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Platelet aggregation, at the site of an atherosclerotic plaque in the coronary arteries has been recognized as a crucial step in the pathogenesis of unstable angina and myocardial infarction. As part of current medical therapy in patients with unstable angina, evolving myocardial infarction and in patients undergoing coronary intervention, platelet aggregation is inhibited partly by administration of aspirin or ticlopidin. In addition, heparin is administered in order to reduce thrombin activity. In spite of such combined antiplatelet and anticoagulant therapy, between 6% and 15% of patients with unstable angina progress to myocardial infarction or death within the first month. Similarly, myocardial damage as assessed by periprocedural enzyme elevation has been reported in 4%– 14% of patients undergoing PTCA. Follow-up studies indicate that larger, but also smaller periprocedural enzyme elevations are associated with impaired long-term outcome. Major progress has been made by development of platelet glycoprotein IIb/IIIa receptor blockers, which block the final common pathway of platelet aggregation, the fibrinogen receptor on the thrombocytes. In this review, the clinical value of treatment with platelet glycoprotein IIb/IIIa receptor blockers is assessed, based on data from medium size and large clinical trials in different groups of patients with unstable angina, evolving myocardial infarction and patients undergoing coronary intervention (Table 1).

Platelet glycoprotein IIB/IIA receptor antagonists An asset for treatment of unstable coronary syndromes and coronary intervention