This review summarizes the current clinical data on antiplatelet, anticoagulant, and specific antithrombin therapies following myocardial infarction.
Guides post-MI antithrombotic selection amid evolving options; leaves open optimal regimens for specific subgroups.
Coronary thrombosis leading to myocardial infarction is a complex process involving the interaction of the arterial wall, the coagulation cascade, and platelets. Increased understanding of the molecular biology of thrombosis has prompted an evolution in antithrombotic therapy, from the early use of warfarin following myocardial infarction to agents targeting specific receptors or modulators in the thrombotic process. The complexity of thrombosis allows for numerous sites of pharmacologic intervention; the multiple pathways leading to platelet aggregation and thrombin formation provide the opportunity for combined therapies. This review presents the current clinical data on antiplatelet, anticoagulant, and specific antithrombin therapies following myocardial infarction.
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Almony et al. (1996) studied this question.
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