Arterial thrombosis in the acute coronary syndromes is precipitated by plaque disruption. This occurs in lesions with a large lipid core, a thin fibrous cap, macrophages infiltrating the fibrous cap, and a lipid core with a high tissue-factor content. This results in acute platelet deposition and rapid growth of mural thrombus which unfavorably influences the rheology of blood flow to produce more thrombus, and propagates additional thrombosis by the high thrombogenicity of the mural thrombus overlying the disrupted culprit arterial lesion. Acute therapy in the hospital and subacute therapy beyond the hospital phase for as long as 1.5-3 months with aspirin plus anti-coagulation, such as low-molecular-weight heparin, or oral anticoagulation, reduces thrombotic occlusion, myocardial infarction, death, and need for coronary revascularization.