Alcoholic Cardiomyopathy: Causes, Symptoms, and Diagnosis

DCM, dilated cardiomyopathy; HF, heart failure; HFrEF, heart failure with reduced ejection fraction; HTx, heart transplant; LVEDD, left ventricular end-diastolic diameter; LVEF, left ventricular ejection fraction; SD, standard deviation. A study in a rat model using an alcohol dehydrogenase transgene that results alcoholic cardiomyopathy symptoms in elevated levels of acetaldehyde demonstrated a change in calcium metabolism at the intracellular level and a decrease in peak shortening and shortening velocity. This was interpreted by the authors as suggesting that acetaldehyde plays a key role in the cardiac dysfunction seen after alcohol intake.

Clinical manifestations and diagnosis of alcohol-induced cardiomyopathy

• In this review, we discuss these mechanisms, as well as the potential importance of drinking patterns, genetic susceptibility, nutritional factors, ethnicity, and sex in the development of ACM.
• However, it has been evidenced that ACM may develop in the absence of protein or caloric malnutrition [38].
• This test will assess the ejection fraction (EF), a measurement that expresses how much blood the LV pumps out with each contraction.
• However, nutritional factors may worsen the natural course of ACM and should be avoided [18,19].
• Chronic alcohol consumption can cause multi-organ damage including myocardial dysfunction.
• This influences the maintenance of cardiac geometry and contractile function, increasing the development of ACM [121].

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. Although analytical markers of alcohol consumption, such as average erythrocyte volume and serum gamma-glutamyltranspeptidase levels, could be an aid to establish abstinence or persistence of alcohol intake in patients, the quantity of alcohol intake is dependent on the patients’ report. Furthermore, in many of these reports, comorbid conditions, especially myocarditis and other addictions https://ecosoberhouse.com/ such as cocaine and nicotine, were not reported. Future studies with a strict classification of non-drinkers and drinkers will help clarify whether complete abstinence is mandatory for ACM patients. 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. Additionally, echocardiographic data suggest that subjects who do not fully withdraw from alcohol consumption, but who reduce it to moderate amounts recover LVEF in a similar manner to strict non-drinkers.

International Patients

Furthermore, the inclusion criteria for ACM were very strict and required a minimum consumption of 8 oz of alcohol (200 g or 20 standard units) each day for over 6 mo. In contrast, European studies focusing on the prevalence of ACM included only subjects diagnosed with DCM and applied the consumption threshold of 80 g/d for ≥ 5 years, finding an ACM prevalence of 23%-47% among idiopathic DCM patients[9-12] (Figure ​(Figure11). Askanas et al[21] found a significant increase in the myocardial mass and of the pre-ejection periods in drinkers of over 12 oz of whisky (approximately 120 g of alcohol) compared to a control group of non-drinkers.

Differential Diagnosis

According to several articles, even moderate alcohol use has comparable effects to abstinence. Goal-directed heart failure therapy, as utilized in idiopathic DCM with low ejection fraction, should be a part of pharmaceutical therapy. If the left ventricular ejection fraction (LVEF) is less than or equal to 40%, this may also comprise a combination of angiotensin blocker-neprilysin inhibitor, diuretics, beta-blockers, diuretics, aldosterone receptor antagonists, and an angiotensin-converting enzyme inhibitor. Some studies have shown that the combination of carvedilol and trimetazidine with other traditional heart failure medications is effective [1-3,7-11,16-20]. 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.

Derangements in Fatty Acid Metabolism and Transport

The Cd36 gene encodes for proteins involved with transport of long-chain fatty acids. The Scd-1 gene encodes for stearoyl-CoA desaturase 1, an enzyme that catalyzes the rate-limiting step in mono-unsaturated fatty acid synthesis. Genes encoding for enzymes important in de novo fatty acid synthesis (e.g., fatty acid synthase) and lipoprotein lipase were unchanged by ethanol consumption (33). Although only examined in the 18% ethanol group, ATP production was significantly decreased (5.18 ± 0.54 pg/ml) compared to the control group (7.40 ± 0.64 pg/ml) (33). One of the relevant facts in ACM is the existence of a clear gender difference, women being more susceptible to the toxic effects of alcohol than men at the same level of lifetime ethanol consumption [93,94].