Morning sudden cardiac death.

A circadian variation of cardiac function with peak in the early morning was documented about twenty years ago. A circadian rhythm of platelet aggregability, in the same time of the day, was demonstrated in healthy young male subjects. The morning hours were also reported as crucial for sympathetic nervous system activity, for heart rate variability, and for the abrupt rise in blood pressure. Altogether, these trigger factors may explain the high incidence of sudden cardiac death during the morning. In the primary prevention of sudden death in patients with high cardiovascular risk, many strategies were proposed, such as implantable cardioverter-defibrillators, antiarrhythmic and antihypertensive therapies, particularly beta-blockers and more recently, aspirin. Also in subjects without cardiovascular risk factors, it is predictable that early and continuous administration of low-dose aspirin, by inhibiting platelet aggregation and thrombin formation, particularly in morning hours, may represent an effective therapy for the prevention of myocardial infarction and morning sudden cardiac death.