Oral platelet glycoprotein IIb/IIIa receptor antagonists: the present challenge is safety.

An indisputable body of angiographic, angioscopic, pathological, and biochemical evidence supports the role of thrombus in the pathogenesis of acute myocardial infarction, unstable angina, and percutaneous coronary intervention. Compelling data from large-scale trials and analyses have established the role of platelet inhibitors in reducing coronary events in patients with the acute coronary syndromes and in maintaining patency of vascular grafts in the long term. Persistent reports of high clinical event rates in the modern era of acute coronary syndromes despite aggressive medical therapy have spurred the development of more effective antiplatelet agents. Despite its efficacy, aspirin is a relatively weak antiplatelet agent, inhibiting only thromboxane A2–mediated platelet aggregation. The final common pathway of platelet aggregation involves activation of the platelet glycoprotein IIb/IIIa (GP IIb/IIIa) receptor to allow fibrinogen binding. Studies involving a number of intravenous inhibitors of GP IIb/IIIa receptors have demonstrated efficacy in reducing ischemic complications after percutaneous angioplasty and in the acute coronary syndromes.