Abstract
BACKGROUND: Currently, the association between sleep pattern and cardiac conduction disease (CCD) remain largely unexplored. In our study, we aimed to investigate the association between sleep patterns and CCD, the mediating role of inflammation, and the modifying effect of genetic susceptibility.</p>
METHOD: Our study included 316,667 participants from UK Biobank. The healthy sleep score (0-5) was calculated through chronotype, sleep duration, insomnia, snoring, and daytime sleepiness. Subsequently, participants were categorized into healthy (≥4), intermediate (2-3), or poor (≤1) sleep patterns. Cox proportional hazards models were performed to evaluate the association between healthy sleep patterns and CCD, atrioventricular block (AVB), left bundle branch block (LBBB) and right bundle branch block (RBBB). For observed associations, we further explore the mediating role of inflammation and calculated polygenic risk score to assess the sleep-gene interaction.</p>
RESULTS: Compared with poor sleep patterns, healthy sleep patterns were associated with a lower risk of CCD (HR = 0.73, 95% CI: 0.65-0.81), AVB (HR = 0.73, 95% CI: 0.61-0.86), LBBB (HR = 0.67, 95% CI: 0.56-0.81), and RBBB (HR = 0.78, 95% CI: 0.64-0.95), with each 1-point sleep score increase linked to a 4-6% reduced risk. Inflammatory biomarkers partially mediated these associations, with the proportion mediated ranging from 1.71% to 7.45%. Sleep-gene interaction analysis showed the protective effect of healthy sleep pattern on LBBB attenuated in participants with high genetic risk compared with those with low genetic risk (Pinteraction = 0.03).</p>
CONCLUSION: Healthy sleep patterns are associated with reduced risks of CCD and its subtypes, partly through inflammatory pathways, and the association with LBBB is modified by genetic susceptibility.</p>