In addition, ethanol is an immunosuppressive drug that is pro-inflammatory and pro-oncogenic 14,15,16,17. Data suggests patients with successful quitting of alcohol have improved overall outcomes with a reduced number of inpatient admissions and improvement in diameter size on echocardiogram. Alcohol use is an important cause for non-ischemic cardiomyopathy and accounts for 10% of all cases of dilated cardiomyopathies. Furthermore, there are conflicting data among studies regarding the prognosis of the condition, with some showing overall mortality near 60% and others showing a mortality rate of only 19% (Table 1). Furthermore, Fernández-Solá et al30, when analysing a population of alcoholics, found a higher prevalence of DCM in alcoholics than among the general population.
5. The effects of Moderate Consumption of Ethanol and Binge-drinking
Heart remodeling is an adaptive mechanism, susceptible to being modified in ACM by the use of cardiomyokines (FGF21, Metrnl) and growth factors (IGF-1, Myostatin) 112,119. Recently, apoptosis and necrosis have been also attributed to autophagy in ACM 18. In order to maintain cardiac homeostasis, the removal of defective organelles and cell debris by autophagy is essential both in physiological and pathological conditions 115. Dysregulated excessive autophagy, together with other factors such as oxidative stress, neurohormonal activation, and altered fatty acid metabolism, contributes to cardiac structural and functional damage following alcoholism. This influences the maintenance of cardiac geometry and contractile function, increasing the development of ACM 121.
Chronic Alcohol and Skeletal Muscle
These changes, though subtle, were similar to those found by Ferrans and Hibbs in eight deceased individuals diagnosed with ACM42,43. On alcoholic cardiomyopathy 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. Also, there were significant size variations in the myofibrils and they showed a relative decrease in the number of striations, in addition to swelling, vacuolisation and hyalinisation.
LIMITATIONS OF ACM STUDIES
- One of the few papers analysing genetic susceptibility in ACM was published by Fernández-Solà et al64 in 2002.
- A doctor can guide someone to resources to help them quit drinking and can make referrals.
- Furthermore, in contrast to nuclear DNA, mitochondrial DNA is susceptible to oxidative stress due to its close proximity to the formation of ROS and the limited protective mechanisms in place to safeguard DNA integrity.
- However, during the time that these haemodynamic changes appeared, some researchers identified a possible decrease in the ejection fraction and other parameters related to systolic function32-39.
Alcoholic cardiomyopathy (ACM) is amphetamine addiction treatment a disease in which the long-term consumption of alcohol leads to heart failure.1 ACM is a type of dilated cardiomyopathy. The major risk factor for developing ACM is chronic alcohol abuse; however, there is no specific cutoff value for the amount of alcohol consumption that would lead to the development of ACM. The diagnosis of ACM is usually one of exclusion in a patient with DCM with no identified cause and a long history of heavy alcohol abuse. According to most studies, the alcohol consumption required to establish a diagnosis of ACM is over 80 g per day during at least 5 years9-12.
- According to the National Institute on Alcohol Abuse and Alcoholism (NIAAA), AUD is a brain disorder that doctors characterize by the inability to stop or control alcohol consumption.
- In this respect, a higher prevalence of excessive alcohol consumption has been reported among individuals diagnosed with DCM than in the general population8.
- According to most studies, the alcohol consumption required to establish a diagnosis of ACM is over 80 g per day during at least 5 years9-12.
- Pathologically, ethanol induces myocytolysis, apoptosis, and necrosis of myocytes, with repair mechanisms causing hypertrophy and interstitial fibrosis.
- Your doctor might prescribe ACE inhibitors and beta-blockers to help lower your blood pressure.
NATURAL HISTORY OF ALCOHOLIC CARDIOMYOPATHY
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. Thus, Nicolás et al73 studied the evolution of the ejection fraction in 55 patients with ACM according to their degree of withdrawal. The population was divided into 3 groups according to their intake volume during the follow-up period. At the end of the first year, no differences were found among the non-drinkers, who improved by 13.1%, and among those who reduced consumption to g/d (with an average improvement of 12.2%).
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 time13. In this review, we evaluate the available evidence linking alcohol consumption with HF and DCM. Anyone with concerns about alcohol consumption or https://ecosoberhouse.com/ heart health needs to consult a doctor for further advice and guidance.
