Sleep Duration and Myocardial Infarction

Study Questions:

Is sleep duration associated with incident myocardial infarction (MI) after accounting for other sleep traits, and genetic risk of coronary artery disease (CAD)?

Methods:

Participants from the UK Biobank (UKB), who were free of relevant cardiovascular disease, were included in the present study. Multivariate adjusted hazard ratios (HRs) were estimated for MI (5,128 incident cases). Sleep duration was grouped into habitual self-reported short duration (<6 hours) or long duration (>9 hours) and compared with the reference group who reported 6-9 hours’ sleep duration. A two-sample Mendelian randomization was conducted for short (24 single nucleotide polymorphisms) and continuous (71 single nucleotide polymorphisms) sleep duration with MI (n = 43,676 cases/128,199 controls), and replicated results in UKB (n = 12,111/325,421).

Results:

A total of 461,347 participants were included in the present analysis, from which 5,218 incident MIs were reported over a median of 7.04 years of follow-up. Participants who reported regularly sleeping 7-8 hours were more likely to be employed and report excellent health and were less likely to report a history of smoking, depression, high cholesterol, or hypertension. Participants who reported a habitually short sleep duration had a 20% higher adjusted risk for incident MI (HR, 1.20; 95% confidence interval [CI], 1.07-1.33) compared with the reference group (6-9 hours’ sleep duration). Among participants who reported habitually longer sleep duration, a 34% higher risk for incident MI was observed (HR, 1.34; 95% CI, 1.13-1.58) compared to sleep durations of 6-9 hours. These associations were independent of other sleep traits. Healthy sleep duration mitigated MI risk even among individuals with high genetic liability (HR, 0.82; 95% CI, 0.68-0.998). Mendelian randomization was consistent with a causal effect of short sleep duration on MI in CARDIoGRAMplusC4D (Coronary ARtery DIsease Genome wide Replication and Meta-analysis plus Coronary Artery Disease Genetics Consortium) (HR, 1.19; 95% CI, 1.09-1.29) and UKB (HR, 1.21; 95% CI, 1.08-1.37).

Conclusions:

The investigators concluded that prospective observational and Mendelian randomization analyses support short sleep duration as a potentially causal risk factor for MI. Investigation of sleep extension to prevent MI may be warranted.

Perspective:

These data support the need for further research related to interventions to promote healthy sleep duration and to further understand the mechanisms between sleep duration and MI risk. The public health implications of these findings are broad given the number of adults who report short sleep duration due to work or other factors. Clinicians may wish to ask about sleep duration and to advise patients that healthy sleep duration may be cardioprotective even among patients at increased genetic predisposition for CAD.

Clinical Topics: Dyslipidemia, Heart Failure and Cardiomyopathies, Prevention, Atherosclerotic Disease (CAD/PAD), Lipid Metabolism, Nonstatins, Hypertension, Smoking, Sleep Apnea

Keywords: Cholesterol, Coronary Artery Disease, Depression, Genetic Predisposition to Disease, Hypertension, Myocardial Infarction, Polymorphism, Single Nucleotide, Primary Prevention, Risk Factors, Smoking, Sleep Apnea Syndromes, Sleep


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