<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>24(9)</volume><submitter>Tu SJ</submitter><funding>Early Career Fellowship from the National Heart Foundation of Australia and the Derek Frewin Lectureship from the University of Adelaide</funding><funding>Mid-Career Fellowship from the Hospital Research Foundation and a Postdoctoral Fellowship from the National Heart Foundation of Australia</funding><funding>Postgraduate Scholarship from the Hospital Research Foundation</funding><funding>National Heart Foundation of Australia</funding><funding>Postdoctoral Fellowship from the University of Adelaide</funding><funding>Practitioner Fellowship from the National Health and Medical Research Council of Australia</funding><funding>Early Career Fellowship from the National Heart Foundation of Australia</funding><funding>Beacon Research Fellowship from the University of Adelaide</funding><funding>Robert J. Craig Lectureship from the University of Adelaide</funding><pubmed_abstract>&lt;h4>Aims&lt;/h4>There is a paucity of epidemiological evidence on alcohol and the risk of bradyarrhythmias. We thus characterized associations of total and beverage-specific alcohol consumption with incident bradyarrhythmias using data from the UK Biobank.&lt;h4>Methods and results&lt;/h4>Alcohol consumption reported at baseline was calculated as UK standard drinks (8 g alcohol)/week. Bradyarrhythmia events were defined as sinus node dysfunction (SND), high-level atrioventricular block (AVB), and permanent pacemaker implantations. Outcomes were assessed through hospitalization and death records, and dose-response associations were characterized using Cox regression models with correction for regression dilution bias. We studied 407 948 middle-aged individuals (52.4% female). Over a median follow-up</pubmed_abstract><journal>Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology</journal><pagination>1469-1474</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9559907</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Alcohol intake and bradyarrhythmia risk: a cohort study of 407 948 individuals.</pubmed_title><pmcid>PMC9559907</pmcid><pubmed_authors>Elliott AD</pubmed_authors><pubmed_authors>Hendriks JML</pubmed_authors><pubmed_authors>Wong CX</pubmed_authors><pubmed_authors>Tu SJ</pubmed_authors><pubmed_authors>Linz D</pubmed_authors><pubmed_authors>Pitman BM</pubmed_authors><pubmed_authors>Lau DH</pubmed_authors><pubmed_authors>Sanders P</pubmed_authors><pubmed_authors>Gallagher C</pubmed_authors></additional><is_claimable>false</is_claimable><name>Alcohol intake and bradyarrhythmia risk: a cohort study of 407 948 individuals.</name><description>&lt;h4>Aims&lt;/h4>There is a paucity of epidemiological evidence on alcohol and the risk of bradyarrhythmias. We thus characterized associations of total and beverage-specific alcohol consumption with incident bradyarrhythmias using data from the UK Biobank.&lt;h4>Methods and results&lt;/h4>Alcohol consumption reported at baseline was calculated as UK standard drinks (8 g alcohol)/week. Bradyarrhythmia events were defined as sinus node dysfunction (SND), high-level atrioventricular block (AVB), and permanent pacemaker implantations. Outcomes were assessed through hospitalization and death records, and dose-response associations were characterized using Cox regression models with correction for regression dilution bias. We studied 407 948 middle-aged individuals (52.4% female). Over a median follow-up</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Oct</publication><modification>2025-04-27T03:38:36.907Z</modification><creation>2025-04-06T18:53:15.42Z</creation></dates><accession>S-EPMC9559907</accession><cross_references><pubmed>35178566</pubmed><doi>10.1093/europace/euac007</doi></cross_references></HashMap>