Impact of acute ethanol intake on cardiac autonomic regulation

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...

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Autores principales: Stefan Brunner, Raphaela Winter, Christina Werzer, Lukas von Stülpnagel, Ina Clasen, Annika Hameder, Andreas Stöver, Matthias Graw, Axel Bauer, Moritz F. Sinner
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Publicado: Nature Portfolio 2021
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Acceso en línea:https://doaj.org/article/eea84573012a4042b020b7cb04f12586
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spelling oai:doaj.org-article:eea84573012a4042b020b7cb04f125862021-12-02T16:05:54ZImpact of acute ethanol intake on cardiac autonomic regulation10.1038/s41598-021-92767-y2045-2322https://doaj.org/article/eea84573012a4042b020b7cb04f125862021-06-01T00:00:00Zhttps://doi.org/10.1038/s41598-021-92767-yhttps://doaj.org/toc/2045-2322Abstract 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’.Stefan BrunnerRaphaela WinterChristina WerzerLukas von StülpnagelIna ClasenAnnika HamederAndreas StöverMatthias GrawAxel BauerMoritz F. SinnerNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 11, Iss 1, Pp 1-7 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Stefan Brunner
Raphaela Winter
Christina Werzer
Lukas von Stülpnagel
Ina Clasen
Annika Hameder
Andreas Stöver
Matthias Graw
Axel Bauer
Moritz F. Sinner
Impact of acute ethanol intake on cardiac autonomic regulation
description 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’.
format article
author Stefan Brunner
Raphaela Winter
Christina Werzer
Lukas von Stülpnagel
Ina Clasen
Annika Hameder
Andreas Stöver
Matthias Graw
Axel Bauer
Moritz F. Sinner
author_facet Stefan Brunner
Raphaela Winter
Christina Werzer
Lukas von Stülpnagel
Ina Clasen
Annika Hameder
Andreas Stöver
Matthias Graw
Axel Bauer
Moritz F. Sinner
author_sort Stefan Brunner
title Impact of acute ethanol intake on cardiac autonomic regulation
title_short Impact of acute ethanol intake on cardiac autonomic regulation
title_full Impact of acute ethanol intake on cardiac autonomic regulation
title_fullStr Impact of acute ethanol intake on cardiac autonomic regulation
title_full_unstemmed Impact of acute ethanol intake on cardiac autonomic regulation
title_sort impact of acute ethanol intake on cardiac autonomic regulation
publisher Nature Portfolio
publishDate 2021
url https://doaj.org/article/eea84573012a4042b020b7cb04f12586
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