Modest, habitual alcohol consumption is associated with an increased risk for atrial fibrillation (AF), indicating that alcohol-reduction strategies may prevent a substantial number of cases of AF, according to research published in the European Heart Journal.

Because researchers considered the effect of alcohol consumption on AF risk ambiguous, they conducted a study to examine the association between alcohol consumption and incident AF in the face of classical risk factors, heart failure (HF), and cardiac biomarkers.

Investigators collected data from 5 community-based cohorts, which included 107,845 individuals who underwent baseline examinations between 1982 and 2010. Risk factor information included BMI, hypertension, systolic blood pressure, diabetes, total serum cholesterol, smoking status, and history of previous cardiac events. The researchers evaluated average alcohol consumption as g/d and measured biomarkers via blood samples to determine serum high-sensitivity troponin (hsTnl) and N-terminal pro-B-type natriuretic peptide (NT-proBNP).

The cohort included 100,092 participants (median age, 47.8 [range, 38-59] years; 51.7% women) without baseline AF. Generally, participants were slightly overweight (median BMI, 25.7 kg/m2) and consumed a median of 3 (mean, 8.7) g/d of alcohol. Over the median follow-up period of 13.9 years, researchers documented 5854 incident cases of AF.


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Results of a Cox regression analysis showed that alcohol consumption was associated positively with incident AF; the hazard ratio (HR) for one 12-g drink/d was 1.16 (95% CI, 1.11-1.22), with a cutoff for statistically significantly increased AF risk for regular alcohol consumption of 2 g/d.

Investigators made additional adjustments for classical cardiovascular risk factors; these adjustments did not notably change the association. The adjusted HR for 1 drink/d was 1.18 (95% CI, 1.12-1.25), and HRs were similar between women and men. Association for incident AF and alcohol consumption did not significantly change after accounting for the competing risk for all-cause mortality.

After excluding participants aged >80 years (n=99,352), researchers noted 5728 cases of incident AF, with an HR of 1.17 (95% CI, 1.11-1.22) for 1 drink/d.

Researchers noted no statistically significant association for subcategories that included former drinkers, occasional drinkers, and persons with alcohol consumption ≤1 drink/d. Higher categories of alcohol intake — between 1 and 2 drinks and >4 drinks — were associated with 28% and 47% increased risks for AF, respectively.

In a joint dataset that included available follow-up for both AF and HF, investigators observed 4995 incident cases of HF (N=69,084). Sex- and cohort-stratified Cox regression analyses showed a J-shaped relationship with incident HF. Researchers found lowest HRs with the consumption of 1.6 drinks/d.

Investigators noted weak correlations between circulating biomarkers and alcohol consumption for both NT-proBNP (r =-0.1) and hsTnl (r =0.12). Cardiac biomarker concentration levels did not significantly change the relationship between alcohol consumption and incident AF.

Study limitations include the potential underreporting of alcohol consumption; the availability of only single-biomarker measurements at baseline; and a lack of availability of baseline electrocardiograms, which may have excluded asymptomatic AF episodes.

“Alcohol consumption is positively associated with risk of AF independent of classical pathophysiological pathways including those related to myocardial wall stress and injury reflected by NT-proBNP and hsTnl,” the researchers concluded. “A strategy of reduction of alcohol consumption might have the potential to prevent a substantial number of cases of AF.”

Disclosure: Several study authors declared affiliations with the pharmaceutical industry. Please see the original reference for a full list of authors’ disclosures.

Reference

Dsengeri D, Sprünker N-A, Di Castelnuova A, et al. Alcohol consumption, cardiac biomarkers, and risk of atrial fibrillation and adverse outcomes. Eur Heart J. 2021;42(12):1170-1177.