Acute excessive alcohol intake may cause the holiday heart syndrome, characterized by cardiac arrhythmias including atrial fibrillation. Since underlying data are scarce, the study aimed to prospectively investigate the temporal course of occurring cardiac arrhythmias following binge drinking in young adults.

A total of 202 volunteers planning acute alcohol consumption with expected peak breath alcohol concentrations (BACs) of ≥1.2 g/kg were enrolled. The study comprised 48 h electrocardiogram monitoring covering baseline (Hour 0), 'drinking period' (Hours 1-5), 'recovery period' (Hours 6-19), and two control periods corresponding to 24 h after the 'drinking' and 'recovery periods', respectively. Acute alcohol intake was monitored by BAC measurements during the 'drinking period'. Electrocardiograms were analysed for mean heart rate, atrial tachycardia, premature atrial complexes, premature ventricular complexes (PVCs), and heart rate variability measures.

Data revealed an increase in heart rate and an excess of atrial tachycardias with increasing alcohol intake. Heart rate variability analysis indicated an autonomic modulation with sympathetic activation during alcohol consumption and the subsequent 'recovery period', followed by parasympathetic predominance thereafter. Premature atrial complexes occurred significantly more frequently in the 'control periods', whereas PVCs were more frequent in the 'drinking period'. Ten participants experienced notable arrhythmic episodes, including atrial fibrillation and ventricular tachycardias, primarily during the 'recovery period'.

The study demonstrates the impact of binge drinking on heart rate alterations and increased atrial tachycardias during 'drinking period', and the occurrence of clinically relevant arrhythmias during the 'recovery period', emphasizing the holiday heart syndrome as a health concern.

Atrial fibrillation (AF), with its significant associated morbidity and mortality contributes to significant healthcare utilisation and expenditure. Given its progressively rising incidence, strategies to limit AF development and progression are urgently needed. Lifestyle modification is a potentially potent but underutilised weapon against the AF epidemic. The purpose of this article is to review the role of lifestyle factors as risk factors for AF, outline potential mechanisms of pathogenesis and examine the available evidence for lifestyle intervention in primary and secondary AF prevention. It will also highlight the need for investment by physicians, researchers, health services and governments in order to facilitate delivery of the comprehensive, multidisciplinary AF care that is required to manage this complex and multifactorial disease.

Atrial fibrillation (AF) is the most common cardiac arrhythmia responsible for significant morbidity and mortality. Its burden on patients and the health care system is only expected to increase. Several studies have established a dose-response relationship between the amount and frequency of alcohol consumption and the incidence of new onset AF independent of sex, age, and other risk factors. This causal relationship is mediated by the impact alcohol consumption has on conduction properties of the atrium, structural and cellular effect on cardiac myocytes, and dysregulation of the autonomic nervous system. This article reviews the current literature supporting the link between alcohol consumption and AF while attempting to provide an insight into pathophysiological mechanisms.

The association between alcohol consumption and abnormalities of heart rate and rhythm has long been recognized. Significant attention has focused on the risk of atrial fibrillation (AF) and sudden cardiac death (SCD) with excessive alcohol intake. Recent studies have advanced our understanding of these relationships and provided additional insights into potentially arrhythmogenic mechanisms. However, considerable uncertainty remains, such as the level of consumption at which harm begins and whether alcohol plays a role in other arrhythmias. This review characterizes the spectrum of conduction abnormalities and heart rhythm disorders in relation to alcohol consumption. In addition, it discusses the latest epidemiologic and experimental evidence, the potential importance of beverage type and constituent ingredients, and conflicting information on drink definitions, thresholds, and recommendations.

Tobacco smoking and alcohol consumption are widespread exposures that are legal and socially accepted in many societies. Both have been widely recognized as important risk factors for diseases in all vital organ systems including cardiovascular diseases, and with clinical manifestations that are associated with atrial dysfunction, so-called atrial cardiomyopathy, especially atrial fibrillation and stroke. The pathogenesis of atrial cardiomyopathy, atrial fibrillation, and stroke in context with smoking and alcohol consumption is complex and multifactorial, involving pathophysiological mechanisms, environmental, and societal aspects. This narrative review summarizes the current literature regarding alterations in the atrial myocardium that is associated with smoking and alcohol.

To evaluate (1) the impact of acute and habitual alcohol consumption on atrial fibrillation (AF) and atrial remodeling and (2) the role of alcohol reduction and/or abstinence in the primary and secondary prevention of AF.

Acute alcohol consumption appears to be a common AF trigger, with animal and human studies demonstrating changes in electrophysiological parameters, autonomic tone, and cellular properties expected to promote AF. Habitual consumption is associated with adverse atrial remodeling, higher risk of incident AF, and AF recurrence. Randomized data suggest that reduction in excessive alcohol consumption may reduce the risk of recurrent AF episodes and AF burden. Alcohol is an increasingly recognized risk factor for both new onset AF and discrete AF episodes. Excessive consumption should be avoided for primary and secondary prevention of AF.

This article summarizes recent experimental and epidemiological data on the toxic and beneficial effects of ethanol and its metabolites (acetaldehyde), and focuses on their immunomodulatory effects. The section dealing with the toxic effects of alcohol focuses on its chronic toxicity (liver disorders, carcinogenic effects, cardiovascular disorders, neuropsychic disorders, addiction and withdrawal syndrome, hematologic disorders, reprotoxicity, osteoporosis) although acute toxicity is considered. The role of oxidative metabolism of ethanol by alcohol dehydrogenase, cytochrome P450 2E1, and aldehyde dehydrogenase, as well as the impact of genetic polymorphism in its physiopathology are also highlighted. The section dealing with the beneficial effects of low to moderate alcohol consumption (on cardiovascular system, diabetes, the nervous system and sensory organs, autoimmune diseases, and rheumatology) highlights the importance of anti-inflammatory and immunomodulatory effects in these observations. This knowledge, enriched by a focus on the immunomodulatory effects of ethanol and its metabolites, in particular on the NLRP3 inflammasome pathway, might facilitate the development of treatments that can reduce ethanol's harmful effects or accentuate its beneficial effects.

Alcohol is one of the most commonly abused substances in the United States. Chronic consumption of ethanol has been responsible for numerous chronic diseases and conditions globally. The underlying mechanism of liver injury has been studied in depth, however, far fewer studies have examined other organs especially the heart and the central nervous system (CNS). The authors conducted a narrative review on the relationship of alcohol with heart disease and dementia. With that in mind, a complex relationship between inflammation and cardiovascular disease and dementia has been long proposed but inflammatory biomarkers have gained more attention lately. In this review we examine some of the consequences of the altered cytokine regulation that occurs in alcoholics in organs other than the liver. The article reviews the potential role of inflammatory markers such as TNF-α in predicting dementia and/or cardiovascular disease. It was found that TNF-α could promote and accelerate local inflammation and damage through autocrine/paracrine mechanisms. Unraveling the mechanisms linking chronic alcohol consumption with proinflammatory cytokine production and subsequent inflammatory signaling pathways activation in the heart and CNS, is essential to improve our understanding of the disease and hopefully facilitate the development of new remedies.

Alcoholic beverages have been consumed for thousands of years, attracting great human interest for social, personal, and religious occasions. In addition, they have long been debated to confer cardioprotective benefits. The French Paradox is an observation of a low prevalence of ischemic heart disease, with high intakes of saturated fat, a phenomenon accredited to the consumption of red wine. Although many epidemiological investigations have supported this view, others have attributed it to beer or spirits, with many suggesting that the drink type is not important. Although excessive consumption of alcoholic beverages is commonly regarded to be detrimental to cardiovascular health, there is a debate as to whether light-to-moderate intake is cardioprotective. Although there is extensive epidemiological support for this drinking pattern, a consensus has not been reached. On the basis of published work, we describe the composition of wine and the effects of constituent polyphenols on chronic cardiovascular diseases.

Most young patients with mild-to-moderate aortic stenosis show no symptoms, and sudden death appears only occasionally. We hypothesised that malignant ventricular arrhythmias could be responsible for the high incidence of sudden death in such patients. If multiple factors such as asymptomatic aortic stenosis in association with arrhythmia-provoking agents are involved, could it be sufficient to account for sudden unexpected death? In this study, eight cases of sudden death in young adults, with ages ranging from 22 to 36 years, who had never reported any symptoms that could be related to aortic stenosis, were investigated. Full autopsies were performed, and congenital aortic stenosis in all eight cases was confirmed. DNA testing for channelopathies was negative. Comprehensive toxicological analyses found an electrolyte imbalance, or non-toxic concentrations of amitriptyline, terfenadine, caffeine, and ethanol. Collectively, these results suggest that congenital asymptomatic aortic stenosis without cardiac hypertrophy in young adults is not sufficient to cause sudden death merely on its own; rather, an additional provoking factor is necessary. According to our findings, the provoking factor may be a state of physical or emotional stress, a state of electrolyte imbalance, or even taking a therapeutic dose of a particular drug.

Alcohol is popular in Western culture, supported by a perception that modest intake is cardioprotective. However, excessive drinking has detrimental implications for cardiovascular disease. Atrial fibrillation (AF) following an alcohol binge or the "holiday heart syndrome" is well characterized. However, more modest levels of alcohol intake on a regular basis may also increase the risk of AF. The pathophysiological mechanisms responsible for the relationship between alcohol and AF may include direct toxicity and alcohol's contribution to obesity, sleep-disordered breathing, and hypertension. We aim to provide a comprehensive review of the epidemiology and pathophysiology by which alcohol may be responsible for AF and determine whether alcohol abstinence is required for patients with AF.

Although several studies have reported an association between atrial fibrillation (AF) and alcohol, the impact of alcohol consumption on the outcome after catheter ablation (CA) for AF has not been discussed. We aimed to elucidate the effect of alcohol consumption on the outcome of CA for paroxysmal AF.

We examined 1361 consecutive patients with paroxysmal AF (mean age, 61±11 years, 334 women) who underwent CA, including 623 (45.8%) patients who consumed alcohol. The clinical characteristics and outcomes of CA were compared between patients who did and did not consume alcohol. No significant differences were seen in the left atrial size, duration of AF history, and incidence of nonpulmonary vein foci between 2 groups (P=NS). Although the AF recurrence-free rate after the initial CA was higher in patients who did not consume alcohol (261/623 [41.9%] versus 252/738 [34.1%]; mean follow-up, 44.4±30.7 months; P=0.003), the outcome after the final CA was similar between 2 groups (patients who consumed alcohol: 111/628 [17.7%] versus patients who did not consume alcohol: 138/738 [18.7%]; mean follow-up, 53.1±25.8 months; P=0.67). The frequency (hazard ratio 1.07 per 1 day/week increase, CI 1.00-1.15, P=0.04) of alcohol consumption was significantly associated with AF recurrence after CA.

The frequency of alcohol consumption may be associated with AF recurrence after the initial CA for paroxysmal AF, but it may not affect the outcome after the final CA.

The effect of alcohol consumption on substrate remodeling and ablation outcome of paroxysmal atrial fibrillation (PAF) remains unknown.

We performed circumferential pulmonary vein isolation (CPVI) and voltage mapping of left atrium (LA) during sinus rhythm in 122 consecutive patients with symptomatic PAF (age, 55.4±9.4 years; 73.8% men). Low-voltage zones (LVZs) were semiquantitatively estimated and presented as low-voltage index (LVI). Each patient's daily alcohol consumption history was recorded at baseline and classified into alcohol abstainers, moderate drinkers, and heavy drinkers based on the National Institute on Alcohol Abuse and Alcoholism definition. Follow-up was ≥12 months for AF recurrence. Alcohol abstainers and moderate and heavy drinkers were 70 (57.4%), 13 (10.6%), and 39 (32.0%), respectively. In total, LVZs were observed in 44 patients (36.1%). Daily alcohol consumption independently predicted presence of LVZs (odds ratio [OR], 1.097; 95% confidence interval [CI], 1.001-1.203; P=0.047). During mean follow-up of 20.9±5.9 months, 40 patients (35.1%) experienced AF recurrence. Success rate was 81.3%, 69.2%, and 35.1% in alcohol abstainers, moderate drinkers, and heavy drinkers, respectively (overall log rank, P<0.001). Multivariate analysis showed that both alcohol consumption and LVI were independent predictors of AF recurrence (hazard ratio [HR], 1.579; 95% CI, 1.085-2.298; P=0.017; HR, 2.188; 95% CI, 1.582-3.026; P<0.001, respectively). Furthermore, mediation analysis revealed that LVZs acted as a partial mediator in effect of alcohol consumption on AF ablation outcomes.

Daily alcohol consumption was associated with atrial remodelling, and heavy drinkers have substantial risk for AF recurrence after CPVI.

Epidemiological data are limited regarding risk factors of atrial fibrillation (AF) in patients with normal-sized left atria (LA). We evaluated whether traditional risk factors of AF differ between patients with normal-sized and dilated LA. This is a cross sectional study of community-dwelling participants of the Atherosclerosis Risk in Communities study. LA volume index was measured by 2-dimensional echocardiography. LA volume index ≥29 mm(3)/m(2) defined dilated LA. Prevalent AF was defined by electrocardiogram and hospital discharge International Classification of Diseases-9 codes. Multivariate adjusted logistic regression analysis was used to examine whether magnitude of association of risk factors with AF differ by LA cavity size. Interaction of risk factors by LA cavity size was evaluated to determine significance of these differential associations. Of 5,496 participants (mean age 75 ± 5 years, women 58%), 1,230 participants (22%) had dilated LA. The prevalence of AF was 11% in patients with normal-sized LA and 15% in patients with dilated LA. Age >75 years (odds ratio [OR] 1.87, 95% confidence interval [CI] 1.49 to 2.35, interaction p = 0.12) and heart failure (OR 5.43, 95% CI 3.77 to 7.87, interaction p = 0.10) were stronger risk factors for AF in normal-sized LA than dilated LA. Female gender (OR 1.67, 95% CI 1.01 to 2.77, interaction p = 0.09), weight (OR 1.32, 95% CI 1.02 to 1.71, interaction p = 0.19), and alcohol use (OR 1.61, 95% CI 1.08 to 2.41, interaction p = 0.004) were stronger risk factors for AF in patients with dilated LA than normal-sized LA. In conclusion, risk factors of AF may differ by left ventricular cavity size.

The measures of nonlinear properties of RR interval and QT interval time series are sensitive to physiologically- or pathologically-induced complexity/regularity changes, but were not used to estimate the effect of alcohol intake. We wanted to examine the potential of these measures to quantify the acute effect of a low dose of red wine in healthy subjects. In separate experiments, fourteen young volunteers drank 200ml of red wine and a control drink with equal concentration of ethanol. ECG in supine position was recorded 20min before and 60min after drink intake. RR interval and QT interval series were extracted from ECG and we calculated variability, scaling exponents (α1 and α2) and sample entropy (SampEn) for both series. Systolic and diastolic blood pressures (BP) were measured every 10min. The immediate effect of both the drinks was equal: HR, BP and QT variability exhibited a sudden increase and then a decrease. However, the prolonged effect of wine and the control drink was different. Wine decreased both BP (p<0.05) and reduced complexity of RR and QT series (increased scaling exponents and decreased SampEn). The control drink prolonged QT and RR intervals (p<0.05). These results point out that the nonlinear properties of RR and QT interval series could be used to differentiate the effect of wine and ethanol. Changes in RR and QT interval series induced by a low dose of red wine are more detectable by methods that quantify the structure of the series than by methods that quantify their variability.

Atrial fibrillation (AF), the most common sustained cardiac arrhythmia encountered in clinical practice, is associated with increased morbidity and mortality. Electrophysiologically, it is characterized by a high rate of asynchronous atrial cell depolarization causing a loss of atrial contractile function and irregular ventricular rates. For a long time, AF was considered as a pure functional disorder without any structural background. Only in recent years, have new mapping and imaging techniques identified atrial locations, which are very often involved in the initiation and maintenance of this supraventricular arrhythmia (i.e. the distal portion of the pulmonary veins and the surrounding atrial myocardium). Morphological analysis of these myocardial sites has demonstrated significant structural remodeling as well as paved the way for further knowledge of AF natural history, pathogenesis, and treatment. This architectural myocardial disarrangement is induced by the arrhythmia itself and the very frequently associated cardiovascular disorders. At the same time, the structural remodeling is also capable of sustaining AF, thereby creating a sort of pathogenetic vicious circle. This review focuses on current understanding about the structural and genetic bases of AF with reference to their classification, pathogenesis, and clinical implications.

The risk of acute heavy alcohol intake on the development of atrial fibrillation (AF), aka ?holiday heart syndrome?, has been well-described. However, whether chronic alcohol intake is also associated with increased risk of AF, or might even be protective as has been observed with other cardiac conditions, is more uncertain. A number of studies, from basic science to large cohort studies have been performed to analyze the association between alcohol and AF. Basic-level studies have found that alcohol causes changes in tissue electrophysiology, ion channels, and circulating hormones, which might promote development and maintenance of AF. Clinical studies have generally shown groups with the highest regular intake of alcohol to be at increased risk, with no association with more moderate use. However, these studies have not always accounted for other AF risk factors, been inconsistent in the assessment and validation of the quantity of alcohol consumed across populations, and been unable to completely separate drinking patterns from overall health of participants. As a result, solid conclusions about a threshold level for ?safe? chronic alcohol intake cannot be made with regard to AF risk, but it appears to be safe within currently recommended limits of 1 drink daily for women and 2 for men. In this review, we discuss these findings, limitations, and conclusions.

The purpose of this meta-analysis is to summarize the estimated risk of atrial fibrillation (AF) related to alcohol consumption.

Results from observational studies examining the relationship between alcohol consumption and AF are inconsistent.

A systematic electronic search of Medline (January 1966 to December 2009) and Embase (January 1974 to December 2009) databases was conducted for studies using key words related to alcohol and AF. Studies were included if data on effect measures for AF associated with habitual alcohol intake were reported or could be calculated. The effect measures for AF for the highest versus lowest alcohol intake in individual studies were pooled with a variance-based method. Linear and spline regression analyses were conducted to quantify the relationship between alcohol intake and AF risk.

Fourteen eligible studies were included in this meta-analysis. The pooled estimate of AF for the highest versus the lowest alcohol intake was 1.51 (95% confidence interval: 1.31 to 1.74). A linear regression model showed that the pooled estimate for an increment of 10 g per day alcohol intake was 1.08 (95% confidence interval: 1.05 to 1.10; R(2) = 0.43, p < 0.001). A spline regression model also indicated that the AF risk increased with increasing levels of alcohol consumption.

Results of this meta-analysis suggest that not consuming alcohol is most favorable in terms of AF risk reduction.

To assess how ethanol in potential lethal serum concentrations affects features of the ECG that may be associated with cardiac arrhythmias.

We included 84 patients, who were hospitalised with assumed acute ethanol intoxication. In the emergency room resting ECG was recorded and blood was collected for serum osmolality measurement used as a proxy for ethanol level. Thirty-two also had ECG recorded at discharge. Twenty-seven hospitalised patients without known alcohol ingestion served as controls. ECG segment durations were compared with controls and related to intoxication level.

In subjects with moderately elevated to high serum osmolality, the P wave and QTc intervals were prolonged compared with sober subjects. P wave, PR, QRS and QTc intervals were longer when the subjects had high blood ethanol levels (at admission) than at discharge (p-values: 0.0001, 0.0002, 0.010 and <0.0001 for P wave, PR, QRS and QTc intervals. n=32).

Ethanol at high to very high blood concentration causes several changes in the ECG that might be associated with increased risk of arrhythmias.

Alcohol is the most consumed drug worldwide. Both acute and chronic alcohol use have been associated with cardiac arrhythmias, in particular atrial fibrillation, or so-called 'holiday heart syndrome'. Epidemiological, clinical and experimental studies have attempted to elucidate the mechanisms involved in this association. However, because most of these studies have shown conflicting results, the connection between ethanol and atrial arrhythmias remains controversial. Historical, epidemiological and pharmacological aspects of alcohol, as well as recent concepts on atrial fibrillation are reviewed. We then examine the literature and provide a critical point of view on the still elusive association between alcohol and atrial fibrillation.

Alcohol has been related to atrial fibrillation (holiday heart syndrome), but its electrophysiologic actions remain unclear.

We evaluated the effects of alcohol in 23 anesthetized dogs at baseline and after 2 cumulative intravenous doses of ethanol: first dose 1.5 ml/kg (plasma level 200 mg/dl); second dose 1.0 ml/kg (279 mg/dl). In 13 closed-chest dogs (5 with intact autonomic nervous system, 5 under combined autonomic blockade and 3 sham controls), electrophysiologic evaluation and monophasic action potential (MAP) recordings were undertaken in the right atrium and ventricle. In 5 additional dogs, open-chest biatrial epicardial mapping with 8 bipoles on Bachmann's bundle was undertaken. In the remaining 5 dogs, 2D echocardiograms and ultrastructural analysis were performed.

In closed-chest dogs with intact autonomic nervous system, ethanol had no effects on surface electrocardiogram and intracardiac variables. At a cycle length of 300 milliseconds, no effects were noted on atrial and ventricular refractoriness and on the right atrial MAP. These results were not altered by autonomic blockade. No changes occurred in sham controls. In open-chest dogs, ethanol did not affect inter-atrial conduction time, conduction velocity, and wavelength. Atrial arrhythmias were not induced in any dog, either at baseline or after ethanol. Histological and ultrastructural findings were normal but left ventricular (LV) ejection fraction decreased in treated dogs (77 vs. 73 vs. 66%; p = 0.04).

Ethanol at medium and high doses depresses LV systolic function but has no effects on atrial electrophysiological parameters. These findings suggest that acute alcoholic intoxication does not directly promote atrial arrhythmias.

Magnetocardiography (MCG) is a method complementary to electrocardiography (ECG). We examined recording and reproducibility of atrial depolarization signal by MCG. Multichannel MCG over anterior chest and orthogonal 3-lead ECG were recorded in 9 patients who had paroxysmal lone atrial fibrillation and in 10 healthy subjects in duplicate at least 1 week apart. Data were averaged using atrial wave template and high-pass filtered at 25, 40, and 60 Hz. Atrial signal duration with automatic detection of onset and offset and root mean square amplitudes of the last portion of atrial signal were determined. Coefficient of variation of atrial signal duration by MCG at 40 Hz was 3.3% and difference between the measurements was 3.5 milliseconds on average. The corresponding figures obtained by signal-averaged ECG (SAECG) were 6.1% and 6.9 milliseconds. Coefficient of variation for root mean square of the last 40 milliseconds of atrial signal were 16% in MCG and 17% in SAECG. Reproducibility was best at 40-Hz filter and similar in patients and healthy subjects. In conclusion, the reproducibility of atrial signal variables in MCG is adequate and somewhat better than in SAECG and equal in patients with lone atrial fibrillation and healthy subjects. Magnetocardiography seems to be a potentially valuable method to evaluate features of atrial depolarization in patient studies.

An alcohol-naive 16-year-old male is presented with alcohol-induced atrial fibrillation. Past medical history, review of systems, and presentation were all otherwise benign. Atrial fibrillation occurred early in the intoxication at an alcohol level slightly higher than the legal limit for intoxication (153 mg/dL). His complete cardiac evaluation was otherwise normal. The atrial fibrillation was not treated aggressively and resolved as the alcohol level quickly fell to zero, consistent with his "nonalcoholic" metabolism. Complete follow-up found the adolescent with no evidence of cardiac or other disease.

We examined the cardiac conduction system of three alcohol abusers who died suddenly. Cases 1 and 2 showed mitral valve disorder (mitral valve prolapse and rheumatic valvular disease), while Case 3 showed mild Ebstein's anomaly. On examination of the conduction system, Cases 1 and 2 showed severe fibrofatty infiltration into the conduction system, and we conclude that these findings were probably a complication of alcohol abuse. Both cases also demonstrated severe small artery disease. The conduction system of Case 3 showed an anomalous location of the bundle of His with its fragmentation. These three cases suggest that such considerable conduction system abnormalities may be significant findings in alcohol abusers with valvular disease. We consider that alcohol intake may be one of the direct accelerating factors for arrhythmogenic potential to the abnormal conduction system in alcohol abusers who have asymptomatic valvular disease.