Results of the How Alcohol Induces Atrial Tachyarrhythmias (HOLIDAY) trial offer insight into the effects of alcohol on cardiac electrophysiology from a randomized, double-blind, placebo-controlled trial.
New data from a randomized trial assessing the effects of intravenous alcohol on the heart demonstrate a direct mechanistic link between alcohol and immediate proarrhythmic effects in the atria.
Results of the study, which included 100 participants, provide further evidence that increased consumption of alcohol is associated with an increased risk of arrhythmias.
"Although epidemiological studies have found an association between self-reported alcohol consumption and the development of an atrial fibrillation diagnosis, ours is the first study to point to a mechanism through which a lifestyle factor can acutely change the electrical properties of the heart to increase the chance of an arrhythmia," said Gregory Marcus, MD, professor of medicine in the Division of Cardiology at UCSF, in a statement.
Despite a multitude of studies finding an association between alcohol intake and increased risk of atrial fibrillation, few have examined the mechanisms behind the changes in cardiac electrophysiology. With this in mind, investigators designed the How Alcohol Induces Atrial Tachyarrhythmias (HOLIDAY) trial to compare the effects of intravenous alcohol versus placebo in patients undergoing pulmonary vein isolation procedures for atrial fibrillation.
In the randomized, double-blind, placebo-controlled trial, a group of 100 patients was randomized in a 1:1 ratio to intravenous alcohol titrated to 0.08% blood alcohol concentration or volume- and osmolarity-matched, masked, placebo. For the purpose of analysis, right, left, and pulmonary vein atrial effective refractory periods (AERPs) and conduction times were measured pre- and post-infusion. Additionally, isoproterenol infusion and burst atrial pacing were used by investigates to assess atrial fibrillation inducibility.
The 50 patients in the alcohol group had a mean age of 58.78±11.27 years, 28% were women, and 88% were white. The 50 patients in the placebo group had a mean age of 61.14±13.08 years, 24% were female, and 90% were white. Investigators pointed out patients in the placebo arm of the trial were more likely to be diabetic (22% vs 4%; P=.007) and to have undergone a prior ablation procedure for atrial fibrillation (36% vs 22%; P=.005).
In their analyses, results indicated pulmonary being AERPs decreased an average of 12 ms (95% CI, 1-22; P=.026) in the alcohol group and no change in the placebo group (P=.98). However, results suggested there were no statistically significant differences observed in continuously assessed AERPs.
Investigators also noted the proportion of AERP sites tested that decreased with alcohol (median, 0.5; IQR, 0.6-0.6) was greater than placebo (median, 0.4; IQR, 0.2-0.6; P=.0043). Additionally, there were no statistically significant differences observed in conduction times or in the proportion with inducible atrial fibrillation.
"We were able to induce AFib in large numbers of patients in both groups, but our artificial methods of inducing AFib may have overwhelmed any observable differences between the groups," Marcus said. "Alternatively, it may be that there is a delay between the change in electrical properties caused by alcohol and the increased likelihood of triggering AFib."
This study, “A Randomized, Double-Blind, Placebo-Controlled Trial of Intravenous Alcohol to Assess Changes in Atrial Electrophysiology,” was published in JACC: Clinical Electrophysiology.