Antiplatelet therapy for treatment of acute coronary syndromes

Acute coronary syndromes and the postpercutaneous coronary intervention state share the common feature of atherosclerotic plaque disruption and subsequent intraluminal thrombus formation. In most cases, vascular patency is maintained but partial occlusion causes myocardial ischemia and can either progress to complete occlusion or result in distal embolization with subsequent small vessel obstruction, the core section of an intraarterial thrombus is platelet-rich and can serve as a nidus for further thrombosis. Aspirin, by virtue of its anticycloxygenase activity inhibits platelet activation and aggregation to a mild degree. Clinically, aspirin has been shown to reduce the rates of myocardial infarction in patients with acute coronary syndromes and to reduce the number of ischemic complications which follow coronary angioplasty. More potent inhibitors of platelet aggregation antagonize the interaction between the platelet surface protein GP IIb-IIIa and fibrinogen. The result is profound inhibition of platelet aggregation. Three intravenous antagonists of platelet GP IIb-IIIa are clinically available and a fourth is under phase III study. When used in addition to aspirin therapy, these agents have been shown to produce further reductions in either peri-interventional infarctions or in recurrent myocardial infarctions in patients with acute coronary syndromes.