Ischemic Heart Disease

Chapter 7 Ischemic Heart Disease


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.

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).

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

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.

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).

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.

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).

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.

Morphology of Coronary Atherosclerosis

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).

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.

Determinants of Coronary Blood Flow

Transient Variations

The coronary system autoregulates its blood flow for transient variations in perfusion pressure. Abrupt increases in perfusion pressure (aortic pressure minus right atrial pressure) result in an equivalent increase in coronary blood flow, which gradually returns toward the initial value as vascular resistance changes. A similar response occurs when there is a quick decrease in perfusion pressure.

The blood flow through both left and right coronary arteries is influenced by the extravascular resistance supplied by the thick-walled left ventricle. In the left coronary artery, most blood flow is in diastole. In left ventricular hypertrophy, left coronary flow may even reverse. In contrast, right coronary blood flow is more constant and occurs quite equally during systole and during diastole. In diseases that increase left ventricular wall tension, resting coronary flow tends to be more phasic. Because left coronary flow occurs mainly during diastole, changes in heart rate can lead to critical alterations in myocardial blood supply. In tachycardia, the diastolic filling period is shortened, so blood flow occurs during a shorter time period. Enhancement of left ventricular contraction, as occurs with aortic stenosis or with sympathetic stimulation, similarly increases the time of the heart in systole and thereby reduces left coronary flow. The opposite effect would occur in a patient on propranolol in whom there is bradycardia and decreased afterload.

Resting coronary blood flow in a normal vascular bed does not decrease until the diameter of the stenosis is at least 80% of the adjacent normal vessel. As a stenosis is gradually increased, the distal vascular bed—mainly at the level of the precapillary arteriole—begins to dilate and thus reduces the vascular resistance. However, if the vasculature is already maximally dilated so that autoregulation is no longer present, coronary flow begins to decrease with a stenosis of 30% to 50%. This effect can be seen after pretreatment with a vasodilator but is also thought to occur in the presence of atherosclerosis. In this latter instance, the precapillary sphincters of the distal vascular bed may theoretically dilate slowly from the growth of proximal stenoses.

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.

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.

Dec 26, 2015 | Posted by in CARDIOVASCULAR IMAGING | Comments Off on Ischemic Heart Disease

Full access? Get Clinical Tree

Get Clinical Tree app for offline access