Coronary Anery Anorulies: A Comprehensfue Approach, edited by P. Angelini. Lippincott Williams & Wilkins, Philadelphia O 1999

CHAPTER 4

Normal and Anomalous Coronary Arteries in Humans Paolo Angelini, Salvador Villason, Albert V. Chan,Jr., andJos6 G. Diez

Part I HISTORICAL BACKGROUND

The presence of a pulmonary circulation organized in series with the systemic circulation had been postulated by isolated early researchers: Ibn-na-Nafis, a 13th-century Arab physician working in Damascus; Miguel Serveto, a passionate 16th-century Spanish theologian; and Cesalpino, a 16thcentury anatomist from Padua, who coined the term "pulmonary circulati on.' 'sz6 Nevertheless, it was not until 1628 that William Harvey (1518-1651), a physician trained in Padua but later active in London, and Cambridge, propounded a clear, complete, organized concept ofthe circulation, thereby founding the discipline of physiologic anatomy. Discovery of the systemic capillary network awaited the introduction of the microscope. It was Marcello Malpighi (1628-1694), operating mainly in Bologna, who first described the circulation of blood through the peripheral capillary network.s26 Regarding the coronary arteries in particular, the founder of descriptive anatomy, the great Flemish anatomist Andreas Vesalius (1514-1564), produced a series offundamental /cbulae anatomicae (Yenice, 1538), that were followed by his comprehensive treatise "De Humani Corporis Fabrica Libri Septem" (Basel, 1543), which became the basic textbook of anatomy for generations of physicians throughout Europe. Interestingly, one famous tabula anatomica showed the right coronary artery GCA) originating from the left coronary artery (LCA) and coursing anterior to the pulmonary outflow tract (Fig.4.2). Similarly, a single coronary ostium was mentioned by Fallopius (Venice, 1562).so8 Not until 1761, did G. P. Morgagni accurately and definitively describe the two main coronary vessels.so8 During the ensuing centuries, var* ious investigators published occasional descriptions of peculiar or unusual coronary anatomic features: the work of A. C. Thebesius and R. Vieussens was especially note-

Interest in coronary anatomy and the nature of the coro-

nary vessels was cautiously aroused in the 16th century, when inquisitive Renaissance scholars began to perform anatomic investigations in the early European medical schools. Until then, anatomic knowledge had been heavily influenced by the philosophical and theological teachings ofthe ancient, rediscovered masters of the Greek and Arabic schools. Aristotle (384-322 BC), the philosophical interpreter of nature, and Galen of Pergamum (129-199 AD), the great physician, were the main authorities whose theories continued to dominate the medical schools of Salerno, Bologna, Padua, and eventually Louvain, Paris, and London during the Renaissance.

Leonardo da Vinci (1452-1519), a lone, ingenious spirit, examined a few animal hearts (probably of oxen) and also briefly touched on coronary anatomy while exploring the arcane viscera of the chest.531 His main interest seemed to be in applying the principles of hydraulic physics to cardiovascular function. Leonardo tended to rely on instinctive curiosity rather than organized, formal methods. He left us

only brief notes, accompanied by precise, faithful sketches of the coronary anatomy, including the aortic trifoliate valve, the right and left coronary ostia, and the proximal course of the right and left coronary arteries (Fig. a.l). He noted that the coronary arteries become progressively smaller as they progress toward the cardiac apex.s3l He also accurately described the coronary veins and the coronary sinus; his observation of the arrangement of these structures supported his assumption that an artery is always accompanied by a vein.s3l Leonardo's approach exemplified the new method of critical, direct observation, which a little more than a century later would allow better-trained, more-disciplined scientists to understand how the circulation works.53l

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With the advent of the 20th century, physicians became increasingly aware of the complexity and variability of the coronary anatomy. In 1926, this concept was reinforced and put into a biologic prospective by Grant and Regnier,ra6 who

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FIGURE 4.1. Leonardo da Vinci's drawings of the heart after removal of the pulmonary trunk above the valve (left drawing: lateral view; right drawing: frontal view). The two coronary arteries are clearly represented, one coursing on each side of the pulmonary outflow tract. The pulmonary sinuses are also precisely and correctly drawn in relation to the aortopulmonary contact point. (Courtesy of The Royal Collection@, Her Majesty Queen Elizabeth ll.)

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into two branches, one of which (transverse) continues on-

ical solutions to be temporarily adopted by common agree-

ward in the groove between the left auricle and ventricle. . . . The other (descending) courses along the posterior interventricular furrow. (Gray's Anatomy, 1901 editionsoe)

ment.

Since the beginning of this century, when the preceding passage was published in a leading textbook of human anatomy, there has been a continuously expanding awareness of the great variability of the coronary anatomy and the difficulty of defining normal coronary arteries. This expanding awareness has mainly been the result of the introduction of selective coronary angiography, coronary bypass surgery, and catheter-based angioplasty. A growing number of coro-

nary features have become clinically relevant, and an increasing number of variants have become apparent. Today, discussions of this subject are far more detailed than would have been considered relevantjust a few decades ago. Moreover, as further developments occur, discussions can be expected to become even more complex in the future. So far, the rich literature on coronary anomalies has been marred by a recurrent, inconclusive debate about the definition of coronary normality: What is normal (or unusual but normal) as opposed to atypical, abnormal, abenant,23a'23s' s05 anomalous, acces sory, ectopic, incidental, I e a v ariant,a a or a less common variant? What is a major or minora2'll5 anomaly or a clinically2e'a 12 or hemodynamically2o'e7'23 t titnificant anomaly? At a time when confusion still governs the terminology and concepts related to coronary anomalies, we would like to propose a method of study and a discipline that may promote a more rational organization of the subject matter. In this method, coronary anomalies are defined by exclusion, on the basis of a description of the normal coro1

nary anatomic features. This fundamental organizational concept, which one of us (PA) proposed in 1989,480 seems

to have been widely validated since that 1i-".82'tos'3oz gnlt by means of a feature-by-feature description of the normal coronary anatomy can coronary anomalies be defined. Some features, such as the presence or absence of a common main trunk of the left coronary artery @CA), are dichotomous; in these cases, normal is easily defined ("normal is to have a common trunk"). Other features are better described on the basis of a continuous spectrum of quantitative data, which can be assessed with a normal, or Gaussian, distribution curve observed in large populations. In such cases, "normal" should probably be defined as the interval between two standard deviations from the mean value, as commonly used in biologic studies. Additionally, the terminology used to distinguish normal and abnormal coronary arteries should be based solely on morphologic grounds and should avoid the issue ofclinical relevance. Clinical or functional repercussions of coronary anomalies are obviously important, and they will be discussed at the end of this chapter (see Pathophysiologic Mechanisms and Clinical Implications of Coronary Anomalies). Unfortunately, some questions cannot yet be resolved on the basis of currently available knowledge; in these cases, one can only propose certain criteria to be tested in further studies or certain empir-

METHODS FOR STUDYING CORONARY MORPHOLOGY

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Traditional descriptions coronary morphology are based on anatomic observations in necropsy specimens. The primary tools are gross inspection and fine dissection with the aid of magnifying loupes. Injection/corrosion methods involve both injection of a semisolid gelatin mass or of chemical fibers (which tend to solidify in response to changes in temperature) and corrosion induced by changes in the chemical environment. Injection of radiopaque media, followed by radiography, is also a well-established method for evaluating autopsy specimens. Each of these observational methodologies has its indications, advantages, and limitations. Gross Anatomic Inspection Gross anatomic inspection-obviously the simplest, most readily available method for examining autopsy specimens-is often quite adequate. It is preferred for studying the coronary ostial anatomy, because it is well suited for describing the location of the ostia with respect to aortic root reference structures (the semilunar leaflets, commissures, and sinotubular junction). Gross anatomic inspection (sometimes with the aid of magnifying lenses) is also preferred for describing the intrinsic anatomic features of the proximal coronary anatomy (for example, slitlike ostial ridges in coronary arteries that originate tangentially with respect to the aortic wall). For evaluating a coronary artery's course, distal distribution, and termination (as in cases of small anomalous fistulous communications), the gross anatomic approach is less appropriate: it is not as precise as injection-corrosion or radiographic methods. The great value of gross anatomic inspection lies in its convenience and negligible cost. Its most obvious limitation is its reliance on necropsy material. Indeed, because of the widespread clinical introduction of precise diagnostic imaging methods (such as computerized axial tomography, nuclear magnetic imaging, echocardiography, and angiogra-

phy), necropsy studies are currently performed with decreased frequency.

Injection-Corrosion Techniques Injection-corrosion techniques are quite satisfactory for showing coronary distribution patterns.le2'3sl'so8 At their most sophisticated level of execution, these techniques can allow visualization of even the finest collateral network. However, because this approach depends on comosion techniques to better delineate the coronary luminal spaces, it is inadequate for determining the relationship between coronary arteries and their adjacent structures (such as the depen-

Nom,rer eNl ANovrerous ConoNapy Anrnrurs dent myocardial segments). Moreover, injection-corrosion techniques are delicate, time-consuming, and expensive, requiring special technical knowledge on the part of the investigator. In recent decades, these techniques have largely been replaced by radiologic methods.

Radiologic Visualization Radiology may be performed in vivo, as well as in cadaveric specimens. In recent decades, in vivo selective coronary angiography has become an unparalleled tool for studying coronary anatomy. 2'48' 1zz' 146 3 s s,37 0,442 Because of this method's safety, its capacity for precise stereoscopic imaging (achieved by combining multiple simultaneous or sequential projections), and its excellent rendition ofcoronary anatomic details in motion (by means of enhanced radiologic techniques, digital enhancement, and electronic magnification), it is currently used in some 2 million patients per year worldwide. Moreover, it has been used in the great majority of recent investigational studies of coronary anatomy. In cadavers, radiologic single-plane coronary angiography inffoduces a serious artifact, related to superimposition of the different planes (the cardiac free walls, septa, atria, and ventricles). This artifact tends to negate the advantage of greater detail during visualization ofthe fine coronary anatomy in a nonbeating heart. To overcome this technical problem, Schlesinger35l proposed an "unrolling technique" by which the ventricular septum and both atrial walls are eliminated, transforming the cadaver heart into a flat surface. Obviously, this technique introduces other artifacts and precludes examination of certain relevant cardiac structures. Nevertheless, it is an expedient means of studying, for example, coronary dominance.

Newer Imaging Techniques Because of its high cost, coronary angiography is not appropriate as a primary screening test for ruling out corona"ry anomalies. For this purpose, noninvasive clinical imaging techniques are safer, more.convenient for the patient, and more cost-efficient-particularly echocardiography6'l 23'1 3 1' 33r but also nuclear magnetic resonance imagingee'lo7'222'41'2' 460'462'463 and computerized axial tomography at rapid rates of image acquisition. These methods can document the presence of a coronary anomaly or at least greatly raise the level of suspicion. For providing a thorough anatomic description, however, they are inferior to coronary angiography, not only because of their intrinsic physical characteristics but also because their basic approach is tomographic (whereas the coronary arteries do not lie in a single plane). Doppler signal interrogation can greatly enhance ultrasonographic imaging by facilitating vessel identification and providing flow velocity data. Echocardiography, magnetic resonance imaging,

and computerized axial tomography can frequently allow diagnosis of the larger coronar:y fistulas and anomalous origination of a coronary artery from the pulmonary artery. Orig-

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31

ination of a coronary artery from an anomalous aorlic location or from the anomalous course of a proximal coronary artery can also be reliably identified with echocardiography,otu especially using the transesophageal approach.aae' 482 OL the contrary, the distal coronary anatomy cannot be adequately visualized with these methods.sle's21 Questions related to myocardial perfusion, especially those aimed at ruling out myocardial ischemia in the presence ofcoronary anomalies, can best be resolved by nuclear myocardial perfusion scintigraphy coupled with exercise or pharmacologic stress testing or by metabolic radioactive tracers coupled with positron emission tomography. In the near future, these testing modalities will become more relevant: they will be used to definitively and categorically establish the clinical relevance of certain coronary anomalies that are still unclear and to guide the management of individual patients, based on objective evidence of reversible segmental ischemia.

NORMAL CORONARY ARTERIES IN HUMANS: DESCRIPTIONS AND DEFINITIONS

A coronary artery is dejined as any artery or arterial brqnch that carries blood to cardiac parenchyma (i.e., any structure located within the pericardial cavity). The cardiac parenchyma includes not only the myocardium but also the semilunar and atrioventricular valves, the great vessels (the proximal aorta, the pulmonary trunk, and a short segment of the superior vena cava), and the visceral pericardium or epicardium. The parietal pericardium should not be included, so the pericardial arteries should not be considered coronary. The name and nature of a coronary artery or branch is defined by that vessel's distal vascularization territory, not by its origin. A coronary afiery that arises from the right anterior sinus of Valsalva and that branches into the left anterior descending (LAD) and circumflex territories is not a right coronary artery (RCA) but, rather, a left main trunk with an ectopic origin. Similarly, the dffirent sinuses of Valsalva are identified not by the coronary arteries that originate from them but, rather, by their own topographic location.

When considering the spectrum of coronary morphologies, "normal" should mean "what is commonly observed,t' 3e4'48o and the terms abnormal or anomalous should be used for any form observed in less than l%o of the general human population.aso This criterion is proposed as the dividing line between (l) normality, which would include the more frequent variations (normal variants), and (2) abnormality, which would consist of relatively infrequent variations ( anomalie s ). In essence, a useful convention is all that, on purely anatomic grounds, distinguishes a normal coronary artery pattern from an abnormal variant. Only cenain anomalies (such as a coronary aneurysm) predispose the patient to a morbid state, and very few anomalies (such as anomalous origination of a coronary artery from the pulmonary artery) consti-

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tute, in themselves, a disease state. Pathophysiologic and clinical considerations should be clearly distinguished from, and subordinate to, anatomic description. With respect to its basic reference framework, the coronary artery anatomy should be related to the aortic sinuses at one extreme and the dependent myocardium at the other. The essential reference for describing the origination of the coronary arteries is the aortic root. Anatomically, the aortic root consists of three equal-sized507 semilunar leaflets, three intercuspal spaces, and three sinuses ofValsalva, as well as the sinotubularjunction, which separates the aortic root from the ascending aorta (Fig. 4.3). In a normal human heart, the aortic valve is situated posterior to-and slightly to the right

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pulmonary valve, just anterior to the recess between the tricuspid and mitral annuli (Fig. 4.4).The posterior wall of the aortic root is the anterior wall of the sinus transversus pericardii, a liquid-filled pericardial space that separates the aorta from the right and left atria (Fig. 4.4). The aortic and pulmonary valves have a single adjacent contact point, which is the consistent remnant of the embryologic aortopulmonary septum (Fig. a.q. This point is a useful reference for describing the semilunar cusps and sinuses. Indeed, the circumference of each semilunar valve is normally divided into three equal 120' sectors, and the aortopulmonary contact point is easlly and consistently locatable and helps identify the site of one (joining or adja-

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FIGURE 4.3. A and B. Diagrammatic representation of the aortic root in crosssection (grossly sagittal, view A) and in rectified form (unrolled root, view B), after excision of the semilunar cusps to reveal the implantation line of the cusps (view B, arrows). The aortic root is limited distally by the sinotubular junction. The sinuses of Valsalva are limited distally by the sinotubular junction and proximally by the implantation line of the cusps. The bottom section of each cusp is shadowed to indicate the underlying muscular septum (view B, solid circle). The intercuspal triangles or spaces (view B, asterisk), have different wall constituents depending on the

anterior fascicle of the bundle of His; AsAO : : left atrial wall; M : section of mitral valve; MS : membranous septum; NC : so-called noncoronary sinus; pp : posterior fascicle of the bundle of His; R : right sinus; STJ : sinotubular junction; TS : transverse septum. View B: ICS : intercuspal space or triangle; IVS : interventricular septum; L : left sinus; MS : membranous septum; MV : anterior leaflet of the mitral valve; NC : so-called noncoronary sinus; R : right sinus; STJ : sinotubular junction; SV - sinus of Valsalva. C. Relationship between the aortic root and the right ventricular cavity. AO : aorta, AP : anterior papillary muscle of the tricuspid valve; AR : anterior right pulmonary cusp; C : crista supraventricularis; MB : moderator band; P : posterior pulmonary cusp; R : raphe of the right ventricular outllow tract (a residual sign of the fusion line between the embryologic conal ridges); RA : right atrial anteriorwall; SM : crista septo-marginalis. Shaded area : membranous ventricular septum. specific location. View A: AF

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Crrarran 4

Origination of the Coronary Ostia Normally (i.e., in more thanl%o of individuals),the human

corondry arteries have two or three coronary ostia.a2r Whereas two ostia (the right and left) are typically present, it is also normal to see a separate aortic ostium for a conal or infundibular branch, or third coronary utt"ry.tto which is present in 23 to 5lVo of normal h"r1r.1e1'3sl'so8 Less frequently, separate origination of the LAD and circumflex arteries from the aorta, in the absence of a common left main trunk, produces a third (or fourth) coronary ostium. This condition was studied by several anatomists, and the reporled frequency of absent left main trunk varied from 0.4 to 8.07o, depending on the criteria used by the different investigators.ea'1e2'3st'3e1'413's08 If the defining criterion is minimal evidence of a common left main trunk, however rudimentary, like a common aortic niche, the lower estimates are correct. In contrast,

if

the criterion is absence of a clearly individualized common trunk, the higher estimates are cor-

rect. The question of whether an absent left main trunk is an anomaly or a normal variant will be discussed again later in this chapter. The coronary ostia are normally located in the middle of the right anterior and left anterior sinuses, just above the upperfree margin of the semilunar leaflets (in the open position) and just below the sinotubular junction. This general rule applies to cases involving two, three, or even four coronary ostia. As already suggested in the literaturs,le'23'227'4tz' 480

a

specific, detailed anatomic study needs to be undertaken

with the aim of establishing, in a large human population with normal hearts, the spectrum of coronary ostial distribution in both the horizontal plane (oriented along the circumference ofthe aortic annulus) and the vertical plane (oriented along the longitudinal axis of the ascending aorta). Only after a precise description becomes available can the standard deviations in the two axes be determined and anomalies be exactly defined (Fig. a.6). Normally, the proximal segment of a coronary artery arises at a nearly orthogonal angle from the aortic wall

FIGURE 4.7. Cross-sectional view of the right coronary cusp, showing four examples of variant coronary origination: 1, normal, grossly orthogonal to the aortic wall; 2, uplifted; 3, downward with a tangential path (in a case of ectopic origination

from the ascending aorta); 4, horizontal (in a case of low, ectopic origination).

Gig. a.1). This angle has never been precisely studied in a large population, and the normal range has never been established, but it is important that distinctly unusual angles of coronary origination be recognized, especially during selective catheterization in clinical studies. Coronary ostia that originate ectopically are consistently associated with acute ( ' 'tangential' ' ) arterial origination from the aortic wall, and only rarely does acute angulation occur in the context of a

normal ostial location. In size, the coronary ostia are typically equal to, or larger than, the proximal segment of the related coronary artery.3ol As the coronary arteries produce side branches and progress downstream, they gradually decrease (but never increase)

in diameter. The course of the coronary arteries is mostly epicardial, l-4D is intramural in 5 to 257o of cases, producing a systolic narrowing or milking effect when observed angiographically (see Intramural Coronary Artery). The coronary arteries normally terat least in humans, although the proximal

minate

in the capillary

network via arteriolar segments,

which are responsible for most of the coronary tree's hemodynamic resistance (see Overview of Coronary Physiology). Direct coronary artery communications with the cardiac cavities or with veins are considered generically abnormal (see Anomalies of Termination: Coronary Fistulas).

Although an ideal "coronary luminal size/dependent myocardial mass ratio" no doubt exists, its normal range has been difficult to define. FIGURE 4.6. Schematic representation of the aortic root and the ascending aorta, showing the conceptual pattern of distribution of the right (R) and left (L) coronary ostia in the vertical (for the right) and horizontal (for the left) planes (vp and hp, respectively). See text.

I

75,20 s,23o,233,217,28 1,3o 1,4o8,428,4ee

It is important that this ratio be clarified, however, to better elucidate anomalies such as coronary ectasia, coronary aneurysm, coronary hypoplasia, or absent coronary artery. The current open debate about how to define these entities stems from the lack of universally accepted parameters of normal

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Cneprrn4

FIGURE 4.11. Relationship between coronary arteries and cardiac structures as seen in the frontal (A), right anterior oblique (B), and left anterior oblique (C) projections. AO : aorta; LV : left ventricle; M : mitral valve; PA : pulmonary artery; RV : right ventricle; T : tricuspid valve.

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coronary angiography, when myocardial blushing is frequently seen, especially in the left anterior oblique projection, during angiography of both the LCA and the

TABLE 4.2. lncidence of coronary anomalies and patterns, as obserued in a continuous series of 1950 angiograms

RCA.

Coronary anomalies (total) Split RCA Ectopic RCA (right cusp) Ectopic RCA (left cusp)

margin of the heart (left ventricle) was identified by recognizing the border of the heart in the left anterior oblique projection (at about 45"; see Figures 4.8 and 4.11). The circumflex artery was identified as the vessel that coursed in the left atrioventricular groove, crossing the obtuse margin of the heart. The larger lateral wall branches, starting from the obtuse margin and moving posteriorly toward the posterior descending artery, were labeled the obtuse marginal I (OMl), obtuse marginal 2 (OM2), and obtuse marginal 3 (OM3). Right coronary branches. We used the following nomenclature for right coronary branches: a. "Infundibular (or conal) branch" (Fig. 4.I2) was

6. The obtuse

used to designate branches that serve the anterior free

wall of the right ventricular outflow tract (grossly

b.

the 3- to 5-cm segment of myocardial territory below the pulmonary valve). These branches may have direct independent aortic origination. Because infundibular branches that originate separately are usually smaller than the tip of the diagnostic catheter, selective catheterization of such independent branches was rarely observed. "Right ventricular branch" was used to designate branches that serve the free wall of the inlet and the

apical portion of the right ventricle. We tried only to identify the acute marginal branch as the artery that lies closest to the acute margin of the heart. The acute margin of the heart was identified angiographically as the lowest point in the "C" described

by the RCA in the left and right anterior oblique

Number

Variable

110

24 22

Fistulas

Absent left main coronary

Percentage 5.64 1.23 1.13

18 17 13

0.92 0.87 0.67

13

o.67

artery

Circumflex arising from right cusp LCA arising from right cusp Low origination of RCA Other anomalies Coronary dominance patterns Dominant RCA Dominant LCA (circumflex) Codominant arteries (RCA, circumllex)

LCA

:

3 2 3

left coronary artery; RCA

0.15 0.1

0.27

1641

89.1

164 48

8.4 2.5

:

right coronary artery.

tuse margin and sometimes including the posterome-

dial papillary muscle (Fig. a.8). Correlations (Table 4.3 )

After identifying the variant anatomic pattems, we related them to the following variables: sex, the presence of coronary disease (criterion: )507o obstruction of vessel with a lumen larger than 1.5 mm), the presence of a primary cardiomyopathy (myocardial systolic dysfunction in the absence ofcoronary disease and/or a clinical history ofmyocardial infarction able tojustify contractile dysfunction). Coronary anomalies were classified according to the scheme

views (Fig. 4.12).

c. "Posterior

descending branch" was used to designate the branch that follows the posterior interventricular groove and is angiographically identified by the posterior septal penetrating branches (Fig. a.I2). Compared with the anterior septal penetrating branches, the posterior ones are shorter, frequently being similar in length to the penetrating branches in the free wall of the left ventricle. For this reason, our favored means of identifying the posterior descending branch (and, hence, the dominant artery) was the myocardial blush phase during coronary angiography in the left anterior oblique projection, especially with a caudal tilt, when available. We used

the term "codominant circumflex and RCA" for cases in which two branches, one from each ofthese

arteries, coursed

into the posterior

descending

groove, providing septal perforators (Table 4.2).

d. "Posterolateral"

was used to designate branches that

provide flow to some portion of the posterolateral wall of the left ventricle, extending as far as the ob-

TABLE 4.3. Correlations Variable

Number

Men with coronary anomalies Women with coronary anomalies Patients with CAD and coronary

66/1 369 44/581 63/1 290

4.82 7.6 4.96

57/1950

8.6

7511950

3.8

anomalies Patients without CAD and coronary anomalies Patients with aortic valve anomalies Patients with aortic valve anomalies and coronary anomalies Patients with cardiomyopathy Patients with cardiomyopathy and coronary anomalies Patients without cardiomyopathy but with coronary anomalies

aP:.90(NS) be:.es1rus;. CAD

:

coronary artery disease

20175

96/1 950

5/96 1

05/1 854

Percentage

26.7

4.924 5.2^'b 5.7b

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TABLE 4.4. Classification of coronary anomalies in (normal) human hearts

A) Anomalies of origination and course 1) Absent left main trunk (split origination of LCA) 2) Anomalous location of coronary ostium within aortic

3)

root or near proper aortic sinus of Valsalva (for each artery): a) High b) Low c) Commissural Anomalous location of coronary ostium outside normal "coronary" aortic sinuses a) Right posterior aortic sinus b) Ascending aorta c) Left ventricle d) Right ventricle e) Pulmonary artery Variants: 1) LCA arising from posterior facing sinus 2) Cx arising from posterior facing sinus 3) LAD arising from posterior facing sinus 4) RCA arising from anterior right facing sinus 5) Ectopic location (outside facing sinuses) of any coronary artery from pulmonary artery . From anterior left sinus . From pulmonary trunk . From pulmonary branch f) Aortic arch g) lnnominate artery h) Right carotid artery i) lnternal mammary artery

j)

Bronchialartery

k) Subclavian artery

l)

Descending thoracic aorta

4) Anomalous origination of coronary ostium from opposite, facing "coronary" sinus (which may involve joint origination or adjacent double ostia). Variants: a) RCA arising from left anterior sinus, with anomalous course: 1) Posterior atrioventricular groove* or retrocardiac 2) Retroaortic" 3) Between aorta and pulmonary arlerya

4)

b)

a

lntraseptal"

5) Anterior to pulmonary outflowa or precardiac 6) Posteroanterior interventricular groovea LAD arising from right anterior sinus, with anomalous course: 1) Between aorta and pulmonary arlery 2) lntraseptal 3) Anterior to pulmonary outflow or precardiac 4) Posteroanterior interventricular groove

c)

d)

Cx arising from right anterior sinus, with anomalous course: 1 ) Posterior atrioventricular groove 2) Retroaortic LCA arising from right anterior sinus, with anomalous course: 1) Posterior atrioventricular groovea or retrocardiac 2) Retroaortica 3) Between aorta and pulmonary arterya

4) lntraseptal' 5) Anterior to pulmonary outflowa or precardiac 6) Posteroanterior interventricular groove" B)

5) Single coronary artery Anomalies of intrinsic coronary arterial anatomy 1) Congenital ostial stenosis or atresia (LCA, LAD, cx)

RCA,

a) Coronary ostial dimple b) Coronary ectasia or aneurysm 2) Absent coronary artery 3) Coronary hypoplasia

4) lntramural coronary artery (muscular bridge) 5) Subendocardial coronary course 6) Coronary crossing 7) Anomalous origination of posterior descending artery from anterior descending branch or septal penetrating branch 8) Absent PD (split RCA) Variants: a) (Proximal + distal) PDs, both arising from RCA 9) Absent LAD (split LAD). Variants: a) LAD + first large septal branch b) LAD, double 10) Ectopic origination of first septal branch C) Anomalies of coronary termination 1 ) lnadequate arteriolar/capillary ramifications? 2) Fistulas from RCA, LCA, or infundibular artery to: a) Right ventricle b) Right atrium c) Coronary sinus d) Superior vena cava e) Pulmonary artery f) Pulmonary vein g) Left atrium h) Left ventricle i) Multiple, right + left ventricles D) Anomalous collateral vessels

lf a single, common ostium is present, the pattern is considered to represent "single" coronary artery. circumflex; LAD left anterior descending coronary artery; LCA left coronary artery; PD posterior descending branch; RCA right coronary artery.

Cx

:

:

:

:

:

11s'287

coronary artery inside the atrial septum. Our proposed classification scheme is based on our own experience as angiogra-

course,"

phers and a thorough review of the pertinent literature. It stresses a meticulous, orderly approach in which each feature of the normal coronary anatomy is viewed as a criterion for potential anomalies. We prefer to combine the traditional headings "anomalies of origin" and "anomalies of

cept in arteries). Rather than favoring alphabetical-numerical listings, we prefer descriptive, clear terminology that identifies each anomaly. Moreover, we prefer to avoid labeling an anomaly with the name of its purported discoverer.

6""urrse a coronary artery's proximal course if that artery's origin is abnormal (exthe case of intramural or subendocardial coronary

can be abnormal only

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Anomalous Location of a Coronary Ostium Outside the Normal ttCoronary" Aortic Sinuses Ectopic Coronary Ostium Located at or near the Right Posterior Aortic Sinus (Noncoronary) The right posterior coronary sinus is commonly termed "noncoronary" because coronary ostia are only rarely, if ever, observed in this rinur.77'2le'28s'13s's26,s27'sze A fundamental condition for including a case in this category is the presence of a normal, trifoliate aortic valve. Some of the patients reported in the literature have had, or could have had, substantial anomalies of the aortic valve, mainly of the bicuspid kind. In most true cases of these anomalies, the ectopic ostium has a commissural location: usually it is the LCA ostium that is located next to the posterior left commissure. In itself, this anomaly is benign unless it involves a tangential origin (as it frequently does), in which case it may carry an increased risk of ostial stenosis and/or enhanced

spasticity. During coronary angiography, this anomaly causes difficult cannulation as a result ofits unexpected location and its tangential or slitlike nature. When this anomaly is suspected after initial unsuccessful attempts to cannulate, biplane aortography is recommended. The right anterior oblique and straight lateral projections are the most contributory ones for establishing posterior origination of the LCA. The relationship between the ostium and the aofiic sinuses should be documented, preferably using the right anterior oblique projection with a cranial tilt and selective iniections. For selective catheterization, the operator must be highly skilled and patient.17e,21e,3oo.s2e The Amplatz or Multipurpose curved catheters offer the best chance of success. Alternatively, the Sones catheter, advanced from the brachial artery, offers a favorable approach. In addition, intravascular ultrasound has recently been used to identify this anomaly (Fig.4.l3).527 This anomaly should be ruled out when selective cannulation cannot be achieved with Judkins left-sided catheters

FIGURE 4.13. A. lntraaortic ultrasound image showing the left main coronary artery (LM, white arrow) originating from the square coronary sinus. B. The artery courses posteriorly around the left coronary sinus and gives rise to the left anterior descending aftery (LAD, white arrow). The ultrasound transducer's position (in the left coronary sinus in view A and the right coronary sinus in view B) is indicated by the dark central square with the surrounding bright halo of ring-down artifact.

The imaging field is scaled by 8-mm divisions. LCC : left coronary cusp; NCC : noncoronary cusp; RCC : right coronary cusp; RVOT : right ventricular outflow tract. (From Lo et al. Anomalous origin of left main coronary artery from the noncoronary sinus: an intravascular ultrasound observation. Cathet Cardiovasc Diagn 1997;42:431. Reprinted with permission.)

In the presence of this anomaly, angioplasty of any LCA's branches would also offer unusual difficulties because of precarious selective cannulation and back-up support. (See Case Reports 4.8 and 4.9 in the Atlas of Case Re-

usually involves the anterior/left surface ofthe aorta.l80'201. In the rare cases reported in the literature, the site of coronary origination has ranged from just above the sinotubular junction to the origin of the innominate artery, several centimeters above the aorlic valve. This condition differs from the previously discussed milder anomalies (page 45) in that, here, the ostium is clearly located above the sinotubular region of the aortic root; the ectopic coronary arteries frequently have slitlike orifices and a tangential proximal course along the aorlic wall, on which they lie, loosely attached to the aortic tissue. Occasionally, the proximal coronary segment is intramural, inside the aortic wall, and is intussuscepted for 0.5 to 5.0 cm.32s Once the ectopic coronary artery reaches the epicardial surface, it regains a normal location and course. The RCA is the most frequently ectopic artery, but the LCA (or, separately, the LAD and circumflex artery) may also originate ectopically. Although an ectopic proximal artery course is not a pathologic condition in itself, the artery may be predisposed to have a more active atherosclerotic buildup, especially at the ostium, per-

ports)

haps because ofrheologic factors and unusual shear stress.4oe

and nonselective angiography shows a longer than usual left

main trunk. The anomaly is generally considered benign,le, 186'411 un6 the literature contains only one case in which origination of the left main artery from the noncoronary sinus led to a clinical event, namely the occurrence of a large, fatal anterior myocardial infarction in a l2-year-old girl.sze The mechanism of coronary occlusion in this case was probably clot formation in the slitlike ostium of the anomalous vessel.

Ectopic Coronary Ostium Arising Outside the Aortic Root, in the Ascending Aorta An ectopic coronary ostium located outside the aortic root,

in the ascending aorta, can be present at different levels but

234'344'3eo

Angiography of this type of anomaly is frequently challenging and incomplete. The basic initial condition that should alert the angiographer is the absence of a coronary ostium at the expected site. In such cases, the first step is to rule out ostial atresia or occlusion, as suggested by retrograde filling of the distal "missing" artery from the contra-

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Ectopic Coronary Artery Arising from the Pulmonary

Artery As a major coronary anomaly that commonly manifests in the pediatric age group,a3'104 ectopic coronary artery originating from the pulmonary urtery is more thoroughly discussed in Chapter 5. The present chapter covers general anatomic and nosologic considerations regarding this condition. Anomalous origination of a coronary artery from the pulmonary artery is defined as that condition in which a coronary artery carrying nutrient flow anatomically arises from the pulmonary main trunk.ae Indeed, a coronary artery is also connected to the main pulmonury artery (or its branches) in some cases of coronary fistulas.26 To further confuse this issue, anomalous origination of a conal branch from the main pulmonary artery may result in a condition that resembles a coronary fistula both angiographically and anatomically. Interestingly, in anomalous origination of a coronary artery from the pulmonary artery, the direction of the fistulous flow is toward the pulmonary artery, 8'113'306'318'33e'452 as seen in coronary-to-pulmonary fistulas. Nevertheless, in the present condition, blood flow originates from the contralateral, normally originating, coronary artery; whereas in coronary-topulmonary fistulas, flow originates from the coronary aortic ostium of the artery that has the fistulous communication. The following forms of ectopic origination of one or more coronary arteries from the pulmonary artery have been rep orted.T

3' r97'27 7'27 a'426

o Anomalous LCA arising from the posterior facing sinus of the pulmonary afiery or from the pulmonary trunk or branches (the most common form, abbreviated as ALcAPA)467

o (Isolated) circumflex artery arising from the pulmonary

clinical manifestations and anatomophysiologic forms are not adequately characterized by the terms "infantile" or "adult" or similar fuzzy descriptors (see Chapter 5) but, rather, require a more complex terminology. ALCAPA varies greatly with respect to clinical presentation, prognostic implications, and the optimal choice and timing of therapy. Its treatment depends on multiple anatomic, functional, and clinical variables, including the fol-

lowing factors:

r o o

o o

. o

The coronary dominance pattern (the larger the RCA, the better the results of simple ligation of the ectopic vessel and the overall prognosis) Obstruction of the ectopic ostium (the more severe the obstruction, the better the natural prognosis) The extent of acquired coronary artery obstructive disease (the more extensive the disease, the more severe the myocardial ischemia) Epicardial versus intramural collateral patterns (the former pattern promotes fistulous flow, and the latter one favors nutrient flow) The myocardial oxygen demand (which is related to left ventricular dilation, diastolic volume overload secondary to a left-to-right shunt and mitral regurgitation, and systemic vasoconstriction) The pulmonary artery pressure (the higher the pressure, the lower the fistulous flow)276 Body weight and lifestyle factors

Less common, clinically different conditions-anomalous origination of the RCA, LAD, or circumflex artery from the pulmonary artery-are presented here, as they are usually compatible with prolonged, frequently asymptomatic, survival in the adult age groupl.

artery (posterior facing sinus) or one of its branchessT'74' 169,292

r

Anomalous Origination of the RCA, I-AD, or Circumflex Artery From the Pulmonary Artery

o

Each of these three anomalies has different pathophysiologic consequences and clinical presentations. Origination of the RCA from the pulmonary artery has been described in several recent isolated case reports.l l7'130'214'226'2st'252' 264'312374347'4o0'416'42,J In most instances, the ectopic ostium was described as being located at the anterior right pulmonary cusp, and the RCA was dominant, with a posterior descending branch. In such cases, collateral circulation be-

(Isolated) LAD arising from the posterior facing sinus of the pulmonary urt"rynt o RCA originating from the anterior facing sinus of the pulmonary artery or from the pulmonary trunk or its branChes

I

o2,25 1,264 37 a,42o

Simultaneous RCA and LCA arising from the pulmonary artery3e8'+sr'+6s'a7a (sometimes originating in a single com-

mon trunkso3)

o Small (right infundibular or conal) branch arising from the anterior facing sinus of the pulmonary artery Occasionally, ostial stenosis involving a ridge or fibrous buildup is observed in the pulmonary arterial wall.2s2 This condition may significantly decrease fistulous flow. Anomalous origination of the entire LCA from the pulmonary aftery (ALCAPA) has distinct clinical features that are discussed in Chapter 5. In the literature and in clinical practice, several taxonomic classification criteria have been proposed, mainly in response to the clinical need for distinguishing between subtypes of ALCAPA that have different prognostic and therapeutic implications. This anomaly's

tween the LCA and the RCA follows the patterns seen in atherosclerotic occlusion of the coronary arteries: the atrial, infundibular, right anterior, and septal branches may contribute to variable degrees in individual cases (Fig.4.l5A). The septal branches are usually the dominant source of collateral flow (from the LAD to the posterior descending artery). These enlarged vessels, with their fistulous flow. are prominently displayed not only during angiography but also during echocardiography with Doppler interrogation (Fig. 4.15). In adults, the condition is typically recognized because of a heart murmur or when angiography is performed for ac-

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CHaprsR.4

aorta with the aid of extracorporeal circulation and transec-

tion of the pulmonary artery (see Chapter 5). The ectopic circumflex artery more typically originates from a pulmonary branch (the proximal right or left), and reimplantation necessitates careful dissection. Unlike in ALCAPA, the ratio of fistulous to nutrient flow seems to favor nutrient flow, so that myocardial ischemic manifestations tend to be more limited and to occur only with maximal exercise. Frequently, a relatively obstructive ectopic coronary ostium will also limit the fistulous flow. The amount of absolute flow probably perpetuates an intrinsic mechanism of progressive enlargement of the involved vessels.

l03

Although ectopic origination of a coronary artery from the pulmonary artery is routinely subjected to surgical repair,

the need for repair has not been well established.l2s In the absence of major clinical manifestations (recurrent angina, myocardial infarction, venfficular arrhythmias, syncope, or aborted sudden death), anomalous origination from the pulmonary artery may not, in itself, be an automatic indication for surgery, especially if the anomalous vessel is a smaller one such as a nondominant RCA or a circumflex artery. In such cases, stress testing is frequently negative forreversible ischemia in adult patients, although mild fixed myocardial uptake defects are frequently found on nuclear images, because of old scar tissue and/or a rich collateral network, which replaces myocardial tissue. 12s'2@ Progressive enlargement of the dilated coronary vessels, with the risk of intimal changes, mural thrombosis, and/or accelerated atherosclerosis, is a possibility in these cases, just as in primary coronary fistula. This factor tends to encourage early intervention (during childhood or the patient's teen years), because otherwise the extremely dilated vessels with increased flow would be transformed, by surgical correction during adult life, into aneurysmatic vessels with normal flow, yielding a persistently poor prognosis because of the risk of mural thrombosis. After correction of this anomaly, coronary ectasia may undergo reversal in young patients but will not generally do so in older ones. The survival of untreated older patients is an indication, if not proof, of the benign nature of the anomaly in such instances. Moreover, the surgical risks may be substantially greater and the potential benefits fewer in older patients, causing many physicians to prefer continued medical treatment and some surgeons to prefer simple ligation (versus the more complex reimplantation) of the ectopic vessel. (See Case Report 4.1

I

in

the Atlas of Case Reports)

Ectopic Coronary Ostium Arising from the Aortic Arch, Innominate Artery, Right Carotid Artery, Internal Mammary Artery, Bronchial Artery, Subclavian Artery, or Descending Thoracic Aorta

descending thoracic aorta63 in humans. Most of these reports mention accompanying major congenital heart defects.63.330 In such cases, the proximal coronary trunk's ectopia reproduces, in humans, the normal coronary pattern seen in various animals (see Chapter 1). Reports of bronchial origination of a coronary artery (see also Coronary-Bronchial Fistula, page62) should be examined critically: because both the bronchial and the coronary arteries are normally subject to the same systemic pressure, no flow could be expected in the absence of a congenital coronary obstruction or a suprasystemic pulmonary pressure with an inverted patent ductus arteriosus (usually in the presence of a hypoplastic left heart syndrome). In cases of uncomplicated extracardiac origination of the coronary arteries from the systemic circu-

lation, no myocardial ischemic effects are generally expected.

Anomalous Origination of a Coronary Artery from the Opposite, Facing Sinus of Valsalva As stated earlier, the right, left, LAD, and circumflex coronary arteries are defined by virtue of their territory of distribution, not by their origination.taT When a coronary artery arises anomalously from the opposite-from-normal sinus of Valsalva, the artery's intrinsic name and nature (or function) remain unchanged, and only its origin and proximal course are anomalous.2o8 Of necessity, the artery's proximal course is abnormal in these cases, as the artery connects with the contralateral, in situ vascular network. Because these anomalies are chNacteized by abnormal origination of an otherwise "normal" coronary artery from the opposite sinus of Valsalva, it is important that the essence of a coronary artery (in contradistinction to, and independently of, its origin)be clearly defined. Indeed, conceptually the human heart has not two, but three, coronary arteries: the RCA, LAD, and circumflex. The essence of each of these arteries was discussed previously (pages 35-38), and it becomes clear in light of the spectrum of possible variations described in this section. The RCA is essentially that artery that courses in the right atrioventricula"r groove and provides nutritive branches to the free wall of the right ventricle. Branches that supply the right ventricular infundibulum, or conus, often originate directly from the right aortic sinus and are not an essential part of the RCA. The same is true of the sinus or atrioventricular nodal arteries and the posterior descending branch: all of these branches may originate anomalously without changing the nature of the RCA. Similarly, the LAD is essentially that artery that courses along the anterior interventricular groove and provides perforating branches to most of the anterior ventricular septum. It is not essential that the LAD provide a diagonal branch

The literature contains rare reports of extracardiac origina-

(although it usually does) or reach the apex, but it is essential

tion of the coronary arteries from the aortic arch,63 innominate artery,86 right carotid artery,63 internal mammary eirtery,32e'zzo bronchial artery,63 subclavian artery,33o or

for the LAD to course mostly in the anterior subepicardial space. Cases in which a large, entirely intramyocardial first septal artery provides most of the anterior perforating

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FIGURE 4.17. Conceptual diagram showing most of the possible paths (1 through 5) by which the RCA, LAD, and circumflex anery (Cx) can potentially connect with the opposite coronary cusps. Paths: 1, retrocardiac; 2, retroaortic; 3, preaortic, or between the aorta and pulmonary artery; 4, intraseptal (supracristal); 5, prepulmonary (precardiac). The aortic and pulmonary cusps are labeled according to

theirpositioninspace: AL:antero-left; AR:antero-right; P:posterior;

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path most commonly associated with this type of anomaly,

specifically involving origination of the circumflex artery from the right sinus of Valsalva.al'334'36s This anomaly's incidence in the general population ranges from 0.1 to 0.9Eo,2t"'4r including cases in which the circumflex artery has a separate origin, adjacent to the RCA ostium, and those in which the circumflex artery arises jointly with the RCA from

a

common short, mixed trunk. The anrmalous retroaor-

tic circumflex path courses just next to the posterior wall of the aorta, in the sulcus between the atria and the aorta (the transverse sinus), and finally reaches a normal location in the left atrioventricular groove, providing pathognomonic angiographic features.ar Cardiac surgeons should be especially aware of this anomalous coronary path, because placement of sutures at the aortic or mitral annulus during valve

replacement might compromise the aberrant vessel. Otherwise, the anomaly, in itself, is not expected to have any

clinical consequences.336 The same retroaortic path can also be observed, although less frequently,32a when the RCA originates from the left sinus (either directly or, more often, from a common mixed trunk), and when the entire LCA originates from the right sinus. The retroaortic path is not seen, however, when the LAD has an isolated ectopic origin. Path 3, the preaortic anomalous path, (Fig. 4. 17) courses "between the aorta and pulmonary artery. " This terminology alludes to the fact that an anomalous RCA or LAD or left main trunk (but never the isolated circumflex atlery) subepicardially crosses the aortopulmonary septum or space. Embryologically, the aortopulmonary septum is initially in-

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TABLE 4.5. Single Coronary Arteries: Classification Criteria Sinus of Origination 1) Right anterior sinus 2) Left anterior sinus 3) Posterior sinus 4) Ectopic sinus, at: A) Ascending aorta B) Systemic artery C) Pulmonary artery Pathways Followed by Each Ectopic Branch Arising From the Proximal Trunk' 1) Retrocardiac (circumflex, LCA or RCA) 2) Retroaortic (circumflex, LCA, or RCA) 3) Preaortic (LCA or RCA) 4) lntraseptal (LCA, LAD, or RCA) 5) Precardiac (LCA, LAD, or RCA) a Any individual case may involve more than one anomalous path.

location, their sequence of origination, and the proximal course of their anomalous coronary branches.362 Excluded from this list are several conditions that resemble single coronary artery but involve ectopic origination of a coronary artery from the opposite cusp, from an additional ostium adjacent to the normal coronary ostium for that cusp. To conclusively establish the diagnosis of single coronary artery, angiographers and anatomists should verify (1) the presence of a single ostium in one sinus, jointly with the absence of an ostium in the opposite sinus, and (2) the lack of origination of any other coronary artery from an ectopic site. This process is usually quite simple for anatomists but may be harder for angiographers, who may encounter difficulties in ascertaining that the arlery in question indeed supplies all ofthe heart and that no additional ectopic coronary artery exists. Functionally, single coronary aftery has essentially the same clinical implications as ectopic coronary origination from the opposite sinus but with separate ostia; nevertheless, a single coronary ar1ery is not as susceptible to tangential origin or ostial ridge pathology as are ectopic coronary a.rteries with independent ostia. Coronary blood flow is not affected by the simple presence of a single proximal trunk that supplies coronary flow to the entire heart, unless congenital or acquired obstructive disease is present in the proximal mixed trunk.22'157 lnsuch a case, the hemodynamic repercussions would be quite severe,24'423 as the whole heart could become ischemic without having any possible source of collateral circulation. Although definitive studies are not available, the incidence of atherosclerotic disease does not appear to be increased in the mixed trunk. An ectopic single coronary ostiuml80'le8 could, indeed, be more susceptible to congenital (ostial) or acquired obstructive disease, but the rarity of this anomaly precludes adequate analysis. During coronary angioplasty, a few minor adjustments are necessary in patients with a single coronary artery.21'rae' 37s'421 1n the presence of a single ostium, even the temporary

creation of an ostial obstruction (by means of a large guiding catheter or any other instrument, such as the bulky directional atherectomy device) would be poorly tolerated and could cause symptoms (angina, dyspnea, light-headedness) and important changes in physiologic variables, including blood pressure. In general, angioplasty of the common trunk is absolutely contraindicated, even with the use ofstents, not only because of the increased perioperative risk but, more importantly, because of the risk of postoperative restenosis resulting in sudden death (a risk that is expected to be even higher than after angioplasty of the left main trunk). During coronary artery bypass surgery, the presence of a single coronary artery should not affect any technical decisions, except fbr suggesting the absolute need for as many arterial conduits as possible. Proximal mixed trunk obstruction is particularly relevant in this regard, because it tends to progress to total occlusion soon after successful bypass surgery. In contrast to venous grafts, arterial grafts are expected to provide longer-lasting conduits. If graft occlusion does eventually occur, it will likely be fatal because of the presence of total occlusion of the native circulation.

ANOMALIES OF INTRINSIC CORONARY ARTERIAL ANATOMY Congenital Ostial Stenosis or Atresia The literature contains occasional repofis3o's l'1 3e'337'423 o1 coronary arteries that are u1aa1i"l60'ass'a7s'4e2 or stenosed because of a membrane or fibrotic ridgeles located at, or near,

the aortic orifice in an otherwise normal heart. In cases of atresia, only a dimple is seen from the aortic side.13 Histologically, when the obstructive element is congenital, it invariably consists of fibrous tissue. A stenosis observed during angiography, surgery, or autopsy may be subject to debate regarding its nature (congenital versus acquired;.13e'337 The condition may be associated with a coronary anomaly, some-

times involving tangential origination

of a coronary

ar-

Indeed, atherosclerotic growth may occur early in life at the site of a congenital ostial fibrotic plaque.2se Coronary ostial or proximal occlusion frequently occurs in the context of pulmonary valve atresia with intact ventricular septum (see Chapter 6); in extreme cases, both the RCA and the LAD may be affected by ostial atresia.3e6 Isolated coronary ostial atresia (total occlusion) probably represents the extreme degree of improper formation of the aortic ostium, and its presence often raises two questions: first, is the condition congenital or acquired, and second and more importantly, is it truly a case of ostial atresia or is it anomalous origination? The congenital cases could be regarded as instances of neonatally or fetally acquired ostial occlusion, which occurs after a normal distal coronary tree has already developed (however, such occlusion would most likely occur after embryologic development). Ostial atresia in the left corona.ry system can potentially occur, not only at the aortic connection site but also at the left main bifurcation, the site tery.326'z+o

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As suggested by R. D. Leachman (oral communication, 1989), some cases of syndrome X (angina and myocardial ischemia in the absence of coronary obstruction) may be caused by a defective number of capillaries per myocardial fiber. This syndrome has never been definitely documented and is not identical with what has been called "absent coror'ary artery" in the literature. On angiographic grounds, the most frequent reasonses for an apparently missing coronary artery are coronary ectopia (misdiagnosed), coronary occlusion with lack of demonstrable collateral retrograde fi.lling,22s'433 or an alternative coronary artery tree pattern that may not be recognized on angiography. Although the literature includes sporadic cases in which an absent coronary artery was reported to cause chest pain,r78 cardiomyopathy,3a or a myocardial infarction,z2a absence of a coronary artery has never been established as a

specific congenital entity. (See Case Report 4.6 in the Atlas of Case Reports)

Coronary Hypoplasia a

Several reports have appeared in the literature alluding to poorly defined entity called coronary hypoplasia.8T'13'7'26t'

322'a2s

Butli"t in this chapter, we discussed the difficulty of

demonstrating congenital inadequacy of coronary vessel size. Normal coronary arterial size should be defined in terms of both resting metabolic needs and coronary reserve. Epicardial coronary branches normally maintain an ideal luminal diameter ratio with respect to the dependent myocar-

dial bed or territory or capillary

network.2os'23o'233'z8t'3ot

Gouldras theorized that flow velocity is the most practical parameter for measuring the adequacy of vessel diameter: a higher than normal flow velocity would imply a vessel size that is restricted in comparison to the distal arteriolar-capillary network. However, this type of measurement was previously quite impractical; it became clinically possible only

recently, with the introduction of flow velocity wires, and has not yet been used to substantiate the claim of coronary hypoplasia. A more practical diagnostic method may be based on the simultaneous (1) angiographic appearance of a "hypoplastic" coronary branch (that has a small diameter with respect to the apparent area of dependent myocardium) and (2) demonstration of local reversible ischemia (reduced coronary reserve) during stress testing with myocardial nuclear scintigraphy. We are not aware of any cases in the literature in which the diagnosis of hypoplasia could be soundly based on such combined evidence, and any report that portrays a small coronary artery as a pathologic congenital entity47z should be viewed with skepticism. In most cases, the terminology is used incorrectly, and the dependent myocardial bed is actually served by alternative sources (unusual coronary patterns),322 or coronary spasm or diffuse disease is present. Roberts and coworkers322 observed "hypoplastic" right or circumflex arteries in 8 of 3400 consecutive autop-

sies (0.00247o), according to the dubious criterion of an "absent dominant vessel" (see Absent Posterior Descending Branch). (See Case Report 4.35 in the Atlas of Case Reports)

Intramural Coronary Artery (Muscular Bridge) On anatomic grounds, the general rule in human hearts

is that large coronary arteries and their branches are situated in the loose connective tissue of the subepicardial space. Nevertheless, the septal penetrating branches are normally intramyocardial, and other usually subepicardial branches are found to be intramural in more than lVo of instances.68'ls7'3

I

6

In several mammals and in birds, most of the coronary arteries are intramyocardial (see Chapter 1), apparently without having adverse functional consequences. Three considerations are relevant in defining and discussing muscular bridges in humans: (1) nosologic considerations (what constitutes a muscular bridge? is it an anomaly?); (2) functional considerations (are muscular bridges able to cause disease?); and (3) prognostic considerations (do muscular bridges lead to unexpected pathologic events such as spasm, thrombosis, or atherosclerotic changes?). An intramural coronary ar.teryl36 is defined

as a coronary artery that has a segment of variable length covered by myocardial fibers but that otherwise lies subepicardially.266 These fibers constitute the "bridge," whereas the underlying coronary segment is not the bridge but, rather, is the "bridged artery." Fine anatomic dissection, with the use of microscopy, has indicated a high incidence of myocardial fibers overriding otherwise subepicardial coronary arteries or branches, as reported in detail by Polacek.306 In clinical angiographic studies, detection of the intramyo-

cardial course

of a coronary artery

compression,e'3o7 a narrowing

depends on systolic of the lumen ("milking ef-

fect")

seen during systolic myocardial contraction. Phasic narrowing of a coronary aftery may also occur in other conditions, such as in the presence of ventricular aneurysms or pericardial fibrous bands.lo This angiographic marker is highly predictive of an intramyocardial coronary course, but it is actually seen in only a minority of anatomically detectable cases. Administration of a vasodilator (typically, intra-

coronary nitroglycerin in a 100- to 300-/rg bolusr2'187) greatly facilitates the angiographic recognition of systolic narrowing. Also, multiple angiographic views of the involved vessel may add relevant information. Systolic narrowing is generally considered to be caused by coronary compression by myocardial fibers that are oriented circumferentially with respect to the heart (and tangentially with respect to the involved vessel). It is usually best seen in projections that are tangential to the cardiac wall over which the involved artery is located (see Case Report 4.36 in the Atlas of Case Reports). A less reliable, indirect indicator of an intramural coronary segment is the "U sign,"12 caused by the artery's subclinically accentuated descent from its

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curiosity, especially during surgery for debridging of a coronary artery, or tricuspid valve replacement or valvuloplasty. The literature includes repofts of cases in which a simple, nonextracorporeal approach to correcting a muscular bridge of the LAD became a surgical nightmare because of perforation of the right ventricle during unroofing of a segment of the intramyocardial LAD in an unexpected subendocardial location.eo Unfortunately, no angiographic clues allow this anomaly to be diagnosed before surgery. A subendocardial coronary artery might be viewed as an intermediate stage in a spectrum of "coronary malpositions" ranging from the normal subepicardial location to intramyocardial coronary artery and to coronaro-cameral fistula.

Coronary Crossing As a rule, epicardial coronary arteries do not cross one another. The literature contains only a few angiographic (but not anatomic) reports2T3 that describe crossing of adjacent branches, apparently at the subepicardial level. This phenomenon should not be confused with superimposition of coronary branches during angiography when the vessels lie in different planes. In almost all reponed cases and in the few cases seen by these authors, the crossed arleries were obtuse marginal branches. By examining this feature in several angiographic views, the observer can occasionally verify that both arteries are indeed subepicardial (instead of papillary muscles, penetrating coronary branches, or subendocardial collateral vessels). Coronary crossing affects secondary vessels and only rarely causes clinical problems, such as difficulty in identifying a branch to be grafted during coro-

nary artery bypass. (See Case Report 4.37 in the Atlas of Case Reports)

Anomalous Origination of the Posterior Descending Artery from the Anterior Descending Branch or a Septal Penetrating Branch According to a consistent rule of coronary morphology, anterior septal penetrating branches do not reemerge on the opposite side of the ventricular septum. In cases of posterior descending artery occlusion, however, they are frequently a source of collateral connection with the facing. posterior septal vessels. Only rarely have cases been reported of an unusually large anterior septal branch that not only penetrates the whole extent of the septum but also reappears, in a subepicardial position, in the posterior interventricular groove? and produces the terminal portion of the posterior descending branch.ss'367 One might doubt the congenital nature of such an anomaly (versus an acquired occlusion of the posterior descending artery with collateral circulation from an anterior septal branch), especially in the context of coronary atherosclerosis. In a more common and clinically relevant pattern, the posterior descending branch originates congenitally from the distal LAD after encircling the cardiac apex (see the next section).

Absent Posterior Descending Branch (Split RCA)

As a rule, the posterior descending branch is a single, continuous vessel that originates from the RCA or circumflex artery, at the crux of the heart, and courses in the posterior interventricular groove. Occasionally, the posterior descending branch comprises two segments: one that originates normally from the distal RCA at the cardiac crux and courses only in the upper posterior portion of the interventricular groove; and another segment that originates from the mid RCA, close to the acute margin of the heart, and reaches the distal posterior portion of the interventricular groove.147'470 Altematively, the LAD or circumflex artery may supply part or all of the posterior descending branch, causing it to appear interrupted or split (Fig. 4.18). This phenomenon is a nosologic curiosity, but it may become clinically relevant in surgical grafting of the "posterior descending branch" or while attempting myocardial scintigraphic/coronary angiographic correlations. (See Case Reports 4.38 and 4.39 Reports)

in the Atlas of

Case

ttAbsent LADt'

In the human heart. the anterior subdivision of the LCA (the LAD) generally features anteroseptal and anterolateral (diagonal) branches as it courses along the anterior interventricular groove and tapers toward the cardiac apex. In some instances, a large subepicardial anterior artery is not encountered in the interventricular groove because one of the following alternative patlerns is present:

1. The proximal anterior descending afieryloo':+s or a supernumerary aortic ostium2e6 gives rise to a single large

first septal branch that supplies most of the secondary anteroseptal branches, leaving a small or absent middistal subepicardial LAD (which is improperly called atretic).

2. The proximal LAD splits into two smaller, parallel branches ("split LAD"l,ttz which run along the anterior interventricular groove. 3. A large diagonal artery originates quite proximally from the LAD and runs parallel to it, giving rise to all the anterolateral branches. Beyond the origin of the first septal branch, the residual distal LAD is left with limited dependent territory and appears as a very small vessel, where a bypass graft could not typically be implanted.

4. A highly dominant RCA gives rise to most of the anterior septal penetrating branches by producing

an anoma-

lous LAD177 (via the direct intraseptals6 or the anterior prepulmonicao'4l8 route, unusually prominent posterior septal branches, or a wrap-around-the-apex posterior de-

scending branch).

In similar cases, the small size of the LAD might lead to the erroneous conclusion that the LAD territory is ischemic because of the unusual coronary pattern. In the absence of

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ANOMALIES OF TERMINATION: CORONARY FISTULAS As the coronary artery tree branches and propagates peripherally, it undergoes continuous tapering until it reaches the arteriolar level (the last segment of the coronary circulation to have a tunica media). The arterioles eventually drain

into the capillary network, and only occasionally do they maintain small communications with sinusoidal intratrabecular spaces. A sizable communication between a coronary artery and (1) a cardiac cavity or (2) any segment of the systemic or pulmonary circulation is generally called a coronary fistula.3" Any structure with a pressure lower than that of the systemic aorta (i.e., equal to the proximal coronary pressure) can drain blood flow from a coronary artery if an abnormal communication occurs, allowing fistulous flow. In reviewing the anatomic literature, starting with the historic early reports ofVieussens (1706) and Thebesius (1708), Baroldi and Scomazzoni5o8 analyzed recurrent, lively discussions525 that have occurred over the centuries about coronaro-cameral communications in the normal heart. These authors concluded that two types of communications normally exist in the human heart, as alternatives to normal drainage into the corona.ry veins/coronary sinus system:

1. Communications originating at the arteriolar level are established indirectly by means of arterio-sinusoidal vessels (which are irregularly shaped, measure 50 to 250 g,m in diameter, lack a tunica media, and drain into any cardiac cavity), or directly by means of arterioluminal vessels (which are 40 to 200 p,m in diameter, have a thin media, and drain into any cardiac cavity).

2. Venous communications or thebesian veins (first described by Thebesius 11686-11321, who injected various substances into the coronary sinus) are direct communications between a coronary vein and a cardiac cavity. They are especially common in the right atrium (where they measure tp to 2 mm in size) and in the right ventricle. The exact nature of these small coronaro-cameral connec-

tions remains unclear. However, they should probably not be called fistulas, because they do not involve substantial fistulous flow. Angiographically, it is usually impossible to visualize the smaller coronary artery to cardiac cavity communications without the use of wedge injections.r28 Baroldi and Scomazzoni found such communications in almost all specimens by injecting the coronary arteries with latex or neoprene, which is fluid at room temperature but solidifies at 40 to 50 "C. The injections were made at 200 mm Hg of continuous pressure and were followed by further manual compression to enhance fluid progression during the 5- to l0-minute preparation period. To visualize veno-cameral communications, these investigators injected the coronary sinus with the same plastic material (of a different color), at 70 mm Hg of pressure, a few minutes after the beginning of the arterial injec-

tions. Appearance of the plastic gel in a cardiac cavity was considered evidence of an arterio- or veno-cameral communication, An important but unproved condition for accurately establishing this diagnosis was that the plastic gel not get past the capillary level. Using these techniques, Baroldi and Scomazzoni5os demonstrated 2O0- pt arterioluminal communications in 867o of the left ventricles and 5O%o of the right ventricles but not in the atria; they also demonstrated 200-pc anatomic channels seen by Baroldi and Scomazzoni in normal hearts. Nevertheless, these channels should be subjected to specific studies, using proper techniques. The definition ofcoronarocameral fistulas is clear when larger vessels are involved, but it is not totally clear when smaller, multiple vessels are involved.s6'170'343 5*u11 angiographic fistulas tend to occur only occasionally in patchy aggregates, affecting the smaller ramifications of several adjoining coronary branches or arteries, and typically involving the apical portions ofboth the left and right ventricles but never the outflow tracts. In such instances, the flow pattern indicates the presence of multiple small communications with limited flow, which is generally only diastolic into the left ventricle but systolo-diastolic into the right ventricle.56'i7o These communications do not cause ectasia of the proximal feeding arteries, nor do they tend to enlarge with time.2el This subject is being discussed extensively herein because of widespread persistent ignorance about the exact nature of the smaller communications between corona.ry vessels and

cardiac cavities.332 The overwhelming current tendency in the literature and in practice is to group these entities under the general heading of coronary fistulas and to imply that nutrient blood is shunted away from the myocardium.lll Numerous reports have been published regarding patients with angina, ischemia, myocardial infarction, or arrhythmias in the presence of multiple small, patchy coronaro-cameral communications. However, overwhelming evidence (based

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nutrient myocardial flow, rather than simply to eliminate the fistulous tract. The absence of nutrient coronary branches arising from a fistulous tract should suggest an alternative diagnosis, namely ruptured aneurysm of an aortic sinus.447 With the larger fistulas , alarge quantity of contrast medium should be injected (about 20 ml/sec for at least 2 seconds), and the fistula should be examined in different projections, depending on its specific anatomy. It is prudent to avoid small-lumened catheters with only end holes (coronary preformed catheters) with high injection pressure and to use large-lumened catheters with side holes (like an NIH@ or a '.6 angiographic catheter). Alternatively, one may use Gensini' a coronary angioplasty guiding catheter (large-lumened), kept in position by a 0.014-inch guidewire. The proximal tract of a fistulous coronary artery should be regarded as an atypical example of a "mixed trunk" rather than as a simple coronary artery (which is defined as a vessel that provides exclusively nutrient flow). Over the years, torrential flow will induce clinically important morphologic changes in the walls of a fistulous coronary artery. The fistulous tract-but not the distal, exclusively nutrient branches-will undergo progressive changes that range from simple dilation (as would be expected because of the increased blood flow) to frank aneurysm formar26.262.28a 3a2.s22 (reco gnizable only because dilation is 1iontg' greater than in the adjacent vessel), intimal ulceration, medial degeneration, intimal rupture, atherosclerotic deposition, calcification,28s side branch (nutrient) obstruction,a3a and mural thrombosis.a5'a3a'aa2 16" ultimate, dreaded but rare, complication of the increased wall stress is coronary rupture into adjacent cardiac structures6l or the pericardium.ls6 Because the vessel wall's reaction to the prolonged increased flow is so variable, the observer should be cautious estimating the amount of fistulous flow on the basis

in

of luminal diameter alone. Vessel size, in itself, may be a fallacious parameter: in the most extreme case, a very large, aneurysmatic fistula could eventually become throm-

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amount of dilation of a fistulous vessel has recently become more relevants2'118'333 than the amount of fistulous flow or symptoms and/or signs of myocardial ischemia. 1 1a'38e 6u15"ter-based26e or surgical63 intervention at an early age is generally recommended for patients with large fistulas, because of the risk of rupture and mural clottinga3a'aaz; moreover, aortic sinus disruption caused by an extremely enlarged coronary ostium can result in aortic insufficiency. Late athero-

sclerotic and thrombotic changes2lS will evolve even after total obliteration of the fistula. With respect to the optimal timing of surgery, another major consideration should be that reversibility of the ectasia is consistently reported only after surgical correction of fistulas in pediatric casesl I 8 and is never observed in older patients.52 Because of these factors, many authorities have concluded that, once a large coronary fistula has been diagnosed, the optimal time for correction

is during the patient's fifth to fifteenth year of life; the timing

of surgery in such cases should not be based on the time of onset of symptoms, the absolute amount of fistulous flow,38e

or signs of congestive failure or myocardial ischemia during stress testing. If the diagnosis is missed in the 5- to l5-year age range (as it frequently is), the indications for, and timing of, intervention may change because of variance of the riskbenefit ratio.ao6 Older patients445'4e5 may still do very well at surgery but may have more frequent complications (especially peri- and postoperative myocardial ischemic events3o3' 311's33 and extracardiac complications); moreover, after normalization of blood flow, their remaining risk of coronary thromboembolic disease in the excessively ectatic coronary segments will at least equal that of patients treated medically.s33 The recent introduction of catheter devices for the obliteration of coronary fistulassT' I 6l'2 I 7'303'3 l'1'3 I s'368'1o2'441 will be further discussed in Chapter 5. Concomitant obstructive coronary disease, in either the affected vessel or an unaffected one, may be the most common reason for clinical recognition of a coronary fistula and for surgical intervention in older patients. Fistulous coronary connections usually involve structures that adjoin the coronary arteries, such as the coronary veins and the four cardiac cavities. I I 8'237'338'381'406'43sAa3Aaa y""" frequently, in otherwise normal hearts, a coronary fistula will drain into an extracardiac structure such as the pulmonary artery or its main branches or the superior vena cava.18' 466 Coronary-to-main pulmonary artery fistulas are usually small, multiple,16 and of no clinical significance. Congenital coronary-pulmonary connections are sometimes seen in the context of other congenital heart defects, especially critical pulmonary valve stenosis or atresia or (even more frequently) pulmonary branch stenosis or atresia, or coarctation of the aorta. Although the literature contains frequent references to t7 t ' 'coronary-to-bronchial artery fistulas ,t; '41'141't7 '347 '366'373 we doubt the existence of such an entity. Both of these arteries are, in fact, systemic in patients with a normal cardiovascular anatomy, and fistulous flow cannot be expected to occur between two vascular sites that have identical pressure regimens. Communications have indeed been observed with special frequency between a coronary artery and a lung segment with a chronic infectionl (bronchiectasia, sequestration, or pseudosequestration); in these cases, the involved vessels behaved more like neovascularizations or collateru1r22o3ae than like fistulas.lT'173 Only occasional reporters have suggested that a "coronary to bronchial anastomosis" exists and can cause a myocardial infarcti on.17'27e In congenitally sequestered pulmonary lobes, the systemic arterial supply is usually derived from the descending or abdominal aorta; in pseudosequestered lobes, however, it may originate from intercostal, mediastinal, subclavian, and pericardial arteries, l7'173'24:'zue .6i"6 probably connect with pulmonary arterial branches,2o not bronchial ones. Coronary-to-pulmonary communications may also appear after cardiac surgery, even heart transplantation (see Case

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