Analysis of the circadian distributions of silent ischemic episodes and myocardial infarction has revealed a circadian variability with peak event incidences in the morning hours after awakening. This morning peak of ischemic events is paralleled by circadian variations of blood pressure and heart rate that reflect an increase of sympathetic activity. The increase in blood pressure and heart rate is accompanied by a morning increase of platelet aggregability and a decrease in endogenous fibrinolytic activity. The increase in sympathetic activity may lead to inadequate vasoconstriction in atherosclerotic coronary arteries, which, in combination with mechanical factors such as elevated blood pressure, may lead to plaque rupture. The enhanced thrombogenicity of the blood might facilitate or accelerate thrombus formation and can help to explain the circadian variability of myocardial infarctions caused by occlusive coronary thrombi. Further characterization of the underlying mechanisms of the circadian variability might ultimately lead to more effective prevention, especially during the vulnerable morning hours.