The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy PMC

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. Chronic alcohol consumption can cause multi-organ damage including myocardial dysfunction. There are no specific targeted histological or immunological biomarkers for the diagnosis of alcohol-induced cardiomyopathy. Various pathophysiological mechanisms have been postulated in the development of cardiomyopathy however one key factor undergoing active research is the role of genetic mutation and susceptibility to develop cardiomyopathy. Due to its significant toxicity, studies have avoided its direct instillation, as it produces indiscriminate cell damage even at low doses.

5. The effects of Moderate Consumption of Ethanol and Binge-drinking

Data suggests patients alcoholic cardiomyopathy is especially dangerous because with successful quitting of alcohol have improved overall outcomes with a reduced number of inpatient admissions and improvement in diameter size on echocardiogram. Alcoholic cardiomyopathy is a leading cause of non-ischemic dilated cardiomyopathy in United States. Myocardial depression secondary to alcohol is initially reversible however prolonged sustained alcohol use leads to irreversible dysfunction. A standard drink contains 10 g of alcohol, equivalent to 100 mL of wine, 300 mL of beer, or 40 mL of spirits.

Diagnosis and Tests

• At present, ACM is defined as a dilated cardiomyopathy of toxic origin with low left-ventricle ejection fraction, chamber dilatation, and progression to congestive heart failure 18,52,53.
• Additionally, the accepted ACM definition does not take into account a patient’s sex or body mass index (BMI).
• 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.
• More than 30% of the myocyte ventricular fraction can be replaced by fibrotic tissue, thus decreasing the heart elasticity and contractile capacity 64 (Figure 2).
• The effect measure for each outcome was conducted using the mean differences effect measure, where the outcomes were assessed in identical units across the various literature reviews used in the study.

Regarding ICD and CRT implantation, the same criteria as in DCM are used in ACM, although it is known that excessive alcohol intake is specifically linked to ventricular arrhythmia and sudden cardiac death71. As it is not uncommon in ACM for patients to experience a significant recovery of systolic function, it is particularly challenging in this disease to decide the most appropriate time to implant an ICD and whether it is necessary to replace a previously implanted device. Future studies in ACM should also address this topic, which has important economic consequences. 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. These changes, though subtle, were similar to those found by Ferrans and Hibbs in eight deceased individuals diagnosed with ACM42,43.

• This activity highlights the role of the interprofessional team in caring for patients with this condition.
• 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.
• We review the current thinking on the pathophysiology, clinical characteristics, and treatments available for alcoholic cardiomyopathy.

Is Alcohol Ever Beneficial to Your Health?

Alternatively, studies have analysed its effect by combining ethanol with cyanamide. This substance is a potent inhibitor of the enzyme acetaldehyde dehydrogenase, so it increases the presence of acetaldehyde, and it promotes its effects.48,50 The harmful effects of this substance have been found to be exerted at various levels, in both animal and human models. The pathophysiology of AC involves a combination of direct toxic effects of alcohol on the myocardium, oxidative stress, mitochondrial dysfunction, https://ecosoberhouse.com/ and genetic susceptibility.

• These include damaging factors such as acetaldehyde or ROS, cardiac fibrosis, or apoptosis.
• Echocardiography may reveal a mild or severe depression of cardiac function and ejection fraction or even show hypertrophy in the beginning 109.
• In the mid-1960s, another unexpected heart failure epidemic among chronic, heavy beer drinkers occurred in two cities in the USA, in Quebec, Canada, and in Belgium.
• This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

In addition, acetaldehyde is able to interact with proteins and produce protein-adduct compounds that are highly reactive and may induce additional inflammatory and immunologic heart damage 78. Therefore, because of its multiple actions, acetaldehyde may influence ACM pathogenesis in addition to ethanol effect itself 20,76,77. The first clinical recognition of ACM was performed by Hippocrates in Greece during the 4th century B.C. However, its modern clinical report was delayed until the 19th century, where specific ACM cases were clinically described in Germany and England 1. During the 20th century, the physiopathological basis for ACM was progressively established 6. At present, ACM is defined as a dilated cardiomyopathy of toxic origin with low left-ventricle ejection fraction, chamber dilatation, and progression to congestive heart failure 18,52,53.

If you have an abnormal heart rhythm, talk with your healthcare provider before drinking. At ultrastructural level, dysfunction on the transition pore in the inner membrane is related to ethanol exposure 111. In addition, ethanol induces mitochondrial-dependent apoptosis pathways with Bax and caspase activation 101. Though they aren’t causes of alcohol-induced cardiomyopathy, other lifestyle choices can make it worse. These include using recreational drugs (especially those that affect your heart, such as cocaine) and tobacco (which has major negative effects on your heart, lungs and circulatory system).