In conditions of acute alcohol toxicity, ethanol has been shown to increase circulating catecholamine, which may play a role in myocardial damage. Alcohol-induced cardiomyopathy remains a relevant health problem, for which the mainstay of treatment is alcohol abstinence. In recent years, basic and clinical research has shed light on its pathogenesis, which includes direct toxic effects of alcohol on the myocardium, oxidative stress, mitochondrial dysfunction, and genetic susceptibility. The pathophysiology of AC involves a combination of direct toxic effects of alcohol on the myocardium, oxidative stress, mitochondrial dysfunction, and genetic susceptibility. Clinical overview, pathogenesis, treatment and prognosis of alcoholic cardiomyopathy.
AMOUNT OF ALCOHOL REQUIRED TO PRODUCE ACM
Pharmacologic therapy should include goal-directed heart failure therapy as used in idiopathic dilated cardiomyopathy with reduced ejection fraction. This includes a combination of beta-blockers, an angiotensin-converting enzyme inhibitor, diuretics, aldosterone receptor antagonist and angiotensin blocker-neprilysin inhibitor (if LVEF is less than or equal to 40%). The use of carvedilol, trimetazidine with other conventional heart failure drugs have been proven to be beneficial in some studies. Most common age population for ACM is males from age with significant history of alcohol use for more than 10 years. Females constitute roughly 14 % of cases of alcohol induced cardiomyopathy however lifetime exposure required for women to develop alcohol induced cardiomyopathy is less compared to men.
Acute vs. chronic
The first paper to assess the natural history and long-term prognosis of ACM was published by McDonald et al69 in 1971. He recruited 48 patients admitted to hospital with cardiomegaly without a clear aetiology and severe alcoholism. The only factor to predict a poor outcome was the duration of symptoms before admission.
Figure 1. Alcohol-induced dilated cardiomyopathy.
Acute can be defined as large volume acute consumption of alcohol promotes myocardial inflammation leading to increased troponin concentration in serum, tachyarrhythmias including atrial fibrillation and rarely ventricular fibrillation. Incidence of alcoholic cardiomyopathy ranges from 1-2% of all heavy alcohol users. It is estimated, approximately 21-36% of all non-ischemic cardiomyopathies are attributed to alcohol. The prevalance of alcoholic cardiomyopathy in addiction units is estimated around %. Overall data with regards to alcohol induced cardiomyopathy is insuffienct and does not illustrate significant available data.
The final damage is an equilibrium between the intensity of damaging effects and the possibility of defense, plasticity, regeneration, and adaptation for every specific organ 29,30,31. Thus, alcohol-dilated cardiomyopathy (ACM) is the result of dosage and individual predisposition 32. The diagnosis of alcohol-induced cardiomyopathy in our patient relied on the absence of known causes of dilated cardiomyopathy, the identification of excessive alcohol consumption and the improvement of cardiac function after the abstention from alcohol ingestion. Specifically, there was no evidence of a preceding viral infection or presence of another toxin.
Table 1. List of literature articles reviewed in this study.
There is also an established link between the development of ACM and apoptosis because of myocardial cell death, which contributes to heart pathology and dysfunction. Previous studies were conducted on rats that are fed alcohol for about eight months. They found that there is about 14% loss of myocardial cells in the left ventricle of those rats. It showed a significant increase in both acute and chronic alcohol intoxication. All previous mechanisms can induce myocyte apoptosis through the induction of mitochondrial damage and oxidative stress 12.
Basic studies on molecular mechanisms of myocardial damage
- One of the most relevant targets of ethanol in the membrane is the disruption of membrane receptor composition and activities 86.
- Elevations in troponin can signify heart damage or an increase in cardiac output that results in demand ischemia.
- However, a possible confusion factor was identified because the group with clinical improvement also exhibited a shorter evolution of the symptoms and the disease.
- Echocardiogram usually reveals left ventricular hypertrophy, depressed left ventricular ejection fraction, and dilation.
- It was described as a form of DCM with severe pericardial effusion, low cardiac output, and purplish skin coloration.
- In addition, the AHA advises against starting to drink alcohol solely for potential health benefits, as the risks can outweigh the advantages.
Half the admissions occurred for cardiovascular etiologies and in‐hospital mortality among all admissions remained fairly unchanged in the absence of a clinically relevant trend. The commonest affected age group was patients in the 45 to 59‐year age group followed by the 60 to 74‐year age group. Comorbidities such as depression are often overlooked and many of these comorbidities could be potentially modifiable risk factors to help curb subsequent cardiovascular sequelae as a result of AC. Further studies are needed to address this subset of the heart failure population and validate the results. Alcohol (ethanol) is contained in a number of beverages consumed all over the world since ancient times. The acute ingestion of large amount of alcohol as well as chronic alcohol abuse induce toxic effects to all organs and tissues 7, particularly to central nervous system, liver and heart 8,9.
Treatment
This section collects any data alcoholic cardiomyopathy symptoms citations, data availability statements, or supplementary materials included in this article. There is a need for basic, observational and clinical trials to improve the knowledge of disease. To date, none of the ACM studies have proposed a treatment for ACM other than that recommended for DCM in current HF guidelines.
- One of the characteristics that makes ethanol harmful is its systemic toxic effect on the human body 10,11.
- In addition, there is a relevant role on each organ, particularly on defense and adaptive mechanisms, with a clear induction of anti-oxidant, metabolic, and anti-inflammatory protective responses as a result of ethanol aggression 18,25,26.
- They try to control myocardial remodeling to avoid the progression of myocyte hypertrophy 39,148 or fibrosis 149 and ventricle dysfunction and dilatation, as well as to increase the degree of myocyte regeneration 150.
- Through a thematic synthesis, we identified common trends, knowledge gaps, and emerging research areas related to ACM.
- Until the second part of the 20th century, there was no scientific evidence on the direct and dose-dependent effect of ethanol on the heart as cause of ACM 6,38.
- In addition to this, there is difficulty in actually making the diagnosis of AC itself clinically due to absence of specific diagnostic criteria and the need to rule out other causes of cardiomyopathy as well.
General Health
Two independent reviewers assessed each article for relevance and eligibility for full-text review. Once the 15 articles were selected (see Appendix Table 1 for the list of included articles), we extracted and organized relevant information from them. The risk of developing alcoholic cardiomyopathy appears to be related to both the amount and duration alcohol intake.