Alcohol and the Electric Atrium, Part 2: When BAC Exceeds the Legal Limit

February 04, 2021

As alcohol intake goes up, so does the likelihood of developing atrial fibrillation (AF), epidemiologic surveys and other studies overwhelmingly suggest, as excessive alcohol use is increasingly seen as a modifiable risk factor for the arrhythmia. The research has generally focused on links between chronic alcohol use and the arrhythmia, with its acute effects as a cause of AF typically the realm of preclinical studies.

On that backdrop, blood alcohol concentrations (BAC) consistent with a legal definition of intoxication were followed by atrial electrophysiologic (EP) changes believed conducive to the genesis of AF in an elegant study of patients in the lab under general anesthesia for an AF ablation.

Atrial refractory periods at the pulmonary vein shortened, possibly setting the stage for arrhythmia, when BAC were maintained at 0.08% during EP studies performed prior to ablation.

The findings "provide functional, mechanistic evidence of electrical changes that certainly could explain a propensity to atrial fibrillation in the setting of alcohol," Gregory M. Marcus, MD, University of California, San Francisco, told theheart.org | Medscape Cardiology. They point to "a modifiable behavior under the control of the patient that has immediate effects on the electrical properties of the heart relevant to generating an arrhythmia."

In the study, published January 27 in JACC: Clinical Electrophysiology with Marcus as lead author, the investigators measured atrial effective refractory periods (AERP) — myocyte recovery time before a next signal transmission — and conduction speeds at left atrial sites in patients about to undergo AF ablation. Shortening of AERP has been long believed to be associated with AF initiation, he noted.

The group had randomly assigned 100 adult patients in the lab for an AF ablation procedure to first undergo the study's EP protocol both before and during a continuous infusion of either ethanol, set to maintain a BAC of 0.08% using a validated titration protocol, or placebo. The latter was administered under conditions that mimicked the ethanol titration procedure.

"Patients, operators, and investigators were blinded, whereas the anesthesiologist and research coordinator(s) administering and overseeing the infusion were not," the report notes.

Although conduction speeds didn't differ significantly in the two groups, shortened AERPs were more prevalent for the 50 patients who received the ethanol infusion.

Mean AERP measured at the pulmonary vein was significantly reduced in the alcohol group but didn't change in the control group; no such AERP shortening on alcohol was seen at other atrial sites.

"Lowering of the AERP was most pronounced in the pulmonary vein in the setting of alcohol," Marcus observed. "There seemed to be some uniquely potent relationship between alcohol and pulmonary vein electrophysiology," which — assuming alcohol does indeed promote AF — is consistent with the status of pulmonary vein isolation as the predominant AF ablation technique.

Global atrial AERP did not change significantly during the infusions in either the alcohol or placebo groups. But AERP at the pulmonary vein dropped a mean of 11.61 ms in the alcohol group (P = .026) and didn't change significantly among the control group.

Solely among those in the alcohol group, mean AERP shortened 25.88 ms further at the pulmonary vein, compared with other atrial sites (P < .001).

"This is a little surprising, but we did not see a difference in induction of atrial fibrillation," Marcus observed, and offered possible explanations. Possibly, he said, the effect of alcohol in promoting AF may be delayed, which is consistent with reports from patients that it often "happens a few hours later."

Another explanation, he said, may be that the study's AF induction technique "was just so overwhelming that it washed out any clear difference between the two groups, because we actually were able to induce atrial fibrillation in the majority of these patients."

Marcus discloses receiving research support from the National Institutes of Health, Patient-Centered Outcomes Research Institute, Medtronic, Eight, Jawbone, and Baylis; and consulting and holding equity interest in InCarda Therapeutics. The other authors reported they have no relevant conflicts.

JACC Clin Electrophysiol. Published online January 27, 2021. Abstract

Follow Steve Stiles on Twitter: @SteveStiles2. For more from theheart.org | Medscape Cardiology, follow us on Twitter and Facebook.

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