Why the study?
Does the adjunct use of glycoprotein IIb/IIIa antagonists with fibrinolytic therapy improve outcomes in patients with acute myocardial infarction?
Does the adjunct use of glycoprotein IIb/IIIa antagonists with fibrinolytic therapy improve outcomes in patients with acute myocardial infarction?
This review discusses the rationale and recent findings regarding the use of glycoprotein IIb/IIIa antagonists as adjuncts to fibrinolytic therapy in acute myocardial infarction.
Does not support routine adjunctive glycoprotein IIb/IIIa use with fibrinolysis in AMI; leaves open need for definitive trials.
The efficacy of fibrinolytic therapy in acute myocardial infarction may be limited by three factors: failure to achieve reperfusion of the epicardial culprit artery, failure to achieve myocardial reperfusion, or reocclusion of the culprit artery following initial reperfusion. Platelet activation plays a central role in the acute thrombotic process, and the adjunct use of aspirin (a relatively weak antiplatelet agent) with fibrinolytic therapy has been shown to reduce mortality and probably reocclusion. In this review, we discuss the rationale for antiplatelet therapy, the importance of the glycoprotein IIb/IIIa receptor on the platelet surface (the final common pathway in platelet activation) and the findings from recent studies using specific glycoprotein IIb/IIIa antagonists as adjuncts to fibrinolytic therapy in acute myocardial infarction.
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Menown et al. (2001) studied this question.
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