[Effects of thrombolysis on platelets and coagulation].

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.