Heart rhythm · 2025
Secondhand tobacco smoke and risk of atrial fibrillation: An observational epidemiologic and gene-environment interaction analysis.
СтатьяНаблюдательное исследованиеПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Rhee Tae-Min, Lee Kyung-Yeon, Choi JungMin, Ahn Hyo-Jeong, Lee So-Ryoung, Choi Eue-Keun, Oh Seil, Lip Gregory Y H
Аннотация
BACKGROUND: The relationship between secondhand tobacco smoke (SHS) and the risk of incident atrial fibrillation (AF) remains controversial.
OBJECTIVE: This study aimed to evaluate the long-term risk of AF associated with SHS exposure and assess potential gene-environment interactions using extensive population-based data.
METHODS: We performed a nationwide population-based cohort study using the UK Biobank database. Participants were categorized into SHS-exposure and nonexposure groups. The primary outcome was the risk of incident AF. We also evaluated the synergistic effect of SHS exposure and the polygenic risk score of AF.
RESULTS: During a median follow-up of 12.5 years, AF occurred in 23,471 (5.9%). The SHS-exposure group (median exposure 0.5 [0.5-1.5] h/wk) was younger and predominantly male. The risk of AF was significantly higher in the SHS-exposure group (multivariable-adjusted hazard ratio 1.06; 95% confidence interval 1.02-1.09; P = .002) than the nonexposure group, suggesting a dose-dependent manner (adjusted hazard ratio of the severe SHS-exposure group 1.11; 1.04-1.18; P = .001). The risk of AF was higher in the SHS-exposure group regardless of the exposure location (home, outside, or workplace). When SHS exposure was combined with the high genetic risk of AF, a significant additive interaction was observed on the risk of AF (synergy index of SHS exposure with the third tertile of AF polygenic risk score 1.13; 1.05-1.21; P = .024).
CONCLUSION: Exposure to SHS is a significant predictor of an increased risk of AF, with a synergistic effect when combined with genetic predisposition. Minimizing SHS exposure, especially in individuals with a heightened genetic susceptibility to AF, may potentially reduce the future risk of AF.
OBJECTIVE: This study aimed to evaluate the long-term risk of AF associated with SHS exposure and assess potential gene-environment interactions using extensive population-based data.
METHODS: We performed a nationwide population-based cohort study using the UK Biobank database. Participants were categorized into SHS-exposure and nonexposure groups. The primary outcome was the risk of incident AF. We also evaluated the synergistic effect of SHS exposure and the polygenic risk score of AF.
RESULTS: During a median follow-up of 12.5 years, AF occurred in 23,471 (5.9%). The SHS-exposure group (median exposure 0.5 [0.5-1.5] h/wk) was younger and predominantly male. The risk of AF was significantly higher in the SHS-exposure group (multivariable-adjusted hazard ratio 1.06; 95% confidence interval 1.02-1.09; P = .002) than the nonexposure group, suggesting a dose-dependent manner (adjusted hazard ratio of the severe SHS-exposure group 1.11; 1.04-1.18; P = .001). The risk of AF was higher in the SHS-exposure group regardless of the exposure location (home, outside, or workplace). When SHS exposure was combined with the high genetic risk of AF, a significant additive interaction was observed on the risk of AF (synergy index of SHS exposure with the third tertile of AF polygenic risk score 1.13; 1.05-1.21; P = .024).
CONCLUSION: Exposure to SHS is a significant predictor of an increased risk of AF, with a synergistic effect when combined with genetic predisposition. Minimizing SHS exposure, especially in individuals with a heightened genetic susceptibility to AF, may potentially reduce the future risk of AF.