Chapter 55

Applied Anatomy of the Heart and Great Vessels

Joseph G. Murphy, M.D.

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.

Pericardium
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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S V C

Parietal pericardium

Ao

Ao
SVC

PA L P V

PA

R 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.)

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 hearts 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.

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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. 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. 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.
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Cardiac Chambers
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

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.

Applied Anatomy of the Heart and Great Vessels R L P V LLPV IAS RA AVS LA

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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.)

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.

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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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.

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.

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

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

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.

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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

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.

PV PB RAA SB RCA P TV A A OS RV R Ao SVC

*
B

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.)

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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.

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 thirdsbasal (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

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 LV RV 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.)

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Basal

Midventricular

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

% LV volume per segment 7.2 6.0 5.3 No. of segments 6 6 4

Level Basal Middle Apical

Total, % 43 36 21

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(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.

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.

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.

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

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C CZ

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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.

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.

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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.
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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. 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 Lambls 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).

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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.
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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

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.

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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.

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Applied Anatomy of the Heart and Great Vessels

G
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

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K
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

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Applied Anatomy of the Heart and Great Vessels

Trachea

Aortic arch

R Common carotid R Subclavian Innominate

L Common carotid L Subclavian Ligamentum arteriosum

RUL RPA PT RML LPA

LUL

Descending thoracic aorta

Ascending aorta

Tubular aorta Sinotubular jct. Aortic sinus Coronary art. Esophageal Diaphragm Bronchial Intercostal

Lingula

RLL

LLL

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

Hepatic

Celiac

Sup. mes. art. R Adrenal R Renal R Gonadal

L Gastric Splenic L Adrenal L Renal L Gonadal

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.

Middle sacral

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.)

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

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

bronchial or other systemic collateral arteries (analogous to total anomalous pulmonary venous connection).

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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.
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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.

Coronary Circulation
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.

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.

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

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Applied Anatomy of the Heart and Great Vessels

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

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.

947

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 m 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 (Kugels 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. 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 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.

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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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

Aorta Pulmonary valve Superior vena cava Sinus node Crista terminalis Fossa ovalis Right atrium Inferior vena cava Atrioventricular node AV (His) bundle RIght bundle branch Septal band Moderator band Right ventricle Anterior papillary muscle

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Ventricular septum Tricuspid valve annulus

Aorta Pulmonary artery

Left bundle branch

Left ventricle

Left atrium

Papillary muscles

Mitral valve annulus

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 supplyfrom 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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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.
q

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.

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.

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

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

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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.
q

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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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 1. Calcification of aortic valve in degenerative aortic stenosis.

Plate 2. Normal aortic valve, opened (left) and closed (right).

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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.

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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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Plate 14. Left ventricle (free wall and septum) with mitral valve on free wall.

Plate 15. Position of atrioventricular node (triangle of Koch).

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Plate 16. Right atrium, showing hemodynamic streaming (superior vena cava to tricuspid valve to inferior vena cava to foramen ovale).

Plate 17. Myocardial bridge, left anterior descending coronary artery.

Plate 18. Myocardial arteriole.

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Plate 19. Septal perforators (coronary cast).

Plate 20. Left anterior descending coronary artery with septal perforators.

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Plate 21. Coronary ostia (conus, right, and left).

Plate 22. Normal aortic valve, closed (left) and opened (right).

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Plate 23. Aortic valve (from below).

Plate 24. Valve fibrosis in rheumatic mitral stenosis.