Cardiovascular diseases are the leading cause of mortality in modern society. According to WHO, they are responsible for approximately 17.9 million deaths annually (1).

The treatment of alcohol-related illnesses also puts a significant burden on the healthcare system. Among psychoactive substances, ethyl-alcohol is one of the most addictive agents, both physically and psychologically (2). Alcohol consumption data shows that annual intake is continuously increasing due to its easy accessibility and the pleasant feeling experienced after consumption, while the harmful effects appear later (3). According to WHO data, alcohol intake contributes to 3 million deaths annually (4). In 2019, an average adult in Hungary consumed 10.8 liters of alcohol per year (5). Alcohol can also have harmful effects on the heart, contributing to the development of various cardiovascular diseases and arrhythmias.

Alcoholic dilated cardiomyopathy (ACM) is the most common form of alcohol-induced heart damage, which can lead to congestive heart failure and various clinically significant arrhythmias (3). Ethanol-induced toxic cardiomyopathy accounts for about one-third of non-ischemic dilated cardiomyopathies (6).

In terms of pathomechanism, ethanol reduces myocardial contractility through its direct toxic effects, which can subsequently lead to cardiac remodeling and ventricular dilatation. At the cellular level, it causes myocytolysis, apoptosis, and myocyte necrosis, while repair mechanisms working against the damage lead to hypertrophy and interstitial fibrosis. Targets of ethanol-induced impairment include cell membranes, receptors, ion channels, structural proteins, mitochondria, ribosomes, DNA, the cytoskeleton, and disruption of sarcomeric contractility (3, 7).

Literature suggests that ethanol-induced cardiomyopathy develops in a dose-dependent manner, significantly influenced by individual risk factors such as gender, ethnicity, comorbidities, genetic factors, and the use of other substances (8). Regarding gender differences, different alcohol metabolism characteristics and pathophysiological mechanisms were observed in women, resulting in increased sensitivity to alcohol-induced damage. Studies indicate that women develop ACM by consuming lower doses of alcohol compared to men (9, 10).

Alcohol consumption can be categorized into three groups based on quantity, with 1 standard drink defined as 12 g of alcohol in American studies:

The dose-dependent effect of ethyl alcohol was discovered in the latter half of the 20th century, revealing that long-term high-dose alcohol consumption is associated with the development of ACM (7). Generally, the risk of evolving asymptomatic ACM increases significantly when consuming more than 90 g of alcohol (7-8 standard drinks, 1 standard drink: 12-15 g alcohol) daily over more than 5 years (12). Moderate-dose alcohol consumption is associated with ACM development after more than 10 years of regular drinking (7). Low-dose alcohol consumption accumulates its effects over time, thereby increasing the likelihood of developing ACM (13). Malignant arrhythmias triggered by heart failure can lead to increased mortality rate. In the case of ACM, complete abstinence offers the possibility of recovery; however, for those who continue high-dose alcohol consumption, the mortality rate can reach up to 10% (3, 7, 14).

Atrial fibrillation (AF) or atrial flutter is the most common symptomatic arrhythmia worldwide. Alcohol consumption can contribute to its development. „Binge drinking” refers to consuming a large amount of alcohol within a short period of time, which is defined by the National Institute on Alcohol Abuse and Alcoholism (NIAAA) in 2004 as consuming >5 standard drinks for men and >4 standard drinks for women within 2 hours, reaching a blood alcohol level exceeding 80 mg/dl (15). „Binge drinking” is an independent risk factor for arrhythmias – most commonly AF and atrial flutter - contributing to the development of „Holiday Heart Syndrome” (11). „Holiday Heart Syndrome” was first described in 1978 by Ettinger and colleagues, who observed various arrhythmias, predominantly AF, in 24 individuals after drinking a large amount of alcohol over a weekend (16). Although AF resulting from „binge drinking” often terminates within 24 hours (Figure 1), Krishnamoorthy et al found that 26% of their patients experienced recurrent AF episodes within one year after repeated alcohol intake (17).

Long time alcohol exposure can cause atrial remodeling, but even occasional consumption can act as a trigger for the onset of AF or atrial flutter. At the cellular level, ethanol, or its metabolite acetaldehyde, has direct toxic effects on myocytes, causing damage to ion channels, electrolyte disturbances, and potentially leading to acute oxidative stress. Alcohol’s autonomic effects include activation of the sympathetic nervous system, reduction in heart rate variability, and inhibition of the vagus nerve. In some cases, parasympathetic activation has been reported to cause newly developed AF as well. The resulting electrophysiological changes create a favorable environment for various arrhythmias (11, 18).

Yan et al shows that alcohol activates c-Jun NH(2)-terminal kinase 2 (JNK2) in cardiomyocytes, which phosphorylates calcium/calmodulin-dependent protein kinase II (CaMKII), increasing its intracellular activity. CaMKII affects the binding of Ca2+ to the sarcoplasmic reticulum, causing pathological Ca2+ leakage, which has a proarrhythmic effect (19).

In addition to its direct effects, regular alcohol consumption is a risk factor for hypertension, left ventricular dysfunction, obesity, and obstructive sleep apnea, which indirectly increase the frequency of AF or atrial flutter (18, 20).

A positive association between the development of AF and alcohol consumption has been observed, regardless of the type of alcohol, regularity of consumption, or gender. Even small amounts of alcohol (2 g/day) significantly increased the likelihood of developing AF, with a non-linear relationship to the amount of alcohol consumed (21). Regarding the type of alcohol, individuals consuming beer or spirits were more likely to experience AF compared to those consuming wine, but the difference was not significant (22).

Since even small amounts of alcohol increase the likelihood of arrhythmias, abstinence or at least reducing the amount of alcohol is substantial for both preventing AF and managing existing arrhythmias (21).

In patients who have undergone pulmonary vein isolation, those who continued to drink alcohol regularly after the procedure had a significantly increased chance of arrhythmia recurrence (23, 24).

There is limited literature on the connection between alcohol and malignant ventricular arrhythmias (ventricular tachycardia, ventricular fibrillation). Tu et al study, which included 408,712 participants, did not find a significant association between general alcohol consumption and the development of ventricular arrhythmias. However, when considering different types of alcohol, in individuals who consumed larger quantities of spirits (>14 standard drinks per week, where 1 standard drink = 8 g of alcohol according to studies conducted in the United Kingdom) there was a significantly higher incidence of ventricular arrhythmias (25). Jabbari and colleagues reported an association between high alcohol consumption (>96 g/week) and the occurrence of ventricular fibrillation in patients after ST-elevation myocardial infarction (26). In individuals suffering from alcoholic cardiomyopathy, a higher rate of ventricular arrhythmias was observed when compared to other forms of non-ischemic dilated cardiomyopathies (27). Regarding the mechanism, significant alcohol consumption has been associated with QT-interval prolongation, as well as electrolyte abnormalities and increased catecholamine release, which may contribute to the development of ventricular arrhythmias (7).

The relationship between sudden cardiac death and alcohol consumption can be represented by a „J”-shaped curve. A study conducted in the United Kingdom found that consuming less than 26 standard drinks per week (8 g of alcohol per standard drink) overall reduced the risk of sudden cardiac death (SCD). When examining types of alcohol, the occurrence of SCD was more frequent among beer and cider drinkers if they consumed more than 26 standard drinks per week. For spirits drinkers, a linear relationship was observed, where even small amounts of spirits increased the risk of SCD, whereas the consumption of white or red wine reduced this risk of SCD (25).

Previous epidemiological studies also suggest that the relationship between alcohol consumption and cardiovascular mortality can also be represented by a „J”-shaped curve. In individuals without other comorbidities, low to moderate alcohol consumption (1-2 standard drinks per day) was associated with a lower incidence of coronary artery disease and mortality compared to non-drinkers (3, 28, 29). When examining types of alcohol separately, red and white wine were observed to have a greater cardioprotective effect compared to beer (30). However, according to a meta-analysis by Stockwell et al, most studies included former alcohol drinkers who were now abstinent for other medical reasons in the abstinent control group, therefore affecting the mortality data due to other risk factors. In studies where former alcohol drinkers were not included in the control group, low-dose alcohol consumption was less effective in reducing mortality risk, and a linear relationship was observed between the amount of alcohol intake and the mortality rate (31). Further meta-analyses and Mendelian randomization studies have also questioned the beneficial cardiovascular effects of regular, mild alcohol consumption (32, 33).

However, „binge drinking” and prolonged high-dose alcohol consumption significantly increase the risk of cardiovascular diseases and mortality (34). The 2021 ESC Guidelines on cardiovascular disease prevention consider the consumption of up to 100 g of pure alcohol per week to still be safe regarding cardiovascular diseases (35).

Alcohol dependence, alcohol-induced cardiovascular diseases, and alcohol-induced diseases affecting other organ systems impose a significant morbidity and mortality burden on the healthcare system. Several studies suggest a cardioprotective effect of low to moderate alcohol intake, with most evidence supporting the consumption of wine. However, prolonged alcohol consumption in a dose-dependent manner increases the risk of developing alcohol-induced cardiomyopathy and various cardiac arrhythmias due to its direct cardiotoxic effects. Additionally, „binge drinking” (consuming large amounts of alcohol in a short period) is dangerous, as it increases the likelihood of developing AF („Holiday Heart Syndrome”). The beneficial effects of low-dose alcohol intake on coronary artery disease and cardiovascular mortality are not clear, but long-term alcohol consumption and high-dose intake significantly increase the negative effects of alcohol, thereby increasing the likelihood of various arrhythmias and the development of alcohol-induced cardiomyopathy. Consequently, from the perspective of preventing arrhythmias, complete abstinence is the only safe approach.