Xiang Li1, Tao Zhou2, Hao Ma3, Tao Huang4, Xiang Gao5, JoAnn E Manson6, Lu Qi7. 1. Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, New Orleans, Louisiana, USA. Electronic address: https://twitter.com/XiangL9. 2. Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, New Orleans, Louisiana, USA; Department of Epidemiology and Biostatistics, School of Public Health (Shenzhen), Sun Yat-sen University, Guangdong, Guangzhou, China. 3. Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, New Orleans, Louisiana, USA. 4. Department of Epidemiology and Biostatistics, School of Public Health, Peking University, Beijing, China. 5. Department of Nutritional Sciences, The Pennsylvania State University, State College, Pennsylvania, USA. 6. Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA; Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA; Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts, USA. 7. Department of Epidemiology, School of Public Health and Tropical Medicine, Tulane University, New Orleans, Louisiana, USA; Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts, USA. Electronic address: lqi1@tulane.edu.
Abstract
BACKGROUND: Emerging evidence has linked sleep behaviors with the risk of cardiac arrhythmias. The various sleep behaviors are typically correlated; however, most of the previous studies only focused on the individual sleep behavior, without considering the overall sleep patterns. OBJECTIVES: The purpose of this study was to prospectively investigate the associations between a healthy sleep pattern with the risks of cardiac arrhythmias. METHODS: A total of 403,187 participants from UK Biobank were included. A healthy sleep pattern was defined by chronotype, sleep duration, insomnia, snoring, and daytime sleepiness. Weighted genetic risk score for atrial fibrillation was calculated. RESULTS: The healthy sleep pattern was significantly associated with lower risks of atrial fibrillation/flutter (AF) (HR comparing extreme categories: 0.71; 95% CI: 0.64-0.80) and bradyarrhythmia (HR: 0.65; 95% CI: 0.54-0.77), but not ventricular arrhythmias, after adjustment for demographic, lifestyle, and genetic risk factors. Compared with individuals with a healthy sleep score of 0-1 (poor sleep group), those with a healthy sleep score of 5 had a 29% and 35% lower risk of developing AF and bradyarrhythmia, respectively. Additionally, the genetic predisposition to AF significantly modified the association of the healthy sleep pattern with the risk of AF (P interaction = 0.017). The inverse association of the healthy sleep pattern with the risk of AF was stronger among those with a lower genetic risk of AF. CONCLUSIONS: Our results indicate that a healthy sleep pattern is associated with lower risks of AF and bradyarrhythmia, independent of traditional risk factors, and the association with AF is modified by genetic susceptibility.
BACKGROUND: Emerging evidence has linked sleep behaviors with the risk of cardiac arrhythmias. The various sleep behaviors are typically correlated; however, most of the previous studies only focused on the individual sleep behavior, without considering the overall sleep patterns. OBJECTIVES: The purpose of this study was to prospectively investigate the associations between a healthy sleep pattern with the risks of cardiac arrhythmias. METHODS: A total of 403,187 participants from UK Biobank were included. A healthy sleep pattern was defined by chronotype, sleep duration, insomnia, snoring, and daytime sleepiness. Weighted genetic risk score for atrial fibrillation was calculated. RESULTS: The healthy sleep pattern was significantly associated with lower risks of atrial fibrillation/flutter (AF) (HR comparing extreme categories: 0.71; 95% CI: 0.64-0.80) and bradyarrhythmia (HR: 0.65; 95% CI: 0.54-0.77), but not ventricular arrhythmias, after adjustment for demographic, lifestyle, and genetic risk factors. Compared with individuals with a healthy sleep score of 0-1 (poor sleep group), those with a healthy sleep score of 5 had a 29% and 35% lower risk of developing AF and bradyarrhythmia, respectively. Additionally, the genetic predisposition to AF significantly modified the association of the healthy sleep pattern with the risk of AF (P interaction = 0.017). The inverse association of the healthy sleep pattern with the risk of AF was stronger among those with a lower genetic risk of AF. CONCLUSIONS: Our results indicate that a healthy sleep pattern is associated with lower risks of AF and bradyarrhythmia, independent of traditional risk factors, and the association with AF is modified by genetic susceptibility.
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