Acute electrical, autonomic and structural effects of binge drinking: Insights into the ‘holiday heart syndrome’

doi:10.1016/j.ijcard.2021.01.071

International Journal of Cardiology

Volume 331, 15 May 2021, Pages 100-105

https://doi.org/10.1016/j.ijcard.2021.01.071 Get rights and content

Highlights

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Binge drinking appears to be is associated with sympathetic activation followed by a ‘rebound’ parasympathetic response.
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Subclinical mechanical atrial dysfunction was seen at 3 days post binge.
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No myocardial inflammation or change in ventricular function were seen up at 3 days post binge.
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Alcohol appears to have a relatively modest effect on burden of atrial ectopy.

Abstract

Background

Binge drinking is a common atrial fibrillation (AF) trigger, however the mechanisms are poorly understood.

Objective

To investigate the effects of alcohol intoxication and hangover with rhythm monitoring and cardiac MRI.

Methods

Patients underwent serial cardiac MRI pre- and post-binge with continuous Holter monitoring. Time periods analyzed: baseline (24 h pre-binge), consumption, hangover (0– 24 h post-consumption) and post-hangover (24–48 h post-consumption).

Results

50 patients (age 49 ± 15 years, 40% paroxysmal AF) completed the study (intake 8.4 ± 3.1 standard drinks). Mean heart rate increased from 72 ± 10 to 80 ± 13 beats per minute (bpm) during consumption (p < 0.001). The hangover period was characterised by higher daily atrial ectopic count (50, IQR 10–132 vs baseline 43, IQR 10–113; p = 0.04) and reduced heart rate variability (SDNN 55 ms, IQR 40–65 versus 62 ms, IQR 51–66; p = 0.007). There was evidence of heightened parasympathetic activity post-hangover with heart rate slowing (mean HR 54 ± 6 bpm; p = 0.03) and increased activity in the High frequency band when separating the complex heart rate variability waveform into its component rhythms (291 ms², 97–538 versus baseline 237 ms², IQR 104–332; p = 0.04). Three patients developed AF 11, 29 and 34 h post-binge. Cardiac MRI (2.7 ± 0.7 days post-binge) demonstrated a decrease in left atrial (LA) emptying fraction (57.9 ± 8.5 to 53.5 ± 6.7%; p = 0.003) but no change in LA volume, left ventricular ejection fraction or markers of ventricular inflammation.

Conclusion

Binge drinking is associated with sympathetic activation followed by a ‘rebound’ parasympathetic response and atrial mechanical dysfunction which may explain the propensity and temporal association between binge drinking and AF.

Introduction

Binge drinking, defined as 5 or more standard drinks (SDs) over a two-hour period, is undertaken by ~33% of adults on an annual basis [1]. This behaviour may result in numerous adverse health-related consequences. The most common cardiac consequence of acute alcohol consumption is atrial fibrillation (AF). Alcohol is the most frequently reported trigger for AF by patients [2], with some series reporting its association with 63% of all emergency department presentations with AF in those less than 65 years old [3]. We recently reported a randomized study in regular drinkers with AF that demonstrated a significant reduction in AF recurrence and burden associated with alcohol abstinence [4]. The ‘Holiday Heart Syndrome’ was first coined by Ettinger et al. who reported a higher incidence of alcohol-related atrial arrhythmias during December and January and following weekends [5]. Interestingly, presentations for HHS peaked on a Monday, consistent with the clinical observation of a temporal delay between alcohol intake and vulnerability to atrial fibrillation.

Proposed mechanisms by which acute intoxication may predispose to AF include shortening of atrial action potential and refractory period, conduction slowing, direct myocyte injury and autonomic perturbations [6]. Excessive alcohol consumption may result in myocardial injury and inflammation [7]. Despite the well appreciated relationship between acute alcohol exposure and AF the responsible mechanisms have not been well defined. We aim to report the acute electrical, autonomic and structural effects of acute alcohol exposure using continuous rhythm monitoring and cardiac magnetic resonance imaging (CMR) in an observational study.

Section snippets

Study design

Between May 2017 and October 2019, we prospectively enrolled 50 participants (30 healthy adult volunteers and 20 patients with a history of AF) with a known history of binge drinking. A binge drinking session was defined as >5 standard alcoholic drinks on a single occasion with the aim of becoming intoxicated. AF patients were required to be in stable sinus rhythm at study commencement without any symptomatic AF episodes in the preceding month. Exclusion criteria included: alcoholic binge

Results

Fifty participants completed the study, consisting of 38 (74%) males with mean age 49 ± 15 years and 20 (40%) with a history of paroxysmal atrial fibrillation. Of the 20 patients with prior AF, 5 (25%) were on sotalol, 3 (15%) were on flecainide and 1 (5%) was on amiodarone. Mean alcohol intake was 8.4 ± 3.1 drinks over the drinking session, with average time from first to last drink of 3.8 ± 1.6 h. Full baseline characteristics and alcohol consumption as part of the study are shown in Table 1.

Discussion

Alcohol intoxication is reported to be responsible for over a third of new-onset emergency presentations with AF [3]. In those with a history of AF, alcohol is the most common trigger reported by 35% of patients. The timeframe during which such arrhythmias have been reported following a binge has not been extensively studied. Earlier studies reported a peak in presentations on a Monday (rather than the weekend). A study of participants during Octoberfest [8] representing the period during the

Conclusion

Binge drinking is associated with changes in autonomic function with initial sympathetic activation followed by a rebound parasympathetic dominance. Acute atrial mechanical dysfunction was demonstrated on cardiac MRI. Alterations in autonomic and mechanical function may in part explain the propensity and temporal association between binge drinking and atrial fibrillation.

Funding sources/conflicts of interest

Dr. Voskoboinik is supported by a National Heart Foundation of Australia Early Career Fellowship. Prof Kalman is supported by a NHMRC practitioner fellowship.

Relationship(s) with industry

Nil.

References (23)

R.W. Hingson et al.
Drinking beyond the binge threshold: predictors, consequences, and changes in the U.S
Am. J. Prev. Med.
(2017)
C.A. Groh et al.
Patient-reported triggers of paroxysmal atrial fibrillation
Heart Rhythm.
(2019)
P.O. Ettinger et al.
Arrhythmias and the “holiday heart”: alcohol-associated cardiac rhythm disorders
Am. Heart J.
(1978)
A. Voskoboinik et al.
Alcohol and atrial fibrillation: a sobering review
J. Am. Coll. Cardiol.
(2016)
F.T. Nishimura et al.
Effects of aldehyde dehydrogenase-2 genotype on cardiovascular and endocrine responses to alcohol in young Japanese subjects
Auton. Neurosci.
(2002)
T. Maki et al.
Effect of ethanol drinking, hangover, and exercise on adrenergic activity and heart rate variability in patients with a history of alcohol-induced atrial fibrillation
Am. J. Cardiol.
(1998)
R.M. Carney et al.
Heart rate variability and markers of inflammation and coagulation in depressed patients with coronary heart disease
J. Psychosom. Res.
(2007)
A. Gallardo-Carpentier et al.
Arrhythmogenic and antiarrhythmic actions of substances of abuse: effects on triggered activity
J. Electrocardiol.
(1997)
S.R. Lowenstein et al.
The role of alcohol in new-onset atrial fibrillation
Arch. Intern. Med.
(1983)
A. Voskoboinik et al.
Alcohol abstinence in drinkers with atrial fibrillation
N. Engl. J. Med.
(2020)

A. Zagrosek et al.

Effect of binge drinking on the heart as assessed by cardiac magnetic resonance imaging

JAMA

(2010)

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Co-consumption of caffeine and binge drinking synergistically promote spontaneous ventricular tachyarrhythmias in rats. Dantrolene treatment can decrease alcohol-enhanced Ca²⁺ sparks in vitro and prevented alcohol and caffeine induced ventricular tachyarrhythmias in vivo.
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Epidemiological evidence has revealed a complex, often paradoxical association between alcohol consumption and cardiovascular diseases including atrial fibrillation, ischemic heart disease, stroke, hypertension, cardiomyopathy, and heart failure [1–4]. Binge drinking contributes to unfavorable pathological impact on the cardiovascular system including disturbed cardiovagal tone and baroreflex, sympathetic activation followed by a “rebound” parasympathetic response, altered myofibrillary architecture, atrial and ventricular mechanical function [5,6]. Nonetheless, inconsistent findings were also reported such that the Norwegian health survey did not find a major contribution from frequent binge drinking in the risk of incident ischemia heart diseases or stroke events [7].
Binge drinking leads to compromised mitochondrial integrity and contractile function in the heart although little effective remedy is readily available. Given the possible derangement of autophagy in ethanol-induced cardiac anomalies, this study was designed to examine involvement of Beclin1 in acute ethanol-induced cardiac contractile dysfunction, in any, and the impact of Beclin1 haploinsufficiency on ethanol cardiotoxicity with a focus on autophagy-related ferroptosis.
WT and Beclin1 haploinsufficiency (BECN^+/−) mice were challenged with ethanol for one week (2 g/kg, i.p. on day 1, 3 and 7) prior to assessment of cardiac injury markers (LDH, CK-MB), cardiac geometry, contractile and mitochondrial integrity, oxidative stress, lipid peroxidation, apoptosis and ferroptosis.
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Citation Excerpt :
Moreover, AF itself may be triggered by simultaneous discharge of both sympathetic and parasympathetic nervous system.86 Voskoboinik et al.,87 Weise et al.,88 and Brunner et al.89 demonstrated a complex autonomic response to alcohol consumption. Whereas the consumption phase as such was associated with an increase in sympathetic activity, demonstrated in a decrease in heart rate variability (HRV), the hangover period was marked by a rebound phase.
Excessive drinking has detrimental effects on the cardiovascular system. Atrial fibrillation (AF) after alcohol binge drinking, also named “holiday heart syndrome,” is well established. However, chronic lower levels of alcohol intake also may increase AF risk. In this review, we aim to provide a comprehensive overview of the epidemiology and pathophysiology by which alcohol may be responsible for AF and discuss whether alcohol abstinence is required for optimal rhythm control as well as to maintain sinus rhythm in patients with AF. The pathophysiologic mechanisms responsible for the relationship between alcohol consumption and AF may include both direct and chronic effects increasing AF burden. Acute effects may include arrhythmogenic changes (such as shortening in atrial refractoriness, slowing in conduction velocity, and increased atrial ectopy) and an autonomic imbalance. Chronic changes contributing to the development of an arrhythmogenic substrate involve atrial structural and functional remodelling processes due to atrial dilation, elevated pressures, and fibrosis formation. In addition, alcohol consumption contributes to developing concomitant AF risk factors such as obesity, sleep-disordered breathing, and hypertension. Alcohol abstinence is associated with a reduction in AF recurrence and overall burden and moreover improves AF risk factor development such as obesity, hypertension, sleep apnea, and AF-related consequences such as stroke. In conclusion, alcohol consumption is associated with atrial arrhythmia and a wide range of cardiovascular comorbidities. Although further evidence is needed, current knowledge indicates that there might not be a safe level of alcohol consumption that does not increase AF risk.
L'excès d'alcool a des effets néfastes sur le système cardiovasculaire. Une fibrillation auriculaire (FA) succédant à une consommation excessive d'alcool, également appelée "syndrome du cœur en vacances", est un phénomène bien établi. Cependant, une consommation chronique d'alcool à des niveaux plus faibles peut également augmenter le risque de FA. Dans cette revue de littérature, nous visons à fournir un aperçu complet de l'épidémiologie et de la pathophysiologie par lesquelles l'alcool peut être responsable de la FA et à discuter si une abstinence d'alcool s'avère nécessaire pour un contrôle optimal du rythme ainsi que pour maintenir un rythme sinusal chez les patients souffrant de FA. Les mécanismes pathophysiologiques responsables de la relation entre consommation d'alcool et FA peuvent inclure des effets directs et chroniques, augmentant le fardeau que constitue la FA. Les effets aigus peuvent inclure des perturbations arythmogènes (telles que le raccourcissement de la période réfractaire au niveau auriculaire, un ralentissement de la vitesse de conduction, et une augmentation d'évènements auriculaires ectopiques) et un déséquilibre du système nerveux autonome. Les changements chroniques contribuant au développement d'un substrat arythmogène impliquent des processus de remodelages structurel et fonctionnel de l'oreillette dus à la dilatation de l'oreillette, aux pressions élevées, et à la formation de fibrose. En outre, la consommation d'alcool contribue à l'apparition de facteurs de risque de FA concomitants tels que l'obésité, les troubles respiratoires du sommeil et l'hypertension. L'abstinence d'alcool est associée à une réduction de la récurrence de la FA et du fardeau qu'elle représente globalement, et elle améliore de surcroît la régulation de facteurs de risque de FA tels que l'obésité, l'hypertension, l'apnée du sommeil et des conséquences liées à la FA telles que l'accident vasculaire cérébral. En conclusion, la consommation d'alcool est associée à l'occurence d'arythmies auriculaires et à un large éventail de comorbidités cardiovasculaires. Bien que des preuves supplémentaires soient nécessaires, les connaissances actuelles indiquent qu'il n'existe peut-être pas de niveau de consommation d'alcool sans danger qui n'augmente pas le risque de FA.

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Acute electrical, autonomic and structural effects of binge drinking: Insights into the ‘holiday heart syndrome’

Highlights

Abstract

Background

Objective

Methods

Results

Conclusion

Introduction

Section snippets

Study design

Results

Discussion

Conclusion

Funding sources/conflicts of interest

Relationship(s) with industry

Am. J. Prev. Med.

Heart Rhythm.

Am. Heart J.

J. Am. Coll. Cardiol.

Auton. Neurosci.

Am. J. Cardiol.

J. Psychosom. Res.

J. Electrocardiol.

The role of alcohol in new-onset atrial fibrillation

Arch. Intern. Med.

Alcohol abstinence in drinkers with atrial fibrillation

N. Engl. J. Med.

Effect of binge drinking on the heart as assessed by cardiac magnetic resonance imaging

JAMA