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Elevations in troponin can signify heart damage or an increase in cardiac output that results in demand ischemia. This is where the heart has an increased need for oxygen that exceeds the body’s ability to supply it. Until the second part of the 20th century, there was no scientific evidence on the direct and dose-dependent effect of ethanol on the heart as cause of ACM 6,38. However, there is a clear personal susceptibility of this effect that creates a wide variability range and supposes significant inter-individual differences 50,66.

• It is crucial to exercise caution and be aware of individual tolerance and personal health circumstances when making decisions about alcohol consumption.
• Moreover, alcohol may reduce the levels of transport proteins and diminish antioxidant activity by decreasing the plasma concentration of antioxidant enzymes.
• Pharmacologic therapy should include goal-directed heart failure therapy as used in idiopathic dilated cardiomyopathy with reduced ejection fraction.
• Alcoholic-dilated Cardiomyopathy (ACM) is the most prevalent form of ethanol-induced heart damage.

Health News

This ethanol misuse at high consumption rates causes a variety of health problems, ethanol being the sixth most relevant factor of global burden of disease and responsible for 5.3% of all deaths 5. Despite this clear epidemiological evidence of ethanol’s unsafe consumption and increased health risk, results of consumption policies are not effective enough. Therefore, the need to establish a more effective control on ethanol consumption has been repeatedly claimed 2. The outlook for people with alcoholic cardiomyopathy varies depending on how long alcohol was abused and how much alcohol was consumed during that time. In cases where the damage to the heart is severe, the chances of complete recovery are low. Once the damage is considered irreversible, alcoholic cardiomyopathy it’s difficult for the heart and rest of the body to recover.

1. The Natural Course of ACM

Specifically in the United States, ACM was declared the leading cause of non-ischemic DCM7; a fact related to the high consumption of alcoholic beverages worldwide, which is particularly elevated in Western countries26 . Prior studies have investigated the impact of ethanol on changes in the activity and levels of oxidative enzymes. Catalase activity is significantly increased marijuana addiction in postmortem heart samples acquired from people who have been diagnosed with ACM. Other studies investigated the catalase levels and activity among rats with ACM with a control group. This may be explained by the fact that the increased catalase activity in those who have a long history of alcohol abuse may represent a protective and adoptive reaction to the persistent high ethanol levels 11. Alcoholic cardiomyopathy (ACM) is a heart disease that occurs due to chronic alcohol consumption.

• The subject with excessive alcohol consumption, after more than 10 years of high ethanol consumption, usually develops subclinical heart functional changes before symptom appearance or signs of heart failure 55,56.
• Therefore, physicians should be aware of the risk of new cardiomyopathy in patients with these overlapping diagnoses 144.
• 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.
• For tens of years, the literature has documented many clinical cases or small series of patients who have undergone a full recovery of ejection fraction and a good clinical evolution after a period of complete alcoholic abstinence.
• This ethanol misuse at high consumption rates causes a variety of health problems, ethanol being the sixth most relevant factor of global burden of disease and responsible for 5.3% of all deaths 5.

General Health

In addition, there is a relevant role on each organ, particularly on defense and adaptive mechanisms, with a clear induction of anti-oxidant, metabolic, and anti-inflammatory protective responses as a result of ethanol aggression 18,25,26. This multi-factorial effect is attributed to genetic factors 27 and ethnic 28 variability. The final damage is an equilibrium between the intensity of damaging effects and the possibility of defense, plasticity, regeneration, and adaptation for every specific organ 29,30,31. Thus, alcohol-dilated cardiomyopathy (ACM) is the result of dosage and individual predisposition 32.

Treatment / Management

• There are no specific targeted histological or immunological biomarkers for the diagnosis of alcohol-induced cardiomyopathy.
• Therefore, efforts for the prevention, early detection, and specific treatment in this relevant disease should be established 45.
• According to current knowledge, prolonged and excessive alcohol consumption plays a significant role in inducing oxidative stress within the myocardium.
• In a national inpatient sample study, some authors have reported ACM to be most common in white males aged between 45 and 59 2.

However, these new strategies have not yet demonstrated their real effectiveness in clinical trials, require further evaluation, and are not approved for clinical use 147. The signs and symptoms of alcoholic cardiomyopathy (ACM) can vary depending on the severity of the condition.6 In the early stages, people with ACM may not experience any symptoms. However, as the condition progresses, they may experience symptoms such as fatigue, shortness of breath, palpitations, and swelling of the legs and ankles.6 They may also experience chest pain, dizziness, and fainting. In some cases, ACM can cause arrhythmias or irregular heartbeats, which can be life-threatening.

Demakis et al70 in 1974 divided a cohort of 57 ACM patients https://ecosoberhouse.com/ according to the evolution of their symptoms during follow-up. 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. However, a possible confusion factor was identified because the group with clinical improvement also exhibited a shorter evolution of the symptoms and the disease.