Unstable angina and non-Q-wave myocardial infarction, part of the acute coronary syndromes, are characterized by coronary arterial plaque rupture and endovascular thrombus formation. Plaque rupture leads to exposure of subendothelial components such as collagen and fibronectin, and these substances are known to cause platelet activation, aggregation, and initiation of the coagulation cascade. Aspirin and heparin have been used as therapeutic mainstays for acute coronary syndromes, acting as antiplatelet and antithrombin agents, respectively. Despite treatment with this conventional anticoagulant strategy and antianginal drugs, substantial morbidity and mortality continue to be associated with unstable angina and non-Q-wave myocardial infarction. Specific antagonists of the platelet glycoprotein IIb/IIIa inhibitor have proved effective in substantially reducing ischemic events following percutaneous coronary revascularization, and several trials using these agents in acute coronary syndromes are now completed. Compared to patients receiving standard therapy (aspirin and heparin), platelet IIb/IIIa antagonists have further reduced the incidence of major ischemic events. Ongoing studies are addressing the optimal extent and duration of platelet inhibition in patients with acute coronary syndromes.