Circadian Variation in the Frequency of Onset of Acute Myocardial Infarction

TLDR

Circadian timing of myocardial infarction may arise from variations in thrombosis tendency when plaque disruption occurs. The study aims to identify rhythmic processes driving myocardial‑infarction onset to enable interventions that delay or prevent events. The authors analyzed pain onset times in 2,999 myocardial‑infarction patients and used CK‑MB elevation in 703 patients to objectively time infarction onset. A marked circadian rhythm was observed, with a threefold higher frequency of onset between 6 a.m. and noon—peaking at 9 a.m.—and no rhythm in patients receiving beta‑adrenergic blockers.

Abstract

To determine whether the onset of myocardial infarction occurs randomly throughout the day, we analyzed the time of onset of pain in 2999 patients admitted with myocardial infarction. A marked circadian rhythm in the frequency of onset was detected, with a peak from 6 a.m. to noon (P<0.01). In 703 of the patients, the time of the first elevation in the plasma creatine kinase MB (CK-MB) level could be used to time the onset of myocardial infarction objectively. CK-MB—estimated timing confirmed the existence of a circadian rhythm, with a threefold increase in the frequency of onset of myocardial infarction at peak (9 a.m.) as compared with trough (11 p.m.) periods. The circadian rhythm was not detected in patients receiving beta-adrenergic blocking agents before myocardial infarction but was present in those not receiving such therapy. If coronary arteries become vulnerable to occlusion when the intima covering an atherosclerotic plaque is disrupted, the circadian timing of myocardial infarction may result from a variation in the tendency to thrombosis. If the rhythmic processes that drive the circadian rhythm of myocardial-infarction onset can be identified, their modification may delay or prevent the occurrence of infarction. (N Engl J Med 1985; 313:1315–22.)