Biologic aspects of vulnerable plaque

Atherosclerosis and its thrombotic complications are the major cause of morbidity and mortality in the industrialized world. The progression of atherosclerotic plaques in coronary circulation is modulated by several risk factors. It is now clear that plaque composition is a major determinant of plaque disruption and superimposed thrombosis. Plaque vulnerability, defined as the propensity of plaques to disrupt, is further determined by intrinsic and extrinsic triggering factors. After disruption, the fatty core of the plaque and its high content of tissue factor provide a powerful substrate for the activation of the coagulation cascade. Plaque disruption can be clinically silent or cause symptoms of ischemia depending on thrombus burden and the degree of vessel occlusion. In addition, plaque disruption and subsequent healing are recognized to play key roles in the rapid plaque progression. This review looks at the mechanisms underlying the development and progression of atherosclerotic plaques, factors leading to plaque rupture and subsequent thrombosis, and their clinical consequences as potential targets for future research.