Physicians' Academy for Cardiovascular Education

Moderate alcohol consumption predisposes to atrial fibrillation

Voskoboinik A et al., JACC 2016

Alcohol and Atrial Fibrillation - A Sobering Review

Voskoboinik A, Prabhu S, Ling L-H, et al.,
JACC 2016. Vol. 68. DOI: 10.1016/j.jacc.2016.08.074
While the link between excessive alcohol drinking and various forms of CV disease is well established, smaller amounts of alcohol may reduce the incidence of coronary disease. However, some evidence may also suggest that modest levels of alcohol intake on a regular basis may increase the risk of atrial fibrillation (AF). The ‘holiday heart syndrome’ (HHS) is a common emergency department presentation, in which AF is precipitated by alcohol in 35% to 62% of cases.
Three large meta-analyses revealed that moderate habitual consumption, even after correcting for binge drinking (at least 5 standard drinks on a single occasion), increases the incidence of AF in a dose-dependent manner. Men and women are equally affected. Generally, alcohol consumption is defined as light (<7 drinks/week), moderate (7-21 drinks/week) and heavy (>21 drinks/week), with 1 standard drink being approximately 12 g of alcohol.

Pathophysiological mechanisms of alcohol-associated AF

Alcohol may act as a trigger for AF, and regular long-term consumption may facilitate atrial remodelling.
Electrophysiological effects of alcohol
Alcohol consumption may induce electrical atrial remodelling, producing a arrhythmogenic substrate. Experiments in rodents have shown shortening of action potential and altered expression of ion channels in response to alcohol administration. A porcine model also suggested a link, since acute intoxication increased AF susceptibility following burst atrial pacing.
Studies in humans have suggested that consumption of ~5-6 standard doses of whisky prolongs the His-ventricular interval and shortened the refractory period. Alcohol appears to slow intra-atrial conduction in everybody, but more so in those with AF. Atrial effective refractory periods were significantly shorter in drinking AF patients as compared to AF patients who do not drinking.
Hypokalemia is also common in heavy drinkers along with hypomagnesemia. Potassium loss can predispose to AF by increasing excitability, since cellular hyperpolarisation lowers the resting membrane potential, which could increase sodium channel recruitment, leading to a faster upstroke.
Autonomic effects of alcohol
Alcohol stimulates the sympathetic nervous system in AF patients, which promotes adrenaline secretion and higher urinary excretion of adrenaline has also been described in AF patients following alcohol consumption. A hyperadrenergic state, in which short-term heart rate variability (HRV) is reduced, appears to persist at least 24 hours after intoxication in those without prior AF. Parasympathetic modulation of autonomic tone (greater high frequency HRV) has also been described. Vagal triggers (rest, sleep, eating) can provoke alcohol-mediated paroxysmal AF.
Vagal activation shortens atrial refractoriness and may result in waves of excitation and fibrillatory conduction, while sympathetic activation increases intracellular calcium and spontaneous release from the sarcoplasmic reticulum.
Simultaneous sympathetic and parasympathetic discharge may itself trigger AF.
Atrial structural effects of alcohol
Alcohol may also cause tissue fibrosis. Reduced myofilament calcium sensitivity and inotrope response and ultrastructural cystic changes in intercalated discs in cardiac muscle have been described in alcoholic animals.
In patients with paroxysmal AF undergoing pulmonary vein isolation, daily drinking independently predicted atrial fibrosis, the hallmark of structural remodelling in AF.
Alcohol and its metabolite acetaldehyde have direct cardiotoxic effects, including impairing excitation-contraction coupling, inhibiting calcium release from the sarcoplasmic reticulum, and it may cause oxidative stress, protein damage and lipid peroxidation. Changes suggestive of acute inflammation in the myocardium have also been observed, but is unknown whether similar processes occur in the atria after binge drinking.

Alcohol and binge drinking: “Holiday Heart Syndrome”

HHS has been described to occur after a binge also in infrequent and non-drinkers. While many patients develop AF during the intoxication, it may also present 12-36 hours later. AF in HHS generally terminates within a day, but about a quarter of patients have recurrences with subsequent binges at 1 year. HHS is generally considered benign, but several links have been described between heavy binge drinking and sudden cardiac death. This is especially true in patients with pre-existing heart disease, possibly via induction of ventricular tachycardia by QTc prolongation.
Alcohol has complex physiological consequences depending on the time point after consumption. A meta-analysis of 23 studies (n=~29500) reported that moderate consumption led to an immediately increased CV risk, which decreased after 24h, and protection against stroke followed within 1 week.

Habitual alcohol consumption as a risk factor for AF

Three large meta-analyses have revealed a dose-dependent relationship between light-moderate habitual consumption and risk of AF.
After exclusion of binge drinkers and adjustment for other AF risk factors, a meta-analysis of 7 prospective studies and a 12-year follow-up of over 850000 persons, found a positive association between alcohol and AF risk, with each extra alcoholic drink per day accounting for an 8% higher AF incidence. For those consuming >14 standard drinks/week, wine (RR: 1.35) and liquor (RR: 1.46), but not beer (RR: 1.03), were significantly associated with increased AF risk. Another meta-analysis of 14 studies reported similar findings, namely 8% higher AF risk for each 6 standard drinks per week. Yet another study also described a dose-response curve, albeit with a higher threshold for AF risk. In those studies, AF risk may be underestimated due to under-reporting of alcohol consumption (self-reported) and non-reporting of asymptomatic AF episodes.
Based on the current review the authors state that they did not find a safe level of daily alcohol intake in patients with AF. Some studies showed that heavy habitual consumption is an even more important risk factor for AF than hypertension and obesity.

Alcohol and other risk factors: an intermediary or a confounding variable?

The interaction of alcohol with other AF risk factors may be understated. Alcohol has been linked to hypertension, and may explain 16% of cases of hypertensive disease.
Obesity is a well-recognised AF risk factor. A relationship between alcohol consumption and obesity has not consistently been shown, nor is the is the effect of limiting alcohol consumption on weight reduction to reduce AF symptoms known.
Sleep-disordered breathing (SDB) is an established AF risk factor, and even modest alcohol consumption before sleep has been described to increase the Apnea Hypopnea Index. Epidemiological studies have confirmed the link between alcohol and SDB, in a dose-dependent manner.
While lighter alcohol intake may reduce the risk of heart failure, habitual heavy drinking may cause development of alcoholic cardiomyopathy. Progress from unexplained left ventricular hypertrophy to overt systolic heart failure may be seen, particularly in long-term consumption of >7 drinks/day. Many heavy-drinkers have diastolic dysfunction that correlated with degree of alcohol consumption, even in absence of systolic dysfunction.

Alcohol and AF: prognostic implications

Progression from paroxysmal to persistent AF is more common in those who continue to consume alcohol. Moderate-heavy alcohol consumption is a strong risk factor for progression and for recurrent AF. Alcohol consumption may also increase the risk of adverse outcomes such as thromboembolism in patients with AF, but contradicting observations have been published.
Over 100 non-randomised studies have indicated a benefit of light-moderate alcohol consumption (7 drinks per week for women and 14 for men) with regard to the risk of new-onset CAD, angina, myocardial infarction and CV mortality. This effect has been postulated to occur through improved lipid profile or reduced platelet aggregation and inflammation. These studies have been conducted in healthy adults and results may not be extrapolated to those with a history of AF or structural heart disease.


Regular consumption of alcohol at moderate levels, as well as binge drinking, predisposes to AF, with an increase in AF recurrence in those who continue to drink. While a small amount of alcohol is generally considered cardioprotective, these benefits to not extend to AF.
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