The pathophysiology of the onset of morning cardiovascular events

Several studies have demonstrated that myocardial infarctions (MI) are at least 3 times more likely to occur in the morning than in the late evening. Similar circadian patterns have been found for transient myocardial ischemia, sudden cardiac death, and stroke. The circadian variation of these events suggests that the onset of MI is often triggered by patient activities. In the MILIS study, 49% of patients with MI reported a possible trigger, including physical exertion and emotional upset. The physiological processes that might result in the morning peak of MI remain unknown. Possible mechanisms include an arterial blood pressure surge and an increase in coronary arterial tone which increase shear stress at the endothelial surface and predispose to plaque rupture. An increase in platelet aggregability (resulting from the assumption of an upright posture) or an increase in blood viscosity with an insufficient countervailing circadian rise in circulating t-PA could produce a state of relative hypercoagulability which would promote coronary thrombus formation. The immediate value of recognizing the circadian variation of MI onset is the emphasis that can be placed on pharmacologic protection during the morning hours for patients already receiving anti-ischemic therapy. Both aspirin and beta-blockers have been shown to significantly reduce the morning peak of MI perhaps by attenuating morning platelet hyperactivity and blood pressure surges respectively. Calcium channel blockers have not been well studied but may modify the morning increase in coronary vascular tone. While as yet unproven, it seems reasonable that longer-acting anti-ischemic agents have an advantage over short-acting agents in providing protection agaistt MI in the morning when the effects of short-acting agent taken the night before may begin to wear off. Further research is required in understanding the mechanisms of triggering.