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From bench to bedside

GP IIb–IIIa inhibitors

From the Coronary Care Unit, Northwestern University School of Medicine, Chicago, Illinois.

Address correspondence and reprint requests to Dr. Dan J. Fintel, Coronary Care Unit, Northwestern University School of Medicine, Wesley Suite 726, 250 E. Superior St., Chicago, IL 60611.

Our understanding of the pathophysiology of acute coronary syndromes (ACS) has now been substantiated by many studies showing that atherothrombosis plays a predominant role. This article reviews the molecular interactions in thrombosis that may serve as therapeutic targets for more effective management of these syndromes. In particular, the discovery of the fact that the glycoprotein (GP) IIb–IIIa receptor plays a central and common role in platelet-mediated thrombosis has focused the therapeutic efforts. Blockade of this receptor has emerged as a new and potent strategy for inhibition of platelet aggregation and thus of clot formation. A number of trials have now corroborated the need for such antithrombotic drugs in the management of patients with non-ST-segment elevation ACS.

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