%0 Journal Article
%T Causal influence of sleeping phenotypes on the risk of coronary artery disease and sudden cardiac arrest: A Mendelian randomization analysis.
%A Chiu YW
%A Su MH
%A Lin YF
%A Chen CY
%A Chen TT
%A Wang SH
%J Sleep Health
%V 9
%N 5
%D 2023 Oct
%M 37429813
%F 4.207
%R 10.1016/j.sleh.2023.05.009
%X <B>OBJECTIVE: </B>To assess the causal influence of sleep and circadian traits on coronary artery disease and sudden cardiac arrest with adjustment for obesity through a two-sample Mendelian randomization study.<BR><B>METHODS: </B>We used summary statistics of 5 sleep and circadian traits for genome-wide association studies, including chronotype, sleep duration, long sleep (≥9 h a day), short sleep (<7 h a day), and insomnia (sample size range: 237,622-651,295). Coronary artery disease genome-wide association studies with 60,801 cases and 123,504 controls, sudden cardiac arrest genome-wide association studies with 3939 cases and 25,989 controls, and obesity genome-wide association studies with 806,834 individuals were also used. Multivariable Mendelian randomization was performed to estimate the causality.<BR><B>RESULTS: </B>After adjusting for obesity, genetically predicted short sleep (odds ratio = 1.87 and p = .02), and genetically predicted insomnia (odds ratio = 1.17 and p = .001) were causally associated with increased odds of coronary artery disease. Genetically predicted long sleep (odds ratio = 0.06 and p = .02) and genetically predicted longer sleep duration (odds ratio = 0.36 for per-hour increase in sleep duration and p = .0006) were causally associated with decreased odds of sudden cardiac arrest.<BR><B>CONCLUSIONS: </B>The findings of this Mendelian randomization study indicate that insomnia and short sleep contribute to the development of coronary artery disease, whereas a longer sleep duration protects from sudden cardiac arrest, independent of the influence of obesity. The mechanisms underlying these associations warrant further investigation.