Thrombosis in Unstable Angina

Abstract

Unstable angina often appears to be due to the disruption of a lipid-filled atherosclerotic plaque, with erosion of the fibrous cap containing monocytes and macrophages that were chemotactically attracted by lipid.¹ More than half of such disruptions occur in coronary arteries with plaques that narrow the vessel lumens by less than 50 to 75 percent of their diameter. These disruptions occur deep within plaques and may involve fissuring toward the lumen, resulting in macroscopic mural thrombus on the surface of the plaque. A large disruption or ulceration of the plaque may lead to total occlusion of the vessel and myocardial . . .