Atheromatous plaque rupture, platelet activation with consequent thrombus formation and impairment of coronary arterial blood flow is a common theme in acute coronary syndromes (ACS) (1–4). The importance of antiplatelet therapy in the treatment of acute myocardial infarction (MI) was amply demonstrated in the second International Study of Infarct Survival (ISIS-2). At present, aspirin and to a lesser extent heparin, are used in nearly all patients with ACS. In spite of the improvements in prognosis that these treatments have brought, the incidence of adverse events in patients with ACS is still significant (5–8) and demonstrates the need for further improvement. There has been a rapid expansion of data from large multicenter trials on the use of IIb/IIIa receptor antagonists in the full spectrum of ACS. This is in part related to a recognition of the limitations of other antiplatelet agents, a better understanding of the mechanisms of platelet activation and aggregation. The realization that the GPIIb/IIIa platelet receptor is the final common pathway through which all the platelet agonists exhibit their effects on platelet aggregation make this receptor a promising target for antiplatelet therapy (9).