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Chapter 55
Applied Anatomy of the Heart
and Great Vessels
Joseph G. Murphy, M.D.
Pericardium
This chapter reviews important topics in cardiovascular anatomy that pertain to the practice of clinical
cardiology. The format of the chapter is to describe
briefly the anatomy followed by the clinical significance in italic type.
The pericardium surrounds the heart and consists of fibrous
and serous portions. The fibrous pericardium forms a tough
outer sac, which envelops the heart and attaches to the great
vessels. The ascending aorta, pulmonary artery, terminal
2 to 4 cm of superior vena cava, and short lengths of the
pulmonary veins and inferior vena cava are intrapericardial
(Fig. 1).
The fibrous pericardium is inelastic and limits the diastolic
distention of the heart during exercise. Cardiac enlargement or chronic pericardial effusions, both of which develop
slowly, will stretch the fibrous pericardium. However, the
fibrous pericardium cannot stretch acutely, and the rapid
accumulation of as little as 200 mL of fluid may produce
fatal cardiac tamponade. Hemopericardium results from
perforation of either the heart or the intrapericardial great
vessels.
The serous pericardium is a delicate mesothelial layer
that lines the inner aspect of the fibrous pericardium (parietal pericardium) and the outer surface of the heart and
intrapericardial great vessels (visceral pericardium). The
visceral pericardium, or epicardium, contains the coronary
arteries and veins, autonomic nerves, lymphatic channels,
and variable amounts of adipose tissue.
Mediastinum
The mediastinum contains, in addition to the heart and great
vessels, the distal portion of the trachea, right and left bronchi,
esophagus, thymus, autonomic nerves (cardiac and splanchnic, left recurrent laryngeal, and bilateral vagal and phrenic),
various small arteries (such as bronchial and esophageal) and
veins (such as bronchial, azygos, and hemiazygos), lymph
nodes, cardiopulmonary lymphatics, and thoracic duct.
Enlargement of a cardiac chamber or great vessel may displace or compress an adjacent noncardiac structure. An
enlarged left atrium may displace the left bronchus superiorly and the esophagus rightward. An aberrant retroesophageal
right subclavian artery indents the esophagus posteriorly and
may cause dysphagia. Mediastinal neoplasms can compress
the atria, superior vena cava, or pulmonary veins.
Sections of the text in italic type are topics related to pathology.
An atlas illustrating the anatomy of the heart is at the end of the chapter (Plates 1-24).
Modified from Edwards WD: Applied anatomy of the heart. In Giuliani ER, Gersh BJ, McGoon MD, Hayes DL, Schaff HV (editors): Mayo Clinic Practice
of Cardiology. Third edition. Mosby, 1996, pp 422-489. By permission of Mayo Foundation.
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Ao
Parietal pericardium
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Fig. 1. Parietal pericardium. A, Anterior portion of the parietal pericardium has been removed to show the intrapericardial segments of the great arteries and
superior vena cava. (Anterior view from 16-year-old boy.) B, Heart has been removed from posterior portion of parietal pericardium to show the great vessels, the transverse sinus (dashed line), and the oblique sinus (arrows). (Anterior view from 13-year-old boy.) (See Appendix at end of chapter for abbreviations.) (A from Mayo Clin Proc 56:479-497, 1981. By permission of Mayo Foundation.)
In obese subjects, excessive epicardial depot fat may
encase the heart, but because pericardial fat is liquid at
body temperature, cardiac motion is generally unhindered.
Focal epicardial fibrosis along the anterior right ventricle
or posterobasal left ventricle (so-called soldiers’ patches)
may result from old pericarditis or perhaps from the trauma
of an enlarged heart’s impact against the sternum or calcified
descending thoracic aorta.
Between the great arteries (aorta and pulmonary artery)
and the atria is a tunnel-like transverse sinus (Fig. 1).
Posteriorly, the pericardial reflection forms an inverted Ushaped cul-de-sac known as the oblique sinus. The ligament of Marshall is a pericardial fold that contains the
embryonic remnants of the left superior vena cava.
A sequential saphenous vein bypass graft to the left coronary system may be positioned posteriorly through the transverse sinus. A persistent left superior vena cava will occupy
the expected site of the ligament of Marshall, along the junction between the appendage and body of the left atrium.
Between the parietal and visceral layers of the serous pericardium is the pericardial cavity, which normally contains
10 to 20 mL of serous fluid that allows the tissue surfaces
to glide over each other with minimal friction.
Thick and roughened surfaces associated with fibrinous pericarditis lead to an auscultatory friction rub, and
organization of such an exudate may result in fibrous adhesions between the epicardium and the parietal pericardium.
Focal adhesions are usually unimportant, but occasionally
they may allow the accumulation of loculated fluid or, rarely,
tamponade of an individual cardiac chamber, usually the
right ventricle. After cardiac surgery, the opened pericardial
cavity may become sealed again if the parietal pericardium
adheres to the sternum; in this setting, the raw pericardial surfaces, which are lined by fibrovascular granulation tissue,
may ooze enough blood to cause cardiac tamponade.
Densely fibrotic adhesions, with or without calcification,
can hinder cardiac motion and may restrict cardiac filling.
The pericardium is thickened in subjects with chronic constriction but not necessarily so in persons with constriction that
develops relatively rapidly. In the setting of constrictive pericarditis, surgical excision of only the anterior pericardium
(between the phrenic nerves) is often inadequate, because
the remaining pericardium surrounds enough of the heart to
maintain constriction.
Most postoperative pericardial adhesions are usually
functionally unimportant, but they may obscure the location
of the coronary arteries at subsequent cardiac operation.
Other pericardial conditions include congenital cysts or
diverticula of the pericardium, or the parietal pericardium
may be focally deficient or absent.
Applied Anatomy of the Heart and Great Vessels
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The fibrous pericardium cannot adequately stretch acutely,
and the rapid accumulation of as little as 200 mL of fluid
may produce fatal cardiac tamponade.
A sequential saphenous vein bypass graft to the left coronary system may be positioned posteriorly through the
transverse sinus.
Great Veins
Bilaterally, the subclavian and internal jugular veins merge
to form bilateral innominate (or brachiocephalic) veins. The
latter then join to form the superior vena cava (or superior
caval vein) (Fig. 2).
Superior Vena Cava
The right internal jugular vein, right innominate vein,
and superior vena cava afford a relatively straight
intravascular route to the right atrium and tricuspid orifice.
Accordingly, this route may be used for passage of a stiff
endomyocardial bioptome across the tricuspid valve and
into the right ventricular apex to obtain a cardiac biopsy specimen. Similarly, both temporary and permanent
transvenous pacemaker leads are inserted via either the
subclavian or the internal jugular vein and are threaded
into the right ventricular apex.
Catheters and pacemakers within the innominate veins
and superior vena cava become partially coated with
thrombus and may be associated with thrombotic venous
obstruction, pulmonary thromboembolism, or secondary
infection. Mediastinal neoplasms, fibrosis, and aortic
aneurysms may compress the thin-walled veins and result
in the superior vena caval syndrome.
Inferior Vena Cava
The inferior vena cava receives systemic venous drainage
from the legs and retroperitoneal viscera and, at the level
of the liver, from the intra-abdominal systemic venous
drainage (portal circulation) via the hepatic veins.
The inferior vena cava, which is retroperitoneal, may
become trapped and compressed between the vertebral
column posteriorly and either an adjacent retroperitoneal
structure (for example, an abdominal aortic aneurysm) or
an intraperitoneal structure (for example, a neoplasm) and
thereby produce the inferior vena caval syndrome.
Venous thrombi in the lower extremities may extend into
the inferior vena cava or may become dislodged and
embolize to the right heart and pulmonary circulation.
Fig. 2. Systemic veins, excluding the portal circulation. (See Appendix at
end of chapter for abbreviations.)
Renal cell carcinomas may extend intravascularly within
the renal veins and inferior vena cava and may even form
tethered intracavitary right-sided cardiac masses.
Hepatocellular carcinomas often involve the hepatic veins
and occasionally may enter the suprahepatic inferior vena
cava or right atrium.
The superior and inferior pulmonary veins from each
lung enter the left atrium. The proximal 1 to 3 cm of the
pulmonary veins contain cardiac muscle within the media
and may thereby function like sphincters during atrial systole as well as when significant mitral valve disease exists.
The thin-walled and low-pressure pulmonary veins may
be compressed extrinsically by mediastinal neoplasms or
fibrosis. Rarely, a primary neoplasm may cause luminal
obstruction in the major pulmonary veins.
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Congenital Abnormalities of the Venous System
Congenital anomalies of the systemic veins include a persistent left superior vena cava (with or without a left innominate vein) joining the coronary sinus or, rarely, the left
atrium; an unroofed or absent coronary sinus; a large
right sinus venosus valve (so-called cor triatriatum dexter);
azygos continuity of the inferior vena cava; and bilateral
subrenal inferior venae cavae.
Cardiac Chambers
Cor Triatriatum
Cor triatriatum (sinistrum) results when the junction
between common pulmonary vein and left atrium is
stenotic. A fenestrated membranous or muscular shelf
subdivides the left atrium into a posterosuperior chamber, which receives the pulmonary veins, and an anteroinferior chamber, which contains the atrial appendage and
mitral orifice.
Right Atrium
The right atrium, along with the superior vena cava, forms
the right lateral border of the frontal chest radiographic cardiac silhouette. It receives the systemic venous return from
the superior and inferior venae cavae and receives most of
the coronary venous return via the coronary sinus and numerous small thebesian veins. The ostium of the inferior vena
cava is bordered anteriorly by a crescentic eustachian valve,
which may be large and fenestrated and form a so-called
Chiari net. The coronary sinus ostium is partly shielded by
a fenestrated thebesian valve. The right atrium consists of
a free wall and septum.
Its free wall has a smooth-walled posterior portion, which
receives the caval and coronary sinus blood flow, and a
muscular anterolateral portion, which contains ridge-like
pectinate muscles and a large pyramid-shaped appendage.
Separating the two regions is a prominent C-shaped muscle
bundle, the crista terminalis (or terminal crest). The right
atrial appendage abuts the right aortic sinus and overlies the
proximal right coronary artery.
The thickness of the right atrial free wall varies considerably. The atrial wall between the pectinate muscles is
paper-thin and can be perforated by a stiff catheter.
When atrial enlargement and stasis to blood flow occur,
mural thrombi may form within the recesses between the
pectinate muscles, particularly in the atrial appendage.
Indwelling cardiac catheters or pacemaker wires tend to
injure the endocardium at the cavoatrial junction and are
often associated with shallow linear mural thrombi. An
atrial pacing lead can be inserted into the muscle bundles
within the appendage.
Mediastinal neoplasms, fibrosis, and aortic aneurysms
may compress the thin-walled veins and result in the
superior vena caval syndrome.
The inferior vena cava may become trapped and compressed between the vertebral column posteriorly and
either an adjacent retroperitoneal structure or an intraperitoneal structure and thereby produce the inferior vena
caval syndrome.
The thin-walled low-pressure pulmonary veins may be
compressed extrinsically by mediastinal neoplasms or
fibrosis.
Connection of one (usually the upper) or both right pulmonary veins to the right atrium commonly accompanies
sinus venosus atrial septal defects.
Atrial Septum
The atrial septum has interatrial and atrioventricular
components (Fig. 3). The interatrial portion contains the
fossa ovalis (or oval fossa), which includes an arch-shaped
outer muscular rim (the limbus or limb) and a central fibrous
membrane (the valve). In contrast to the fossa ovalis, the
foramen ovale (or oval foramen, which is patent throughout
fetal life) represents a potential interatrial passageway, which
courses between the anterosuperior limbic rim and the valve
of the fossa ovalis and then through the natural valvular perforation (ostium secundum, or second ostium) into the left
atrium. In approximately two-thirds of subjects, the foramen ovale closes anatomically during the first year of life
as the valve of the fossa ovalis becomes permanently sealed
Anomalous Venous Connection
In total anomalous pulmonary venous connection, the confluence of pulmonary veins does not join the left atrium but
rather maintains connection to derivatives of the cardinal
or umbilicovitelline veins, such as the left innominate vein,
coronary sinus, or ductus venosus. An interatrial communication must also be present.
In partial anomalous pulmonary venous connection, only
some veins (usually from the right lung) lack left atrial
connections. Connection of the right pulmonary veins to
the right atrium commonly accompanies sinus venosus atrial
septal defects, whereas connection of these veins to the
suprahepatic inferior vena cava is usually part of the scimitar
syndrome.
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Applied Anatomy of the Heart and Great Vessels
R
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IAS
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LV
Fig. 3. Atrial anatomy. The atrioventricular septum lies anterior to the interatrial septum and posterior to the interventricular septum; note also the
infolded nature of the limbus (arrows) and the relative thinness of the valve
of the fossa ovalis (open arrow). (Four-chamber view from 15-year-old
boy.) (See Appendix at end of chapter for abbreviations.)
to the limbus. In the remaining third, this flap-valve closes
functionally only when left atrial pressure exceeds right atrial pressure; this constitutes a so-called valvular-competent
patent foramen ovale.
Through a patent foramen ovale, systemic venous emboli
may enter the systemic arterial circulation. Such paradoxic
emboli may be thrombotic (e.g., from the legs) or nonthrombotic (e.g., air emboli).
Pronounced atrial dilatation may so stretch the atrial
septum that the limbus no longer covers the ostium secundum in the valve of the fossa ovalis. As a result, interatrial
shunting may occur across the valvular-incompetent patent
foramen ovale (acquired atrial septal defect). In some
subjects, aneurysms of the valve of the fossa ovalis may
develop and may undulate during the cardiac cycle. Atrial
dilatation also stimulates the release of natriuretic peptide.
The atrioventricular component of the atrial septum,
which separates the right atrium from the left ventricle, is
primarily muscular but also has a small fibrous component
(the atrioventricular portion of the membranous septum).
Triangle of Koch
The atrioventricular septum corresponds to the triangle of
Koch, an important anatomical landmark that contains the
atrioventricular node and bundle; it is bound by the septal
tricuspid annulus, the coronary sinus ostium, and the tendon
of Todaro.
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Tendon of Todaro
The tendon of Todaro is a subendocardial fibrous cord that
extends from the eustachian-thebesian valvular commissure
to the anteroseptal tricuspid commissure (at the membranous septum); it very roughly corresponds to the level of the
mitral annulus.
The thickness of the atrial septum varies considerably.
The valve of the fossa ovalis is a paper-thin translucent
membrane at birth but becomes more fibrotic with time and
may achieve a thickness of 1 to 2 mm. The limbus of the
fossa ovalis ranges from 4 to 8 mm in thickness; however,
lipomatous hypertrophy may produce a bulging mass more
than three times this thickness. The muscular atrioventricular
septum forms the summit of the ventricular septum and
may range from 5 to 10 mm in thickness; this may be greatly
increased in the setting of hypertrophic cardiomyopathy or
concentric left ventricular hypertrophy. The membranous
septum generally is less than 1 mm thick.
Left Atrium
The left atrium, a posterior midline chamber, receives
pulmonary venous blood and expels it across the mitral orifice
and into the left ventricle. The esophagus and descending thoracic aorta abut the left atrial wall. Thus, the left atrium, atrial septum, and mitral valve are particularly well visualized
with transesophageal echocardiography. The body of the
left atrium does not contribute to the frontal cardiac silhouette; however, the left atrial appendage, when enlarged, may
form the portion of the left cardiac border between the left ventricle and the pulmonary trunk. Normally the appendage,
shaped like a windsock, abuts the pulmonary artery and overlies the bifurcation of the left main coronary artery.
With chronic obstruction to left atrial emptying (for
example, rheumatic mitral stenosis), the dilated left atrium
may shift the atrial septum rightward and in severe cases
may actually form the right cardiac border roentgenographically. Moreover, the esophagus can be shifted rightward, and the left bronchus may be elevated. Mural thrombi
often develop within the atrial appendage or, less commonly,
the atrial body, and in severe cases can virtually fill the
chamber except for small channels leading from the pulmonary veins to the mitral orifice. In contrast to left atrial
mural thrombi, which tend to involve the free wall, most
myxomas arise from the left side of the atrial septum.
Comparison of Atria
The right atrial free wall contains a crista terminalis and
pectinate muscles, whereas the left atrial free wall has neither.
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The right atrial appendage is large and pyramidal, in contrast
to the windsock-like left atrial appendage. Finally, the atrial
septum is characterized by the fossa ovalis on the right side
and by the ostium secundum on the left.
Owing to hemodynamic streaming within the right atrium
during intrauterine life, superior vena caval blood is directed
toward the tricuspid orifice, and inferior vena caval blood,
carrying well-oxygenated placental blood, is directed by
the eustachian valve toward the foramen ovale. As a result,
the most-well-oxygenated blood in the fetal circulation is
directed, via the left heart, to the coronary arteries, the upper
extremities, and the brain. Even postnatally, the superior
vena cava maintains its orientation toward the tricuspid
annulus, and the inferior vena cava maintains its orientation toward the atrial septum (Fig. 4).
Consequently, an endomyocardial biopsy specimen of
the right ventricular apex is much more easily obtained via
a superior vena caval approach than an inferior vena caval
approach. In contrast, the passage of a catheter from the
right atrium into the left atrium via the foramen ovale is
much more easily performed via an inferior vena caval
approach. In subjects in whom the foramen ovale is anatomically sealed, the valve of the fossa ovalis may be intentionally perforated (transseptal approach); however, this
membrane becomes thicker and more fibrotic with age.
Atrial Septal Defect
A secundum atrial septal defect involves the fossa ovalis
region of the interatrial septum. It is the most common form
of atrial septal defect and often is an isolated anomaly.
A primum atrial septal defect involves the atrioventricular septum and represents a malformation of the endocardial cushions; it is almost invariably associated with
mitral and tricuspid abnormalities, particularly a cleft in
the anterior mitral leaflet.
A sinus venosus atrial septal defect involves the
posterior aspect of the atrial septum and is usually associated with anomalous right atrial connection of the right
pulmonary veins. A coronary sinus atrial septal defect
is usually associated with an absent (unroofed) coronary
sinus and connection of the left superior vena cava to the
left atrium.
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Most myxomas arise from the left side of the atrial
septum.
A secundum atrial septal defect involves the fossa ovalis
region of the interatrial septum.
A coronary sinus atrial septal defect is usually associated
SVC
RV
IVC
Fig. 4. Right atrial hemodynamic streaming. Superior vena caval blood is
directed toward the tricuspid orifice, and inferior vena caval blood is directed toward the fossa ovalis. (Opened right atrium from 31-year-old man.) (See
Appendix at end of chapter for abbreviations.) (From Edwards WD:
Anatomy of the cardiovascular system. In Clinical Medicine. Vol. 6, Chap
1. Spittell JA Jr [editor]. Harper & Row Publishers, 1984, p 8. By permission of Lippincott-Raven Publishers.)
with an absent coronary sinus and connection of the left
superior vena cava to the left atrium.
Right Ventricle
The right ventricle does not contribute to the borders of the
frontal cardiac silhouette roentgenographically. It is crescentshaped in short-axis and triangular-shaped when viewed in
long-axis.
Conditions, such as pulmonary hypertension, that impose
a pressure overload on the right ventricle cause straightening of the ventricular septum such that both ventricles
attain a D shape on cross-section. In extreme cases, such
as Ebstein’s anomaly or total anomalous pulmonary venous
connection, leftward bowing of the ventricular septum may
result not only in a circular right ventricle and crescentic
left ventricle but also in possible obstruction of the left ventricular outflow tract.
The right ventricular chamber consists of three regions—
inlet, trabecular, and outlet. The inlet region receives the
tricuspid valve and its cordal and papillary muscle attachments. A complex meshwork of muscle bundles characterizes the anteroapical trabecular region. In contrast, the
outlet region is smoother-walled and is also known as the
infundibulum, conus, or right ventricular outflow tract.
Along the outflow tract, an arch of muscle separates the tricuspid and pulmonary valves. The arch consists of a parietal
Applied Anatomy of the Heart and Great Vessels
band, outlet septum, and septal band (Fig. 5), known
collectively as the crista supraventricularis (supraventricular crest).
During right ventricular endomyocardial biopsy, the
bioptome is directed septally, not only to avoid injury to the
cardiac conduction system and tricuspid apparatus but also
to prevent possible perforation of the relatively thin free
wall. Tissue is more often procured from the meshwork of
apical trabeculations than from the septal surface per se.
When permanent transvenous pacemaker electrodes are
inserted into the right ventricle, the apical trabeculations
trap the tined tip and thereby prevent dislodgment.
During vigorous cardiopulmonary resuscitation in which
ribs are fractured, the jagged-edged bones may be forced
through the parietal pericardium, anteriorly, and may lacerate an epicardial coronary artery or may perforate the
right atrial or ventricular free wall. Furthermore, if cardiopulmonary resuscitation is exerted along the midsternum rather than the xiphoid area, the right ventricular
outflow tract may be compressed and this can result in
high right ventricular pressure, which may produce apical
rupture.
Left Ventricle
The left ventricle forms the left border of the frontal cardiac silhouette roentgenographically. It is circular in shortaxis views and is approximated in three dimensions by a
truncated ellipsoid.
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Pressure Overload
Conditions such as aortic stenosis and chronic hypertension, which impose a pressure overload on the left ventricle,
induce concentric left ventricular hypertrophy without appreciable dilatation. Although the short-axis chamber diameter does not increase significantly, the wall thickness
generally increases 25% to 75%, and the heart weight may
double or triple.
Volume Overload
Disorders that impose a volume overload on the left ventricle, such as chronic aortic or mitral regurgitation or
dilated cardiomyopathy, are attended not only by hypertrophy but also by chamber dilatation. They thereby produce a globoid heart with increased base-apex and short-axis
dimensions. Although the heart weight may double or triple,
the left ventricular wall thickness generally remains within
the normal range because of the thinning effect of dilatation. Accordingly, when the left ventricle is dilated, wall
thickness cannot be used as a reliable indicator of hypertrophy (Fig. 6). The term “volume hypertrophy” is favored
in this situation. Hypertrophy, with or without chamber
dilatation, decreases myocardial compliance and impairs
diastolic filling.
Like the right ventricle, the left ventricle can be divided
into inlet, apical, and outlet regions. The inlet receives the
mitral valve apparatus, the apex contains fine trabeculations, and the outlet is angled away from the remainder of
PV
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Fig. 5. Ventricular anatomy. A, The right ventricle has a heavily trabeculated anteroapical region and exhibits muscular separation between the tricuspid
and pulmonary valves. *Moderator band; arrow, papillary muscle of the conus. B, In contrast, the left ventricle (shown in long-axis) has fine apical trabeculations
and is characterized by direct continuity between the mitral and aortic valves. (See Appendix at end of chapter for abbreviations.) (A, from Schapira JN, Charuzi
Y, Davidson RM [editors]: Two-Dimensional Echocardiography. Williams & Wilkins Company, 1982, p 131. By permission of Mayo Foundation.)
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the chamber. Inflow and outflow tracts are separated by
the anterior mitral leaflet, which forms an intracavitary curtain between the two (Fig. 5).
The anterior mitral leaflet is also in direct contact, at its
annulus, with the left and posterior aortic valve cusps. For
comparison, the membranous septum abuts the right and
posterior aortic cusps, and the outlet septum lies beneath
the right and left aortic cusps.
For practical purposes, the base-apex length of the left
ventricle is divided into thirds—basal (corresponding to
the mitral leaflets and tendinous cords), midventricular
(corresponding to the mitral papillary muscles), and apical
levels. Each level is then further divided into segments,
thus forming the basis for regional analysis of the left ventricle (for example, the evaluation of regional wall motion
abnormalities) (Fig. 7 and Table 1).
Hypertrophic cardiomyopathy is characterized by asymmetric (nonconcentric) left ventricular hypertrophy that
disproportionately involves the septum. Cardiac amyloid
may mimic hypertrophic cardiomyopathy.
In the normal elderly heart, left ventricular geometry is
altered (septum is more sigmoid in shape) and in concert
with mild fibrosis and calcification of the aortic and mitral
valves may contribute to the low-grade systolic ejection
murmurs that are so common in the elderly. With advancing age, the aortic annulus dilates appreciably and tilts
rightward and less posteriorly, thereby altering the shape and
direction of the left ventricular outflow tract, which may
simulate hypertrophic cardiomyopathy.
Left ventricular trabeculae carneae are small, and permanent apical entrapment of a tined transvenous pacemaker electrode is difficult to achieve and may necessitate
the placement of epicardial electrodes (for example, in
patients with corrected transposition of the great arteries
or with complete transposition of the great arteries and a previous Mustard or Senning operation).
When left ventricular endomyocardial biopsy is performed, care must be taken not to injure the mitral apparatus
or left bundle branch and not to perforate the apex.
In some persons, apical or anteroseptal trabeculae carneae
may form a prominent spongy meshwork that may be misinterpreted as apical mural thrombus on imaging studies.
Comparison of Ventricles
Normally, left ventricular wall thickness is three to four times
that of the right ventricle. In short-axis, the left ventricle is
circular and the right is crescentic. Whereas the tricuspid and
pulmonary valves are separated from one another, the mitral
and aortic valves are in direct continuity. The right ventricular apex is much more heavily trabeculated than the left.
By two-dimensional echocardiography, ventricular morphology is best inferred by the morphology of the atrioventricular valves, particularly by differences in their annular
levels at the cardiac crux (Fig. 3).
RV
RV
RV
LV
LV
LV
Fig. 6. Compared with a normal heart (center), the heart with pressure hypertrophy (left) has a thick left ventricular wall, but the heart with volume hypertrophy (right) has a normal wall thickness. Both hypertrophied hearts weighed more than twice normal. (Left, from 64-year-old man with aortic stenosis.
Right, from 50-year-old man with idiopathic dilated cardiomyopathy.) (See Appendix at end of chapter for abbreviations.)
Applied Anatomy of the Heart and Great Vessels
Basal
Midventricular
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Apical
Fig. 7. Regional analysis of the left ventricle. Short-axis views show the recommended 16-segment system. (See Appendix at end of chapter for abbreviations.)
Ventricular Septal Defect
The most common ventricular septal defect, either isolated or associated with other cardiac anomalies, is the membranous (perimembranous) type, which involves the
membranous septum. An infundibular (outlet; supracristal;
subarterial) ventricular septal defect is commonly encountered in tetralogy of Fallot and truncus arteriosus. A
malalignment ventricular septal defect occurs when one of
the great arteries overrides the septum and attains biventricular origin, or both great arteries arise from one ventricle. Muscular defects involve the muscular septum and
can be solitary or multiple (so-called Swiss cheese septum).
A defect of the atrioventricular septum is considered to be
an atrioventricular canal defect, and straddling of an atrioventricular valve most commonly occurs across a defect of
this type.
Tetralogy of Fallot
Within the spectrum of cyanotic congenital heart disease is
a group of anomalies that share in common a maldevelopment of the conotruncal septum. Tetralogy of Fallot, the
most common anomaly in this group, results from displacement of the infundibular septum and is characterized
by a large malalignment ventricular septal defect, an overriding aorta, and variable degrees of infundibular and valvular pulmonary stenosis. When the pulmonary valve is atretic,
pulmonary blood flow may come from the ductus arteriosus
or systemic collateral arteries.
Transposition of the Great Arteries
Complete transposition of the great arteries is associated
with abnormal conotruncal septation and parallel rather
than intertwined great arteries, such that the aorta arises
from the right ventricle and the pulmonary artery emanates
from the left ventricle; a ventricular septal defect is present
in about one-third of cases.
Truncus Arteriosus
Truncus arteriosus implies absent conotruncal septation
and is characterized by a single arterial trunk from which
the aorta, pulmonary arteries, and coronary arteries arise;
the ventricular septal defect is of membranous or infundibular type.
Double-Outlet Right Ventricle
Double-outlet right ventricle is characterized by the origin
of both great arteries from the right ventricle, a malalignment ventricular septal defect, and infundibular septal displacement that differs from the type observed in tetralogy.
Myocyte Response to Injury
Myocardial cells are by volume one-half contractile elements
and one-third mitochondria. They are exquisitely sensitive
to oxygen deprivation, and ischemia represents the most
common form of myocardial injury. Other injurious agents
include viruses, chemicals, and excessive cardiac workload
(volume or pressure).
Table 1.—Percentage of Regional Left Ventricular
(LV) Mass
Level
Basal
Middle
Apical
% LV volume
per segment
7.2
6.0
5.3
No. of
segments
6
6
4
Total, %
43
36
21
936
Applied Anatomy of the Heart and Great Vessels
The heart has only a limited response to stress or injury.
Adaptive responses include hypertrophy and dilatation,
whereas sublethal cellular injury is characterized by various degenerative changes. Necrosis is the histologic hallmark of lethal cellular injury, and it elicits an inflammatory
response with subsequent healing by scar formation.
Hypertrophy of cardiac muscle cells is accompanied by
degenerative changes, an increase in interstitial collagen,
and a decrease in ventricular compliance. In dilated hearts,
hypertrophied myocytes are also stretched, but with relatively normal diameters. In dilated hearts, the best histologic
indicators of hypertrophy are nuclear alterations.
Acute myocardial ischemia is characterized by intense
sarcoplasmic staining with eosin dyes, prominent sarcoplasmic contraction bands, and, occasionally, stretched and wavy
myocardial cells. When ischemic cells are irreversibly injured,
the changes of coagulative necrosis appear. Nuclei fade away
(karyolysis) or fragment (karyorrhexis), and the sarcoplasm
develops a glassy homogeneous appearance, although in
many cases the cross-striations remain intact for several days.
Necrotic myocardium elicits an inflammatory infiltrate of
neutrophils and macrophages, which serves histologically to
differentiate acute infarction from acute ischemia. Because
myocardial cells cannot replicate, healing is by organization,
with scar formation.
Cardiac Valves
Atrioventricular Valves
The right (tricuspid) and left (mitral) atrioventricular valves
have five components, three of which form the valvular
apparatus (annulus, leaflets, commissures) and two of which
form the tensor apparatus (chordae tendineae and papillary
muscles).
Valve Annulus
The annulus of each atrioventricular valve is saddle-shaped.
As part of the fibrous cardiac skeleton at the base of the
heart, each annulus electrically insulates atrium from ventricle. Since the tricuspid annulus is an incomplete fibrous
ring, loose connective tissue maintains insulation at the
points of fibrous discontinuity. The mitral annulus, in contrast, constitutes a continuous ring of fibrous tissue.
Valve Leaflet
The valve leaflets are delicate fibrous tissue flaps that close
the anatomical valvular orifice during ventricular systole
(Fig. 8). The leading edge of each leaflet is its free edge,
and its serrated appearance results from direct cordal insertions into this border. The closing edge, in contrast, represents a slightly thickened nodular ridge several
millimeters above the free edge. When the valve closes,
apposing leaflets contact one another along their closing
edges, and interdigitation of these nodular ridges ensures
a competent seal. Each leaflet comprises two major
layers—namely, the fibrosa, which forms the strong structural backbone of the valve, and the spongiosa, which acts
as a shock absorber along the atrial surface, particularly
at the closing edge (rough zone), where one leaflet coapts
with an adjacent leaflet.
Chordae Tendineae
The chordae tendineae are strong, fibrous tendinous cords
that act as guidewires to anchor and support the leaflets.
They restrict excessive valvular excursion during ventricular
systole and thereby prevent valvular prolapse into the atria.
Most tendinous cords branch one or more times, so that
generally more than 100 cords insert into the free edge of
each atrioventricular valve. By virtue of these numerous
cordal insertions, the force of systolic ventricular blood is
evenly distributed throughout the undersurface of each
leaflet.
Papillary Muscles
The papillary muscles, which may have multiple heads, are
conical mounds of ventricular muscle that receive the
majority of the tendinous cords. Because of their position
directly beneath a commissure, each papillary muscle
receives cords from two adjacent leaflets. As a result, papillary muscle contraction tends to pull the two leaflets toward
each other and thereby facilitates valve closure.
In the elderly, mild mitral annular dilatation may occur,
with or without atrial dilatation. Leaflets become thicker,
with increasing nodularity of the rough zone and with mild
hooding deformity of the entire leaflet. Contributing to the
latter is a decrease in ventricular base-apex length which
makes the thickened cords appear relatively longer than necessary, thus simulating mitral valve prolapse.
Tricuspid Valve
The plane of the tricuspid annulus faces toward the right
ventricular apex. Along the free wall, the annulus inserts
into the atrioventricular junction, whereas along the septum,
it separates the atrioventricular and interventricular portions
of the septum.
Applied Anatomy of the Heart and Great Vessels
937
C
CZ
*
RZ
A
B
Pap M
Fig. 8. Components of an atrioventricular valve (from the mitral valve of an 8-year-old girl). A, Each leaflet has a large clear zone (CZ) and a smaller rough
zone (RZ) between its free edge (arrow) and closing edge (dotted line). B, Each commissure (C) separates two leaflets and overlies a papillary muscle (Pap
M); a fan-like commissural tendinous cord (*) connects the tip of the papillary muscle to the commissure.
In living subjects, the tricuspid annular circumference
varies with the cardiac cycle: it is maximum during
ventricular diastole (about 11 cm2) and decreases by about
30% during ventricular systole. The reduction in area is
due to contraction of the underlying basal right ventricular
myocardium, since the incomplete tricuspid annulus cannot adequately constrict by itself.
The three tricuspid leaflets are not always well separated
from one another. The septal (medial) leaflet lies parallel
to the ventricular septum, and the posterior (inferior) leaflet
lies parallel to the diaphragmatic aspect of the right ventricular free wall. In contrast, the anterior (anterosuperior) tricuspid leaflet forms a large sail-like intracavitary
curtain that partially separates the inflow tract from the outflow tract.
Because of differences in leaflet size and cordal length,
the excursion of the posterior and septal leaflets is less than
that of the anterior leaflet. In the setting of annular dilatation,
leaflet excursion is inadequate to effect central coaptation,
and valvular incompetence results. Because the tricuspid
annulus is incomplete, and because the basal right ventricular myocardium forms a subjacent muscular ring,
dilatation of the right ventricle commonly produces annular dilatation and tricuspid regurgitation. Right atrial dilatation alone, as in constrictive pericarditis, usually does not
cause significant tricuspid insufficiency.
Valvular incompetence also may be observed in conditions that limit leaflet and cordal excursion, such as
rheumatic disease (fibrosis and scar retraction), carcinoid
endocardial plaques (thickening and retraction), and
eosinophilic endomyocardial diseases (thrombotic adherence to the underlying myocardium). In normal hearts,
mild degrees of tricuspid regurgitation commonly exist.
Tricuspid stenosis involves commissural and cordal fusion
and may occur in rheumatic or carcinoid heart disease.
Mitral Valve
Mitral Annulus
The plane of the mitral annulus faces toward the left
ventricular apex. The orifice changes shape during the
cardiac cycle, from elliptical during ventricular systole to
more circular during diastole. In living subjects, the normal
mitral annular circumference is maximum during ventricular diastole (about 7 cm2) and decreases 10% to 15%
during systole.
Mitral annular calcification almost invariably involves
only the posterior mitral leaflet and forms a C-shaped ring
of annular and subannular calcium which may impede basal
ventricular contraction and thereby produce mitral regurgitation. Similarly, inadequate basal ventricular contraction may contribute to valvular incompetence in the setting
of pronounced left ventricular dilatation; however, because
only part of the mitral annulus is in direct contact with the
basal ventricular myocardium, dilatation of the ventricle
rarely increases annular circumference more than 25%.
Secondary left atrial dilatation may contribute to the progression of preexisting mitral incompetence by displacing
the posterior leaflet and its annulus and thereby hindering
the excursion of this taut leaflet.
938
Applied Anatomy of the Heart and Great Vessels
Mitral Leaflets
The mitral leaflets form a continuous funnel-shaped veil
with two prominent indentations, the anterolateral and
posteromedial commissures. Although the two commissures do not extend entirely to the annulus, they effectively
separate the two leaflets. In contrast to the three other cardiac
valves, which each comprise three leaflets or cusps, the
mitral valve has only two leaflets. At midleaflet level, the
mitral orifice is elliptic or football-shaped, and its long axis
aligns with the two commissures and their papillary muscles.
Although the anterior leaflet occupies only about 35%
of the annular circumference, its leaflet area is almost identical to the area of the posterior leaflet, about 5 cm2. The
total mitral leaflet surface area is 10 cm2, nearly twice that
necessary to close the systolic annular orifice, 5.2 cm2.
However, some folding of leaflet tissue is needed to ensure
a competent seal, and the normal leaflets are not as redundant as they might appear.
The myxomatous (or floppy) mitral valve is characterized by annular dilatation, stretched tendinous cords, and
redundant hooded folds of leaflet tissue, which are prone
to prolapse, incomplete coaptation, cordal rupture, and
mitral regurgitation. In contrast, rheumatic mitral insufficiency results from scar retraction of leaflets and cords. In
the setting of infective endocarditis, virulent organisms may
perforate the leaflet tissue and produce acute mitral regurgitation. In hypertrophic cardiomyopathy, the anterior
mitral leaflet contacts the ventricular septum during systole
and contributes both to left ventricular outflow tract obstruction and to mitral incompetence.
In chronic aortic insufficiency, the regurgitant stream
may impact on the anterior mitral leaflet and produce not
only a fibrotic jet lesion but also the leaflet flutter and premature valve closure that are so characteristic echocardiographically.
commissural fusion, which obliterate the secondary intercordal orifices and narrow the primary valve orifice. Cordal
rupture may occur in a myxomatous (floppy) valve, an
infected valve, or, rarely, an apparently normal valve and lead
to acute mitral regurgitation.
The mitral papillary muscles occupy the middle third of
the left ventricular base-apex length. Two prominent muscles
originate from the anterolateral and posteromedial (inferomedial) free wall, beneath their respective mitral commissures. Trabeculations not only anchor the papillary muscles
but also may form a muscle bridge between the two papillary groups and thereby contribute to valve closure.
The anterolateral muscle is a single structure with a midline groove in 70% to 85% of cases, whereas the posteromedial muscle is multiple or is bifid or trifid in 60% to 70%.
The anterolateral muscle is generally larger and extends
closer to the annulus than the posteromedial muscle.
Occasionally, an accessory papillary muscle is interposed
between the two major muscles along the free wall. No
papillary muscles or tendinous cords originate from the
septum and terminate on the mitral leaflets. However, in
about 50% of subjects, one or more cord-like structures,
known as left ventricular false tendons, or pseudotendons,
arise from a papillary muscle and insert either onto the septal
surface or onto the opposite papillary muscle.
Chronic postinfarction mitral regurgitation is associated
with papillary muscle atrophy and scarring, thinning and
scarring of the subjacent left ventricular free wall, and left
ventricular dilatation. Acute postinfarction mitral regurgitation may be associated with rupture of a papillary muscle
(almost invariably the posteromedial) and can involve the
entire muscle or only one of its multiple heads.
Competent function of the mitral valve requires the harmonious interaction of all valvular components, including
the left atrium and left ventricle.
Papillary Muscles
A fan-shaped cord emanates from the tip of each of the two
papillary muscles and inserts into its overlying commissure
and into both adjacent leaflets (Fig. 8B). Similarly, a smaller commissural cord inserts into each minor commissure
between their posterior scallops. Two particularly prominent
cords insert along each half of the ventricular surface of the
anterior mitral leaflet, and these so-called strut cords offer
additional support for this mid-cavitary leaflet that also
forms part of the wall of the left ventricular outflow tract.
Cordal length is generally 1 to 2 cm.
Rheumatic mitral stenosis is characterized by cordal and
●
●
●
●
●
Right atrial dilatation alone usually does not cause significant tricuspid insufficiency.
In normal hearts, mild degrees of tricuspid regurgitation
commonly exist.
Secondary left atrial dilatation may contribute to the progression of preexisting mitral incompetence.
In hypertrophic cardiomyopathy, the anterior mitral leaflet
may contact the ventricular septum during systole and
contribute both to left ventricular outflow tract obstruction and to mitral incompetence.
Chronic postinfarction mitral incompetence is associated
with papillary muscle atrophy and scarring.
Applied Anatomy of the Heart and Great Vessels
Semilunar Valves
The right (pulmonary) and left (aortic) semilunar valves, in
contrast to the atrioventricular valves, have no tensor apparatus and, therefore, are structurally simpler valves. They
consist of annulus, cusps, and commissures. Behind each
cusp is an outpouching of the arterial root, known as a sinus
(of Valsalva). There are three aortic sinuses and three pulmonary sinuses, which impart a cloverleaf shape to the arterial
roots.
The annuli of the semilunar valves are part of the fibrous
cardiac skeleton. They are nonplanar structures, shaped
like a triradiate crown.
The cusps are half-moon-shaped (semilunar), pocketlike flaps of delicate fibrous tissue which close the valvular
orifice during ventricular diastole. The leading edge of
each cusp is its free edge. The closing edge, in contrast,
represents a slightly thickened ridge that lies a few millimeters below the free edge, along the ventricular surface
of the cusp. At the center of each cusp, the closing edge
meets the free edge and forms a small fibrous mound, the
nodule of Arantius. When the valve closes, apposing cusps
contact one another along the surfaces between their free
and closing edges (that is, the lunular areas), forming a
competent seal.
Like the atrioventricular valves, the semilunar valves
contain two major layers histologically. The fibrosa forms
the structural backbone of the valve and is continuous
with the annulus, whereas the spongiosa acts more as a
shock absorber along the ventricular surface, especially
at the closing edge. Cusps contain little elastic tissue and,
accordingly, have no appreciable elastic recoil. The
opening and closing of the semilunar valves is a passive
process that entails cusp excursion and annulocuspid
hinge-like motion.
In the elderly, degenerative changes in the aortic valve
may result in low-grade systolic ejection murmurs. The
closing edges become thickened and, along the nodules of
Arantius, may form whisker-like projections called Lambl’s
excrescences. Lunular fenestrations also tend to develop
with increasing age.
Disease processes that tend to increase cusp rigidity,
such as fibrosis or calcification, or that lead to commissural fusion, such as rheumatic valvulitis, tend to narrow the
effective valvular orifice and, as a consequence, produce
stenosis. In contrast, processes that straighten the cuspid line
between commissures and thereby hold the commissures
open, such as arterial root dilatation or rheumatic cuspid
scar retraction, tend to produce regurgitation.
939
Pulmonary Valve
The plane of the pulmonary annulus faces toward the left
midscapula with an area of about 3.5 cm2. The cusps are usually similar in size, although minor variations are commonly
observed.
Pulmonary incompetence occurs in conditions that
produce dilatation of the pulmonary artery and annulus,
such as pulmonary hypertension or heart failure. Combined
pulmonary stenosis and incompetence are features of carcinoid heart disease, in which the annulus becomes constricted and stenotic and in which the cusps are also retracted
and insufficient. Pure pulmonary stenosis is almost always
congenital in origin.
Aortic Valve
The plane of the aortic valve faces the right shoulder. In
the living subject, the normal aortic annular area averages
about 3 cm2.
Unoperated symptomatic aortic stenosis has a worse
prognosis than many malignancies. The vast majority of
stenotic aortic valves are calcified. Most commonly, the
valve represents either degenerative (senile) calcification or
a calcified congenitally bicuspid valve. Only rarely are heavily calcified valves the site of active infective endocarditis.
Aortic root dilatation stretches open the commissures
and thereby produces aortic insufficiency in either a tricuspid or a bicuspid aortic valve. Acute aortic regurgitation
may be produced by infective aortic endocarditis with cuspid perforation or by acute aortic dissection with commissural prolapse. Chronic aortic regurgitation with coexistent
aortic stenosis is most commonly associated with
postrheumatic cuspid retraction, which yields a fixed triangular orifice.
Among cases of infective endocarditis, perhaps none present so varied a clinical spectrum as those associated with
aortic annular abscesses. The possible clinical presentations
depend to a great extent on the particular cusp(s) involved.
Subvalvular extension may involve the anterior mitral leaflet,
left bundle branch, or ventricular septal myocardium;
involvement of the ventricular septal myocardium may
produce a large abscess cavity or result in rupture into a
ventricular chamber with the formation of either an aortoright ventricular or aorto-left ventricular fistula. An aortic
annular abscess may expand laterally and enter the
pericardial cavity and thereby produce purulent pericarditis or fatal hemopericardium, or it may burrow into adjacent
cardiac chambers or vessels and produce various fistulas
(aorto-right atrial, aorto-left atrial, or aortopulmonary).
940
Applied Anatomy of the Heart and Great Vessels
Fibrous Cardiac Skeleton
At the base of the heart, the fibrous cardiac skeleton encircles the four cardiac valves. It comprises not only the four
valvular annuli but also their intervalvular collagenous
attachments (the right and left fibrous trigones, the intervalvular fibrosa, and the conus ligament) and the membranous septum and tendon of Todaro. This fibrous scaffold is
firmly anchored to the ventricles but is rather loosely attached
to the atria. Thus, the cardiac skeleton not only electrically
insulates the atria from the ventricles but also supports the
cardiac valves and provides a firm foundation against which
the ventricles may contract.
Because of the intervalvular attachments of the fibrous
cardiac skeleton, disease or surgery on one valve can affect
the size, shape, position, or relative angulation of its neighboring valves and also can affect the adjacent coronary
arteries or cardiac conduction system. Tricuspid annuloplasty or replacement may be complicated by injury to the
right coronary artery or atrioventricular conduction tissues,
whereas mitral valve replacement may be attended by trauma
to the circumflex coronary artery, coronary sinus, or aortic
valve. At aortic valve replacement, the anterior mitral leaflet,
left bundle branch, or coronary ostia may be injured inadvertently.
Most congenital anomalies of the pulmonary valve are
associated with stenosis. Isolated pulmonary stenosis is
almost always due to a dome-shaped acommissural valve,
with congenital fusion of all three commissures. However,
forms of pulmonary stenosis which are associated with other
cardiac malformations, such as tetralogy of Fallot, usually
result from a bicuspid or unicommissural valve (often with
a hypoplastic annulus) or from a dysplastic valve with three
thickened cusps.
Congenitally bicuspid aortic valves affect 1% to 2% of the
general population and constitute the most common form of
congenital heart disease. Although they usually are neither
stenotic nor insufficient at birth, most bicuspid valves will
become stenotic during adulthood as the cusps calcify, and
some will become insufficient as a result of infective endocarditis or aortic root dilatation. In contrast, the congenitally unicommissural aortic valve is usually stenotic at birth
and becomes progressively more obstructive as calcification develops in adulthood. Aortic atresia is associated with
the hypoplastic left heart syndrome and is usually fatal
during the first week of life. All congenital anomalies of the
aortic valve are much more common in males than in
females.
In truncus arteriosus, the truncal valve most commonly
comprises three cusps and resembles a normal aortic valve.
However, it may be quadricuspid, bicuspid, or, rarely,
pentacuspid and may contain one or more raphes; such
nontricuspid valves are often incompetent, particularly if
the truncal root is dilated.
●
●
●
●
●
●
Disease processes that tend to increase cusp rigidity tend
to narrow the effective valvular orifice and produce
stenosis.
Processes that straighten the cuspid line between commissures tend to produce regurgitation.
Pulmonary incompetence occurs in conditions that
produce dilatation of the pulmonary trunk and annulus,
such as pulmonary hypertension or heart failure.
Pure pulmonary stenosis is almost always congenital in
origin.
An aortic annular abscess may expand laterally and enter
the pericardial cavity.
Congenitally bicuspid aortic valves affect 1% to 2% of
the general population.
Figure 9 shows the anatomy of the heart as seen on magnetic resonance imaging.
Great Arteries
Pulmonary Arteries
The pulmonary artery arises anteriorly and to the left of the
ascending aorta and is directed toward the left shoulder. In
adults, it is slightly greater in diameter than the ascending
aorta, although its wall thickness is roughly half that of the
aorta. At the bifurcation, the right pulmonary artery travels
horizontally beneath the aortic arch and behind the superior vena cava, and the left pulmonary artery courses over
the left main bronchus (Fig. 10). The main and left
pulmonary arteries contribute to the left border of the frontal
cardiac silhouette roentgenographically.
In pulmonary hypertension, especially in children with
pliable tracheobronchial cartilage, the tense and dilated
pulmonary arteries can compress the left bronchus and
the left upper and right middle lobar bronchi and thereby contribute to recurrent bronchopneumonia in those
lobes. Furthermore, the dilated pulmonary artery may
displace the aortic arch rightward and secondarily produce tracheal indentation and, occasionally, hoarseness
as a result of compression of the left recurrent laryngeal
nerve.
Applied Anatomy of the Heart and Great Vessels
A
B
C
D
941
Fig. 9. Transverse (A through D), sagittal (E through H), and coronal (I through L) planes of the heart shown in analogous magnetic resonance images (at
left) and anatomic sections (at right). aAo, ascending aorta; Ao, aortic arch; AoR, aortic root; AV, aortic valve; AzV, azygos vein; CS, coronary sinus; dAo,
descending thoracic aorta; IA, innominate artery; LA, left atrium; LAA, left atrial appendage; LAD, left anterior descending coronary artery; LB, left
bronchus; LCC, left coronary cusp; LCCA, left common carotid artery; LCX, left circumflex coronary artery; LCX-OM, left circumflex coronary artery, obtuse
marginal branch; LIV, left innominate vein; LLPV, left lower pulmonary vein; LMA, left main coronary artery; LPA, left pulmonary artery; LPV, left pulmonary vein; LSA, left subclavian artery; LSV, left subclavian vein; LUPV, left upper pulmonary vein; LV, left ventricle; MPA, main pulmonary artery;
MV, mitral valve; PS, pericardial sac; PV, pulmonary valve; RA, right atrium; RAA, right atrial appendage; RCA, right coronary artery; RCCA, right common carotid artery; RIV, right innominate vein; RJV, right internal jugular vein; RPA, right pulmonary artery; RSV, right subclavian vein; RV, right ventricle; RVOT, right ventricular outflow tract; SVC, superior vena cava; T, trachea; TV, tricuspid valve; VS, ventricular septum. (From Mayo Clin Proc
62:573-583, 1987. By permission of Mayo Foundation.)
Aorta
The aorta arises at the level of the aortic valve annulus
and terminates at the aortic bifurcation, approximately at
the level of the umbilicus and the fourth lumbar vertebra.
The aorta has four major divisions: ascending aorta, aortic
arch, descending thoracic aorta, and abdominal aorta (Fig.
11).
The ascending aorta lies almost entirely within the pericardial sac and includes sinus and tubular portions, which
are demarcated by the aortic sinotubular junction. The
aortic valve leaflets are related to the three sinuses, and the
right and left coronary arteries arise from the right and left
aortic sinuses, respectively. The ascending aorta lies posterior and to the right of the pulmonary artery.
With age or with the development of atherosclerosis, the
aortic sinotubular junction can become heavily calcified,
particularly above the right cusp, and may produce coronary
ostial stenosis. Among the causes of aortic root dilatation,
perhaps aging, mucoid medial degeneration (so-called cystic
medial necrosis), and chronic hypertension are the most
common and may produce an ascending aortic aneurysm,
aortic valvular regurgitation, or acute aortic dissection.
942
Applied Anatomy of the Heart and Great Vessels
E
G
F
H
Fig. 9 continued
The aortic arch travels over the right pulmonary artery
and the left bronchus. From its superior aspect emanate the
innominate (or brachiocephalic), left common carotid, and
left subclavian arteries, in that order. In 11% of subjects,
the innominate and left common carotid arteries form a
common ostium, and in 5%, the left vertebral artery arises
directly from the aortic arch, between the left common
carotid and left subclavian arteries. The ligamentum arteriosum represents the obstructed fibrotic or fibrocalcific
remnant of the fetal ductus arteriosus (ductal artery), which
joins the proximal left pulmonary artery to the undersurface of the aortic arch. The aortic arch contributes to the
left superior border of the frontal cardiac silhouette and
forms the roentgenographic aortic knob.
Aortic Dissection
When aortic dissections do not involve the ascending aorta
(type III or type B), the intimal tear is commonly near the
Applied Anatomy of the Heart and Great Vessels
I
J
K
L
943
Fig. 9 continued
ligamentum arteriosum or the ostium of the left subclavian
artery. By virtue of severe torsional and shear stresses placed
on the heart and great vessels during nonpenetrating decelerative chest trauma, as can occur in motor vehicle accidents, the aorta may be transected at the junction between
the aortic arch and the descending thoracic aorta. When
the tear is incomplete, a posttraumatic pseudoaneurysm can
develop with time. Aneurysms of the aortic arch may be
associated with hypertension, atherosclerosis, or aortitis, or
they may be idiopathic.
Descending Thoracic Aorta
The descending thoracic aorta abuts the left anterior surface
of the vertebral column and lies adjacent to the esophagus
and the left atrium. Its posterolateral branches are the bilateral
intercostal arteries, and its anterior branches include the
bronchial, esophageal, mediastinal, pericardial, and superior
phrenic arteries. The bronchial arteries, most commonly
two left and one right, nourish the bronchial walls and the
pulmonary arterial and venous walls. Uncommonly,
bronchial arteries may arise from intercostal or subclavian
Trachea
RUL
LUL
R Subclavian
Lingula
L Common carotid
L Subclavian
Innominate
Ligamentum
arteriosum
Tubular aorta
Bronchial
Sinotubular jct.
Aortic sinus
Intercostal
Coronary art.
Esophageal
LLL
Diaphragm
Fig. 10. Pulmonary and bronchial arteries. The right and left pulmonary arteries do not exhibit mirror-image symmetry. (See Appendix at end of chapter for abbreviations.)
Abdominal Aorta
The abdominal aorta travels along the left anterior surface
of the vertebral column and lies adjacent to the inferior vena
cava. The major lateral (retroperitoneal) branches include
the renal, adrenal, right and left lumbar, and inferior phrenic
arteries. The gonadal arteries arise somewhat more anteriorly but remain retroperitoneal. The intraperitoneal branches
arise anteriorly and include the celiac artery (with its left
gastric, splenic, and hepatic branches) and the superior and
inferior mesenteric arteries. The distal aortic branches
include the right and left common iliac arteries and a small
middle sacral artery.
Atherosclerotic abdominal aortic aneurysms are most
commonly infrarenal. They tend to bulge anteriorly and
thereby stretch and compress the gonadal and inferior
mesenteric arteries. Such aneurysms are generally filled
with laminated thrombus and so their residual lumens often
Abdominal aorta
arteries or, rarely, from a coronary artery. The bronchial
veins drain not only into the azygos and hemiazygos veins
but also into the pulmonary veins.
If the bronchial circulation is adequate, pulmonary emboli
usually do not cause pulmonary infarction. In several forms
of pulmonary hypertension, the bronchial arteries become
quite enlarged and tortuous.
Aneurysms of the descending thoracic aorta may be
associated with aortic dissection, aortitis, atherosclerosis,
hypertension, or trauma. They may or may not extend
below the diaphragm.
Hepatic
Celiac
Sup. mes. art.
R Adrenal
R Renal
R Gonadal
Middle sacral
Descending thoracic aorta
PT
RLL
R Common carotid
LPA
RPA
RML
Aortic arch
Applied Anatomy of the Heart and Great Vessels
Ascending aorta
944
L Gastric
Splenic
L Adrenal
L Renal
L Gonadal
Inf. mes. art
L Common iliac
R Ext. iliac
L Ext. iliac
L Int. iliac
R Int. iliac
Fig. 11. Systemic arteries. The aorta may be divided into ascending, arch,
descending thoracic, and abdominal regions. (See Appendix at end of chapter for abbreviations.)
appear normal or even narrowed rather than dilated.
Rupture of an atherosclerotic abdominal aortic aneurysm
may be associated with extensive retroperitoneal hemorrhage, with or without intraperitoneal hemorrhage.
Aortopulmonary Window
An aortopulmonary septal defect represents a large opening between the ascending aorta and the pulmonary trunk
and hemodynamically resembles a patent ductus arteriosus.
Rarely, one pulmonary artery may originate from the ascending aorta or ductus arteriosus, while the other arises
normally from the pulmonary trunk. Congenital stenosis
of the pulmonary arteries is usually associated with maternal
rubella during the first trimester. In pulmonary atresia with
ventricular septal defect, the pulmonary arteries may be
derived from the right or left ductus arteriosus and from
Applied Anatomy of the Heart and Great Vessels
945
Coronary Circulation
The left coronary artery arises from the left aortic sinus
and tends to arise at an acute angle and to travel parallel to
the aortic sinus wall. When the left main artery is
exceptionally short, its ostium may assume a double-barrel
appearance.
Among the various causes of coronary ostial stenosis,
perhaps the most common is degenerative calcification of
the aortic sinotubular junction, which often affects the right
aortic sinus. Stenosis of the right coronary ostium occurs
six to eight times more often than that of the left. Aortitis
associated with syphilis or ankylosing spondylitis also may
be complicated by coronary ostial obstruction. Iatrogenic
ostial injury may complicate coronary arteriography, intraoperative coronary perfusion, or aortic valve replacement.
The right coronary artery travels within the right atrioventricular sulcus (or groove) (Fig. 12). In 50% of subjects,
the first anterior branch is the conus artery, which nourishes
the right ventricular outflow tract; in the remainder, this
artery arises independently from the right aortic sinus. The
descending septal artery, which arises from the proximal
right coronary artery or, rarely, from the conus artery or
right aortic sinus, supplies the infundibular septum and, in
some individuals, the distal atrioventricular (His) bundle.
Along the acute cardiac margin, from base to apex, courses
a prominent acute marginal branch, and between this vessel and the conus artery, several smaller marginal branches
arise and travel parallel to the acute margin; these vessels
nourish the lateral two-thirds of the anterior right entricular
free wall.
Beyond the acute margin, along the inferior surface of
the heart, the length of the right coronary artery varies
inversely with that of the circumflex coronary artery.
However, in 90% of human hearts, the right coronary artery
gives rise not only to the posterior descending artery, which
travels in the inferior interventricular sulcus, but also to
branches that supply the inferior left ventricular free wall.
Accordingly, these arteries nourish the inferior third of the
ventricular septum (the inlet septum), including the right
bundle branch and the posterior portion of the left bundle
branch, and the inferior left ventricular free wall, including
the posteromedial mitral papillary muscle.
Right Coronary Artery
The right coronary artery arises nearly perpendicularly from
the right aortic sinus. In 50% of subjects, one or more conus
arteries also originate from the right aortic sinus, anterior to
the right coronary ostium. Rarely, the descending septal artery
or the sinus nodal artery may originate directly from the aorta.
Left Main Coronary Artery
The left main coronary artery travels between the pulmonary
artery and the left atrium and is covered in part by the left
atrial appendage. In two-thirds of subjects, it bifurcates into
left anterior descending and circumflex branches, and in the
remaining one-third, it trifurcates into the aforementioned
bronchial or other systemic collateral arteries (analogous
to total anomalous pulmonary venous connection).
Aortic Arch Congenital Abnormalities
Various anomalies result from faulty development of the
aortic arches. A right aortic arch results from persistence
of the right fourth aortic arch and disappearance of its left
counterpart; it most commonly accompanies tetralogy of
Fallot, pulmonary atresia with ventricular septal defect,
and truncus arteriosus. A double aortic arch results from
persistence of both fourth aortic arches. An aberrant retroesophageal right subclavian artery is a relatively common
anomaly, which may cause dysphagia; it probably results
from persistence of the right dorsal aorta and resorption of
the right fourth aortic arch.
Ductus Arteriosus
The patent ductus arteriosus may be isolated or may accompany other cardiac malformations. A left ductus arteriosus
joins the proximal left pulmonary artery to the aortic arch,
whereas a right ductus arteriosus joins the proximal right
pulmonary artery to the right subclavian artery; in cases of
right aortic arch with mirror-image brachiocephalic branching, the opposite pertains.
Coarctation of the Aorta
Coarctation of the aorta represents an obstructive infolded
ridge just distal to the left subclavian artery and opposite the
ductus arteriosus; it is associated with a congenitally bicuspid aortic valve in at least half of the cases.
●
●
Acute aortic dissection is commonly associated with an
intimal tear above the right aortic cusp and with eventual
rupture into the pericardial sac.
When aortic dissections do not involve the ascending
aorta (type III or type B), the intimal tear is commonly
near the ligamentum arteriosum or the ostium of the left
subclavian artery.
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Applied Anatomy of the Heart and Great Vessels
A
B
Fig. 12. Coronary arteries. A, Base of heart. B, Superior and inferior views of the heart. (See Appendix at end of chapter for abbreviations.)
branches and an intermediate artery (ramus intermedius),
which follows a course similar to that of either the first diagonal or first marginal branch.
Left Anterior Descending Coronary Artery
The left anterior descending coronary artery travels within
the anterior interventricular sulcus (or groove) and, after
wrapping around the apex, may ascend a variable distance
along the inferior interventricular sulcus. Septal perforating
branches nourish not only the anterosuperior two-thirds and
entire apical one-third of the ventricular septum but also the
atrioventricular (His) bundle and the right and anterior left
bundle branches. The proximal septal perforators anastomose with the descending septal artery. Epicardial branches,
called diagonals, nourish the anterior left ventricular free
wall and the medial third of the anterior right ventricular
free wall. Myocardial bridges may be demonstrated
angiographically in 12% of subjects and almost invariably
involve the anterior descending artery; they produce critical
systolic luminal narrowing in only 1% to 2% of hearts and
probably have a benign prognosis in most cases.
Left Circumflex Coronary Artery
The (left) circumflex coronary artery travels within the left
atrioventricular sulcus (or groove) and often terminates just
beyond the obtuse marginal branch. The circumflex artery
nourishes the lateral left ventricular free wall; however, in
the 10% of subjects in whom the circumflex artery gives
rise to the posterior descending branch, it also supplies the
inferior left ventricular free wall and the inferior third of the
ventricular septum. The circumflex and anterior descending
arteries nourish the anterolateral mitral papillary muscles, and
the circumflex and right coronary arteries supply the
posteromedial mitral papillary muscles.
The four major epicardial coronary arteries occupy only
two planes of the heart. The right and circumflex arteries
delineate the plane of the atrioventricular sulcus (cardiac
base), and the left main artery and anterior and posterior
descending arteries delineate the plane of the ventricular
septum.
The origin of the posterior descending artery determines
the blood supply to the inferior portion of the left ventricle
and thereby defines coronary dominance. In 70% of hearts,
the right coronary artery crosses the crux and gives rise to
this branch, and right coronary dominance pertains. In 10%,
the circumflex coronary artery terminates as the posterior
descending branch and thereby establishes left coronary
dominance. Both the right and circumflex arteries supply
the cardiac crux in the remaining 20% and constitute socalled shared coronary dominance. The dominant coronary
artery, however, does not supply most of the left ventricular
myocardium. In subjects with right coronary dominance,
for example, the anterior descending artery supplies about
45% of the left ventricle and the circumflex and right coronary arteries nourish about 20% and 35%, respectively.
Blood Supply of the Cardiac Conduction System
The sinus nodal artery arises from the right coronary artery
in 60% of subjects and from the circumflex artery in 40%,
but its artery of origin does not depend on patterns of coronary arterial dominance. The atrioventricular nodal artery
originates from the dominant artery and, accordingly, arises
from the right coronary in 90% and the circumflex in 10%.
The atrioventricular nodal artery and the first septal perforator of the anterior descending artery offer dual blood supply
to the atrioventricular (His) bundle. Other septal perforating
Applied Anatomy of the Heart and Great Vessels
947
branches of the anterior descending artery supply the anterior aspect of the left bundle branch, and septal perforators
of the posterior descending branch, an extension of the dominant artery, supply the posteroinferior portion of the left
bundle branch. The right bundle branch receives a dual
blood supply from the septal perforators of the anterior and
posterior descending arteries.
recognized along the relatively smooth atrial walls but are
difficult to identify in the trabeculated ventricles.
During cardiac electrophysiologic studies among patients
with Wolff-Parkinson-White syndrome and left-sided bypass
tracts, a catheter electrode may be positioned within the
coronary sinus and great cardiac vein, adjacent to the mitral
annulus, to localize the aberrant conduction pathways.
Coronary Collateral Circulation
In the human heart, the major epicardial coronary arteries
communicate with one another by means of anastomotic
channels 50 to 200 µm in diameter. Normally, these small
collateral arteries afford very little blood flow. However,
if arterial obstruction induces a pressure gradient across
such a channel, then with time the collateral vessel may
dilate and provide an avenue for significant blood flow
beyond the stenotic lesion. Such functional collaterals may
develop between the terminal branches of two coronary
arteries, between the side branches of two arteries, between
branches of the same artery, or within the same branch (via
the vasa vasorum). They are most numerous in the
ventricular septum (between septal perforators of anterior and
posterior descending arteries), in the ventricular apex
(between anterior descending septal perforators), in the
anterior right ventricular free wall (between anterior
descending and right or conus arteries), in the anterolateral
left ventricular free wall (between anterior descending
diagonals and circumflex marginals), at the cardiac crux
(between the right and circumflex arteries), and along the
atria (Kugel’s artery between right and circumflex arteries).
Smaller subendocardial anastomoses also exist.
The most common sites for high-grade atherosclerotic
lesions are the proximal one-half of the anterior descending and circumflex arteries and the origin and entire length
of the right coronary artery. The distribution and severity
of atherosclerotic plaques do not differ significantly among
patients with angina pectoris, acute myocardial infarction,
end-stage ischemic heart disease, or sudden death.
Congenital malformations of the coronary arteries include
anomalous ostial origin, anomalous arterial branching
patterns, and anomalous arterial anastomoses.
Cardiac Lymphatics
Myocardial lymphatics drain toward the epicardial surface,
where they are joined by lymphatic channels from the
conduction system, atria, and valves. Larger epicardial lymphatics then travel in a retrograde manner with the coronary
arteries back to the aortic root, where a confluence of right
and left cardiac lymphatics drains into a pretracheal lymph
node and eventually empties into the right lymphatic duct.
The coronary veins and cardiac lymphatics work in concert to remove excess fluid from the myocardial interstitium
and pericardial sac. Accordingly, obstruction of either
system or of both systems may result in myocardial edema
and pericardial effusion.
Coronary Veins
The venous circulation of the heart comprises a coronary
sinus system, an anterior cardiac venous system, and the
thebesian venous system (Fig. 13). Small thebesian veins
drain directly into a cardiac chamber, particularly the right
atrium or right ventricle; the ostia of these veins are easily
Cardiac Conduction System
Sinus Node
The sinus node is the primary pacemaker of the heart. It is
an epicardial structure that measures approximately 15 by
5 by 2 mm and is located in the sulcus terminalis (intercavarum) near the superior cavoatrial junction (Fig. 14).
Through its center passes a relatively large sinus nodal artery.
Sinus nodal function is greatly influenced by numerous
sympathetic and parasympathetic nerves that terminate
within its boundaries.
Histologically, the sinus node consists of specialized
cardiac muscle cells embedded within a prominent collagenous stroma. Its myocardial cells are smaller than ventricular muscle cells and contain only scant contractile elements.
Ultrastructurally, the sinus node comprises transitional cells
and variable numbers of P cells centrally and atrial myocardial cells peripherally. The P cells are thought to be the
source of normal cardiac impulse formation.
Because the sinus node occupies an epicardial position,
its function may be affected by pericarditis or metastatic
neoplasms. In the setting of cardiac amyloidosis, the sinus
node may be involved by extensive fibrosis or amyloid deposition. Although the sinus node is rarely infarcted, its function can be altered by adjacent atrial infarction.
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Applied Anatomy of the Heart and Great Vessels
Fig. 13. Coronary veins. Superior and inferior views of the heart. (See Appendix at end of chapter for abbreviations.)
Internodal Tracts
There are no morphologically distinct conduction pathways
between the sinus and the atrioventricular nodes by light
microscopy, but electrophysiologic studies support the concept of three functional preferential conduction pathways.
By ultrastructural studies, some investigators have observed
specialized cardiac muscle cells in these internodal tracts.
Lipomatous hypertrophy of the atrial septum may interfere with internodal conduction and induce various atrial
arrhythmias. Because the functional preferential pathways
travel only in the limbus and not in the valve of the fossa
ovalis, internodal conduction disturbances do not occur
with intentional septal perforation at cardiac catheterization
(transseptal approach), with the Rashkind balloon atrial
septostomy, or with the Blalock-Hanlon partial (posterior)
atrial septectomy. With the Mustard operation for complete
transposition of the great arteries, in which the entire atrial
septum is resected and in which the surgical atriotomy may
disrupt the crista terminalis, severe disturbances of internodal conduction may result.
Atrioventricular Node
The atrioventricular node is a subendocardial right atrial
structure that measures approximately 6 by 4 by 1.5 mm.
It is located within the triangle of Koch (bordered by the
tendon of Todaro, septal tricuspid annulus, and coronary
sinus ostium) and abuts the right fibrous trigone (central
fibrous body). The atrioventricular nodal artery courses
near the node but not necessarily through it. Sympathetic
and parasympathetic nerves enter the atrioventricular node
and greatly influence its function.
Like the sinus node, the atrioventricular node histologically consists of a complex interwoven pattern of small
specialized cardiac muscle cells within a fibrous stroma.
With advanced age, the atrioventricular node acquires progressively more fibrous tissue, although not as extensively
as the sinus node.
The so-called mesothelioma of the atrioventricular node
is a small and rare primary neoplasm which, by virtue of
its position, produces various arrhythmias and may cause
sudden death. Metastatic neoplasms may rarely infiltrate
the atrioventricular node but do not necessarily alter its
function. Sarcoid granulomas tend to involve the basal
ventricular myocardium and may destroy the atrioventricular conduction system. Because of its subendocardial position, the atrioventricular node may be ablated nonsurgically
at the time of electrophysiologic study.
Atrioventricular Bundle
The atrioventricular (His) bundle arises from the distal
portion of the atrioventricular node and courses through the
central fibrous body to the summit of the muscular ventricular septum, adjacent to the membranous septum. It
affords the only normal physiologic avenue for electrical
conduction between ventricles. By virtue of its position
within the central fibrous body (right fibrous trigone), the
Applied Anatomy of the Heart and Great Vessels
949
Aorta
Pulmonary valve
Superior vena cava
Atrioventricular node
AV (His) bundle
Sinus node
RIght bundle branch
Septal band
Crista terminalis
Moderator band
Fossa ovalis
Right ventricle
Anterior papillary
muscle
Right atrium
Inferior vena cava
Ventricular septum
Tricuspid valve annulus
A
Aorta
Pulmonary artery
Left bundle branch
Left ventricle
Left atrium
Mitral valve annulus
Papillary muscles
B
Ventricular septum
Fig. 14. Cardiac conduction system. A, Right heart. The sinus and AV nodes are both right atrial structures. B, Left heart. The left bundle branch forms a
broad sheet that does not divide into distinct anterior and posterior fascicles. (From Edwards WD: Anatomy of the cardiovascular system. In Clinical
Medicine. Vol. 6, Chap 1. Spittell JA Jr [editor]. Harper & Row Publishers, 1984, p 8. By permission of Lippincott-Raven Publishers.)
atrioventricular bundle is closely related to the annuli of the
aortic, mitral, and tricuspid valves. The atrioventricular
bundle has a dual blood supply—from the atrioventricular
nodal artery and the first septal perforating branch of the
anterior descending artery. In some subjects, a septal branch
of the proximal right coronary artery also nourishes the
atrioventricular bundle.
The atrioventricular bundle is made up of numerous
parallel bundles of specialized cardiac muscle cells, which
are separated by delicate fibrous septa. The entire atrioventricular bundle is insulated by a collagenous sheath.
With increasing age, the fibrous septa become thicker, and
the functional elements may be partially replaced by adipose tissue. Ultrastructurally, the atrioventricular bundle
contains Purkinje cells and ventricular myocardial cells in
parallel arrangement.
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Applied Anatomy of the Heart and Great Vessels
In some subjects, alternate conduction pathways exist
between the atria and the ventricles, either within the existing atrioventricular conduction system or elsewhere along
the fibrous cardiac skeleton, and may produce various
arrhythmias. Atrionodal bypass tracts (of James) connect
the atria to the distal atrioventricular node, and atriofascicular tracts (of Breckenmacher) connect the atria to the
atrioventricular bundle. Nodoventricular and fasciculoventricular bypass fibers (of Mahaim) connect the atrioventricular node and atrioventricular bundle, respectively,
to the underlying ventricular septal summit. These bypass
fibers are quite commonly observed histologically and are
apparently nonfunctional in most persons, although they
may produce ventricular preexcitation in some instances.
Ventricular preexcitation is usually associated with aberrant atrioventricular bypass tracts that bridge the tricuspid
or mitral annuli. These tracts often travel within the adipose tissue of the atrioventricular sulcus rather than through
a defect in the valvular annuli. Such bypass tracts can be
single or multiple and may be identified by electrophysiologic mapping.
Acquired complete heart block may involve the atrioventricular node and bundle or both bundle branches. That
occurring with acute myocardial infarction is usually transient
and more commonly complicates inferoseptal than anteroseptal infarction. Usually the atrioventricular node and atrioventricular bundle are edematous, or the bundle branches
are focally infarcted. Acute heart block also can complicate
aortic infective endocarditis. Chronic heart block may be
associated with ischemic heart disease or with fibrocalcific
disorders of the aortic or mitral valves, but it is most
commonly due to idiopathic fibrosis of the atrioventricular
bundle and bilateral bundle branches. Heart block may also
complicate aortic or mitral valve replacement.
Congenital complete heart block presents as persistent
bradycardia in utero and can represent an isolated anomaly
or may accompany other cardiac malformations. It results
from interruption of atrioventricular conduction pathways,
either at the junction between atrial muscle and the
atrioventricular node or at the junction between the atrioventricular node and the atrioventricular bundle. The
different embryologic origins of these three regions account
for the specific sites of disrupted conduction tissue.
Bundle Branches
As an extension of the atrioventricular bundle, the right
bundle branch forms a cordlike structure, approximately 50
mm in length and 1 mm in diameter, which courses along
the septal and moderator bands to the level of the anterior
tricuspid papillary muscle. The left bundle branch forms a
broad fenestrated sheet of conduction fibers which spreads
along the septal subendocardium of the left ventricle and
separates incompletely and variably into two or three indistinct fascicles. The fascicles travel toward the left ventricular
apex and both mitral papillary muscle groups. The bundle
branches are nourished by septal perforators arising from
the anterior and posterior descending coronary arteries.
Histologically, the bundle branches consist of parallel tracts
of specialized cardiac muscle cells which are insulated by a
delicate fibrous sheath. Ultrastructurally, Purkinje cells and
ventricular myocardial cells form the bundle branches.
Right bundle branch block may be idiopathic or be associated with ischemic heart disease, chronic systemic hypertension, or pulmonary hypertension. Right ventriculotomy
usually produces the electrocardiographic features of right
bundle branch block, even though the bundle may not have
been transected.
Chronic left bundle branch block may be associated with
fibrocalcific degeneration of the ventricular septal summit
as a result of chronic ischemia, left ventricular hypertension, calcification of the aortic or mitral valves, or any form
of cardiomyopathy.
●
●
●
●
The sinus node comprises transitional cells and variable
numbers of P cells centrally and atrial myocardial cells
peripherally.
With the Mustard operation for complete transposition
of the great arteries, in which the entire atrial septum is
resected, severe disturbances of internodal conduction
may result.
The atrioventricular bundle has a dual blood supply—
from the atrioventricular nodal artery and the first septal perforating branch of the anterior descending artery.
Acute heart block may complicate aortic infective endocarditis.
Cardiac Innervation
Because the embryonic heart tube first forms in the future
neck region, its autonomic innervation also arises from this
level. From the cervical ganglia originate three pairs of cervical sympathetic cardiac nerves, which intermingle as they
join the cardiac plexus, between the great arteries and the
tracheal bifurcation. Several thoracic sympathetic cardiac
nerves arise from the upper thoracic ganglia and also join the
cardiac plexus. From the parasympathetic vagus nerves
emanate the superior and inferior cervical vagal cardiac
Applied Anatomy of the Heart and Great Vessels
nerves and the thoracic vagal cardiac nerves, which likewise interweave within the cardiac plexus. The various
sympathetic and parasympathetic nerves then descend from
this plexus onto the heart and thereby innervate the coronary arteries, cardiac conduction system, and myocardium.
Furthermore, afferent nerves concerned with pain and various
reflexes ascend from the heart toward the cardiac plexus.
The transplanted human heart is completely denervated
and responds only to circulating (humoral) substances and not
to autonomic impulses. Similarly, afferent pathways are also
lost, including pain tracts and various reflexes. Consequently,
if chronic cardiac transplant rejection produces diffuse coronary arterial obstruction, subsequent myocardial ischemia
951
and infarction will be asymptomatic.
The asplenia syndrome is characterized by bilateral rightsided symmetry and is generally associated with right atrial
isomerism, right pulmonary isomerism, abdominal situs
ambiguus, and, in some instances, bilateral sinus nodes. In
contrast, the sinus node may be congenitally absent or malpositioned in cases of polysplenia with left atrial isomerism.
●
●
The transplanted heart is completely denervated and
responds only to circulating (humoral) substances and
not to autonomic impulses.
Congenital complete heart block may present as persistent bradycardia in utero.
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Applied Anatomy of the Heart and Great Vessels
Appendix
Abbreviations Used in Figures
A
Ao
Art.
AL
AS
AV
AVS
CS
Desc
Ext
I
IAS
IL
Inf
Int
IS
IVC
IVS
L
LA
LAD
LCX
LLL
LLPV
LMA
LPA
LPV
LUL
LV
LVOT
Anterior
Aorta
Artery
Anterolateral
Anteroseptal
Atrioventricular
AV septum
Coronary sinus
Descending
External
Inferior
Interatrial septum
Inferolateral
Inferior
Internal
Inferoseptal (Fig. 7 only)
Inferior vena cava
Interventricular septum
Left
Left atrium
Left anterior descending coronary artery
Left circumflex coronary artery
Left lower lobe
Left lower pulmonary vein
Left main coronary artery
Left pulmonary artery
Left pulmonary vein
Left upper lobe
Left ventricle
Left ventricular outflow tract
Mes
MV
OS
P
PA
PB
PL
PM
Post.
PS
PT
PV
R
RA
RAA
RCA
RLL
RLPV
RML
RPA
RPD
RPV
RUL
RV
S
SB
Sup
SVC
TV
Mesenteric
Mitral valve
Outlet septum
Posterior
Pulmonary artery
Parietal band
Posterolateral
Posteromedial
Posterior
Posteroseptal
Pulmonary trunk
Pulmonary valve
Right
Right atrium
Right atrial appendage
Right coronary artery
Right lower lobe
Right lower pulmonary vein
Right middle lobe
Right pulmonary artery
Right posterior descending coronary artery
Right pulmonary vein
Right upper lobe
Right ventricle
Septal
Septal band
Superior
Superior vena cava
Tricuspid valve
Applied Anatomy of the Heart and Great Vessels
Plate 1. Calcification of aortic valve in degenerative aortic stenosis.
Plate 2. Normal aortic valve, opened (left) and closed (right).
953
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Applied Anatomy of the Heart and Great Vessels
Plate 3. Four valves at base of heart.
Plate 4. Thin valve of foramen ovale (transilluminated).
Plate 5. Normal atria.
Plate 6. Tricuspid and mitral valves in profile on four-chamber view of the
heart. Note that the normal tricuspid valve takes origin below that of the
mitral valve, allowing the possibility of a right atrial-to-left ventricular shunt.
Plate 7. Pulmonary valve.
Applied Anatomy of the Heart and Great Vessels
955
Plate 8. Right ventricle, showing marked trabeculation and tricuspid valve.
Plate 9. Mitral valve leaflets and annulus (short-axis).
Plate 10. Mitral valve papillary muscles (short-axis).
Plate 11. Mitral valve leaflets and chords (short-axis).
Plate 12. Mitral valve commissural cords.
Plate 13. Left ventricle with membranous septum (transilluminated).
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Applied Anatomy of the Heart and Great Vessels
Plate 14. Left ventricle (free wall and septum) with mitral valve on free wall.
Plate 15. Position of atrioventricular node (triangle of Koch).
Applied Anatomy of the Heart and Great Vessels
Plate 16. Right atrium, showing hemodynamic streaming (superior vena
cava to tricuspid valve to inferior vena cava to foramen ovale).
Plate 18. Myocardial arteriole.
957
Plate 17. Myocardial bridge, left anterior descending coronary artery.
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Applied Anatomy of the Heart and Great Vessels
Plate 19. Septal perforators (coronary cast).
Plate 20. Left anterior descending coronary artery with septal perforators.
Applied Anatomy of the Heart and Great Vessels
Plate 21. Coronary ostia (conus, right, and left).
Plate 22. Normal aortic valve, closed (left) and opened (right).
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Applied Anatomy of the Heart and Great Vessels
Plate 23. Aortic valve (from below).
Plate 24. Valve fibrosis in rheumatic mitral stenosis.