By Michael H. Crawford, MD, Editor
Synopsis: A small study of continuous electrocardiogram and breath alcohol concentration in young volunteers during acute excessive alcohol consumption has shown that heart rate and ventricular premature beats increased during the drinking period. During recovery (six to 19 hours), significant arrhythmias such as atrial fibrillation occured in 5% of the subjects. The observed changes in heart rate variability and breath alcohol concentration suggest that these effects are the result of increased sympathetic nervous system activity associated with excess blood alcohol concentrations.
Source: Brunner S, Krewitz C, Winter R, et al. Acute alcohol consumption and arrhythmias in young adults: The MunichBrew II study. Eur Hear J. 2024;45(46):4938-4949.
Chronic consumption of large amounts of alcohol has been associated with adverse cardiac outcomes, including hypertension, cardiomyopathy, and arrhythmias. Prior studies, including the large MunichBREW study during Octoberfest, were cross-sectional and, consequentially, lack data on the time course of any arrhythmias. Thus, the MunichBREW II study is of interest.
The study was conducted between 2016 and 2017 and enrolled volunteers aged 18 years or older who were planning to indulge in acute alcohol consumption. Excluded were subjects with a history of atrial fibrillation (AF), an implantable cardiac device, contraindications to alcohol consumption, or who were pregnant or breastfeeding. The type and amount of alcohol consumed was not specified, and breath alcohol concentration (BrAC) was measured at baseline and hourly for eight hours.
A three-lead electrocardiogram (ECG) patch monitor was placed at baseline and was capable of recording the heart rhythm continuously for up to 72 hours. The following rhythms were analyzed: mean heart rate and supraventricular tachycardias, premature atrial complexes (PAC), and premature ventricular complexes (PVC). The rhythms were analyzed during three time periods: the drinking period (one to five hours), the recovery period (six to 19 hours,) and two control periods 24 hours after the drinking and recovery periods, respectively. Also, heart rate variability was assessed as a measure of autonomic tone.
In 2024, a late follow-up was conducted by an online questionnaire. For each comparison, the outcome of interest was the ECG measure and the predictor was BrAC. The comparisons were adjusted to account for age, sex, and body mass index. After applying the exclusion criteria, 202 subjects were enrolled and nine subjects were further excluded because of uninterpretable ECG recordings, leaving a final study population of 193: mean age 30 years, 36% women. They consumed an average of 6.8 standard drinks per week and during the past six months had an average of five binge-drinking sessions. Their average peak alcohol BrAC during the drinking period was 1.4 g/kg. (Germany measures BrAC as g/kg of blood. In the United States, BrAC is measured as g/210 L of air, which is equivalent to g/mL of blood volume rather than the kg weight of blood.)
With increasing alcohol intake during the drinking period and the recovery period, there was an increase in heart rate and reduced heart rate variability indicating increased sympathetic tone. Thereafter, parasympathetic tone predominated. Premature ventricular beats were more common during drinking and premature atrial complexes were more common during the control periods. AF, ventricular tachycardia, or various degrees of atrioventricular block occurred in 10 subjects (5%) during the recovery period. The late questionnaire (seven years) was returned by 75% of the participants. Two developed AF: one with AF during the study and one de novo AF.
About 20% of participants reported recurring symptoms of palpitations and rapid heart rate, which were not categorized further. The authors concluded that during acute excess alcohol consumption increases in heart rate were observed, but clinically significant arrhythmias were uncommon and occurred during the recovery period immediately after excess alcohol consumption.
Commentary
The presumed increase in sympathetic tone is not a new finding. It is known that the principal metabolite of ethanol is acetaldehyde, which stimulates sympathetic nerve endings and the adrenal medulla. Interestingly, in the MunichBrew II study, it took 48 hours to fully recover parasympathetic tone. The observation that PACs were more common in the control periods than in the drinking period is likely because of their suppression by increasing heart rate. However, PVCs were more common during the drinking period, suggesting that ethanol has a toxic effect on the myocardium. Noteworthy arrhythmias were seen in about 5% of the subjects in the 12- to 36-hour post-drinking periods. Although not a high incidence, it is considerably higher than what was observed in a British biobank study in this age group of 2.42/1,000 person-years over a six-year period.1
The main strength of MunichBrew II is the prospective, longitudinal design with continuous ECG and BrAC monitoring until full recovery from the binge drinking episode.
There are caveats and weaknesses. The two episodes of transient third-degree block were probably caused by emesis, which can stimulate the vagal nerve. Also, the participants were studied outside a medical facility, so measures of potassium, magnesium, and other biomarkers were not assessed. Their medical history was self-reported and not verified.
Since ECG monitoring was for 48 hours, we do not know if there were any late arrhythmias. In addition, the subjects were relatively young and predominantly white, so the results may not apply to other groups and older subjects with more comorbidities. Finally, there was no randomized control group who went to the party but abstained.
Michael H. Crawford, MD, is Professor of Medicine and Consulting Cardiologist, University of California Health, San Francisco.
A small study of continuous electrocardiogram and breath alcohol concentration in young volunteers during acute excessive alcohol consumption has shown that heart rate and ventricular premature beats increased during the drinking period. During recovery (six to 19 hours), significant arrhythmias such as atrial fibrillation occured in 5% of the subjects. The observed changes in heart rate variability and breath alcohol concentration suggest that these effects are the result of increased sympathetic nervous system activity associated with excess blood alcohol concentrations.
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