Alcoholic cardiomyopathy: The result of dosage and individual predisposition PMC

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. According to current knowledge, prolonged and excessive alcohol consumption plays a significant role in inducing oxidative stress within the myocardium. This can occur through direct means, by promoting the generation of free radicals, or indirectly, by triggering the release of hormones, such as angiotensin II, or activating other systems.

• Recent data favored a role for micro RNA, such as the involvement of miR-378a-5p in cardiomyocyte apoptosis and ACM development through ALDH2 gene suppression 120.
• 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.
• Kino et al22 found increased ventricular thickness when consumption exceeded 75 mL/d (60 g) of ethanol, and the increase was higher among those subjects who consumed over 125 mL/d (100 g), without specifying the duration of consumption.
• In fact, ACM is related to systemic damage induced by ethanol misuse and its global biological response 10,11,31.

Diagnosis

The risk of ACM significantly increases with alcohol intake exceeding 80 g per day for a minimum of five years 3. According to the American Heart Association (AHA) and other US-based guidelines, alcohol intake recommendations are provided to promote responsible drinking habits and maintain overall health. The AHA suggests moderate alcohol consumption for those who choose to drink, defining moderation as up to one drink per day for women and up to two drinks per day for men. It is important to note that these guidelines apply to healthy adults and should be adjusted for individuals with certain health conditions or those taking specific medications.

Natural history and prognosis of alcohol-induced cardiomyopathy

The relationship of alcohol with heart disease or dementia is complicated by the fact that moderate alcohol consumption was shown not only to be detrimental but to a certain degree also protective against cardiovascular disease 14 or to cognitive function in predementia. Ballester specifically analysed the effects of alcohol withdrawal on the myocardium using antimyosin antibodies labelled with Indium-11172. This radiotracer has been acknowledged as an indicator of irreversible myocardial damage. 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 and in only 32% of those who had withdrawn from consuming alcohol.

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The result is a type of dilated cardiomyopathy, in which the heart changes shape because its muscles are stretching too https://ecosoberhouse.com/ much. 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. 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.

Clinical manifestations and diagnosis of alcohol-induced cardiomyopathy

• It’s very important to stick with the treatment plan and to stop drinking alcohol during recovery.
• In their autopsies, he described finding dilated cavities of the heart and fatty degeneration of the ventricular walls14.
• 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.
• While this disease appears most often among men between the ages of 35 and 50, other demographics are affected as well.
• The sub-group of patients in whom symptoms improved was made up of a larger proportion of non-drinkers (73%), compared to 25% in the group who did not improve, or 17% in the group whose condition worsened.
• The liver is the most affected organ, since ethanol is mostly metabolized there 11,13, but gastrointestinal, central, and peripheral nervous systems; the heart and vascular system; endocrinological systems; nutrition; and musculo-skeletal systems are clearly affected 10.

If you are dependent on or addicted to alcohol, it can be tough to moderate your consumption. Reach out to a trusted alcohol addiction treatment center to help you quit drinking for the sake of your health. If you’re concerned about alcohol’s impact on your health, talk with your healthcare provider.

ACTIONS

The available research shows that if you limit your alcohol intake to a certain amount, you’re less likely to develop alcohol-related health problems, including alcohol-induced cardiomyopathy. Alcohol-induced cardiomyopathy is a condition where your heart changes shape because of long-term heavy alcohol use. The changes to your heart’s shape cause long-term damage, leading to heart failure and severe problems. Abstaining from alcohol may help some people recover, but others will need medication or even surgery.

• Drinking, especially binge drinking, can raise blood pressure and heart rate, increase your risk for heart attack, and even lead to a condition called alcoholic cardiomyopathy, a type of heart failure.
• This activity describes the pathophysiology of ACM, its causes, presentation and the role of the interprofessional team in its management.ACM is characterized by increased left ventricular mass, dilatation of the left ventricle, and heart failure (both systolic and diastolic).
• Enzymatic activity changes which are seen in the idiopathic cardiomyopathy including decreased activity of oxygen reduction mitochondrial enzymes, increased fatty acid uptake and increased lysosomal/microsomal enzyme activity can be seen.

Myocardial impairment following chronic excessive alcohol intake has been evaluated using echocardiographic and haemodynamic measurements in a significant number of reports. In these studies, haemodynamic and echocardiographic parameters were measured in individuals starting an alcohol withdrawal program. The findings were analysed taking into account the amount and chronicity of intake and they were compared with the same parameters measured in a control group of non-drinkers. Alcoholic cardiomyopathy (ACM) is a disease in which the long-term consumption of alcohol leads to heart failure.1 ACM alcoholic cardiomyopathy is especially dangerous because is a type of dilated cardiomyopathy. One relevant question concerning ethanol cardiac toxicity is if ethanol itself or its active metabolite acetaldehyde causes cardiac damage 73,74.

It is therefore possible that patients with ACM could also harbour a genetic substrate that predisposes them to this form of cardiomyopathy. The suspicion that there may be an individual susceptibility to this disease is underscored by the finding that only a small group of alcoholics develop ACM, and that a proportional relationship between myocardial damage and alcohol intake has not been proven. 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. The existence of a direct causal link between excessive alcohol consumption and the development of DCM is a controversial issue. While some consider that this toxin alone is able to cause such a disease18,19, others contend that it is just a trigger or an agent favouring DCM3,21,22. 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.