Alcoholic cardiomyopathy: What is known and what is not known

Epidemiological studies analysing the relationship between excessive alcohol consumption and the development of DCM have found the existence of a reciprocal link between both disorders. Finally, it should be noted that a large majority of studies on the long-term prognosis of ACM used the cut-off point of 80 g/d for a minimum of 5 years to consider alcohol as the cause of DCM. In this review, we evaluate the available evidence linking alcohol consumption with HF and DCM. 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]).

Interestingly, angiotensin II administration induces skeletal muscle atrophy in rodents, and mechanisms include increased expression of the E3 ligases atrogin-1/MuRF-1 (70). Alcohol can exacerbate many other underlying problems common in patients with CHF. For example, it can have a pressor effect, cause hypertension, and increase left ventricular mass [34]. Those who drink heavily may experience substantial increases in their blood pressure.

Medical Professionals

In Munich, the annual consumption of beer reached 245 l per capita and year in the last quarter of the 19th century. In 1884, the pathologist and veterinarian Otto von Bollinger (Fig. 2a) described the “Munich beer heart” with fibrosis, hypertrophy, and fatty degeneration in postmortem cardiac tissue of alcoholics who consumed an estimated average of 432 liters of beer per year (Fig. 2b; [23]). 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.

Evidence of oxidative stress is found after short periods of alcohol consumption (2 to 18 weeks), at least in animal models. These data suggest that antioxidant defense mechanisms that attempt to protect the heart against oxidative damage appear to be initiated soon after drinking alcohol. Also, as noted below, data from other studies demonstrate the protective role of administered antioxidants, such as a synthetic compound that mimics the native superoxide dismutase enzyme, called a superoxide dismutase mimetic.

Alcoholism—use and abuse

They do not pass readily through cell membranes, and they are major components of very-low-density lipoproteins (VLDLs), which are converted in the blood to LDLs. High levels of triglycerides in the blood have therefore been linked to atherosclerosis, heart disease, and stroke. Researchers have found evidence of mitochondrial dysfunction or impaired bioenergetics related to alcohol consumption. This is not surprising, because mitochondria are a major target for free-radical injury.

• Zhang et al. found significant increases in myocardial protein carbonyl and superoxide levels in mice fed an ethanol (4% v/v) diet for 6 weeks (22).
• Certain individuals with DNA or gene mutations may be more prone to the damaging impacts of alcohol; however, it is not known exactly how these genetic factors create a higher risk.

Electrographic measurements have demonstrated that a variety of abnormalities may underlie this propensity to arrhythmia. In particular, prolongation of conduction times and heterogeneous increases in refractory period have been reported, especially https://ecosoberhouse.com/ in patients with cardiomyopathy. Investigators found increased levels of catecholamines, altered myocardial refractory periods and conduction times. Therefore, β-blockers are often successfully introduced as treatment for these arrhythmias.

Life expectancy and recovery of alcoholic cardiomyopathy

In this study, the only independent predictor of cardiac death was alcohol abstinence. One of the few papers analysing genetic susceptibility in ACM was published by Fernández-Solà et al[64] in 2002. He compared the prevalence of different polymorphisms of the angiotensin-converting enzyme gene in 30 ACM patients and in 27 alcoholics with normal ventricular function. Furthermore, 89% of the alcoholics with a DD genotype developed ACM, whereas only 13% of those with an II or ID genotype developed this condition.

Endothelial dysfunction is an early indicator of blood vessel damage and atherosclerosis, as well as a strong prognostic factor for future CV events (Deanfield et al. 2007; Ras et al. 2013). Low-to-moderate levels of alcohol consumption may initially improve endothelial function, whereas high daily levels and binge drinking may impair it. Alcohol-induced toxicity leads to non-ischemic dilated cardiomyopathy characterized by loss of contractile function and dilatation of myocardial ventricles.

Clinical work-up for alcoholic cardiomyopathy

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 %.

G., in medieval times, when people took advantage of the vasodilating properties of alcohol to treat angina pectoris or heart failure. 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]. Cardiac percussion and palpation reveal evidence of an enlarged heart with a laterally displaced and diffuse point of maximal impulse. Auscultation can help to reveal the apical murmur of mitral regurgitation and the lower parasternal murmur of tricuspid regurgitation secondary to papillary muscle displacement and dysfunction.

Although the most common cause of heart failure is coronary artery disease, ischemic cardiomyopathy is unlikely in the absence of a clear history of prior ischemic events or angina and in the absence of Q waves on the ECG strip. In most patients, exercise or pharmacologic stress testing with echocardiographic or nuclear imaging is an appropriate screening test for heart failure due to coronary artery disease. In patients with dilated cardiomyopathy, if additional questions remain after a history is obtained and noninvasive testing is performed, cardiac catheterization may be used to help exclude other etiologies of heart failure. Results from serum chemistry evaluations have not been shown to be useful for distinguishing patients with alcoholic cardiomyopathy (AC) from those with other forms of dilated cardiomyopathy (DC).

These findings are coupled with a clinical history of heavy alcohol use in the absence of coronary artery disease as a supportive etiology. In all ACM studies, inclusion of patients is based on patients’ self-reported alcohol drinking habits, which may lead to an underestimation of the prevalence of ACM together with problematic identification of patients who abstain and those who continue drinking. Furthermore, in many of these reports, comorbid conditions, especially myocarditis and other addictions such as cocaine and nicotine, were not reported. Alterations caused by 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].