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. 2019 Sep 10;74(10):1304-1314.
doi: 10.1016/j.jacc.2019.07.022.

Sleep Duration and Myocardial Infarction

Iyas Daghlas  1 , Hassan S Dashti  1 , Jacqueline Lane  2 , Krishna G Aragam  3 , Martin K Rutter  4 , Richa Saxena  2 , Céline Vetter  5
Affiliations

Sleep Duration and Myocardial Infarction

Iyas Daghlas et al. J Am Coll Cardiol. .

Abstract

Background: Observational studies suggest associations between extremes of sleep duration and myocardial infarction (MI), but the causal contribution of sleep to MI and its potential to mitigate genetic predisposition to coronary disease is unclear.

Objectives: This study sought to investigate associations between sleep duration and incident MI, accounting for joint effects with other sleep traits and genetic risk of coronary artery disease, and to assess causality using Mendelian randomization (MR).

Methods: In 461,347 UK Biobank (UKB) participants free of relevant cardiovascular disease, the authors estimated multivariable adjusted hazard ratios (HR) for MI (5,128 incident cases) across habitual self-reported short (<6 h) and long (>9 h) sleep duration, and examined joint effects with sleep disturbance traits and a coronary artery disease genetic risk score. The authors conducted 2-sample MR 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: Compared with sleeping 6 to 9 h/night, short sleepers had a 20% higher multivariable-adjusted risk of incident MI (HR: 1.20; 95% confidence interval [CI]: 1.07 to 1.33), and long sleepers had a 34% higher risk (HR: 1.34; 95% CI: 1.13 to 1.58); 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 to 0.998). MR 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 to 1.29) and UKB (HR: 1.21; 95% CI: 1.08 to 1.37).

Conclusions: Prospective observational and MR analyses support short sleep duration as a potentially causal risk factor for MI. Investigation of sleep extension to prevent MI may be warranted.

Keywords: Mendelian randomization; UK Biobank; coronary artery disease; genetic risk score; myocardial infarction; sleep duration.

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Figures

Central illustration.
Central illustration.. Associations of sleep duration with coronary disease: Observational and 2-sample mendelian randomization.
Magnitude of effects observed for effects of phenotypic and genetically varying sleep duration. Note, that while the clocks show variable sleep timing for short and long sleep, the observed effects are independent of self-reported sleep timing preference.
Figure 1.
Figure 1.. Study sample flow diagram.
Exclusions undertaken for creation of an incident MI (for epidemiologic analyses) and a combined prevalent/incident CAD cohort (for MR analyses). CAD: coronary artery disease; MI: myocardial infarction; MR: mendelian randomization.
Figure 2.
Figure 2.. Concomitant associations of sleep duration and CAD GRS with risk of incident MI (n=310,917).
The comparator group is low genetic risk and favorable sleep duration. To maximize power, sleep durations of <6 or >9 hours per night were combined into ‘unfavorable sleep,’ and six to nine hours of habitual sleep duration was defined as ‘favorable sleep.’ Sleep and genetic liability additively increase risk, but do not have statistical interaction. Bars represent 95% CI. Low genetic risk: 1st quartile of CAD GRS; Medium genetic risk: 2nd and 3rd quartile of CAD GRS; High genetic risk: 4th quartile of CAD GRS; Favorable sleep duration: 6-9h; Unfavorable sleep duration: <6h or >9h. CAD: coronary artery disease; CI: confidence interval; GRS: genetic risk score; MI: myocardial infarction.
Figure 3.
Figure 3.. MR estimates of short and continuous sleep duration against MI in CARDIoGRAMPlusC4D (n=43,676 cases / 128,199 controls) and in UKB (n=12,111 cases / 325,421 controls).
Two-sample MR results reflect fixed-effects inverse variance weighted associations with MI risk. One-sample MR results reflect association of the weighted sleep genetic instrument with MI risk using individual-level data from UKB. Short sleep duration associations reflect the increase in MI risk concomitant with a doubling in the odds of short sleep duration. Continuous sleep duration associations reflect the effect of increasing sleep duration by 1 hour. CI: confidence interval; MI: myocardial infarction; OR: odds ratio; SNP: single nucleotide polymorphism.
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