The observation that acute myocardial infarction and sudden cardiac death are more frequent in the morning indicates that the onset of these cardiovascular events is not random, and provides a clue to mechanism. An atherosclerotic plaque is exposed to systemic physiologic processes that could increase the likelihood of plaque rupture and thrombosis in the presence of a vulnerable plaque. Many of these processes increase in intensity in the morning, including plasma catecholamine levels, sympathetic activity, heart rate, blood pressure, vascular tone, platelet aggregability and blood viscosity increase, whereas some protective factors such as vagal activity and fibrinolytic activity are decreased. Similar changes may also occur after stressful activities. The ability of beta-adrenergic blocking agents and aspirin preferentially to reduce the incidence of myocardial infarction in the morning supports the hypothesis that sympathetic activation and increased platelet aggregability contribute to the circadian pattern of acute cardiovascular disease. Although the extent of atherosclerosis changes slowly with time under the influence of chronic risk factors, it is proposed that stress, particularly in the morning, may produce a combination of transient hemodynamic, vasoconstrictive and prothrombotic forces that can be considered acute risk factors for plaque disruption and thrombosis, the final pathway of most myocardial infarctions.