Abstract
Platelet activation is central to the formation of thrombus, which precipitates most unstable coronary syndromes. The angiographic severity of coronary stenoses may not predict the occurrence of acute cardiac events, since rupture of atheromatous plaque and subsequent thrombosis in slightly stenosed vessels may underlie many myocardial infarctions. Normally, the intact endothelium prevents platelet activation, but intimal injury associated with endothelial denudation and plaque rupture exposes subendothelial collagen and von Willebrand factor, supporting prompt platelet adhesion and activation. Local platelet activation then promotes the recruitment of platelets and the formation of thrombus.The importance of platelet-dependent thrombosis has made activated platelets . . .