The pathophysiology of acute coronary syndromes, ranging from unstable angina to non–Q-wave to Q-wave myocardial infarction (MI) has been elucidated over the past 2 to 3 decades. Treatments involving clot lysis and antiplatelet therapy have reduced the morbidity and mortality rates of these syndromes. In patients with persistently elevated ST segments, treatment with thrombolytic agents is well established. In patients with unstable angina and non–Q-wave MI, there is ongoing investigation of the use of antithrombins and antiplatelet agents. Unfortunately, these treatments do not come without risk. The use of cardiac troponins is currently under intensive investigation because of their specificity to cardiac muscle and sensitivity in the determination of minimal myocardial injury. Troponin T and troponin I are more sensitive than CK-MB and are likely able to detect microinfarctions in patients with unstable angina. Most important is the ability of troponin T and troponin I to identify patients with unstable angina without ST elevations who are at high risk for cardiac events, including MI and cardiac death. Early risk stratification in the emergency department with the cardiac troponins allows for more appropriate decisions for admission and therapeutic triage of admitted patients. One such use currently being studied is the ability of the troponins to identify patients who will benefit from glycoprotein IIb/IIIa receptor inhibitors. (Am Heart J 1999;138:S6-S11)