Kamat S G, Kleiman N S
Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
Cardiol Clin. 1995 Aug;13(3):435-47.
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.
血小板及富含血小板的血栓在急性心肌梗死发病机制中起关键作用。破裂的动脉粥样硬化斑块引发由血小板、其膜受体、黏附配体、血小板激动剂的存在或生成以及伴随纤维蛋白生成的凝血级联激活所介导的止血反应。血小板与凝血系统及纤溶系统的相互作用复杂；然而，急性心肌梗死溶栓期间药理学控制血小板反应能力方面新的、令人兴奋的进展将增进我们对这些相互作用的理解，并最终转化为临床益处。
