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ALCOHOL USE AND ARRHYTHMIAS
Atrial Fibrillation
Meta-analyses have concluded that heavier alcohol con-
sumption predicts a heightened risk of developing atrial
fibrillation (AF).54,55 Instrumental variable analyses have
suggested causal relationships between alcohol expo-
sure and AF in large populations.56–58 No clear threshold
effect has been identified, nor has any one type of alco-
holic drink been differentially implicated; the relationship
appears to be fairly linear.55 Data remain conflicting as to
whether 1 drink/day on average influences AF risk.59,60
Alcohol abstainers appear to be at a lower risk of AF than
those who continue to drink,61 and a prospective, random-
ized trial of Australians consuming at least 10 drinks/
week demonstrated a substantial reduction in AF burden
among those instructed to abstain.62 Patients with parox-
ysmal AF fitted with continuous alcohol sensors demon-
strated a heightened odds of AF occurring within hours of
a drinking event,63 and a per-protocol analysis of random-
ized N-of-1 trials of AF triggers found alcohol to be the
only prespecified trigger associated with AF.30
Alcohol consumption has been associated with left
atrial enlargement and fibrosis, both potential mediators
of the alcohol-AF relationship.64–66 More often, those with
alcohol-related AF may also have vagally mediated epi-
sodes.67 A randomized, double-blind, placebo-controlled
study in humans demonstrated that alcohol acutely
shortened pulmonary vein refractory periods.68
Supraventricular Tachycardia
There is no evidence that alcohol substantially influences
the risk of supraventricular tachycardia.58,67,69
Premature Ventricular Contractions, Ventricular
Tachycardia, and Ventricular Fibrillation
There is no consistent evidence that alcohol directly influ-
ences the risk of premature ventricular contractions, 70,71
ventricular tachycardia, or ventricular fibrillation.72,73
Sudden Death
Long-term consumption of ≈1 drink/day has been as-
sociated with the lowest risk of sudden death, whereas
heavy alcohol consumption may be associated with a
heightened risk of sudden death. 49,72,74,75 Because sud-
den deaths are now known to have multiple causes,76 the
underlying mechanisms may be related to alcoholic car-
diomyopathies, MI, or other noncardiac causes of death.77
Bradycardias
Longitudinal cohort studies have not found a relationship
between alcohol consumption and a higher risk of sinus
node disease.78,79 However, moderate alcohol consump-
tion has been associated with a lower risk of developing
sinus node disease.78 Longitudinal cohort studies also
suggest that alcohol either has no effect or has a protec-
tive effect on atrioventricular conduction disease.69,78,80,81
ALCOHOL USE, CARDIOMYOPATHY, AND
HF
Long-term excessive alcohol use is associated with
the development of a dilated left ventricle, normal or
reduced left ventricular wall thickness and mass, and, in
advanced stages, HF with reduced left ventricular ejec-
tion fraction. 16 Current cardiomyopathy schemas recog-
nize excessive alcohol use as a nongenetic cause of
dilated cardiomyopathy but also note that alcohol may
act as an epigenetic trigger in the presence of underly-
ing genetic variants. 82 In the United States, prevalence
estimates are elusive and vary among reports. Data
from the National Inpatient Sample show that among
352 million estimated hospitalizations of adults, 68 per
100 000 were associated with the diagnosis of alcohol-
ic cardiomyopathy (ACM). This prevalence was higher
among men than women. 83 The average age of hos-
pitalization is similar for men and women (≈56 years);
however, when stratified by race, both Hispanic men
and women were hospitalized at a younger mean age
(53 years).
The exact amount and duration of alcohol consump-
tion associated with the development of ACM remain
unknown. Data derived chiefly from case-control studies
suggest that consuming ≈7 to 15 standard drinks/day
over a 5- to 15-year period is associated with adverse
changes in systolic or diastolic ventricular function. 84
Recently, however, in an observational cross-sectional
study, Daka et al85 reported that as few as 4 drinks/week
(in the past month) was associated with an increased
odds of diastolic dysfunction.
The risk of ACM among those who consume alco-
hol is highly heterogeneous, suggesting important
interactions with other environmental exposures or
genetic factors. The presence of truncating variants
in the gene encoding the giant sarcomeric protein titin
(the most common cause of a dilated cardiomyopathy),
may represent a genetic predisposition and increasedDownloaded from http://ahajournals.org by on July 8, 2025
CLINICAL STATEMENTS
AND GUIDELINESCirculation. 2025;152:e7–e21. DOI: 10.1161/CIR.0000000000001341 July 8, 2025 e13Piano et al Alcohol Use and Cardiovascular Disease
vulnerability to ACM, particularly in individuals report-
ing a history of alcohol intake at ≈6 drinks/day over a
5-year period. 86 Women appear to be at risk of ACM
when exposed to lower amounts and shorter durations
of alcohol use compared with men. 87
Controversy exists on the relationship between alco-
hol use and the risk of developing HF. Several meta-
analyses and prospective cohort studies reported that
<1 and 1 to 2 drinks/day were inversely associated with
incident HF. 88–90 In contrast, an MR study reported both
the absence of an association and an inferred increased
risk of HF attributed to alcohol.42 In the same MR study,
when abstainers were excluded, exceeding 7 to 10
drinks/week was associated with an increased risk of
incident HF.42 Similarly, studies of individual participant
data from large-scale sources and 19 high-income
countries revealed that usual alcohol consumption of <7
drinks/week was not associated with increased HF risk,
whereas levels of ≈21 drinks/week were associated with
an ≈50% increase in HF risk. 33
Among studies and different populations, there
appears to be a consensus that exceeding 21 drinks/
week is associated with an increased risk of HF. Recently,
and similar to others, Wong and colleagues91 reported
that there was no protective or adverse association
between alcohol consumption (≤5 drinks/week) and the
risk of developing HF. However, in patients with struc-
tural or functional cardiac abnormalities, alcohol use (≥5
drinks/week) was associated with an increased risk of
progression of asymptomatic left ventricular dysfunction
and symptomatic HF (odds ratio, 5.0 [95% CI, 1.7–15.5])
over a mean follow-up of 5.4 years.9
Piano MR, Marcus GM, Aycock DM, et al,;on behalf the American Heart Association Council on Lifestyle and Cardiometabolic Health; Council on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology; and Stroke Council. Alcohol Use and Cardiovascular Disease: A Scientific Statement From the American Heart Association. Circulation. 2025 Jul 8;152(1):e7-e21.
Powell-Wiley TM, Poirier P, Burke LE, et al; American Heart Association Council on Lifestyle and Cardiometabolic Health; Council on Cardiovascular and Stroke Nursing; Council on Clinical Cardiology; Council on Epidemiology and Prevention; and Stroke Council. Obesity and Cardiovascular Disease: A Scientific Statement From the American Heart Association. Circulation. 2021 May 25;143(21):e984-e1010.