Common prohibitions against caffeine to reduce arrhythmia risk are likely unwarranted, with coffee drinkers not at heightened risk of developing cardiac arrhythmias, a large UK cohort study found.
Instead, each cup of coffee was associated with a 3% lower risk of incident arrhythmia among UK Biobank (a large-scale biomedical database and research resource) participants with a mean follow-up of 4.5 years. Small reductions were observed for atrial fibrillation and/or flutter and supraventricular tachycardia, in particular.
Additionally, a Mendelian randomisation study did not show that caffeine metabolism-related genes modify the relationship between coffee consumption and arrhythmias, reported Dr Gregory Marcus of University of California San Francisco, and colleagues in JAMA Internal Medicine.
“These data suggest that common prohibitions against caffeine to reduce arrhythmia risk are likely unwarranted,” the authors said. They noted that their results are in line with those of other recent studies showing no link between coffee consumption and increased tachyarrhythmias.
Marcus’ group cited some potential mechanisms for coffee's observed anti-arrhythmic effects in the study, namely its prolongation of left atrial effective refractory periods, blocking of adenosine receptors, antioxidant and anti-inflammatory properties, and catecholaminergic properties.
“Health care professionals can reassure patients that there is no evidence that drinking coffee increases the risk for developing arrhythmias. This is particularly important for the many patients with benign palpitations who are devastated when they think, or are told, that they have to stop drinking coffee,” according to their commentary.
The UK Biobank included more than 500,000 participants. Median coffee consumption was 2 cups per day, though 22.1% did not drink coffee.
Marcus and colleagues counted 386,258 people (mean age 56; 52.3% women; over 90% white) without a prior diagnosis of arrhythmia in their analysis. People who drank more coffee were more likely to be older, white, and male. As a group, they also tended to report more peripheral artery disease, cancer, smoking, and alcohol drinking.
Study authors acknowledged that residual or unmeasured confounding could not be excluded given the observational nature of their study.
Another major caveat was their reliance on self-reported coffee intake at a single point in time. “Not only can this lead to recall bias, but subsequent and substantial changes in coffee consumption are also possible, including reductions due to new signs or symptoms (i.e., patients with palpitations may avoid coffee),” the authors warned.
“Finally, it is important to recognise the distinction between coffee and caffeine. Caffeine is only one element of coffee, which contains other bioactive compounds such as diterpene alcohols and chlorogenic acids. As such, the mendelian randomisation analysis is truly centred on caffeine, not coffee exposure.
“The current study suggests that we can tell patients that waking up to a cup of coffee is not a dangerous ritual. However, it will be more important to listen to patients about their symptoms in association with coffee or caffeine exposure and engage in shared decision-making on an individual level.”
Coffee Consumption and Incident Tachyarrhythmias Reported Behavior, Mendelian Randomization, and Their Interactions
Eun-jeong Kim, Thomas J. Hoffmann, Gregory Nah, Eric Vittinghoff, Francesca Delling, Gregory M. Marcus
Published in JAMA, 19 July 2021
Is moderate, habitual coffee intake associated with the risk of arrhythmia, and is that association modified by genetic variants that affect caffeine metabolism?
In this large, prospective, population-based community cohort study of more than 300 000 participants, each additional daily cup of coffee was associated with a 3% reduced risk of developing an arrhythmia; these associations were not significantly modified by genetic variants that affect caffeine metabolism. A mendelian randomisation study leveraging a polygenic score to capture inherited caffeine metabolism patterns did not reveal evidence that caffeine consumption increases the risk of incident arrhythmias.
Neither habitual coffee consumption nor genetically mediated differences in caffeine metabolism was associated with a heightened risk of cardiac arrhythmias.
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.
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. The main outcomes and measures: any cardiac arrhythmia, including atrial fibrillation or flutter, supraventricular tachycardia, ventricular tachycardia, premature atrial complexes, and premature ventricular complexes.
A total of 386 258 individuals (mean [SD] age, 56  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 randomisation 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 randomisation failed to provide evidence that caffeine consumption was associated with arrhythmias.
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