Acute Myocardial Infarction and Daylight Saving Time Transitions: Is There a Risk?

Abstract

Available evidence on the risk of acute myocardial infarction (AMI) in the days after the spring daylight saving time (DST) transition suggests either a modest increase or no risk increase. Partial sleep deprivation and enhanced circadian clock misalignment have been implicated as the underlying mechanisms for increased AMI risk, probably via enhanced thrombo-inflammatory processes and activation of the sympathetic nervous system. Most of the studies, as we suggest as a perspective here, have used potentially inappropriate control periods, including the two post-transitional weeks, because adjustment after the spring DST transition lasts at least four weeks for all chronotypes and probably even beyond this period for late chronotypes. The most plausible conclusions, at the moment, for the risk of AMI after the spring DST transition are: (1) the risk is increased, (2) a relatively modest risk increase could be currently underestimated or in some studies undetected, (3) late chronotypes and/or individuals with high levels of social jetlag (a proxy for circadian clock misalignment) could be more affected by the phenomenon, and (4) underlying pathophysiological mechanisms should be further explored. As a significant part of world's population continues to be affected by the biannual clock change, the question of increased AMI risk in the post-transitional period remains an intriguing public health issue.

Keywords: acute myocardial infarction; chronotypes; circadian misalignment; daylight saving time; sex; sleep deprivation.

Figure 1

Circadian misalignment in relation to the spring daylight saving time (DST) transition in early and late chronotypes. Late chronotypes at baseline have relatively greater levels of circadian misalignment. Control periods (CPs) are shown as applied in the majority of studies on the post-DST incidence of acute myocardial infarction. Physiological adaptation is expected to be longer, in late chronotypes more than four weeks, and the two post-transitional CP weeks fall within this period. Instead of being used as CP, those weeks could represent the hazard period of an increased cardiovascular risk.

Figure 2

Mechanisms of increased risk of acute myocardial infarction in the period after the spring daylight saving time (DST) transition. Increased inflammation coupled with enhanced hemodynamic and biomechanical forces induced by sympathetic nervous system arousal can cause destabilization of vulnerable coronary atherosclerotic plaque. As those processes accompany the circadian clock misalignment and partial lack of sleep and last over a several week period, they could initiate a superficial erosion of the intimal surface or rupture of a vulnerable plaque. Increased inflammation and sympathetic nervous system activity can also initiate formation of an overlaying thrombus and/or facilitate enhanced thrombus growth, to produce a more significant coronary occlusion during the infarction onset.