Journal
JAMA INTERNAL MEDICINE
Volume 181, Issue 9, Pages 1185-1193Publisher
AMER MEDICAL ASSOC
DOI: 10.1001/jamainternmed.2021.3616
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Funding
- Welsh Assembly Government
- British Heart Foundation
- Diabetes United Kingdom, Northwest Regional Development Agency, Scottish Government
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In a prospective cohort study using data from the UK Biobank, it was found that higher habitual coffee consumption was associated with a lower risk of arrhythmia, and genetically mediated caffeine metabolism did not affect this association. Mendelian randomization did not provide evidence of a significant association between caffeine consumption and arrhythmias.
IMPORTANCE The notion that caffeine increases the risk of cardiac arrhythmias is common. However, evidence that the consumption of caffeinated products increases the risk of arrhythmias remains poorly substantiated. OBJECTIVE To assess the association between consumption of common caffeinated products and the risk of arrhythmias. DESIGN, SETTING, AND PARTICIPANTS This prospective cohort study analyzed longitudinal data from the UK Biobank between January 1, 2006, and December 31, 2018. After exclusion criteria were applied, 386 258 individuals were available for analyses. EXPOSURES Daily coffee intake and genetic polymorphisms that affect caffeine metabolism. MAIN OUTCOMES AND MEASURES Any cardiac arrhythmia, including atrial fibrillation or flutter, supraventricular tachycardia, ventricular tachycardia, premature atrial complexes, and premature ventricular complexes. RESULTS A total of 386 258 individuals (mean [SD] age, 56 [8] years; 52.3% female) were assessed. During a mean (SD) follow-up of 4.5 (3.1) years, 16 979 participants developed an incident arrhythmia. After adjustment for demographic characteristics, comorbid conditions, and lifestyle habits, each additional cup of habitual coffee consumed was associated with a 3% lower risk of incident arrhythmia (hazard ratio [HR], 0.97; 95% CI, 0.96-0.98; P < .001). In analyses of each arrhythmia alone, statistically significant associations exhibiting a similar magnitude were observed for atrial fibrillation and/or flutter (HR, 0.97; 95% CI, 0.96-0.98; P < .001) and supraventricular tachycardia (HR. 0.96; 95% CI, 0.94-0.99; P = .002). Two distinct interaction analyses, one using a caffeine metabolism-related polygenic score of 7 genetic polymorphisms and another restricted to CYP1A2 rs762551 alone, did not reveal any evidence of effect modification. A mendelian randomization study that used these same genetic variants revealed no significant association between underlying propensities to differing caffeine metabolism and the risk of incident arrhythmia. CONCLUSIONS AND RELEVANCE In this prospective cohort study, greater amounts of habitual coffee consumption were inversely associated with a lower risk of arrhythmia, with no evidence that genetically mediated caffeine metabolism affected that association. Mendelian randomization failed to provide evidence that caffeine consumption was associated with arrhythmias.
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