Arora Nikhil, Brumpton Ben Michael, Åsvold Bjørn Olav, Loennechen Jan Pål, Malmo Vegard, Bhatta Laxmi, Skarpsno Eivind Schjelderup, Richmond Rebecca Claire, Strand Linn Beate
HUNT Center for Molecular and Clinical Epidemiology, Department of Public Health and Nursing, Norwegian University of Science and Technology, Trondheim, Norway.
Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom.
Eur J Prev Cardiol. 2025 Feb 6. doi: 10.1093/eurjpc/zwaf062.
Sleep disturbances can induce alterations in functional and electrical properties of the heart, thereby increasing susceptibility to atrial fibrillation (AF). We aimed to test the causal role of different sleep traits and their joint effects on the risk of AF.
We used an observational cohort study design along with one-sample and factorial Mendelian randomization (MR) approaches to test for individual and joint associations of sleep traits (i.e., insomnia symptoms, sleep duration and chronotype) on the risk of AF using UK Biobank and the second survey of the Trøndelag Health Study (HUNT2).
One-sample MR analysis showed that genetic predisposition to insomnia symptoms (hazard ratio (HR) 1.14; 95% confidence interval (CI) 1.07, 1.21) and short (≤6 h vs. 7-8 h) sleep duration (HR 1.14; 95% CI 1.04, 1.26) increased the risk of AF in UK Biobank. However these findings (HR 0.95; 95% CI 0.81, 1.11 for insomnia symptoms and HR 1.41; 95% CI 0.57, 3.46 for short sleep duration) were not consistent in HUNT2. Factorial MR analysis showed participants with genetic predisposition to both insomnia symptoms and short sleep duration (HR 1.08; 95% CI 1.03, 1.12) had the highest risk of AF, although there was no evidence of interaction (relative excess risk due to interaction (RERI 0.03; 95% CI -0.03, 0.09). However, this finding (HR 0.96; 95% CI 0.89, 1.04) was not consistent in HUNT2. Participants with genetic predisposition to both a morning chronotype and insomnia symptoms (HR 1.08; 95% CI 1.04, 1.13) and a morning chronotype and short sleep (HR 1.06; 95% CI 1.02, 1.10) had the highest risk of AF in UK Biobank, although there was no evidence of interaction (RERI -0.01; 95% CI -0.07, 0.04 and RERI 0.06; 95% CI -0.01, 0.12, respectively).
Our study indicates that insomnia symptoms and short sleep duration are causal risk factors for AF. However, having two sleep traits in combination does not increase risk beyond the additive risk of each individual trait. This reinforces clinical and public health efforts to effectively manage insomnia symptoms and short sleep, in order to mitigate the risk of AF and improve overall cardiovascular health.
睡眠障碍可导致心脏功能和电生理特性改变，从而增加心房颤动（AF）易感性。我们旨在检验不同睡眠特征及其联合作用对AF风险的因果关系。
我们采用观察性队列研究设计以及单样本和析因孟德尔随机化（MR）方法，利用英国生物银行和特隆赫姆健康研究（HUNT2）的第二次调查，检验睡眠特征（即失眠症状、睡眠时间和昼夜节律类型）与AF风险的个体关联和联合关联。
单样本MR分析显示，在英国生物银行中，失眠症状的遗传易感性（风险比（HR）1.14；95%置信区间（CI）1.07，1.21）和短睡眠时间（≤6小时与7 - 8小时相比）（HR 1.14；95% CI 1.04，1.26）会增加AF风险。然而，这些结果（失眠症状的HR为0.95；CI为95% 0.81，1.11；短睡眠时间的HR为1.41；CI为95% 0.57，3.46）在HUNT2中并不一致。析因MR分析显示，具有失眠症状和短睡眠时间遗传易感性的参与者（HR 1.08；95% CI 1.03，1.12）患AF风险最高，尽管没有交互作用的证据（交互作用导致的相对超额风险（RERI）0.03；95% CI -0.03，0.09）。然而，这一结果（HR 0.96；95% CI 0.89，1.04）在HUNT2中并不一致。在英国生物银行中，具有晨型昼夜节律和失眠症状遗传易感性的参与者（HR 1.08；95% CI 1.04，1.13）以及具有晨型昼夜节律和短睡眠时间遗传易感性的参与者（HR 1.06；95% CI 1.02，1.10）患AF风险最高，尽管没有交互作用的证据（分别为RERI -0.01；95% CI -0.07，0.04和RERI 0.06；95% CI -0.01，0.12）。
我们的研究表明，失眠症状和短睡眠时间是AF的因果风险因素。然而，同时具有两种睡眠特征并不会使风险增加超过每个个体特征的相加风险。这强化了临床和公共卫生方面为有效管理失眠症状和短睡眠时间所做的努力，以降低AF风险并改善整体心血管健康。
