A
rich supply of vagal afferents from the inferior and posterior aspects of the ventricles mediates
important cardiac reflexes, whereas the abundant vagal efferent fibers to the SA and AV nodes
are active in modulating electrical impulse initiation and conduction.
Cardiac Vessels
The cardiac vessels consist of the coronary arteries and veins and the lymphatics. The largest
components of these structures lie within the loose connective tissue in the epicardial fat.
Coronary Arteries
The heart muscle is supplied with oxygen and nutrients by the right and left coronary arter-
ies, which arise from the root of the aorta just above the aortic valve cusps (Fig. 1-7; see also
Fig. 1-5B). After their origin, these vessels pass anteriorly, one on each side of the pulmonary
artery (see Fig. 1-7).
The large left main coronary artery passes between the left atrium and the pulmonary
trunk to reach the AV groove. There it divides into the left anterior descending (LAD) coro-
nary artery and the circumflex artery. The LAD travels within the anterior interventricular
groove toward the cardiac apex. During its descent on the anterior surface, the LAD gives off
septal branches that supply the anterior two thirds of the interventricular septum and the
apical portion of the anterior papillary muscle. The LAD also gives off diagonal branches that
supply the anterior surface of the left ventricle. The circumflex artery continues within the
left AV groove and passes around the left border of the heart to reach the posterior surface. It
gives off large obtuse marginal branches that supply the lateral and posterior wall of the left
ventricle.
The right coronary artery (RCA) travels in the right AV groove, passing posteriorly
between the right atrium and ventricle. It supplies blood to the right ventricle via acute
marginal branches. In most people, the distal RCA gives rise to a large branch, the posterior
descending artery (see Fig. 1-7C). This vessel travels from the inferoposterior aspect of the
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Normal Cardiac Structure and Function 9
Pulmonary artery
Left main
coronary artery
Aorta
Left circumflex
coronary artery
Left anterior
Right coronary descending
artery coronary artery
Left anterior
descending
coronary artery
Right Obtuse
coronary Diagonal marginal
artery branch branches Right
coronary
artery
Acute
marginal branch Posterior descending
B coronary artery
FIGURE 1-7. Coronary artery anatomy. A. Schematic representation of the right and left coronary arteries demonstrates
their orientation to one another. The left main artery bifurcates into the circumflex artery, which perfuses the lateral and
posterior regions of the left ventricle (LV), and the anterior descending artery, which perfuses the LV anterior wall, the
anterior portion of the intraventricular septum, and a portion of the anterior right ventricular (RV) wall. The right coronary
artery (RCA) perfuses the right ventricle and variable portions of the posterior left ventricle through its terminal branches.
The posterior descending artery most often arises from the RCA. B. Anterior view of the heart demonstrating the coronary
arteries and their major branches. C. Posterior view of the heart demonstrating the terminal portions of the right and
circumflex coronary arteries and their branches.
heart to the apex and supplies blood to the inferior and posterior walls of the ventricles and
the posterior one third of the interventricular septum. Just before giving off the posterior
descending branch, the RCA usually gives off the AV nodal artery.
The posterior descending and AV nodal arteries arise from the RCA in 85% of the population,
and in such people, the coronary circulation is termed right dominant. In approximately 8%,
the posterior descending artery arises from the circumflex artery instead, resulting in a left dom-
inant circulation. In the remaining population, the heart’s posterior blood supply is contributed
to from branches of both the RCA and the circumflex, forming a codominant circulation.
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10 Chapter 1
The blood supply to the SA node is also most often (70% of the time) derived from the
RCA. However, in 25% of normal hearts, the SA nodal artery arises from the circumflex
artery, and in 5% of cases, both the RCA and the circumflex artery contribute to this vessel.
From their epicardial locations, the coronary arteries send perforating branches into the
ventricular muscle, which form a richly branching and anastomosing vasculature in the walls
of all the cardiac chambers. From this plexus arise a massive number of capillaries that form
an elaborate network surrounding each cardiac muscle fiber. The muscle fibers located just
beneath the endocardium, particularly those of the papillary muscles and the thick left ven-
tricle, are supplied either by the terminal branches of the coronary arteries or directly from the
ventricular cavity through tiny vascular channels, known as thebesian veins.
Collateral connections, usually less than 200 μm in diameter, exist at the subarteriolar level
between the coronary arteries. In the normal heart, few of these collateral vessels are visible.
However, they may become larger and functional when atherosclerotic disease obstructs a
coronary artery, thereby providing blood flow to distal portions of the vessel from a nonob-
structed neighbor.
Coronary Veins
The coronary veins follow a distribution similar to that of the major coronary arteries. These
vessels return blood from the myocardial capillaries to the right atrium predominantly via the
coronary sinus. The major veins lie in the epicardial fat, usually superficial to their arterial
counterparts. The thebesian veins, described earlier, provide an additional potential route for
a small amount of direct blood return to the cardiac chambers.
Lymphatic Vessels
The heart lymph is drained by an extensive plexus of valved vessels located in the subendo-
cardial connective tissue of all four chambers. This lymph drains into an epicardial plexus
from which are derived several larger lymphatic vessels that follow the distribution of the
coronary arteries and veins. Each of these larger vessels then combines in the AV groove to
form a single lymphatic conduit, which exits the heart to reach the mediastinal lymphatic
plexus and ultimately the thoracic duct.
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Normal Cardiac Structure and Function 11
Sarcoplasmic
Myofibril reticulum Sarcolemma T tubule
Mitochondrion
FIGURE 1-8. Myocardial cell. Top. Schematic
representation of the ultrastructure of
the myocardial cell. The cell consists of
multiple parallel myofibrils surrounded by
mitochondria. The T tubules are invaginations
of the cell membrane (the sarcolemma) that
increase the surface area for ion transport
and transmission of electrical impulses. The
intracellular sarcoplasmic reticulum houses
most of the intracellular calcium and abuts
the T tubules. (Modified from Katz AM.
Physiology of the Heart. 2nd ed. New York, NY:
Raven Press; 1992:21). Bottom. Expanded
view of a sarcomere, the basic unit of
contraction. Each myofibril consists of serially
connected sarcomeres that extend from one Z
line to the next. The sarcomere is composed
of alternating thin (actin) and thick (myosin) Z Actin Myosin Titin Z
myofilaments. Titin is a protein that tethers
myosin to the Z line and provides elasticity. Sarcomere
The myocardial cell membrane is named the sarcolemma. A specialized region of the mem-
brane is the intercalated disk, a distinct characteristic of cardiac muscle tissue. Intercalated disks
are seen on light microscopic study as darkly staining transverse lines that cross chains of cardiac
cells at irregular intervals. They represent the gap junction complexes at the interface of adjacent
cardiac fibers and establish structural and electrical continuity between the myocardial cells.
Another functional feature of the cell membrane is the transverse tubular system (or
T tubules). This complex system is characterized by deep, fingerlike invaginations of the
sarcolemma (Fig. 1-9; see also Fig. 1-8). Similar to the intercalated disks, transverse tubular
membranes establish pathways for rapid transmission of the excitatory electrical impulses
that initiate contraction. The T tubule system increases the surface area of the sarcolemma
T tubule
Sarcolemma
Ca++ Ca++
Ca++
Ca++ Ca++
FIGURE 1-9. Schematic view Ca++
of the tubular systems of the
myocardial cell. The T tubules, Sarcoplasmic
reticulum
invaginations of the sarcolemma, ATPase
abut the sarcoplasmic reticulum
Ca++
at right angles at the terminal Ca++ Ca++ Ca++
cisternae sacs. This relationship Ca++
is important in linking membrane
excitation with intracellular
release of calcium from the
sarcoplasmic reticulum. Terminal cisternae
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