The pathological basis of angina pectoris.

Coronary stenoses may be either concentric without any potential for variation in the degree of obstruction to flow or eccentric, where the cross-sectional area of the lumen can alter with vasomotor tone. Variable obstruction at eccentric stenoses is due to the retention of an arc of normal vessel wall opposite the plaque. Abnormal vasomotor responses are a feature of both human and experimental atheromatous coronary arteries; such an abnormality is likely to reflect endothelial dysfunction with loss or neutralization of endothelial-derived relaxant factor (EDRF). Structural studies show that superficial intimal injury, with migration of monocytes and focal endothelial denudation leading to deposition of small numbers of platelets on the exposed intimal collagen, is found in both experimental and human atheroma. Such endothelial changes may be responsible for arterial constriction leading to transient myocardial is-chemia in both patients with stable exertional angina and in those without overt ischemic heart disease. Larger coronary thrombi are associated with deep intimal tears or fissures that extend into the lipid pool of an atheromatous plaque. The resultant thrombi, large enough to be seen angiographically, project into the arterial lumen and are associated with un-stable angina of the abrupt-onset crescendo type. Nonoccluding mural thrombi in a coronary artery are a source of distal microemboli into the myocardium.