Chest Radiograph

The initial plain chest film in patients undergoing acute myocardial infarction is obtained to search for signs of left ventricular failure and to screen for some of the complications of infarction. Nearly half the patients admitted to a coronary care unit have radiologic signs of pulmonary venous hypertension within the first 24 hours after an acute myocardial infarction. Even though many films are taken with portable technique in the supine position, the signs of pulmonary edema have a rather good correlation with the pulmonary capillary wedge pressure. The usual caveat, that low lung volumes can mimic signs of pulmonary edema, is appropriate. Indistinct hilar structures represent early engorgement of the vasculature and dilatation of the rich mediastinal lymphatics. You will occasionally see dilatation of upper lobe vessels even on supine films before the reticular pattern of interstitial edema develops. The width of the vascular pedicle above and adjacent to the aortic arch is frequently a good indicator of the intravascular volume. Increase in the size of the azygos vein and superior vena cava on serial films suggest an increase in intravascular blood volume and the need for treatment of left ventricular failure.

Heart Size

Initially, most patients undergoing myocardial infarction have a normal heart size. The assessment of an enlarged heart on a supine portable chest film is rather inaccurate and usually not necessary for clinical management. Severe cardiomegaly generally indicates long-standing coronary artery disease with previous infarction or with a major complication (Fig. 7-1).

FIGURE 7-1 Large left ventricular scar. The arc of calcium (arrow) along the anterolateral and apical walls of the left ventricle denotes dystrophic changes in a large scar of several years’ duration. The anterolateral wall is thin. There is no outward bulge to indicate an aneurysm.

Aneurysms and Ruptures

In addition to chronic left ventricular failure, left ventricular enlargement may also be the result of a true or false aneurysm, chronic mitral regurgitation, or rarely cardiac rupture. Heart enlargement is not a feature of acute mitral regurgitation or rupture of the interventricular septum because the left ventricle needs several hours to several days to dilate enough to be visible on the chest film. The most frequent site of a true left ventricular aneurysm is in the anterolateral and apical wall. Although left ventricular aneurysms may involve any wall segment, aneurysms in the posterolateral wall are frequently false aneurysms. A false left ventricular aneurysm exists when the left ventricle ruptures into a site of previous pericardial adhesions so that the rupture is contained by the pericardium. An increase in size of the left ventricular aneurysm on serial studies is suggestive of a false aneurysm and warrants urgent, definitive evaluation. Calcification of the anterolateral and apical region of the left ventricle usually takes several years after the myocardial infarction that produced the scarring (Fig. 7-2).

FIGURE 7-2 Computed tomography scan of calcified left ventricular apex. The linear calcification at the left ventricular apex is in an old infarct. The polypoid component represents a calcified thrombus. The patient recently had a coronary bypass operation so that anterior mediastinal and pericardial drains, a small pericardial effusion, and bilateral effusions are present.

Both papillary muscle rupture and rupture of the interventricular septum produce nearly identical findings on the chest radiograph. Both complications typically have moderate interstitial pulmonary edema with mild enlargement of the pulmonary arteries. There is a mild increase in heart size with signs of enlargement of all four cardiac chambers.

Coronary Angiography

Uses and Analysis

Asymptomatic Patients or Mild Angina

The majority of patients with asymptomatic ischemia or mild angina should be treated medically. However, for physically active middle-aged individuals with moderate ischemia or objective evidence by both treadmill testing and ambulatory monitoring of significant myocardial ischemia, revascularization with percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) surgery may be considered and may reduce their risk of serious or fatal cardiac events.

Patients with Angina Class II to IV or Unstable Angina

Many patients with moderate or severe stable angina or unstable angina do not respond adequately to medical therapy. PCI or CABG surgery may even improve their left ventricular systolic function. Coronary angiography is used mainly to identify atherosclerotic coronary stenosis, and less often, congenital anomalies and manifestations of other diseases. Each coronary artery is opacified so that its origin, course, and termination are visualized at least in two orthogonal projections. The orthogonal projections are necessary because atherosclerotic stenoses tend to be eccentric; a minor plaque in one projection may appear as a major stenosis in the opposite oblique view (Fig. 7-3).

FIGURE 7-3 Necessity for multiple projections. Coronary angiography must be performed in two orthogonal projections because the atherosclerotic lesion is eccentric. In A, the lumen projects a 77% stenosis, whereas in B, only a 5% stenosis is seen.

The analysis of a coronary arteriogram for coronary artery disease consists of four tasks. First, the extent and location of stenoses must be determined. Second, the severity of each stenosis is graded so that a clinical decision can be made regarding both treatment and prognosis. Third, the morphology of the atherosclerotic plaque is graded. Fourth, the size of the vessel distal to the stenosis is evaluated to see if it is a suitable recipient for a bypass graft or stent placement at the stenosis.

Progression of Atherosclerosis

Coronary atherosclerosis begins as lipid deposition in the arterial wall, which appears grossly as a raised, fatty streak. As the lesion progresses, a fibrous cap develops over the endothelial lipid deposit. Disruption of an atherosclerotic plaque results in fissuring and intraluminal thrombosis (Fig. 7-4). The thrombus may lead to intermittent vessel occlusion and unstable angina. Large ulcers at the site of the plaque can cause formation of a fixed thrombus and a chronic occlusion resulting in acute myocardial infarction. Severe stenoses tend to progress to total occlusion about three times more frequently than less severe lesions.

FIGURE 7-4 Unstable angina. Right coronary angiogram showed a proximal ruptured plaque (solid arrow) associated with an endoluminal defect (open arrow) consistent with a thrombus, just distal to the stenosis. The midposterior descending artery is occluded by a distal emboli (arrowhead).

In patients with unstable angina, most coronary stenoses are only of moderate degree. It is the mild to moderate coronary stenosis that commonly precedes most coronary occlusions in patients with unstable angina. Angiography during acute myocardial infarction usually shows a thrombus in the infarct-related artery. After thrombolysis, many of these patients have an underlying lesion with less than 70% stenosis. Those stenoses that later progress usually have eccentric shapes with overhanging edges and are thought to represent plaque disruption. Therefore, the state of the atherosclerotic plaque—whether it is covered with a fibrin cap or has deep fissures that may lead to thrombus—is an important angiographic observation.

Current imaging techniques for ischemic heart disease are used increasingly to differentiate viable from nonviable myocardium in patients with coronary artery disease and left ventricular dysfunction. Acute coronary occlusion generally results in reduced regional myocardial contraction. An acute reduction of blood flow of 80% below a control value in a coronary artery causes akinesis in that segment of the left ventricle, whereas a 95% reduction causes dyskinesis. Akinesis of a segment of the left ventricle, however, does not reliably distinguish viable myocardium from scar.

Myocardial stunning is a segmental wall motion abnormality that returns to its normal contractile state after reversal of a brief episode of severe ischemia.

Myocardial hibernation is a related state in which left ventricular wall motion abnormalities from chronic ischemia return to normal after relief of the ischemia by angioplasty or grafting. The myocardium remains viable during chronic ischemia even though the wall motion is decreased.

These two conditions of reversible left ventricular dysfunction are important to recognize because vigorous treatment of the thrombus or spasm in myocardial stunning and relief of the obstruction in myocardial hibernation may reverse the impaired ventricular performance and potentially salvage the jeopardized myocardium. Stress echocardiography is the modality of choice to assess left ventricular wall motion abnormalities. Stress cardiac magnetic resonance imaging (CMRI) has demonstrated better sensitivity and specificity, but is less available. Furthermore, CMRI is capable of providing useful information about left ventricular viability (Fig. 7-5).

FIGURE 7-5 Gadolinium-enhanced cardiac magnetic resonance imaging in short axis. A, First pass of contrast. The myocardium of the left ventricle should be homogeneously enhanced. In the anteroseptal myocardium, there is a defect in enhancement (arrows), demonstrating impaired perfusion. B, Late phase. The gadolinium is enhancing the same anteroseptal myocardium, delineating a myocardial infarction in the left anterior descending territory.

(Courtesy Dr. Ricardo Cury and Dr. Cesar Cattani, Beneficiancia Portuguesa Hospital, São Paolo, Brazil.)

Extent and Location of Stenoses

Common Lesion Sites

Most coronary stenoses occur in the proximal portion of both arteries. The distribution of lesions is rather uniform in the three major arteries. The distribution of coronary stenoses with greater than 50% stenosis is: right coronary artery, 37%; left circumflex artery, 28%; left anterior descending artery, 33%; and left main artery, 3%.

In the right coronary artery, most severe stenoses develop in its proximal half, although there are occasional severe plaques at the bifurcation of the posterior descending and posterior left ventricular arteries (Fig. 7-6). The right ventricular marginal branch frequently has a severe stenosis at its origin.

FIGURE 7-6 Right coronary stenoses. A, In lateral projection, there is a 90% stenosis of the proximal right coronary artery (arrow), just before a second large marginal branch. B, Right coronary angiogram. A midright irregular stenosis (arrow) is depicted. C, Right coronary angiogram showing diffuse atherosclerotic disease with a distal right stenosis (solid arrow) and an ostial/proximal stenosis of the posterior descending (PD) artery (open arrow). D, In the lateral projection, there is a severe ostial right coronary artery stenosis (solid arrow), associated with two proximal and one mid stenosis (open arrows). An ulcer is demonstrated just before the origin of the posterior descending artery (arrowhead). M, right ventricular marginal artery; PLV, posterolateral left ventricular artery.

The left main coronary artery should not taper. It is usually narrowed either at its ostium or at the bifurcation of the left anterior descending and circumflex arteries. Occasionally, the entire main arterial segment may be uniformly narrowed but usually one of its ends is more severely involved. Detection of plaques in this segment is particularly important because severe lesions are associated with an increased mortality during cardiac catheterization (Fig. 7-7).

FIGURE 7-7 Left main coronary artery stenosis (arrows). Cranially angled left anterior oblique views show a discrete (A) and diffuse (B) stenosis. C, In the right anterior oblique view the left main artery is smaller than the left anterior descending artery, a sign of diffuse atherosclerosis. D, diagonal artery; L, left anterior descending artery.

Left Main Equivalent Disease

Left main equivalent disease describes the combination of stenoses that would cause a decrease in blood supply similar to that caused by a single stenosis in the left main coronary artery. This concept is applied so that a stenosis at the origin of both the left anterior descending and left circumflex arteries is not a left main equivalent. Either of these stenoses may become more severe but may follow a separate time course. Occlusion of one of these would not result in as large an area of myocardium becoming ischemic as would a single event in the left main coronary artery.

An example of a left main equivalent lesion would be a severe left anterior descending artery stenosis when an occluded right coronary artery is supplied by collaterals from the left anterior descending artery. Here one lesion controls the blood supply to the bulk of the heart. A similar example would be a stenosis in a long left anterior descending artery that extends completely around the apex in place of the usual posterior descending artery. Here also a significant percentage of myocardium is affected by a single stenosis.

Clinically, loss of 40% of the left ventricular myocardium produces cardiogenic shock. A left main or left main equivalent coronary stenosis usually affects this much of the myocardium. If collateral vessels supply an adequate perfusion to an occluded vessel, other combinations of coronary stenoses may produce a situation in which one lesion controls the blood supply to a major portion of the left ventricle.

In the left anterior descending artery, stenoses before or after the first large septal branch may have different clinical implications. Patients with chronic stable angina who have a severe stenosis before the first septal branch have a statistically higher mortality when compared with patients who have a stenosis distal to this branch (Fig. 7-8). The first septal branch can supply nearly half of the interventricular septum and a contractile portion of the ventricle and is closely related to the conduction system. A stenosis before the first septal branch also frequently involves a large diagonal branch that supplies a portion of the lateral wall. This correlation does not hold in unstable angina pectoris, where there is no association between severe plaques before and after the first septal branch.

FIGURE 7-8 Left anterior descending artery stenoses (arrows). A, Left coronary angiogram showing an 80% proximal left anterior descending artery (LAD) stenosis before the first septal branch (S). B, A tapering 90% stenosis in the middle segment of the left anterior descending artery distal to the septal branch. LCX, left circumflex artery; LM, left main coronary artery.

Morphology of Coronary Atherosclerosis

Angiographic Appearance

The angiographic appearance of coronary atherosclerosis ranges from a single focal plaque to multiple diffuse stenoses with eccentric and ulcerated margins. Isolated stenoses are usually discrete irregularities in the vessel wall, rarely more than 10 mm long. Multiple focal stenoses may be present in series with one another. Diffuse atherosclerosis is occasionally difficult to recognize because no normal-sized vessel is adjacent to the narrowing for comparison.

Atherosclerotic plaques tend to have eccentric and sharp edges that help distinguish them from spasm, which is usually smooth and fusiform. Thrombus within the artery may be distinguished from plaques if contrast medium flows on both sides of the lucency (Fig. 7-9). Occlusive thrombi may be impossible to distinguish from a fibrosed artery, but sharp, slanting edges are more typical of thrombus.

FIGURE 7-9 Coronary thrombus (arrows). A, In the left anterior oblique view the right coronary artery is occluded by a thrombus. Contrast medium tracks on both sides of the filling defect. B, Thrombus (filling defect) has formed on the downstream side of a severe left anterior descending artery (LAD) stenosis. The blood flow through the left anterior descending artery and its branches is impaired compared to the filling of the left circumflex artery (LCX). The angiogram is a caudal right anterior oblique projection.

Relationship to Coronary Syndrome

Both clinical and angiographic studies have confirmed that angiographic morphology is correlated with unstable coronary syndromes. Simple plaques with a smooth fibrous covering, smooth borders, and an hourglass configuration are associated with stable angina. Complex lesions with plaque rupture, intraplaque hemorrhage, and irregular borders in eccentric stenoses are associated with unstable angina and myocardial infarction (Fig. 7-10).

FIGURE 7-10 Simple and complex stenoses (arrows). A, The left anterior descending artery (LAD) has a proximal smooth 95% stenosis in the cranial right oblique view. B, The right coronary artery has two complex stenoses, one after the first marginal branch (M₁), which is ulcerated (arrow), and one irregular, after the second marginal branch (M₂·; arrowhead). LCX, left circumflex artery; LM, left main coronary artery; M, marginal branch.

Myocardial Infarctions

Multiple myocardial infarctions result from extensive coronary disease and occur with greater frequency in persons with diabetes. You are more likely to find a decreased ejection fraction in patients with diabetes mellitus but patients with diabetes and those without do not differ significantly in number and extent of severe stenosis. Type II hyperlipoproteinemia is associated with extensive coronary calcifications and severe involvement of the distal distribution of the coronary arteries (Fig. 7-11). These patients may have an unusual edge in the left sinus of Valsalva at the ostium of the left coronary artery, which can make catheterization difficult. Patients with type IV hyperlipoproteinemia have a distribution of stenoses similar to that in patients with normal lipid findings.

FIGURE 7-11 Diffuse coronary disease in type II hyperlipoproteinemia. A, An ostial left main stenosis is common. B, Slight calcification (arrows) in the aortic root is distinctive of this lipid abnormality.

Other Causes of Stenosis

There are many causes of coronary stenosis other than atherosclerosis. Frequently, the cause can only be determined by clinical correlation with a systemic disease (Box 7-2). Even then, in the adult age range, it is often impossible to exclude coexisting atherosclerosis. The clinical constellation of chest pain, a positive exercise test, and a normal coronary arteriogram is referred to as syndrome X. The cause of the syndrome is unknown, is not related to large vessel spasm, and may be related to abnormalities in precapillary vessels that are too small to be seen with coronary angiography. In contrast, myocardial infarction can occur with a normal coronary arteriogram. This event is rare and has been caused by thrombosis with recanalization, coronary spasm, cocaine abuse, viral myocarditis, chest trauma, and carbon monoxide intoxication.

Interpretation of Arterial Stenoses on Angiography

Determining Severity

What degree of arterial narrowing constitutes a severe stenosis? Many studies have correlated the degree of stenosis with the ultimate clinical or pathologic outcome. Severe stenoses correlate well with an impairment in the left ventriculogram. Early clinical studies by Likoff and Proudfit demonstrated a good association between arteriographic evidence of one-, two-, and three-vessel disease with the clinical signs and symptoms of ischemic heart disease. Comparison of arteriograms with postmortem examinations demonstrates a rough correlation with a 50% arterial reduction or 75% area reduction in a coronary artery associated with a transmural myocardial infarct. Because it is easier to measure the greatest percentage diameter reduction in a coronary artery from serial views, the diameter and not the area reduction is measured. The severity of the obstructive disease is assessed in each coronary artery segment by comparing the arterial diameter at a point of maximum lumen reduction with a proximal or distal “normal-appearing” artery. A coronary stenosis is graded as the highest percentage of stenosis seen in all projections.

Because atherosclerotic plaques tend to be eccentric, coronary angiography must be performed in two orthogonal projections so the maximal arterial narrowing can be identified (Fig. 7-12). This system has many limitations. The normal-appearing artery may itself be diffusely diseased. A similar percentage of stenosis in a smaller distal artery is ascribed the same physiologic consequence, even though flow through a larger proximal arterial segment must be quite different. In a large artery with a greater cross-sectional area, the amount of myocardium supplied by its coronary flow is proportionate to the smaller area supplied by a distal coronary artery. A similar degree of narrowing of a small distal coronary artery produces the same profusion deficit as does the same percentage of stenosis in a large or proximal artery. The length of a coronary stenosis is important but is difficult to subjectively evaluate as to severity of a lesion reducing distal flow. Given these limitations, a 50% or greater stenosis in a patient with ischemic heart disease is defined as a significant stenosis.

FIGURE 7-12 Necessity for multiple projections. The severe stenosis (arrow) is not clearly visible in the lateral view (A), but is nicely demonstrated in the mid left anterior descending artery (LAD) in the cranial right anterior oblique projection (B). D, diagonal branch; LCX, left circumflex artery; S, septal branch.

Determinants of Coronary Blood Flow

Flow Reserve

Coronary flow reserve is the maximal flow divided by the resting flow. The “50% significant stenosis” is then a rough approximation to this physiologic model. The maximal flow is that which occurs when the coronary vascular bed has undergone maximal vasodilatation. Fig. 7-13 shows the relation between coronary blood flow and a focal stenosis in an artery at rest and after maximal vasodilatation.

FIGURE 7-13 Hemodynamically significant stenosis—a stenosis that reduces flow in the distal artery. A, The model is an isolated coronary artery in which a plaque is growing progressively larger. B, At rest, when the coronary vasculature is moderately constricted, coronary flow is unchanged until an 80% stenosis is reached because of autoregulation of the vasculature, mainly at the precapillary sphincters. When the experiment is repeated with a vasodilating agent such as exercise, so that the flow is triple the previous resting value, then a 40% stenosis begins to cause a decrease in downstream flow.

If a significant stenosis is defined as that which causes coronary blood flow to decrease, a significant stenosis at rest is roughly 80% reduction in diameter. However, after maximal vasodilatation, a significant stenosis changes to 40%. The interpretation of these results indicates that stenoses greater than 80% cause a reduction in flow under all circumstances, whereas stenoses less than 40% are not significant even under conditions in which there is maximal vasodilatation. The border zone between 40% and 80% represents the limitation of this method. Unfortunately for clinical decision making, most stenoses fall in this middle zone.

Fractional Flow Reserve

Fractional flow reserve (FFR) is an invasive index of the functional severity of a stenosis determined from coronary pressure measurement during coronary catheterization. A 0.014-in pressure wire is advanced, after calibration, into the relevant coronary segment. It is positioned distally to the stenosis. Adenosine is administered intravenously to induce maximal hyperemia. FFR is calculated as the ratio of mean hyperemic distal coronary pressure measured by the pressure wire to mean aortic pressure measured through the guiding catheter. In patients with coronary stenosis of moderate severity, FFR appears to be a useful index of the functional severity of the stenosis and the need for coronary revascularization. An FFR value of less than 0.75 demonstrates a reversible myocardial ischemia (Fig. 7-14) with a sensitivity of about 90% and a specificity of 100%.

FIGURE 7-14 Fractional flow reserve. A, A 0.014-in pressure wire (solid arrow) is positioned distal to a stenosis (open arrow) in the proximal right coronary artery. B, After pharmaceutical hyperemia, pressure measurements are obtained distally to the stenosis and proximally into the aorta. Fractional flow reserve (FFR) is measured at 0.70, given a hemodynamically significant stenosis. Stent implantation was then performed.

Effects of Stenosis Length and Diameter

The length of the coronary stenosis also determines blood flow, although its effect is complex. When the diameter is constricted by less than 50%, stenoses of up to 15 mm in length have little effect on flow during reactive hyperemia. As the diameter of a stenosis is increased to 70%, a stenosis 10 mm long results in a reduction in distal flow. Long stenoses in the presence of borderline reduction in diameter (40% to 70%) may greatly alter coronary hemodynamics during stress. Although Poiseuille’s equation suggests that the length of a stenosis would decrease flow linearly, this cannot be precisely observed because there are neural and biochemical factors and collateral flow that also regulate blood flow. Moreover, the distal coronary vascular bed may vasodilate in a nonuniform manner from endocardium to epicardium. Because a proximal stenosis reduces coronary pressure, the endocardium becomes anoxic before the epicardium does, and there is increased lactate production and a fall in highenergy phosphate mediators. The end result is that vascular resistance distal to a stenosis in an ischemic myocardium varies in a complex way.

Cumulative Effects of Stenosis

Multiple consecutive stenoses are frequently encountered in clinical practice, and therefore their cumulative effects need to be considered. If a critical stenosis is in series with a mild stenosis, flow is governed by the more severe stenosis. If two critical (i.e., severe enough to reduce blood flow) stenoses are in the same artery, their combined effect is additive.

Coronary Collateral Vessels

Angiographic Appearance

The angiographic appearance of an epicardial collateral is usually a serpentine, corkscrew artery that goes from the end of an adjacent artery to the end of the occluded artery. Collaterals through the interventricular septum appear differently: They are straight and connect the septal branches from the anterior descending to the posterior descending artery (Fig. 7-15).

FIGURE 7-15 Septal collaterals. The left anterior descending artery (white arrows) is occluded just after the septal branch. The first septal branch (large black arrow) serves as a collateral pathway (small black arrows) through other septal branches to the distal anterior descending artery and diagonal branches.

There are many pathways in the heart for collateral vessels. Intracoronary collaterals bridge an occluded artery from its proximal to its distal end (Fig. 7-16). This kind may be difficult to distinguish from a recanalized thrombus. Intercoronary collaterals develop between the terminal branches of different arteries (Fig. 7-17). Frequent collateral pathways are from the conus artery of the right coronary artery to the left anterior descending artery (Vieussens’ ring). Kugel’s artery is a collateral that connects the sinoatrial nodal artery to the atrioventricular nodal artery through the interatrial septum. Because the sinoatrial nodal artery can come from either the right coronary or left circumflex artery, and the atrioventricular nodal artery can originate from either a right or left dominant posterior left ventricular artery, there are four pathways that collaterals can take through the atria that can be called Kugel’s artery (Fig. 7-18).

FIGURE 7-16 Intracoronary collaterals. A, Caudal right oblique projection. B, Caudal left anterior oblique view. The collateral flow around the occlusion in the right coronary artery goes through the conus artery, the collateral vessel (arrow) in the anterior wall of the right ventricle, and then in a retrograde direction in the posterior descending artery (PD) and distal right coronary artery.

FIGURE 7-17 Intercoronary collaterals. A, Large, serpentine collateral connects the right coronary artery (curved arrow) to the left anterior descending artery (straight arrow). This pathway is called Vieussens’ ring. B, A collateral vessel as large as the distal left anterior descending artery connects to the posterior descending artery. C, A collateral through the crista supraventricularis (thick arrow) connects the left anterior descending artery (thin arrow) to the distal right coronary artery (curved arrow). D, The left circumflex artery serves as collateral supply (arrows) to the occluded posterior left ventricular branch of the right coronary artery.

FIGURE 7-18 Kugel’s artery. Kugel’s artery (arrows) connects the proximal right coronary artery to the atrioventricular nodal artery through the atrial septum. The middle segment of the right coronary artery is occluded. A, Right anterior oblique view. B, Left anterior oblique view.

Collaterals are rarely visible angiographically in the first few days after myocardial infarction but may develop over the following 2 weeks. Several months after a myocardial infarction, most patients develop visible collaterals unless the infarct has organized into a dense scar.

Coronary Artery Spasm

Dynamic forms of coronary obstruction have been recognized for centuries as causing angina and myocardial infarction. In his original description of angina pectoris Heberden wrote in 1768 that chest pain occasionally occurs without exertion. In 1910, Osler speculated that spasm of a coronary artery could cause anginal pain. In 1959, Prinzmetal described an unusual syndrome of cardiac pain that occurs almost exclusively at rest, is not precipitated by exertion, and is associated with electrocardiographic ST-segment elevations. Myocardial perfusion scanning and coronary arteriography have shown that spasm may reduce or stop segmental myocardial blood flow.

Angiographic Appearance

Coronary spasm is one of a number of causes of myocardial infarction with angiographically normal coronary arteries. The angiographic definition of spasm is a focal stenosis that changes during sequential arterial injections (Fig. 7-19). Occasionally an entire artery will have severe vasoconstriction, but spasm typically is a focal, changeable stenosis. Coronary artery spasm in Prinzmetal variant angina has been seen in the left main, left anterior descending, and circumflex arteries, but spasm in the right coronary artery is more frequent.

FIGURE 7-19 Right coronary spasm. A, The first angiogram of the right coronary artery did not show any stenosis. This second view demonstrated a spasm on the mid right (arrow). B, Severe vasoconstriction occurred during the next view. Immediate intracoronary nitroglycerin relieved the coronary spasm and the patient’s symptoms.

Catheter-Induced versus Prinzmetal Syndrome

The distinction between catheter-induced spasm and that in Prinzmetal syndrome is difficult, but one caused by a catheter occurs proximally, adjacent to the catheter tip (Fig. 7-20). Catheter-induced spasm is usually seen at the origin of the right coronary artery as a short area with smooth fusiform narrowing. Focal spasm frequently occurs at the site of an atherosclerotic plaque, which may make it difficult to distinguish from fixed disease. Spasm may be slight or it may completely occlude the artery. Because the coronary endothelium has potent factors that can cause spasm and thrombus after intimal injury, spasm is frequently seen after percutaneous coronary angioplasty. In this situation, the artery has a sawtooth appearance, which is reversed with nitroglycerin.

FIGURE 7-20 Catheter-induced coronary spasm. Initial injection (A) into the right coronary artery produced severe narrowing that was almost completely reversed (B) after intracoronary nitroglycerin.

Coronary Aneurysms

Coronary artery aneurysms are occasionally discovered during angiographic evaluation of ischemic heart disease and are usually a variant of coronary atherosclerosis (Fig. 7-21). This lesion will frequently be found in the same artery with stenoses and occlusions. Atherosclerosis can produce diffuse ectasia from degeneration of the media and associated elastic elements (Fig. 7-22). To distinguish an ectatic artery or poststenotic dilatation from an aneurysm, a useful definition of coronary aneurysm is a dilatation of 50% greater than the preceding normal artery. Most atherosclerotic coronary aneurysms have an adjacent severe stenosis. The saccular aneurysm may overlap and hide the stenosis during angiography so that at least one angiographic projection should profile the neck of the aneurysm.

FIGURE 7-21 Coronary aneurysms (arrows). A, The left anterior descending artery aneurysm is twice the size of the normal artery. B, A caudal left anterior oblique projection (spider view) shows an aneurysm in the left anterior descending artery (L). C, The left circumflex artery in the caudal right anterior oblique view has a fusiform aneurysm after a severe stenosis in a segment that becomes the left posterior descending artery. D, Multiple segmental plaques with an intervening normal vessel (open arrow) is not to be confused with an aneurysm. C, left circumflex artery.

FIGURE 7-22 Diffuse ectasia of the right coronary artery with distal saccular aneurysm.

Causes

Coronary aneurysms are a major manifestation of many systemic diseases. The history of associated cardiac lesions may implicate syphilis, polyarteritis nodosa, trauma, bacterial infections, neoplasm, and a congenital etiology. Rupture of an atherosclerotic aneurysm is rare. Rupture is associated with bacteria-infected aneurysm, congenital aneurysm of large size, and arteritis diseases. Diffuse aneurysms have been seen in transplanted hearts that underwent immunologic rejection.

Kawasaki disease is a childhood acute multisystem vasculitis that includes cervical lymphadenopathy, fever, and a rash in the mouth and on the hands and feet. Also called mucocutaneous lymph node syndrome, Kawasaki disease involves a myocarditis and pericarditis that may cause congestive heart failure. Aneurysms of the coronary arteries are frequent (Fig. 7-23) and may cause coronary thrombosis, myocardial infarction, and sudden death. About half of the children with coronary aneurysms have angiographically normal-appearing arteries 2 years later. Some aneurysms may be quite large, and rupture is a fatal complication. See Table 7-1 for prognosis of aneurysms in Kawasaki disease.

FIGURE 7-23 Kawasaki disease. A, Coronary aneurysms in the origin of the right coronary artery. B, The left main coronary artery in the same 5-year-old child 2 years after an episode of fever and mucocutaneous signs.

TABLE 7-1 Prognosis of aneurysms in Kawasaki disease

Size	Prognosis
<4 mm	Regress to normal size
4-8 mm	Tend to become smaller
>8 mm	Progress to obstruction or stenosis

Myocardial Bridging

An intramyocardial bridge is a coronary artery that dips into the myocardium and is completely surrounded by cardiac muscle (Fig. 7-24). This segment of the coronary artery narrows dynamically during systole and returns to its baseline size during diastole. Bridges are seen in about 0.5% to 7.5% of angiographic studies, usually in the left anterior descending artery, although diagonal and marginal arteries may be affected. The bridges may be as deep as 10 mm and usually are 10 to 30 mm long. The bridge segment rarely has atherosclerosis, but plaques are seen both proximately and distally. Because narrowing takes place during systole and most coronary flow occurs in diastole, mural coronary arteries were initially considered a minor anomaly. However, chest pain and myocardial infarction may occur when the bridge narrows more than 75% in systole. Because the bridge is usually eccentric, views in at least two orthogonal projections should be obtained.

FIGURE 7-24 Computed tomography coronary arteriogram obtained in a 74-year-old man with occasional chest discomfort. A, Multiplanar reformatted figure depicting the left anterior descending coronary artery. A small, nonobstructing mixed fatty (arrow 2) and calcific (arrow 1) plaque is seen in the proximal artery. There is a long segment intramyocardial bridge in the mid portion of the artery. Note the left ventricular myocardium on both sides of the arterial segment (arrowheads) reflecting the passage of the artery through the myocardium. B, Image reconstructed at right angles to the intramyocardial arterial segment. The high attenuation of the arterial lumen (long arrow) is separated from the low attenuation of the epicardial fat by a band of intermediate attenuation left ventricular myocardium (arrowheads).

The septal arteries, which are also intramural, normally show no change in size between systole and diastole. Septal arteries from the left anterior descending artery may occlude during systole in diseases that increase left ventricular wall tension, such as aortic stenosis, hypertensive heart disease, and idiopathic hypertrophic subaortic stenosis.

Coronary Dissection

The angiographic appearance of dissection is a linear or spiral lucency within the arterial lumen, which represents the intimal flap (Fig. 7-25). The dissection may occlude the distal artery or, as in the aorta, have a false channel with stasis of the contrast medium. Spontaneous dissection occurs in the coronary arteries as it does in most medium-sized arteries (Fig. 7-26). It is seen in pregnancy, Marfan syndrome, and chest trauma. Coronary dissection may occur secondary to an aortic dissection with a retrograde tear. The angiographic catheter may lift a plaque and initiate the downstream tear. After transluminal angioplasty, a short dissection cleft is frequently seen but rarely extends beyond the length of the balloon.

FIGURE 7-25 Coronary artery dissection. Spontaneous dissection of the distal right coronary artery (arrows), starting just before the posterior descending artery (PD), with the membrane of the dissection extending into posterior left ventricular branches (PLV). M, marginal branch.

FIGURE 7-26 Aortic dissection. Patient with type A aortic dissection and ischemic signs on admission electrocardiogram. The aortic dissection involved also the ostium (arrows) of the left main coronary artery (LM) and impaired the coronary blood flow, especially in the left anterior descending artery (LAD). LCX, left circumflex artery.

Anomalies of Origin

Although the usual origin of the left and right coronary arteries is the left and right sinuses of Valsalva, respectively, ectopic coronary arteries can arise above the sinuses in the ascending aorta, within the posterior (noncoronary) sinus, low within the sinus adjacent to the leaflet, within the commissure, or in a subvalvular location. The conus artery frequently originates as a separate ostium in the right sinus of Valsalva. There may be no left main artery if the left anterior descending and circumflex arteries arise separately from the left sinus of Valsalva. A common anomaly is the left circumflex artery arising from the right sinus of Valsalva and passing behind the aorta into the left atrioventricular groove (Fig. 7-27). When the left coronary artery originates from the right sinus of Valsalva, it may:

FIGURE 7-27 Anomalous left circumflex artery. A, Selective injection into the left coronary artery visualized only the left anterior descending artery. B, Right coronary artery injection demonstrates a retroaortic left circumflex artery (arrows). C, A left ventriculogram shows the position of the anomalous circumflex artery (arrow). (A small ventricular apical aneurysm secondary to an old infarct is also present.)

FIGURE 7-28 Origin of the left coronary artery from the right sinus of Valsalva. A, Injection into the right sinus opacifies both the right and left coronary arteries. B, In the right anterior oblique projection, an intimal ridge (arrow) is visible as the left coronary artery leaves the right sinus.

Similarly, when the right coronary artery originates from the left sinus of Valsalva by passing between the aorta and the right ventricular infundibulum, it forms an acute angle at its ostium and may be compressed by the two great vessels. If the anomalous right coronary, originating from the left sinus of Valsalva, courses anteriorly to the aorta, it should not produce any symptom, unless it is diseased (Fig. 7-29). Rarely a left coronary artery arises from the right sinus of Valsalva, assumes an intramyocardial course by traversing through the crista supraventricularis, then continues as the left anterior descending and circumflex arteries in their usual locations.

FIGURE 7-29 Patient with positive stress test in the inferior territory. A, No lesion could be depicted on the left coronary artery, shown here in the “spider” view. B, The right coronary artery could not be found in the right sinus of Valsalva. The ostium of the right coronary artery (RC) was found near the left main artery (LM) in the left sinus of Valsalva. Two stenoses were demonstrated and were successfully stented, as shown in C. LAD, left anterior descending artery; LCX, left circumflex artery; arrow, intermediate branch.

The coronary arteries may have ectopic origins from structures other than the aorta. In this situation, the anomalies include:

The most common of these is the left coronary origin from the pulmonary artery. This entity, the Bland-White-Garland syndrome, is seen in infants who have a myocardial infarction in the first few months of life. Coronary arteriography shows an empty left sinus of Valsalva. The right coronary artery supplies collaterals to the left coronary artery, which fills in a retrograde direction to opacify the pulmonary arteries (Fig. 7-30). The infantile left ventricle may have a segmental wall motion abnormality like that seen in coronary disease in the adult. Left ventricular aneurysms and mitral regurgitation can produce congestive heart failure. Left ventricular aneurysms may completely regress after corrective coronary surgery.

FIGURE 7-30 Anomalous origin of the left coronary artery from the pulmonary artery. A, Initial aortogram in the cranially angled left oblique projection disclosed absence of the left coronary artery from its usual origin at the left sinus of Valsalva. B, The path of coronary filling during cineangiography was right coronary through septal collaterals, to the left anterior descending artery, and then to the pulmonary artery. A catheter in the pulmonary artery helps locate this structure.

Anomalies of Origin and Course

Major coronary anomalies of location are those that go behind the aorta, between the aorta and the pulmonary artery, or anterior to the right ventricular infundibulum (Fig. 7-31). The anomaly that can cause angina and sudden death is the aberrant coronary artery that goes between the aorta and the pulmonary artery. These two great arteries expand during systole and may compress the aberrant coronary artery and constrict its flow. This type of anomaly usually has a stenosis at its origin because of an acute angle with the sinus of Valsalva. A prime example of this group is the isolated single coronary artery, which can originate from either the left or right sinus of Valsalva (Fig. 7-32).

FIGURE 7-31 Classification of single coronary arteries in relation to the aorta and pulmonary artery. LAD, left anterior descending artery; LCA, left coronary artery; LCf, left circumflex artery; RCA, right coronary artery.

FIGURE 7-32 Single right coronary artery with connecting segment to the left anterior descending artery going between the aorta and the right ventricular infundibulum. A, Shallow right oblique view shows anterior connecting segment (arrow) to the left coronary artery. B, Lateral view of artery (arrow) between the aorta, which has the angiographic catheter, and the right ventricular outflow tract through which the pulmonary artery catheter passes. C, Left oblique view. D, Left ventriculogram shows the left coronary artery (arrow) to be anterior to the aorta.

The most common anomaly is origin of the left circumflex artery from the right coronary artery with a course that goes behind the aorta before supplying the usual circumflex territory. You can usually see this retroaortic course on a right anterior oblique left ventriculogram, and it will alert you to the anomaly. Other common variations include the left anterior descending artery coming from the conus artery and the posterior descending artery continuing around the apex as a long left anterior descending artery (Fig. 7-33).

FIGURE 7-33 Single right coronary artery. In the left anterior oblique view, the posterolateral branch (P) of the distal right coronary continues in the left atrioventricular groove to become the circumflex artery. A bridging artery (arrow) from the origin of the right coronary to the vestigial left anterior descending artery (L) joins the left circumflex artery to form an arterial ring.

Noninvasive imaging modalities, such as gadolinium magnetic resonance angiography and electrocardiogram-gated (ECG-gated) 64-detector computed tomography (CT), represent efficient imaging techniques for demonstrating coronary anomalies. They can provide pertinent information on the shape of the vessel orifice and course of the anomalous vessel, such as its relationship with the great vessels, especially before surgery or eventually coronary intervention.

Anomalies of Termination

Coronary artery fistula is a rare congenital anomaly but is significant in the differential diagnosis of a continuous murmur. A coronary fistula may occur to any adjacent vascular bed. Fistulas may connect to all four cardiac chambers, the coronary sinus, the right or left superior vena cava, the pulmonary artery, and the systemic arteries (Fig. 7-34). In aortic atresia and pulmonary atresia, there are frequently large coronary artery sinuses and fistulas to the ventricles.

FIGURE 7-34 Coronary artery fistula. A and B, Left coronary angiogram. Contrast media is seen to “leak” into the left ventricle, which showed contrast enhancement. Diminished venous return opacification was noted at the end of the acquisition. Coronary fistula to the left ventricle was demonstrated (arrows).

Complications

As in other parts of the body, fistulas can be the site of bacterial arteritis, ischemia to distal tissues, and rupture. Complications in the heart are congestive heart failure, infective endocarditis, myocardial infarction, and fistula rupture.

These fistulas are best studied with selective coronary arteriography. Congenital coronary arteriovenous fistulas have a large tortuous artery and vein down to the point of termination (Fig. 7-35). In contrast, acquired fistulas from either trauma or endocarditis have a normal or slightly dilated artery proximal to the fistula. The arterial bed distal to the fistula may be hypoperfused (a vascular steal), and if long-standing, may have collaterals supplying this lesion. Acute traumatic fistulas initially have normal-sized arteries and veins, but if they are uncorrected both these vessels will dilate. If a fistula opens into the right heart, a left-to-right shunt is present.

FIGURE 7-35 Congenital coronary artery fistulas in two patients. A and B, Right coronary and left circumflex arteries terminate in the right ventricle (arrow). C and D, Left circumflex artery terminates in the coronary sinus.

Internal Mammary Artery Grafts

The most common procedure is to attach the left internal mammary artery to the proximal left anterior descending artery (Fig. 7-36). Either the right or left internal mammary artery may be used for grafting, but usually not both together, to prevent sternal osteonecrosis. Occasionally these arteries are sequentially grafted to the left anterior descending and to the diagonal artery. The patency rate of the internal mammary grafts is higher than that of saphenous vein grafts, even though the arterial graft has a slower flow than the venous graft. Unlike the vein graft, the internal mammary arteries do not form intimal hyperplasia, which occurs in all vein grafts during the first year after surgery.

FIGURE 7-36 Multiplanar reformatted computed tomography coronary arteriogram of a left internal mammary artery bypass graft to the distal left anterior descending (LAD) coronary artery. The artery arises from the proximal portion of the left subclavian artery (arrow 1), viewed in cross section in this reconstruction. The graft courses along the interface of the low attenuation, air-filled lung and slightly higher attenuation mediastinal fat, anterior to the main pulmonary artery (MP), to anastomose with the distal LAD (arrow 2). There is backfilling (arrow 3) to the level of the LAD obstruction.

Saphenous Vein Grafts

Saphenous vein grafts have a proximal anastomosis to the ascending aorta several centimeters above the aortic valve. Vein grafts may be constructed so that one or more side-to-side anastomoses are connected with diagonal and marginal arteries that lie in proximity. A side limb can be placed to a saphenous vein graft so that several coronary arteries at a distance from one another may be supplied by a single proximal graft (Fig. 7-37). This type of graft resembles an inverted Y.

FIGURE 7-37 Complex aortocoronary grafts. A, Saphenous vein “Y”-graft has one limb to the left anterior descending artery and the other limb to a diagonal branch. B, The left internal mammary artery in the right anterior oblique projection has a side-to-side anastomosis (thin arrow) to the left anterior descending artery and an end-to-side anastomosis (thick arrow) on a diagonal artery.

Complications

Complications in venous grafts are usually at the proximal aortic anastomosis or the distal coronary anastomosis. Graft complications in coronary surgery are the same as complications to grafts elsewhere. Occlusion and focal or diffuse stenosis are common (Fig. 7-38), whereas pseudoaneurysm at either anastomosis is unusual. Over time, saphenous grafts develop a diffuse stenosis from intimal hyperplasia (Fig. 7-39). Degenerated venous grafts can look like severe atherosclerosis with ragged ulcerated plaques. Unlike coronary artery stenoses, which can be graded by a percentage reduction in diameter, this method is not accurate when applied to a stenosis in a vein graft because vein grafts are larger than the supplied coronary artery. In a graft four times the size of the native artery a stenosis must have an 80% diameter before it reduces distal flow, but in a graft of the same size as the coronary artery, distal flow would be reduced by about 50% at rest. Because of these difficulties, a thallium exercise test is required to assess the severity of a graft stenosis.

FIGURE 7-38 Graft stenosis. A proximal stenosis (arrow) is demonstrated in the vein graft to the left descending artery. Successful treatment was obtained with stent implantation.

FIGURE 7-39 Aortocoronary reversed saphenous vein graft stenoses (arrows). Selective injection into a graft to the left circumflex marginal artery has a moderate stenosis in its middle segment and a severe stenosis distally. These changes are intimal hypertrophy and graft degeneration from development of atherosclerosis in the neointima of the vein. A Carpentier-Edwards valve prosthesis is present.

Imaging Techniques

Bypass grafts can be visualized by angiography, multidetector computed tomography (MDCT), and magnetic resonance imaging (MRI). Angiography of bypass grafts is performed by selective injection in the internal mammary artery or in the aortic anastomosis of the vein graft. The flow into the native coronary artery from a graft should occur in both antegrade and retrograde directions (Fig. 7-40). If there is no flow into the proximal coronary artery from the graft, that artery is usually occluded. Injection into a coronary artery that has a distal graft may show an apparent occlusion in the “watershed” region between the proximal coronary artery and graft insertion. When the coronary artery is stenotic and not occluded before the graft, the graft will fill in a retrograde direction. These complex flow patterns in the graft and the adjacent coronary arteries depend on how much pressure is applied by the angiographer when injecting the graft or artery, and the hemodynamic variables in the arterial system. Collaterals to a grafted artery are not seen when the graft is functioning. Collateral vessels that were present before surgery, unless quite large, no longer are visualized, presumably because the collaterals have involuted or because the graft reduces the pressure gradient between the ends of the collateral channels, thereby slowing flow to the collateral.

FIGURE 7-40 Imaging criteria for a normal aortocoronary bypass graft. The saphenous vein graft to the posterior descending artery (P) has no stenosis in either the aortic anastomosis or the coronary anastomosis. In this left anterior oblique view, there is both antegrade flow in the posterior descending artery and retrograde flow into the distal right coronary artery (R). M, right ventricular marginal artery.

Ventriculogram Analysis

The ventriculogram is a classic example of “information overload.” It images many structures that are usually moving in different directions at different velocities. Even among experienced observers, one person’s dyskinetic wall motion may be another’s normal motion. Therefore, it is useful to develop a schema for interpreting the ventriculogram by isolating the components and separately judging their shape and motion. The basis for analyzing the left ventriculogram follows.

Aorta

Mitral valve

Left ventricular wall

Regional Wall Motion

Regional wall abnormalities are a distinguishing characteristic of coronary artery disease and occur in acute myocardial infarction, myocardial ischemia without infarction, areas of myocardial scar from a remote infarction, aneurysms, and regions of muscle in which there are some viable myocytes interlaced with areas of scar. These changes in wall contraction can occur after only a few minutes of acute coronary occlusion. As ischemia progresses to infarction, first hypokinesis, then akinesis, and then dyskinesis develop. Dyskinesis can represent acute or chronic ischemia as well as an aneurysm or large scar.

Correlation with Coronary Artery Disease

As a general rule, asynergy is noted in areas of previous myocardial infarction and is more common in regions of severely stenosed vessels. However, perfusion, as determined by thallium-201 scintigraphy, correlates more closely with segmental wall motion abnormalities than does coronary anatomy. On the other hand, it is not uncommon to find normal wall motion in a segment of the left ventricle supplied by a severely stenotic coronary artery. These segments tend to have good collaterals and have not had an infarct.

In both acute and chronic myocardial infarction, there are compensatory mechanisms that tend to restore the cardiac output even though a portion of the ventricle is not contracting. These are manifested in a hyperkinetic performance of wall segments that are not involved in the region of ischemia. For example, in anteroseptal infarction, the posterolateral wall may have an excursion twice the normal range.

Left Ventricular Thrombus

Mural thrombi of the left ventricle occur in the area adjacent to healed myocardial infarcts without aneurysm, in segmental wall aneurysms, and with idiopathic dilated cardiomyopathy with poor wall motion. Left ventricular thrombi do not occur if the wall is contracting normally. The thrombi are usually at the apex, although they may be elsewhere, particularly along the inferior wall and, occasionally, within a false aneurysm.

Approximately half of all patients with postinfarction ventricular aneurysm have left ventricular thrombi that are seen at surgery or on necropsy study; however, the angiographic detection of these thrombi is only moderately sensitive and specific. Simpson and colleagues found that roughly 74% of mural thrombi found at surgery are not detected by angiography and in 10% of patients diagnosed as having thrombi no thrombi are present at operation. Even during echocardiography of the left ventricle, it can be difficult to diagnose mural thrombi. Gadolinium magnetic resonance angiography or ECG-gated multirow detector CT can precisely characterize or delineate the thrombus (Fig. 7-43). Furthermore, echocardiography and noninvasive imaging techniques do not have the risk of dislodging mural thrombi when compared to angiography.

FIGURE 7-43 Left ventricular thrombus. Contrast enhanced chest computed tomography showing an apical infarction of the left ventricle (arrows), associated with a thrombus (*).

Calcifications

Left ventricular thrombi may be calcified, particularly when there is calcification of adjacent structures, such as an aneurysm or infarcted papillary muscle. Filling defects that are typical of thrombus may have several appearances (Fig. 7-44). A polypoid shape usually arises in an akinetic apex. This angiographic configuration is a harbinger of systemic embolization. A truncated apex with an adjacent shaggy wall may also indicate thrombus formation. Because the wall of an aneurysm is thin, the presence of a normal or thick wall to the aneurysm indicates a thrombus within the aneurysm.

FIGURE 7-44 Left ventricular thrombus. The left ventricle in mid systole has a dyskinetic apex and diaphragmatic wall. The thrombus is polypoid (arrows) and is attached at the apex.

Cardiac Rupture

Although rupture of the heart may be catastrophic, certain types of rupture may be contained so that the patient can have diagnostic imaging and undergo surgical repair (Box 7-3). Cardiac rupture usually occurs after a myocardial infarct; trauma is less common. Free rupture into the pericardium typically is fatal. Rupture through the interventricular septum, of a papillary muscle, or development of a false aneurysm is a serious complication but may have a longer time course to allow treatment.

Left Ventricular True and False Aneurysm

Definition and Pathologic Correlation

Left ventricular aneurysms appear to develop early in the course of myocardial infarction. In more than 50% of patients who develop an aneurysm, it will be present within 24 to 48 hours of the onset of infarction and frequently will still be present 3 months later. In the Coronary Artery Surgery Study (CASS), roughly 8% of patients with coronary artery disease had well-defined left ventricular aneurysms. Although aneurysms can develop with single-artery disease, most left ventricular aneurysms have multivessel coronary disease with severe obstructions. Patients with an anterior aneurysm usually have a greater than 90% stenosis of the proximal left anterior descending artery.

A left ventricular aneurysm (Box 7-4) is a segment of a left ventricular wall that protrudes from the expected diastolic outline of the ventricular chamber. The wall motion may be either akinetic or dyskinetic. The wall of the aneurysm is generally smooth without the usual trabecular pattern. This definition of a left ventricular aneurysm overlaps with several features of reversible ischemia. During an acute myocardial infarction, the wall segment involved has a dyskinetic motion, which may return to normal if a transmural infarction does not occur.

Box 7-4 Characteristics of left ventricular aneurysms

FUNCTIONAL ANEURYSM

Contour bulge in diastole

Normal contour in systole

Occurs in spasm, ischemia, or infarct

May be reversible after revascularization

Rare thrombus, never calcification

TRUE ANEURYSM

Contour bulge in diastole and systole

Typically occurs anterolateral, apical, and septal walls

Large scar that rarely ruptures

Junction between normal muscle and aneurysm is poorly defined

Thrombus and calcification common

FALSE ANEURYSM

Contour bulge in diastole and systole

Typically occurs in inferior or anterolateral wall

Propensity to expand and rupture

Junction between normal muscle and aneurysm is sharply defined

Thrombus and calcification uncommon

When the wall thins, a large myocardial scar may develop the appearance of an aneurysm. On imaging studies, a large scar or a small aneurysm may have the same appearance. A functional aneurysm has a normal diastolic contour but a dyskinetic systolic bulge in the region of a large acontractile segment and may contain either reversible ischemic myocardium or scar. In contrast, an anatomic aneurysm has an abnormal protrusion during both systole and diastole because the wall is entirely a scar that has stretched (Fig. 7-45).

FIGURE 7-45 Types of ventricular aneurysm. The functional aneurysm has a normal diastolic contour but has an acontractile segment that bulges outward during systole, representing an ischemic wall segment or small scar. The anatomic aneurysm has an abnormal bulge during both systole and diastole from an infarcted wall. The false aneurysm has a discrete neck and typically is saccular, representing the ventricular perforation into the pericardium. The solid lines outline end diastole and the dashed lines outline end systole.

Imaging Signs of Aneurysm

Anatomic aneurysms that have been present for more than several months may have a thin rim of calcium outlining their extent. This type of aneurysm may be either akinetic or dyskinetic. The wall of a true aneurysm is quite thin, reflecting the fact that the scar extends from the endocardium through to the pericardium (Fig. 7-46). The aneurysmal segment has a large neck, comparable in size to its internal circumference. Within the aneurysm, the wall is usually smooth unless a thrombus is present. The boundaries of the aneurysm are usually discrete and easily discernible.

FIGURE 7-46 True left aneurysm. A, A thin rim of calcium outlines the abnormal left ventricular contour over the anterolateral wall. B, On the lateral view, the aneurysm has a broad base and partially projects anteriorly over the right heart.

The chest film is not a sensitive test to screen for left ventricular aneurysm. Only one third of angiographically diagnosed aneurysms show contour abnormalities on the chest film. Part of the explanation for this discrepancy is that the septum is not visible on the chest film and small aneurysms at the apex are obscured by the fat pad. The left ventricle is usually dilated and the remaining wall is hyperkinetic to maintain cardiac output. The uninvolved ventricular wall is frequently hypertrophied, which probably reflects the fact that about half of patients with aneurysms also have systemic hypertension. Most true aneurysms are in the anterolateral and apical walls (Fig. 7-47), although the inferior and posterolateral walls occasionally have isolated aneurysms. Echocardiography depicts left ventricular aneurysm quite well and should be the first modality of choice.

FIGURE 7-47 Left ventricular true aneurysm. A, A diastolic frame shows the filling of the left ventricle. B, The end-systolic frame demonstrates a large aneurysm with a broad base involving the anterolateral, apical and diaphragmatic walls (arrows).

False Aneurysm

When the pericardium rather than myocardium composes the wall of the aneurysm, it is a false aneurysm or pseudoaneurysm. The usual cause is a rupture of the left ventricle into the pericardial space after myocardial infarction. Because of adhesions from previous pericarditis, the pericardium attaches locally to the epicardium. This opportunely prevents the ventricular blood from extending into the remaining pericardial space and causing tamponade. Causes that are less common but have a nearly identical appearance include abscess from bacterial endocarditis, surgical ventriculotomy (Fig. 7-48), and penetrating trauma. In contrast to true aneurysms, most false aneurysms resulting from myocardial infarct are on the posterolateral and diaphragmatic sides of the left ventricle (Fig. 7-49).

FIGURE 7-48 False left ventricular aneurysm after ventriculotomy. The extraluminal collection of contrast (arrows) at the apex occurred at the site of a puncture to vent air as the patient came off coronary bypass. The blood is constrained by the adjacent pericardium and mediastinal scarring.

FIGURE 7-49 Contour abnormality in left ventricular false aneurysm. The patient had a false aneurysm develop at the site of a true aneurysm. A, The anterolateral and apical location is typical of a true aneurysm. B, The lateral chest film shows an aneurysm in the posterolateral wall (arrow), more typical of a false aneurysm. The chest film cannot distinguish between the types of aneurysm but is more useful for diagnosing their presence and whether they have increased in size.

The left ventriculogram demonstrates a discrete saccular aneurysm whose neck is considerably smaller than the internal circumference of the saccule. Contrast material may not flow into the false aneurysm until late in systole, and it may oscillate into and out of the neck of the aneurysm without exiting from the left ventricle. Because of the narrow communication with the left ventricular chamber, the opacification of the false aneurysm may persist for many seconds after the injection has ended (Fig. 7-50). Frequently the false aneurysm is bigger than the left ventricle, and in fact, may enlarge over serial examinations. This has prognostic significance in that false aneurysms have a high propensity to rupture. Rupture of a true aneurysm is rare, occurring in less than 4% of several necropsy series. In contrast, postmortem series indicate that approximately 45% of false aneurysms rupture. Echocardiography is also the first modality of choice when a false aneurysm is suspected.

FIGURE 7-50 Left ventricular false aneurysm. Left anterior oblique ventriculogram shows a posterolateral aneurysm with a narrow neck. The wall thickness is only 3 mm (arrow).

The coronary arteries in patients with false aneurysms are also severely diseased. However, reflecting the posterior and diaphragmatic location of most false aneurysms, there is frequent occlusion of the right coronary artery, whereas, with true aneurysm, occlusion is more common in the left coronary artery.

Cardiac false aneurysm (or changes that look like aneurysms) may result from diseases other than coronary artery disease. Congenital diverticula of the left ventricle may be confused with false aneurysm but they usually are smaller and occur at the apex. The African cardiomyopathies that have apical aneurysms usually can be distinguished by both their clinical course and the absence of coronary disease. The rare submitral aneurysms found in black Africans are not caused by ischemia. These aneurysms have a narrow neck originating between the mitral annulus and the posteromedial papillary muscle. The large sac lies beneath the left atrium and displaces it superiorly.

Clinical Presentation

Rupture of the interventricular septum is an uncommon complication of myocardial infarction that occurs in about 1% of those who sustain infarction. If not surgically treated, more than 90% of those with rupture die within 1 year. The appearance of a new systolic murmur within hours to weeks after myocardial infarction, particularly if associated with biventricular failure or cardiogenic shock, suggests ventricular septal defect or ruptured papillary muscle.

Common abnormalities in chest radiographs of patients with a ruptured septum are signs of interstitial or alveolar pulmonary edema and left ventricular enlargement (Table 7-2). Enlargement of other chambers is inconstant. Almost half will show pleural effusions, enlargement of the pulmonary arteries, and signs of pulmonary venous hypertension. Occasionally, an unusual configuration of the heart will suggest the presence of an aneurysm in addition to the septal rupture (Fig. 7-51).

TABLE 7-2 Chest radiographic abnormalities in rupture of the interventricular septum

Modified with permission from Miller SW, Dinsmore RE, Greene RE, et al.: Coronary, ventricular, and pulmonary abnormalities associated with rupture of the interventricular septum complicating myocardial infarction, Am J Roentgenol 131:571, 1978.

FIGURE 7-51 Typical chest film in rupture of interventricular septum. The heart is enlarged with an aneurysm in the anterolateral and apical segments. There is redistribution of blood to the upper lobes and slight interstitial pulmonary edema manifested by Kerley B lines and shaggy bronchovascular walls. The pulmonary vasculature reflects the left ventricular failure and not the left-to-right shunt that is present.

Left Ventricular Signs

Doppler echocardiography is a good noninvasive technique to demonstrate ventricular septal rupture. During left ventriculography, almost all patients have at least one segment with akinesis or dyskinesis. The posterolateral wall is hyperkinetic in some patients, suggesting that the exaggerated motion is partly compensating for the other segments of the ventricle. The septum is always akinetic or dyskinetic.

In the right anterior oblique view, you will see opacification of the pulmonary artery during left ventriculography. This view superimposes the two ventricles. The most inferior wall visible is the diaphragmatic wall of the right ventricle. If the left ventricular diaphragmatic wall is akinetic, the adjacent right ventricular wall behaves similarly. In the left anterior oblique projection, contrast material passes through the rupture to opacify the right ventricle (Fig. 7-52). The margins of the rupture may be difficult to identify, but they always are in a region of severe segmental wall motion abnormality. Occasionally, the right ventricular anterior wall will also be akinetic and represent an extension of the diaphragmatic infarct.

FIGURE 7-52 Rupture of the interventricular septum. In a left anterior oblique left ventriculogram, contrast material pours through most of the apical septum of the left ventricle (LV) into the dilated right ventricle (RV). The RV is large and akinetic with an aneurysm involving most of the anterior wall.

After myocardial infarction, ventricular septal defects occur in the muscular septum either posteriorly adjacent to the mitral valve or anteriorly near the apex. The margins of the rupture are irregular and the flow of contrast media in that region is slow. However, the site of rupture is always in a region of severe segmental wall motion abnormality. Anterolateral and apical akinesis uniformly correspond with an anterior rupture near the apex, whereas posterobasal and diaphragmatic akinesis occur with posterior rupture adjacent to the mitral annulus. The cranial left anterior oblique view elongates the septum and helps to distinguish apical from basal ruptures.

Left ventricular aneurysm, mitral regurgitation, or both are found in roughly three quarters of patients with septal rupture. These exaggerate extensive wall motion abnormalities. The aneurysm may be in the region of the septal rupture or in a separate portion of the ventricle. The mitral regurgitation is the result of a variety of factors, including left ventricular dilatation and papillary muscle dysfunction. Both these lesions contribute to poor left ventricular performance and make catheterization difficult. However, their recognition is essential for proper surgical management.

Extensive coronary artery stenoses are usually present with septal rupture. Severe two- and three-vessel disease is common with rupture of the interventricular septum, yet about 30% with rupture have a significant stenosis in only one coronary artery, either the right coronary or the left anterior descending artery. When only one coronary artery is involved, that portion of the artery distal to the occlusion is generally not visualized. This indicates that it is completely occluded or that bridging collateral vessels either have not formed or are not currently functioning. The absence of collaterals and the lack of visualization of the coronary artery distal to a proximal occlusion in a patient with septal rupture is presumably associated with a sizable area of muscle infarction that was present before the septum ruptured. On the other hand, in the absence of a septal rupture or aneurysm, the distal segment of an occluded coronary artery is almost always opacified through collateral vessels. It is possible that edema in the ischemic zone around the infarct compresses existing collateral vessels and that these small vessels might be visible when the edema regresses.

Pathologic Causes

The mechanism of mitral regurgitation in coronary artery disease is related to the impairment of the left ventricular wall containing the papillary muscles. This pathologic process has been labeled the papillary muscle dysfunction syndrome, although the papillary muscles and their blood supply are only a partial explanation. The arterioles supplying the papillary muscles are either end arteries or are at the termination of a long arterial path. The posteromedial papillary muscle is supplied by left circumflex marginal branches to the posterolateral wall or by branches of the distal right coronary artery; the anterolateral papillary muscle receives blood mainly from diagonal branches of the left anterior descending artery.

During systole, the papillary muscles contract and either initiate the action or assist in the support of the mitral apparatus to withstand systolic pressure. Clinically, under situations in which the papillary muscles are ischemic, the adjacent left ventricular wall is also ischemic. Congestive heart failure leading to left ventricular dilatation will change the orientation of the papillary muscles to the mitral leaflets but causes only a trace amount of regurgitation because the muscle around the mitral orifice contracts slightly during systole. Under these circumstances mitral regurgitation of mild to severe degree may result because of incomplete mitral leaflet closure.

The spectrum of papillary muscle disorders includes ischemic processes involving both the papillary muscle and its adjacent left ventricular free wall. For example, hypokinesis, akinesis, or aneurysm may produce any degree of mitral regurgitation (Fig. 7-53).

FIGURE 7-53 Papillary muscle dysfunction. Mitral regurgitation (arrow) has resulted from akinesis of the inferior wall after an infarct.

Complete rupture of a necrotic papillary muscle is quite rare, and because of its acute severity, usually causes the death of the patient. Recent surgical advances have made survival possible for some individuals if this lesion is recognized early. The more frequent clinical event is rupture of only one head of the papillary muscle, allowing the attached chordae to partially support both mitral leaflets and to limit somewhat the amount of regurgitation.

Ventriculographic Signs

The left ventriculographic signs of papillary muscle dysfunction include left ventricular enlargement, an akinetic wall that contains a papillary muscle or an adjacent left ventricular aneurysm, calcification in a papillary muscle, and any degree of mitral regurgitation. The papillary muscle may be quite large, swollen with edema associated with myocardial infarction. In the setting of free mitral regurgitation after myocardial infarction, one or both heads of a papillary muscle must have ruptured, indicating the need for emergent mitral valve replacement. Echocardiography should be performed immediately following acute myocardial infarction if mitral valve regurgitation is suspected.