A literature review published in Cureus reinforced the strong association between binge alcohol intake and new-onset atrial fibrillation, a pattern that reliably appears during holidays and weekends when rapid, high-volume drinking is common, known as Holiday Heart Syndrome.
Across 11 cohort, observational, and case-control studies involving sample sizes from 14 to about 400,000 adults without known cardiovascular disease, binge-drinking—defined as 5 or more drinks within 2 hours—consistently preceded atrial fibrillation (AF). Arrhythmias emerged within 24 hours in most reports, with a second diagnostic window 12 to 36 hours after heavy intake. Physiologic signatures included sympathetic surges, reduced vagal tone, elevated heart rates, shortened atrial refractory periods, and measurable declines in heart rate variability.
The structured PubMed and Cochrane search through August 2024 excluded chronic alcohol–focused studies and identified transient reductions in left atrial emptying fraction without persistent structural abnormalities. Dose-response patterns varied across studies, ranging from linear increases in AF incidence to J-shaped associations, but all identified excessive episodic intake as the principal trigger. The lowest AF risk was observed at five drinks per week in one large cohort study, with risk increasing sharply at higher consumption levels.
Alcohol type further modified risk. Whiskey was frequently linked to rapid AF onset and persistent ECG changes, beer was associated with higher AF likelihood than wine or spirits, and women consuming spirits showed greater susceptibility than those drinking wine. Episodes typically resolved within 24 hours of abstinence and often required no specific treatment unless patients developed symptoms such as shortness of breath or chest pain. Arrhythmias recurred only with renewed heavy intake. Although men predominated in heavy-drinking cohorts, binge exposure increased AF risk in both sexes.
A complementary review in the Romanian Journal of Legal Medicine expanded mechanistic context, noting AF may develop even after a single drink in predisposed adults and has occasionally been associated with cardiac arrest in structurally normal hearts. Genetic factors may influence susceptibility. Proposed contributors included acetaldehyde-mediated catecholamine release, alcohol-related electrolyte loss, increased free fatty acids, and sodium-channel inhibition—an arrhythmogenic environment that may persist after sobriety. Additional findings included conduction delays, P-wave and QRS widening, increased beta-adrenoreceptor density, and sleep apnea–related adrenergic surges. Cardioversion within 48 hours is recommended, with anticoagulation initiated beforehand if the arrhythmia exceeds this interval.
Together, the two reviews underscore the importance of detailed alcohol histories, including drink type and timing, as well as electrolyte assessment when evaluating palpitations during peak festive drinking periods. Physicians should routinely screen for alcohol use in patients with arrhythmias and counsel on abstinence or moderation.
The Cureus review authors reported no financial relationships or competing interests, and the authors of the Romanian Journal of Legal Medicine article similarly disclosed no conflicts of interest.
Sources: Cureus, Romanian Journal of Legal Medicine
