B-PO02-152 ELECTROCARDIOGRAPHIC CHANGES IN A DOUBLE-BLIND, PLACEBO-CONTROLLED RANDOMIZED TRIAL OF ETHANOL VERSUS PLACEBO

Abstract

Alcohol is implicated as a common trigger for discrete atrial fibrillation (AF) episodes, but the mechanism by which this occurs remains unknown. Changes in the 12-lead surface electrocardiogram (ECG) can reflect aberrations in conduction time (changes in P wave and QRS durations), autonomic tone (PR interval) and refractoriness (QT interval). We sought to compare ECG changes between two groups randomly assigned to intravenous alcohol versus placebo. To determine the effect of acute ethanol exposure on 12-lead ECGs in human subjects. We performed a secondary analysis of the HOLIDAY (How Alcohol Induces Atrial Tachyarrhythmias) randomized trial. Briefly, 100 participants in sinus rhythm undergoing ablation procedures for AF were randomly assigned to intravenous ethanol titrated to 0.08% blood alcohol concentration versus double-blind, osmotic and volume equivalent placebo infusion. Pre versus post-infusion P wave, PR, QRS, and QT durations were assessed. No significant differences in baseline ECG intervals between ethanol versus placebo groups were observed. Participants receiving the ethanol infusion exhibited a trend towards an increased P wave duration (3.89 ms ± 13.09, p = 0.055), a lengthening in the QRS (3.14 ± 10.06, p = 0.045), and an increase in the PR interval (5.25 ms ± 15.05, p = 0.026), while none of these measurements meaningfully changed in the placebo group. The QTc increased significantly in both the alcohol and control groups (21.55 ms ± 27.37, p <0.001 and 15.52 ms ± 27.50, p <0.001). Acute exposure to ethanol resulted in an increase in the PR interval, potentially reflecting an increase in vagal tone, accompanied by a trend towards a longer P wave duration and a significant lengthening of the QRS interval, indicative of conduction slowing. These data suggest that autonomic changes and changes in conduction velocity may play important in roles in the initiation of alcohol-related AF.