Mortality rates in patients after myocardial infarction (MI) have decreased from a high of >50% in the 1930s to 10-15% currently, and even lower in some clinical trials. At present, much of the research is focused on (1) identifying patients at high risk despite the lack of typical prognosticators of a severe event; and (2) delineating the optimal therapy for patients with unstable angina or non-Q-wave MI. Clinicians are now focusing on acute coronary syndrome. Patients present with (1) minor electrocardiographic abnormalities; (2) chest pain; and (3) possible abnormalities in creatine kinase, creatine kinase-myocardial band, and troponin. The primary goal for these patients is to prevent plaque rupture and its associated morbidity and mortality. Aspirin and heparin are clearly indicated. The glycoprotein (GP) IIb/IIIa receptor inhibitors are even more effective in inhibiting platelet activation. Under what circumstances should these agents be used, and which of the 3 currently available agents is superior? Analysis of the trials addressing these questions clearly demonstrates the importance of these agents in this setting. The choice of agent is still unclear, pending a randomized, interdrug comparison. It also remains to be demonstrated whether low-molecular-weight heparin is superior to standard heparin in this setting and which patients should undergo angiography.