Acute alcohol exposure and electrocardiographic changes: Finding from the HOLIDAY trial

• Published in: Journal of electrocardiology Vol. 83; pp. 26 - 29
• Main Authors: Ciuffo, Luisa, Tung, Monica, Dukes, Jonathan W., Vittinghoff, Eric, Moss, Joshua D., Lee, Randall J., Lee, Byron K., Tseng, Zian H., Vedantham, Vasanth, Olgin, Jeffrey E., Scheinman, Melvin M., Hsia, Henry, Ramchandani, Vijay A., Gerstenfeld, Edward P., Marcus, Gregory M.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01-03-2024
• Subjects: Alcohol; Atrial fibrillation; ECG; ECG; Alcohol; Atrial fibrillation
• ISSN: 0022-0736; 1532-8430
• DOI: 10.1016/j.jelectrocard.2024.01.003

Alcohol consumption is associated with a higher increased risk of atrial fibrillation (AF), but the acute effects on cardiac electrophysiology in humans remain poorly understood. The HOw ALcohol InDuces Atrial TachYarrhythmias (HOLIDAY) Trial revealed that alcohol shortened pulmonary vein atrial effective refractory periods, but more global electrophysiologic changes gleaned from the surface ECG have not yet been reported.
This was a secondary analysis of the HOLIDAY Trial. During AF ablation procedures, 100 adults were randomized to intravenous alcohol titrated to 0.08% blood alcohol concentration versus a volume and osmolarity-matched, masked, placebo. Intervals measured from 12‑lead ECGs were compared between pre infusion and at infusion steady state (20 min).
The average age was 60 years and 11% were female. No significant differences in the P-wave duration, PR, QRS or QT intervals, were present between alcohol and placebo arms. However, infusion of alcohol was associated with a statistically significant relative shortening of the JT interval (r: −14.73, p = 0.048) after multivariable adjustment.
Acute exposure to alcohol was associated with a relative reduction in the JT interval, reflecting shortening of ventricular repolarization. These acute changes may reflect a more global shortening of refractoriness, suggesting immediate proarrhythmic effects pertinent to the atria and ventricles.