ABSTRACT
A great variation exists in the stability of coronary atherosclerotic plaques. When coronary flow is limited by plaque, patients have angina develop, which can be stable for years. However, abrupt disruption of previously stable coronary plaques with superimposed thrombosis is the main cause of acute coronary events, such as unstable angina pectoris, sudden coronary death, and acute myocardial infarction (1-4). Therefore, for event-free survival, the vital question is not why atherosclerosis develops but rather why some plaques remain rupture-resistant and innocuous, whereas other plaques, after years of indolent growth, become rupture-prone and life-threatening (5). There are two major mechanisms of plaque disruption (6, 7): through and through rupture of the fibrous cap of a lipid-rich plaque (8) and superficial denudation and erosion of the endothelial surface (9, 10).
