Alcohol is neither a risk factor nor a protective factor for sudden cardiac death and/or fatal ventricular arrhythmia: A population-based study with genetic traits and alcohol consumption in the UK Biobank

被引:0
作者
Park, Chan Soon [1 ]
Choi, Jaewon [2 ]
Choi, JungMin [1 ]
Lee, Kyung-Yeon [1 ]
Ahn, Hyo-Jeong [1 ]
Kwon, Soonil [1 ]
Lee, So-Ryoung [1 ]
Choi, Eue-Keun [1 ,3 ]
Kwak, Soo Heon [1 ,3 ]
Oh, Seil [1 ,3 ]
机构
[1] Seoul Natl Univ Hosp, Dept Internal Med, Seoul, South Korea
[2] Seoul Natl Univ Hosp, Innovat Biomed Technol Res Inst, Div Data Sci Res, Seoul, South Korea
[3] Seoul Natl Univ, Coll Med, Dept Internal Med, 101 Daehak Ro, Seoul 03080, South Korea
关键词
Alcohol consumption; Genetic predisposition to alcohol metabolism; Death; Sudden; Cardiac; Fatal ventricular arrhythmia; ATRIAL-FIBRILLATION; HEART-FAILURE; EPIDEMIOLOGY; DISEASE;
D O I
10.1016/j.hrthm.2024.04.097
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
BACKGROUND The association between alcohol consumption and the risk of sudden cardiac death and/or fatal ventricular arrhythmia remains controversial. OBJECTIVE We analyzed the association between alcohol consumption, genetic traits for alcohol metabolism, and the risk of sudden cardiac death and/or fatal ventricular arrhythmia. METHODS We identified 397,164 individuals enrolled between 2006 and 2010 from the UK Biobank database and followed them until 2021. Alcohol consumption was categorized as current nondrinkers (nondrinkers and ex-drinkers), mild drinkers, moderate drinkers, or heavy drinkers. Genetic traits of alcohol metabolism were stratified according to the polygenic risk score ter- tiles. The primary and secondary outcomes were a composite of sudden cardiac death and fatal ventricular arrhythmia as well as their individual components. RESULTS During follow-up (median 12.5 years), 3543 cases (0.89%) of clinical outcomes occurred. Although mild, moderate, and heavy drinkers showed deceased risks of outcomes compared with current nondrinkers, there was no prognostic difference among nondrinkers, mild drinkers, moderate drinkers, and heavy drinkers. Ex-drinkers showed an increased risk in univariate analysis, but the significance was attenuated after adjusting covariates (hazard ratio 1.19; 95% confidence interval 0.94-1.50). As a continuous variable, alcohol consumption was not associated with clinical outcomes (hazard ratio 1.01; 95% confidence interval 0.99-1.02). Consistent with these findings, there was no association between genetic traits for alcohol metabolism and the risk of clinical outcomes. CONCLUSION Alcohol consumption was neither a protective factor nor a risk factor for sudden cardiac death or fatal ventricular arrhythmia. Genetic traits of alcohol metabolism were not associated with the clinical prognosis.
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收藏
页码:1820 / 1826
页数:7
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