Coronary atherosclerosis and thrombosis.

The relationship of thrombus to atherosclerosis is complex and far more wide-reaching than the obvious causal association of a thrombotic occlusion in a coronary artery with myocardial infarction. An atherosclerotic plaque may be eccentric (localized primarily along one segment of the arterial wall) or concentric (localized circumferentially) and is a complex structure composed of connective tissue, calcium, inflammatory cells and lipid in proportions differing from plaque to plaque. The consistency of plaques depends on the proportion of their component elements: a heavily fibrotic and calcified plaque is hard, whereas a plaque composed predominantly of cholesterol-ester and lipid-containing macrophages is soft. Plaques with a soft lipid core may be covered by a relatively thin cap of fibrous connective tissue separating the plaque material from the luminal blood flow. A rupture or fissure of this cap allows blood to enter the plaque causing dissection of its structure and deposition of fibrin in the plaque. Fissuring commonly promotes thrombosis also in the lumen of the artery and may be followed by thrombus fragmentation and embolization. Mural thrombi may wax and wane, causing intermittent occlusions and fleeting, minor clinical symptoms. Further episodes of thrombosis increase the mass of the mural thrombus in the already restricted lumen and may herald the onset of ischemic symptoms, abruptly aggravate a stable clinical state and produce the crescendo type of unstable angina, dysrhythmias, myocardial infarction or sudden coronary death. The episodic dynamic progress of atherosclerotic disease and local thrombosis governs the episodic evolution of the clinical course.