Antiplatelet therapy is the cornerstone of pharmacotherapeutic management of acute coronary syndrome (ACS), a general term for the cardiac events that can result from atherosclerotic plaque-related vascular occlusion. Aspirin has long been recommended as initial therapy for ACS and is known to reduce morbidity and mortality. The benefit of aspirin in secondary prevention of cardiovascular disease (CVD) is undisputed. Despite this fact, fatal and non-fatal cardiovascular (CV) events occur while patients are receiving aspirin. Recent literature indicates that some patients may be "resistant" to the effects of aspirin and that this pattern of resistance varies over time. Current guidelines for treatment of patients with ACS recommend the use of dual antiplatelet therapy (aspirin and the thienopyridine, clopidogrel). This study will characterize the effects of aspirin on platelet aggregation and thromboxane formation in outpatients on dual antiplatelet therapy after an ACS admission. The effect of aspirin on platelets will be ascertained after 30 days of aspirin 81 mg and clopidogrel 75 mg with the PFA-100® system and thromboxane B2 levels. Decreased aspirin responsiveness will be confirmed with light transmission aggregometry (LTA). In order to assess compliance with the aspirin regimen, structured interviews will be conducted and salicylate levels drawn at each follow-up visit. When decreased aspirin responsiveness is confirmed with LTA, patients will be instructed to increase their aspirin dose to 325 mg daily. PFA-100® will be repeated after 30 days on the new regimen. The results should lead to better understanding of aspirin response in typical ACS patients being treated according to current guidelines. In addition, data on the ability to overcome aspirin nonresponsiveness by increasing aspirin dose could greatly impact patient management.