Aspirin is effective in, treating patients with unstable angina or myocardial infarction. However, questions remain about the optimal dose of aspirin and aspirin-resistance in subgroups of patients. Heparin also has beneficial effects mostly during the acute phase of unstable angina, but thrombolytics are effective only in acute myocardial infarction and not in unstable angina. Recently, low molecular weight heparins have proved to be as effective (FRIC trial) or more effective (ESSENCE trial) than unfractionated heparin in unstable angina. Ongoing studies (TIMI 11B) are evaluating the efficacy of a prolonged administration of low molecular weight heparin to alter the chronic process of unstable angina. The new antiplatelet drugs directed against GP IIb/IIIa receptors are now available to improve the acute results of high risk percutaneous transluminal angioplasty (PTCA). This new drug (c7E3) binds rapidly to GP IIb/IIIa and prevents fibrinogen binding to the receptor. This very potent and irreversible effect prevents platelet aggregation and decreases the incidence of acute occlusions following PTCA. especially in patients with unstable angina. The counterpart is an increased risk of hemorrhage, knowing that patients receive simultaneously aspirin and heparin. The first results of the EPILOG study also demonstrate a better outcome in elective angioplasty without significant increase of serious bleeding, thanks to a low dose heparin regimen. In contrast to thrombolytics, the GP IIb/IIIa antagonist does not increase the risk of intracranial bleeding. The results of the CAPTURE trial also confirm the clinical benefit obtained with this drug in refractory unstable angina. The reduction of death and myocardial infarction is very consistent throughout the studies performed with c7E3. The Kaplan-Meier curves of freedom of death and myocardial infarction diverge immediately after start of study medication. The acute benefits are preserved at 3 years in the EPIC trial. Similar trends were present during the acute phase with other compounds (tirofiban, integrelin), meaning that a class effect may exist but the long term results are disappointing. The results with new direct antithrombins such as hirudin, or hirulog in acute myocardial infarction or in PTCA for unstable angina are negative. The development of new potent oral antiplatelet drugs might change the treatment of acute coronary syndromes in the future. The current progress made with antithrombotic drugs should improve the prognosis of acute coronary syndromes.