At a pathological level, sarcomere Z-line distortion and disruption of the sarcomere pattern leads to myocytolysis [107,129]. Myocytolysis is evident through focal myofiber dissolution, cell vacuolization, and fiber disarray [19] (Figure 2). The sarcomere complex is early affected by ethanol, decreasing the titin content, a protein that is responsible for sarcomere relaxation and LV distensibility [130]. This damage first induces diastolic dysfunction, which is initially subclinical and later clinically apparent [57]. In addition, contractile sarcomere proteins such as Myosin, Actin, and Troponin are also affected by ethanol, causing the functional progressive depression of myocyte contractility, inducing progression to heart failure [56,104,131]. One relevant question concerning ethanol cardiac toxicity is if ethanol itself or its active metabolite acetaldehyde causes cardiac damage [73,74].

It was suspected that malnutrition, frequently related to chronic alcohol misuse, was the origin of ACM [6,67]. However, it has been evidenced that ACM may develop in the absence of protein or caloric malnutrition [38]. However, nutritional factors may worsen the natural course of ACM and should be avoided [18,19]. It has been said that ethanol is the “perfect drug” because of its pleasant effects but damaging long-term effect [1,6]. It is distributed worldwide, with easy social access, and is pleasant when consumed, with positive sensations of welfare, but its negative effects, which include depressive and damaging noxious health effects, are reserved for later. This dual effect creates an additional difficulty to achieve an effective control.

Is this condition only a chronic (long-term) problem?

In spite of the high prevalence of excessive alcohol consumption and of its consideration as one of the main causes of DCM, only a small number of studies have analysed the long-term natural history of ACM. Unfortunately, all the available reports were completed at a time when a majority of the current heart failure therapies were not available (Table ​(Table11). In the Caerphilly prospective heart disease study, platelet aggregation induced by adenosine diphosphate was also inhibited https://ecosoberhouse.com/ in subjects who drank alcohol [99]. Assessing differences between various forms of alcoholic beverages it should be noted that resveratrol leads in vitro to platelet inhibition in a dose-dependent manner [100] and has shown effects on all-cause mortality in a community-based study [101]. Polyphenols of red barrique wines and flavonoids have been shown to inhibit endothelin-1 synthase [102] and PDGF-induced vasoproliferation thus also contributing to cardiovascular protection [103].

• In fact, patients with ACM who abstain from alcohol have a better long-term prognosis than subjects with idiopathic dilated CMP [54].
• It’s very important to stick with the treatment plan and to stop drinking alcohol during recovery.
• These findings are coupled with a clinical history of heavy alcohol use in the absence of coronary artery disease as a supportive etiology.

Your heart’s shape is part of how that timing works, and when parts of your heart stretch, it can disrupt that timing. If it takes too long — even by tiny fractions of a second— that delay can cause your heart to beat out of sync (a problem called dyssynchrony). Similarly, alcohol can have a toxic effect on your heart and cause scar tissue to form. That scar tissue can also cause potentially life-threatening arrhythmias (irregular heart rhythms). Alcohol-induced cardiomyopathy can affect anyone who consumes too much alcohol, even those who don’t have alcohol use disorder.

Treatment

In addition, ethanol is an immunosuppressive drug that is pro-inflammatory and pro-oncogenic [14,15,16,17]. Ethyl alcohol, also known as “ethanol” or usually just as “alcohol”, is the most consumed drug in human history [1]. At present, its consumption rates are still very high, with a widespread worldwide distribution, in a global uncontrolled scenario with easy access [2]. In fact, there is an increasing consumption in particular groups, such as adolescents and young people [3,4]. You will receive the first heart failure and transplantation email in your inbox shortly.

• The myocyte mitochondria in the hearts of persons exposed to alcohol are clearly abnormal in structure, and many believe that this may be an important factor in the development of AC.
• Steatotic liver disease develops in about 90% of people who drink more than 1.5 to 2 ounces of alcohol per day.
• Specifically, ethanol disturbs the ryanodine Ca2+ release, the sarcomere Ca2+sensitivity [102,103], the excitation–contraction coupling and myofibrillary structure, and protein expression, decreasing heart contraction [86].
• Furthermore, in many of these reports, comorbid conditions, especially myocarditis and other addictions such as cocaine and nicotine, were not reported.

Indeed, the first account of the possible harmful effects of alcohol specifically on heart muscle was reported in the latter half of the 19th century. Expressions referring to “the heart of a wine drinker in Tubingen” and particularly a “Munich beer heart” were used and known in Germany during this time[13]. As a net effect, negative inotropism may result and contribute to heart failure. For more than 3000 years, alcoholic beverages have been consumed in multiple societies through the centuries and cultures. In the 16th century Paracelsus Theophrastus Bombastus from Hohenheim used this term for distilled liquor and called it alcohol [15].

Histologic Findings

According to recent data, a genetic form of DCM could be present in up to 50% of idiopathic DCM cases, and other specific forms of DCM such as peripartum cardiomyopathy have been shown to have a genetic basis in a significant number of cases[68]. It is therefore possible that patients with ACM could also harbour a genetic substrate that predisposes them to this form of cardiomyopathy. Alcohol abuse coinciding with myocarditis was reported in 1902 by McKenzie [26]. In endomyocardial biopsies of alcoholics up to 30 % of patients were found to exhibit sparse lymphocytic infiltrates with myocyte degeneration and focal necrosis and increased HLA (human leukocyte antigen) or ICAM (intercellular adhesion molecule) expression (Fig. 3; [16, 84]).

Growth factors and cardiomyokines are relevant molecules that may modify this process. Cardiac transplantation is the final measure in end-stage ACM but is limited to those subjects able to achieve abstinence. Since ethanol consumption of the global population is not currently under control [2], the incidence of alcoholic cardiomyopathy is expected to be maintained in the future, especially in specific population groups, such as adolescents and young people [3]. Therefore, efforts for the prevention, early detection, and specific treatment in this relevant disease should be established [45]. The direct dose-dependent effect between alcohol intake and development of ACM is clearly established [50,52], women being more sensitive than men to the toxic effects of ethanol on the heart [46].

Interestingly, the strength of this association was not consistent across different geographic regions. Alcohol use was protective against CHD for subjects in most countries, except for people of South Asian ethnicity living in South Asia (India, Bangladesh, Nepal, Pakistan, and Sri Lanka). INTERHEART results also suggested that the protective effect of any alcohol use against MI was greater in women and those over age 45. Finally, data from INTERHEART support the finding that the risk of MI is increased in the 24 hours after consumption of 6 or more drinks, suggesting that binge drinking increases MI risk (table 1). In fact, the particular effects that ethanol produces in a specific organ depend on several factors [18,19]. One is the physical characteristics of ethanol itself, with a low molecular size, high distribution capacity, and high tissue reactivity.

• According to recent data, a genetic form of DCM could be present in up to 50% of idiopathic DCM cases, and other specific forms of DCM such as peripartum cardiomyopathy have been shown to have a genetic basis in a significant number of cases[68].
• Several pathophysiological mechanisms have been proposed at the basis of alcohol-induced damage, most of which are still object of research.
• Also, low to moderate daily alcohol intake was proved to be a predictor of better prognosis for both ischemic cardiomyopathy and heart failure regardless of the presence of coronary disease[1,2].
• Abstinence is the preferred goal, although controlled drinking may still improve cardiac function.
• At that time every 10th necropsy in men at the Munich pathology institute named cardiac dilatation and fatty degeneration as “Bierherz” being its underlying cause.

Additionally, the accepted ACM definition does not take into account a patient’s sex or body mass index (BMI). As women typically have a lower BMI than men, a similar amount of alcohol would reach a woman’s heart after consuming smaller quantities of alcohol. Data on the amount of alcohol consumption required to cause ACM are limited and controversial. Biomarkers of heart failure such as NT-proBNP and of myocardial necrosis such as the troponins and CKMB indicate heart failure or myocytolysis.

Results from evaluations of mean cell volume, aspartate aminotransferase levels, alanine aminotransferase levels, lactate dehydrogenase (LDH) levels, and gamma-glutamyltransferase levels have been shown to be similar in persons with AC to those in persons with other forms of DC. However, results from tissue assays have been shown to be potentially helpful in distinguishing AC from other forms of DC. Physical examination findings in alcoholic cardiomyopathy (AC) are not unique compared with findings in dilated cardiomyopathy from other causes. Elevated systemic blood pressure may reflect excessive intake of alcohol, but not AC per se. The onset of symptoms is usually insidious, but acute decompensations are also observed, especially in patients with asymptomatic left ventricular dysfunction who develop atrial fibrillation or other tachyarrhythmia and, because of this, are unable to increase their cardiac output. Some studies have suggested that a genetic vulnerability exists to the myocardial effects of alcohol consumption.