Smoking Cessation and Incident Atrial Fibrillation in a Longitudinal Cohort
- PMID: 39269397
- DOI: 10.1016/j.jacep.2024.06.019
Smoking Cessation and Incident Atrial Fibrillation in a Longitudinal Cohort
Abstract
Background: Although smoking heightens the risk of AF, it remains unknown if that risk is amenable to modification after smoking cessation.
Objectives: This study sought to evaluate the association between smoking cessation and atrial fibrillation (AF) risk in a large longitudinal cohort.
Methods: After excluding those with prevalent AF and no history of smoking at baseline, we evaluated 146,772 UK Biobank participants with serial smoking assessments. We compared AF risk between former smokers at baseline and those who quit smoking during the study to current smokers. Incident AF was ascertained from outpatient and inpatient encounters and identified using International Classification of Diseases codes. Cox models were used to compare the risk of incident AF among current and former smokers as well as those who quit smoking during the study while controlling for age, sex, race, body mass index, education, cardiovascular comorbidities, alcohol use, and pack-years.
Results: Among the 146,772 participants (48.3% female; age: 57.3 ± 7.9 years), 37,377 (25.5%) currently smoked; 105,429 (72.0%) were former smokers; and 3,966 (2.7%) quit smoking during the study. Over a mean 12.7 ± 2.0 years of follow-up, 11,214 (7.6%) participants developed AF. Compared to current smokers, the adjusted risk of AF was 13% lower in former smokers (HR: 0.87; 95% CI: 0.83-0.91) and 18% lower in those who quit smoking during the study (HR: 0.82; 95% CI: 0.70-0.95).
Conclusions: Compared to those who continue to smoke, smoking cessation was associated with a lower risk of AF.
Keywords: UK Biobank; atrial fibrillation; cohort study; modifiable risk factors; smoking cessation; tobacco use.
Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.
Conflict of interest statement
Funding Support and Author Disclosures This research was conducted using the UK Biobank resource. UK Biobank is supported by its founding funders the Wellcome Trust and UK Medical Research Council, as well as the British Heart Foundation, Cancer Research UK, Department of Health, Northwest Regional Development Agency, and Scottish Government. Dr Marcus receives funding from the National Institutes of Health, Patient-Centered Outcomes Research Institute, and California Tobacco-Related Disease Research Program and is a consultant for and owns equity in InCarda. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.
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