Using glycoprotein IIb/IIIa antagonists as adjuncts to fibrinolytic therapy holds promise

After fibrinolytic therapy for acute myocardial infarction full antegrade perfusion (TIMI 3 flow) at 90 minutes occurs in only 29-54% of patients,1 while reocclusion occurs in at least 12%, with increased morbidity and mortality.2 Fibrinolytic therapy may itself be prothrombotic through releasing clot bound thrombin, which in turn stimulates platelet activation Preclinical and early clinical trials have suggested that glycoprotein IIb/IIIa receptor antagonists (which prevent fibrinogen binding to platelets) used as adjuncts to fibrinolytic therapy may improve early patency and reduce the incidence of reocclusion. Though there are as yet no data showing a reduction in mortality from such use of these antagonists, a large randomised trial has recently confirmed the early findings on patency and suggests that adjunct treatment with glycoprotein IIb/IIIa receptor antagonists may hold promise for the better management of myocardial infarction.

Over 100 agonists, including adenosine diphosphate, thrombin, and adrenaline, may activate platelets. All act via a final common pathway of activating the glycoprotein IIb/IIIa receptors on the platelet surface; binding of fibrinogen to these receptors then leads to platelet aggregation. Aspirin acts synergistically with fibrinolytic therapy to reduce mortality3 and may reduce reocclusion.4 But aspirin is a relatively weak antiplatelet agent, and platelet activation may still continue via pathways independent of thromboxane A2. However, studies have shown that …