Alcohol consumption, sinus tachycardia, and cardiac arrhythmias at the Munich Octoberfest: results from the Munich Beer Related Electrocardiogram Workup Study (MunichBREW)

Abstract

Aims: Alcohol is a risk factor for cardiac arrhythmias. Retrospective analyses suggest supraventricular arrhythmias consecutive to acute alcohol consumption, but prospective data are limited. We intended to prospectively associate acute alcohol consumption with cardiac arrhythmias.

Methods and results: At the 2015 Munich Octoberfest, we enrolled 3028 voluntary participants who received a smartphone-based ECG and breath alcohol concentration (BAC) measurements. ECGs were analysed for cardiac arrhythmias (sinus tachycardia, sinus arrhythmia, premature atrial/ventricular complexes, atrial fibrillation/flutter) and respiratory sinus arrhythmia. By multivariable adjusted logistic regression we associated BACs with cardiac arrhythmias. Similarly, we analysed 4131 participants of the community-based KORA S4 Study (Co-operative Health Research in the Region of Augsburg) and associated cardiac arrhythmias with chronic alcohol consumption. In our acute alcohol cohort (mean age 34.4 ± 13.3 years, 29% women), mean BAC was 0.85 ± 0.54 g/kg. Cardiac arrhythmias occurred in 30.5% (sinus tachycardia 25.9%; other arrhythmia subtypes 5.4%). Breath alcohol concentration was significantly associated with cardiac arrhythmias overall (odds ratio (OR) per 1-unit change 1.75, 95% confidence interval (CI) 1.50-2.05; P < 0.001) and sinus tachycardia in particular (OR 1.96, 95%CI 1.66-2.31; P < 0.001). Respiratory sinus arrhythmia measuring autonomic tone was significantly reduced under the influence of alcohol. In KORA S4, chronic alcohol consumption was associated with sinus tachycardia (OR 1.03, 95%CI 1.01-1.06; P = 0.006).

Conclusions: Acute alcohol consumption is associated with cardiac arrhythmias and sinus tachycardia in particular. This partly reflects autonomic imbalance as assessed by significantly reduced respiratory sinus arrhythmia. Such imbalance might lead to sympathetically triggered atrial fibrillation resembling the holiday heart syndrome.

Clinicaltrials.org accession number: NCT02550340.

© The Author 2017. Published by Oxford University Press on behalf of the European Society of Cardiology.

Figures

Figure 1

Alcohol consumption. A. Distribution of breath alcohol concentration (BAC) across the acute alcohol cohort in g/kg. Results presented for the entire cohort, and stratified by sex and quartiles of age. B. Distribution of chronic alcohol consumption in KORA S4 in g/d. Results presented for the entire cohort, and stratified by sex and quartiles of age. Outliers truncated at 80 g/d. C. Day-by-day variability of mean BAC for each of the 16 days of the Octoberfest. D. Circadian variability of mean BAC across recruitment days at the Octoberfest.

Figure 2

Examples and Prevalence of Cardiac Arrhythmias. A–E. Representative ECG recordings obtained in our acute alcohol cohort. ECG recordings show sinus rhythm (A), sinus tachycardia (B), premature atrial complex (C), premature ventricular complex (D), atrial fibrillation (E). F–G. Clustered bars represent the prevalence of the primary outcome of any cardiac arrhythmia (F) and sinus tachycardia (G) in our acute alcohol cohort by quartiles of BAC. Within each cluster, bars represent the overall cohort (green), and sex-stratified results for men (blue) and women (red). Clusters compared by χ2 test for trend.

Figure 3

MunichBREW study conclusions. The figure summarizes the study procedures and results in the panel shaded in green. These findings influence the generated hypothesis on ‘Holiday Heart Syndrome’ pathophysiology illustrated in the panel shaded in red. Importantly, additional research is warranted to support this hypothesis.