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Mayo Applied Cardiac Anatomy
Mayo Applied Cardiac Anatomy
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.
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.
927
928
Ao
Parietal pericardium
S
V
C
Ao
PA
SVC
R
P
V
PA
L
P
V
RA
RV
IVC
Diaphragm
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.)
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.
929
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).
930
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.
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
LA
AVS
RV
IVS
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.)
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.
931
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.
932
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.)
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 Ebsteins 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
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.
933
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
PB
RV
OS
RAA
Ao
SB
RCA
SVC
TV
A
PM
A
LA
CS
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.)
934
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.)
Basal
Midventricular
935
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.)
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).
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
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
layersnamely, 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.
937
C
CZ
*
RZ
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.
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
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.
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
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.
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
Fig. 9 continued
Aortic Dissection
When aortic dissections do not involve the ascending aorta
(type III or type B), the intimal tear is commonly near the
943
Fig. 9 continued
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
Hepatic
Celiac
Middle sacral
PT
RLL
R Common carotid
LPA
RPA
RML
Aortic arch
Ascending aorta
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L Gastric
Splenic
L Adrenal
L Renal
L Gonadal
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.)
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
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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.
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Fig. 12. Coronary arteries. A, Base of heart. B, Superior and inferior views of the heart. (See Appendix at end of chapter for abbreviations.)
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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.
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
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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
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
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Aorta
Pulmonary valve
Superior vena cava
Atrioventricular node
AV (His) bundle
Sinus node
Crista terminalis
Moderator band
Fossa ovalis
Right ventricle
Anterior papillary
muscle
Right atrium
Inferior vena cava
Ventricular septum
Tricuspid valve annulus
Aorta
Pulmonary artery
Left ventricle
Left atrium
Papillary muscles
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.)
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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
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
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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
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Plate 14. Left ventricle (free wall and septum) with mitral valve on free wall.
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Plate 20. Left anterior descending coronary artery with septal perforators.
Plate 22. Normal aortic valve, closed (left) and opened (right).
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