Structurally, hypertrophy of myocytes is seen in the early stages to avoid contractile depression [52,107,125]. The heart output is progressively lower in a dose-dependent relationship with the lifetime accumulated total dose of alcohol consumed [38]. Several growth factors and cardiomyokines exert an autocrine or paracrine effect that tries to compensate for this heart damage [119,133]. Antioxidant, anti-inflammatory, anti-apoptotic, and antifibrogenic mechanisms try to avoid myocyte necrosis and heart fibrosis [14,30,58]. The final result is that achieved from the equilibrium between the degree of damage and the capacity of heart repair mechanisms in each specific individual [31,56]. This ethanol misuse at high consumption rates causes a variety of health problems, ethanol being the sixth most relevant factor of global burden of disease and responsible for 5.3% of all deaths [5].

Both the absence of a direct correlation and the theory of the existence of a threshold dose (above which some alcoholics develop ACM) require the presence of individual susceptibility to alcohol induced cardiac damage[63]. It is unknown whether individual susceptibility would be related to increased vulnerability at the myocardial level and/or to impaired alcohol metabolism. Alterations caused by alcoholic cardiomyopathy heavy alcohol intake have also been studied from the perspective of histopathology. Emmanuel Rubin analysed muscle biopsies from individuals who were previously non-drinkers and were submitted to a balanced diet with heavy alcohol intake during one month[41]. These changes, though subtle, were similar to those found by Ferrans and Hibbs in eight deceased individuals diagnosed with ACM[42,43].

Apoptosis and ACM

It is thought that 1-2% of all heavy drinkers develop alcoholic cardiomyopathy, while in addiction units research suggests around 21-32% of people needing admission to specialist units for alcohol problems are affected. 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]). In Munich, the annual consumption of beer reached 245 l per capita and year in the last quarter of the 19th century.

It should be noted that a moderate drinker included in this latter group showed an improvement of his ejection fraction. 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].

4. Ethanol Disruption of Transients and SR Activation

So Hildegard von Bingen (1098–1179), one of the most prominent mysticians of her time, recommended her heart wine as a universal remedy. One liter of wine was cooked for 4 min with 10 fresh parsley stems, 1 spoon of vinegar, and 300 g honey and then filtered [11]. Chronic ethanol misuse clearly depresses protein synthesis and degradation, involving both structural and non-structural heart proteins [104,128].

• Cardiomyopathy is a condition characterized by abnormal heart muscle that makes it harder for the heart to pump blood throughout the body.
• Ethanol may induce changes in nuclear regulation of transcription with a dose-dependent translocation of NFkB into the nucleus [106].
• Despite this clear epidemiological evidence of ethanol’s unsafe consumption and increased health risk, results of consumption policies are not effective enough.
• Among the ACM patients, no differences between the patients in the death and survival groups were observed at baseline with respect to age, disease duration, smoking status, presence of syncope, heart rate, gender, and blood test results.
• This observation led to the erroneous belief that alcohol is an immediate coronary vasodilator.
• There are a number of options available, but safely detoxing from alcohol is a priority.

In the interim it seems appropriate to continue discouraging any alcohol consumption in these patients, as it would be difficult for them to maintain a limited alcohol intake considering their history of alcohol dependence and abuse. In their autopsies, he described finding dilated cavities of the heart and fatty degeneration of the ventricular walls[14]. As the name suggests, alcoholic cardiomyopathy is caused by alcohol alone, and accounts for 10% of all cases of dilated cardiomyopathies. People who drink a dangerous amount of alcohol have a higher risk of developing alcoholic cardiomyopathy, as well as damaging other organs in the body.

What is the long-term outlook for someone with alcoholic cardiomyopathy?

Abstinence is the preferred goal, although controlled drinking may still improve cardiac function. New strategies are addressed to decrease myocyte hypertrophy and interstitial fibrosis and try to improve myocyte regeneration, minimizing ethanol-related cardiac damage. Growth factors and cardiomyokines are relevant molecules that may modify this process.