Etiology and Pathogenesis

The presence of risk factors for atherosclerosis—advanced age, genetic predisposition, male sex, hypertension, diabetes mellitus, renal disease, hyperlipidemia, and cigarette smoking—all result in a propensity for the normally thin intima of coronary arteries to increase in both thickness and smooth muscle cell content. This earliest stage of atherosclerosis is caused by the proliferation of smooth muscle cells; the formation of a tissue matrix of collagen, elastin, and proteoglycan; and the accumulation of intracellular and extracellular lipids. Thus, the first phase of atherosclerotic lesion formation is focal thickening of the intima with an increased presence of smooth muscle cells and extracellular matrix. Intracellular lipid deposits also accumulate. Next, lesions called fatty streaks form. A fatty streak is an accumulation of intracellular and extracellular lipid that is visible in diseased segments of affected arteries. As the lesion evolves, a fibrous plaque can form from continued accumulation of fibroblasts covering proliferating smooth muscle cells laden with lipids and cellular debris. Plaques progress in complexity as ongoing cellular degeneration leads to ingress of blood constituents and calcification. The plaque’s necrotic core may enlarge and become calcified. Hemorrhage into the plaque may disrupt the smooth fibrous surface, causing thrombogenic ulcerations. Clot organization on the plaque surface often occludes, or nearly occludes, the arterial lumen, further decreasing blood flow (see also Chapter 2).

Just as the rapidity of atherosclerotic lesion formation varies from individual to individual, the presentation of ischemic heart disease also varies. Objective evidence of myocardial ischemia is identified with concurrent coronary angiographic evidence of flow-limiting atherosclerotic lesions. The need for surgical treatment usually arises from presentation of an individual with an acute coronary syndrome and multivessel coronary artery disease (CAD) or with stable but debilitating angina (see Chapters 13 and 14). Examples of indications for urgent CABG include postinfarction angina, ventricular septal defect, acute mitral regurgitation, free wall rupture, and/or cardiogenic shock in patients admitted to the hospital with acute MI. Each of these acute conditions warrants surgical intervention and revascularization.

Differential Diagnosis

The differential diagnosis of myocardial ischemia includes atherosclerotic and nonatherosclerotic causes of epicardial coronary artery obstruction. Nonatherosclerotic causes include congenital anomalies, myocardial bridges, vascularities, aortic dissection, aortic valve stenosis, granulomas, tumors, and scarring from trauma, as well as vasospasm and embolism. Many of these entities may also be indications for CABG.

Other diseases mimicking angina include esophagitis due to gastrointestinal reflux, peptic ulcer disease, biliary colic, visceral artery ischemia, pericarditis, pleurisy, thoracic aortic dissection, and musculoskeletal disorders.

Diagnostic Approach

Although patients with ischemic heart disease present with a spectrum of clinical urgency, diagnostic evaluation relies on objective evidence of ischemia, assessment of disease burden, and determination of whether the coronary anatomy is amenable to surgical revascularization. The diagnostic approach begins with a complete history and extensive physical examination (see Chapter 1). It is important to note that the physical examination is an insensitive tool and may not assist in the diagnosis of chronic ischemic heart disease. Many patients with chronic ischemic heart disease have no physical findings related to the disease, and even when present, physical findings are often not specific for CAD. Because coronary atherosclerosis is common, any physical finding suggestive of heart disease should raise the suspicion of chronic ischemic heart disease.

Diagnostic evaluation includes multiple approaches. Laboratory studies should be performed to assess for the presence of cardiac risk factors such as diabetes mellitus, hyperlipidemia, renal insufficiency, hepatic insufficiency, and hyperthyroidism. Electrocardiography can document myocardial ischemia during chest pain or with physiologic or pharmacologic stress testing. A stress test may also be used to detect CAD or assess the functional importance of coronary lesions. Test results are positive if the patient has signs or symptoms of angina pectoris with typical ischemic ECG changes. The predictive value of the ECG for detecting myocardial ischemia varies in different clinical settings, but the sensitivity and specificity of electrocardiography are typically less than 70%. The predictive value of stress testing is improved by combining electrocardiography with nuclear or echocardiographic imaging. In individuals who cannot exercise, stress can be induced by administration of the synthetic catecholamine dobutamine, which mimics exercise. Vasodilator drugs such as dipyridamole and adenosine are often used to accentuate flow variations that can occur in individuals with CAD. With vasodilation, these drugs also can cause increased heart rate, increased stroke volume, and an increase in myocardial oxygen demand. Wall motion abnormalities at rest or with stress may be assessed by transthoracic echocardiography, nuclear imaging, or by MRI (see Chapters 3, 7, and 8).

The gold standard for evaluating coronary anatomy to determine the suitability for surgical revascularization is coronary angiography. Coronary angiography allows accurate assessment of coronary atherosclerosis, including quantification of disease location and severity. Studies on the relationship between coronary artery stenoses and myocardial ischemia support the notion that lesions that reduce the coronary artery’s cross-sectional area by 70% or more (50% in diameter) significantly limit flow, especially during periods of increased myocardial oxygen demand. If detected, such lesions are considered compatible with symptoms or other signs of myocardial ischemia. Because atherosclerosis is not uniform, coronary angiography is, to a certain degree, imprecise. The coronary artery’s cross-sectional area at the point of atherosclerotic lesion must be estimated from two-dimensional diameter measurements and in several planes. When compared with autopsy findings, stenosis severity is usually underestimated by coronary angiography. Additionally, coronary angiography does not consider that serial coronary artery lesions may incrementally reduce flow to distal beds by more than is predicted by any single lesion. A series of apparently insignificant lesions may reduce myocardial blood flow substantially.

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