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Adjuvant antiplatelet strategies in coronary thrombolysis.

M ounting experimental and clinical evidence, coupled with a growing understanding of coronary arterial thrombogenesis, supports the hypothesis that the benefits of thrombolytic therapy in acute myocardial infarction depend primarily on achieving rapid recanalization and maintaining patency of the infarct-related vessel. To achieve these goals it presently appears that, in addition to administration of effective thrombolytic agents, the implementation of adjunctive pharmacological strategies designed to inhibit either platelet activity or thrombin generation will be required. Although there are a number of potential mechanisms by which platelets may be inhibited, Yasuda et all describe in this issue of Circulation a unique antiplatelet agent, kistrin, which blocks the platelet GPIIb/IIIa receptor. Coronary artery thrombi consist of both plateletrich and erythrocyte-rich zones, with the former predominating in most instances. A platelet-rich zone exists at the site of atherosclerotic plaque rupture, and erythrocyte-rich zones develop both proximal and distal to the area of vascular injury.