Helft G, Abdelouahed M, Vacheron A, Lecompte T, Samama M M
Clinique Cardiologique, Hôpital Necker, Paris.
Ann Cardiol Angeiol (Paris). 1995 Sep;44(7):354-60.
Rupture of an atherosclerotic plaque is often the trigger of the clotting process, via the activation of platelets which immediately adhere, aggregate and initiate coagulation on their surface. The final step of platelet aggregation involves membrane glycoprotein IIB-IIIA which has become available. Antibodies directed against this membrane receptor are currently under evaluation. They possess definite antithrombotic properties. Complex interactions between thrombolysis, leading to generation of plasmin, and platelet functions have been identified. Depending on its concentration and possibly successively, and according to in vitro experimental conditions, plasmin may be a platelet proaggregant or antiaggregant. Correlations have also been recently demonstrated between thrombolytic activity and coagulation, as, paradoxically, it has been shown that plasmin, the final step of thrombolysis, activates the intrinsic pathway of coagulation, predisposing to the formation of thrombin. This activation is involved in the efficacy of heparin therapy following intravenous thrombolysis during the acute phase of myocardial infarction. This paradoxical action of thrombolysis could also play a role in reocclusions after effective thrombolysis during the acute phase of myocardial infarction. A better understanding of the thrombolysis process and its interactions with platelets and coagulation is important in order to improve the results of this treatment, which are correlated with patient survival.
动脉粥样硬化斑块破裂通常是凝血过程的触发因素，通过激活血小板，血小板会立即黏附、聚集并在其表面启动凝血。血小板聚集的最后一步涉及已可用的膜糖蛋白IIB-IIIA。针对这种膜受体的抗体目前正在评估中。它们具有明确的抗血栓形成特性。已确定溶栓（导致纤溶酶生成）与血小板功能之间存在复杂的相互作用。根据其浓度以及可能相继出现的情况，并根据体外实验条件，纤溶酶可能是血小板促聚集剂或抗聚集剂。最近还证明了溶栓活性与凝血之间的相关性，矛盾的是，已表明纤溶酶（溶栓的最后一步）激活凝血的内源性途径，易导致凝血酶形成。这种激活参与了心肌梗死急性期静脉溶栓后肝素治疗的疗效。溶栓的这种矛盾作用也可能在心肌梗死急性期有效溶栓后的再闭塞中起作用。为了改善与患者生存相关的这种治疗结果，更好地理解溶栓过程及其与血小板和凝血的相互作用很重要。
