Platelets and platelet inhibitors in acute myocardial infarction.
Review
Overview
abstract
Platelets and platelet-rich thrombi play a pivotal role in the pathogenesis of acute myocardial infarction. A ruptured atherosclerotic plaque evokes a hemostatic response that is mediated by platelets, its membrane receptors, adhesive ligands, the presence or generation of platelet agonists, and the activation of the coagulation cascade with fibrin generation. The interaction of platelets with the coagulation and the fibrinolytic systems is complex; new and exciting developments, however, in the ability to pharmacologically control platelet responses during thrombolysis in acute myocardial infarction will enhance our understanding of these interactions and will eventually translate into clinical benefit.
