Key result
Acute intravenous alcohol administration significantly increased periodic repolarization dynamics from 0.85 to 1.92 deg2 and decreased deceleration capacity, indicating autonomic imbalance.
Why the study?
Acute alcohol intake may facilitate cardiac arrhythmias underlying Holiday Heart Syndrome, and autonomic imbalance is known to promote atrial arrhythmias.
Does acute parenteral alcohol administration alter cardiac autonomic regulation in healthy individuals?
Does acute parenteral alcohol administration alter cardiac autonomic regulation in healthy individuals?
Absolute Event Rate: 1.92% vs 0.85%
p-value: p=0.001
Acute alcohol intake causes autonomic imbalance by increasing sympathetic and reducing parasympathetic activity, providing a potential physiological mechanism for 'Holiday Heart Syndrome'.
Acute alcohol alters autonomic tone in healthy volunteers; leaves open mechanistic relevance to Holiday Heart Syndrome.
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) deg 2 vs. 0.85 (0.69–1.48) deg 2 ; 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’.
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Brunner et al. (2021) studied Healthy volunteers (n=15). Acute intravenous alcohol administration vs. Baseline (pre-alcohol) was evaluated on Periodic repolarization dynamics (PRD) at maximum alcohol concentration (p=0.001). Acute intravenous alcohol administration significantly increased periodic repolarization dynamics from 0.85 to 1.92 deg2 and decreased deceleration capacity, indicating autonomic imbalance.
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