PubMed · 5205852
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R A Luttring. 1971. Circadian rhythms.. https://pubmed.ncbi.nlm.nih.gov/5205852/
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We analyzed spontaneous ventricular tachycardias treated by antitachycardia pacing during long-term follow-up in 138 recipients of an implantable cardioverter-defibrillator. An inverse circadian variation of the antitachycardia pacing termination and acceleration rates with the worst antitachycardia pacing success during the time period with the highest episode frequency (morning hours) was demonstrated.
BACKGROUND: Although 250,000 myocardial infarctions and 38,000 sudden cardiac deaths occur at night annually, this public health problem is underappreciated and poorly understood. We examined whether the incidence of myocardial infarction, sudden cardiac death, and automatic implantable cardioverter-defibrillator (AICD) discharge was nonuniform, a result that may implicate physiological triggers such as sleep-state dependent changes in autonomic nervous system activity. METHODS AND RESULTS: We conducted a review of the circadian pattern of the onset of myocardial infarction (n=19), sudden cardiac death (n=12), and AICD discharge (n=7). The nighttime period was chosen a priori as midnight to 5:59 AM. These reports documented 11,633 nocturnal myocardial infarctions (20% of the total myocardial infarctions), 1981 nocturnal sudden cardiac deaths (14.6% of the total sudden cardiac deaths), and 1200 nocturnal AICD discharges (15.0% of the total discharges). The distributions of myocardial infarction, sudden cardiac death, and AICD discharge were each significantly nonuniform (P<.001). The peak incidence of myocardial infarction and AICD discharge occurred between midnight and 0:59 AM, whereas the peak incidence of sudden cardiac death was between 1:00 and 1:59 AM. The trough in incidence occurred between 4:00 and 4:59 AM for sudden cardiac death and between 3:00 and 3:59 AM for myocardial infarction and AICD discharge. CONCLUSIONS: Nocturnal myocardial infarction, sudden cardiac death, and AICD discharge exhibit nonuniform distributions. This finding is consistent with the hypothesis that sleep-state dependent fluctuations in autonomic nervous system activity may trigger the onset of major cardiovascular events and provides further impetus for more directly testing this hypothesis at population, individual, and mechanistic levels. A better understanding of nocturnal triggers may make it possible to reduce the incidence of myocardial infarction, ventricular tachyarrhythmias, and sudden cardiac death during the nocturnal period.