Alcoholic cardiomyopathy natural history, complications and prognosis

This review will provide an updated view of this condition, including its epidemiology, pathogenesis, diagnosis, and treatment (Graphical Abstract). Alcoholic cardiomyopathy is best managed with an interprofessional approach with the involvement of primary care physician and cardiology. To date, none of the ACM studies have proposed a treatment for ACM other than that recommended for DCM in current HF guidelines.

Direct toxic effect of ethanol

Of the 56 patients included in the study, 28 were former drinkers and 28 continued consuming alcohol during the study. Absorption levels of Indium-111 were high in 75% of patients who continued drinking alcoholic cardiomyopathy is especially dangerous because and in only 32% of those who had withdrawn from consuming alcohol. A second set of studies that are quoted when addressing this topic are those conducted in individuals who started an alcohol withdrawal program21-24.

Clinical profile

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. At present ACM is considered a specific disease both by the European Society of Cardiology (ESC) and by the American Heart Association (AHA)18,19. In the ESC consensus document on the classification of cardiomyopathies, ACM is classified among the acquired forms of DCM19. This section collects any data what is Oxford House citations, data availability statements, or supplementary materials included in this article.

Alcoholic consumption and heart failure

The majority of the echocardiographic studies performed on asymptomatic alcoholics found only mild changes in their hearts with no clear impairment of the systolic function. For example, a slight increase in the pre-ejection period/left ventricular ejection time ratio (PEP/LVET) was found by some authors, suggesting a sub-clinical impairment of systolic function21,33. Mathews and Kino found a small, but significant increase in left ventricular mass in individuals consuming at least 12 oz of whisky during 6 years and 60 g of ethanol per day, respectively22,40.

• Categorical data were expressed as percentages and groups were compared using the chi-square (χ²) test.
• 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.
• At present ACM is considered a specific disease both by the European Society of Cardiology (ESC) and by the American Heart Association (AHA)18,19.
• Alcohol-induced cardiomyopathy remains a relevant health problem, for which the mainstay of treatment is alcohol abstinence.
• By inhibiting NOX2 (the most important superoxide-producing enzyme) with apocynin, they observed a decrease in ethanol- and acetaldehyde-induced superoxide levels.

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 month41. Although no significant changes were found using conventional microscopy, when electron microscopy was employed he discovered intracellular swelling, glycogen and lipid accumulation, and alterations in the structure of the sarcoplasmic reticulum and of the mitochondria (Figure 2). These changes, though subtle, were similar to those found by Ferrans and Hibbs in eight deceased individuals diagnosed with ACM42,43. On histological examination, various degrees of fibrosis, patchy areas of endocardial fibroelastosis, intramural blood clots and focal collections of swollen cells in both the epicardium and endocardium were found.

• 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.
• LVEF, QRS duration and CTP Scoring at the time of presentation were found to be the independent prognostic markers of patients with ACM.
• These authors found a relationship between the reduction or cessation of alcohol consumption and higher survival rates without a heart transplant.
• On comparing tribal with non-tribal population, no differences were observed at baseline in terms of age and sex.
• For example, a slight increase in the pre-ejection period/left ventricular ejection time ratio (PEP/LVET) was found by some authors, suggesting a sub-clinical impairment of systolic function21,33.

This was questioned by other authors, who pointed out that these conclusions could not be drawn, as alcohol itself also induces changes in the pre-load and after-load conditions, which influence cardiac contractility35. However, in this https://ecosoberhouse.com/ context, experimental in vitro studies using cardiomyocytes have shown that alcohol depresses the contractile capacity of the myocardium, regardless of the sympathetic tone and the haemodynamic conditions36. Alcohol-induced cardiomyopathy remains a relevant health problem, for which the mainstay of treatment is alcohol abstinence.