Impact of acute ethanol intake on cardiac autonomic regulation

Stefan Brunner,Christina Werzer,Axel Bauer,Raphaela Winter,Matthias Graw,Moritz F Sinner,Andreas Stöver,Lukas Von Stülpnagel,Ina Clasen,Annika Hameder

doi:10.1038/s41598-021-92767-y

Abstract

Acute alcohol consumption may facilitate cardiac arrhythmias underlying the ‘Holiday Heart Syndrome’. Autonomic imbalance is promoting atrial arrhythmias. We analyzed the effects of alcohol on measures of the cardiac autonomic nervous system and their relation to arrhythmias. In 15 healthy individuals, alcohol was administered parenterally until a breath alcohol concentration of 0.50 mg/l. High-resolution digital 30-min ECGs were recorded at baseline, at the time of maximum alcohol concentration, and after alcohol concentration returned to near baseline. Using customized software, we assessed periodic repolarization dynamics (PRD), deceleration capacity (DC), standard measures of heart rate variability (SDNN; RMSSD; LF; HF), and standard ECG parameters (mean heart rate; PQ; QRS; QTc interval). At the maximum alcohol concentration, PRD levels were significantly increased compared to baseline [1.92 (IQR 1.14–3.33) deg2 vs. 0.85 (0.69–1.48) deg2; p = 0.001]. PRD levels remained slightly increased when alcohol concentrations returned to baseline. DC levels were significantly decreased at the maximum alcohol concentration compared to baseline [7.79 (5.89–9.62) ms vs. 9.97 (8.20–10.99) ms; p = 0.030], and returned to baseline levels upon reaching baseline levels of alcohol. Standard HRV measures were reduced at maximum alcohol concentration. The mean heart rate increased significantly during alcohol administration. QRS and QTc duration were significantly prolonged, whereas PQ interval showed no change. Our findings revealed an increase of sympathetic activity and a reduction of parasympathetic activity under the influence of alcohol administration, resulting in autonomic imbalance. This imbalance might ultimately trigger arrhythmias underlying the ‘Holiday Heart Syndrome’.

Highlights

Acute alcohol consumption may facilitate cardiac arrhythmias underlying the ‘Holiday Heart Syndrome’
Median Post Alc periodic repolarization dynamics (PRD) levels decreased to 1.44 [IQR 1.09 d eg2; 2.31 d eg2] (p = 0.09) after breath alcohol concentration dropped to 0.05 mg/l
The first main finding of our study is a significant increase of PRD levels at the time of maximum alcohol concentration and a slight, but not significant decrease after alcohol concentration dropped to near baseline levels

Summary

Introduction

Acute alcohol consumption may facilitate cardiac arrhythmias underlying the ‘Holiday Heart Syndrome’. Our findings revealed an increase of sympathetic activity and a reduction of parasympathetic activity under the influence of alcohol administration, resulting in autonomic imbalance This imbalance might trigger arrhythmias underlying the ‘Holiday Heart Syndrome’. Acute excessive alcohol consumption (“binge drinking”) may cause cardiac rhythm disturbances in otherwise healthy individuals, often referred to as ‘Holiday Heart Syndrome’ Both ventricular and supraventricular arrhythmias, predominantly atrial fibrillation, have been described[1]. In the Munich BREW study, we recently demonstrated in over 3,000 visitors of the Munich Octoberfest that acute alcohol consumption results in both an increase of sinus tachycardia and a reduction of respiratory sinus a rrhythmia[2,3] Recent studies in heart failure patients could demonstrate that increased PRD was strongly associated with ventricular arrhythmias and sudden d eath[8,9,10]

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Discussion

Conclusion