Data on the amount of alcohol consumption required to cause ACM are limited and controversial. According to the NIAAA, many people with AUD recover, although setbacks are common among those receiving treatment. Individuals who completely quit alcohol generally have improved overall outcomes.

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Clinical overview, pathogenesis, treatment and prognosis of alcoholic cardiomyopathy. DCM, dilated cardiomyopathy; HF, heart failure; HFrEF, heart failure with reduced ejection fraction; HTx, heart transplant; LVEDD, left ventricular end-diastolic diameter; LVEF, left ventricular ejection fraction; SD, standard deviation. Alcoholic cardiomyopathy is a form of dilated cardiomyopathy (heart disease) caused by chronic alcohol consumption or long-term alcohol abuse. Alcoholic cardiomyopathy is a form of heart disease caused by alcohol abuse.

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They typically require fewer hospitalizations and show improved heart function on ECG readings. A 2023 article notes that ACM carries a more positive outlook than ischemic cardiomyopathy, which refers to heart damage that typically occurs due to CAD. As a point of reference, consuming 80 grams of alcohol daily for at least 5 years can significantly increase the risk of ACM. Moreover, ranolazine prevents ethanol-induced https://ecosoberhouse.com/ atrial arrhythmias both in vitro and in vivo by blocking the late sodium current, which is activated by CaMKII.112 Its effect on preventing the decrease of LVEF in AC is currently unknown. Biomarkers of heart failure such as NT-proBNP and of myocardial necrosis such as the troponins and CKMB indicate heart failure or myocytolysis.

Data Availability

This article provides a clear and compassionate overview of alcoholic cardiomyopathy, covering its risk factors, symptoms, diagnostic tests, treatments, and lifestyle changes that can help manage the condition. By understanding this condition better, patients can take steps to improve their heart health and overall well-being. First, we devised a search strategy to retrieve relevant articles from PubMed. Next, we established inclusion and exclusion criteria to determine the eligibility of articles. Inclusion criteria encompassed articles that focused on ACM or the relationship between alcohol abuse and cardiac dysfunction, involved human subjects or relevant animal models, were written in the English language, and were published within the last 10 years.

To assess the quality and validity of the included studies, we performed a critical appraisal using appropriate tools such as the Newcastle-Ottawa Scale for observational studies or the Cochrane Risk of Bias tool for clinical trials. This assessment allowed us to evaluate the methodological rigor of each study and determine its overall quality and potential impact on the literature review. Finally, we analyzed and presented the synthesized literature, along with relevant findings and conclusions from the included studies, in a coherent manner. We identified main themes and sub-themes to provide a comprehensive overview of the current state of knowledge regarding ACM. By following this methodology, we aim to contribute to the existing body of knowledge on ACM, providing a reliable and up-to-date understanding of its pathogenesis, clinical features, diagnostic approaches, treatment options, and potential preventive strategies. As a net effect, negative inotropism may result and contribute to heart failure.

• Long-term alcohol abuse weakens and thins the heart muscle, affecting its ability to pump blood.
• Alcohol can directly affect the heart’s electrical system, leading to abnormal rhythms like atrial fibrillation or ventricular tachycardia.
• Your doctor might prescribe ACE inhibitors and beta-blockers to help lower your blood pressure.
• “Sola dosis facit venenum” is an old Latin proverb that means “the dose makes the poison”, a conclusion that defines the basic principle of today’s toxicology.

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After a follow-up period of 47 mo, a significantly higher survival rate was observed among patients with DCM compared to patients with ACM. In this study, the only independent predictor of cardiac death was alcohol abstinence. 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. In their autopsies, he described finding dilated cavities of the heart and fatty degeneration of the ventricular walls14. Orthopnea, or difficulty breathing while lying flat, affects around 40-50% of patients with alcoholic cardiomyopathy.

• More than 1.8 million individuals in Germany with a total population of 81 million inhabitants are alcohol dependant.
• Elevations of the transaminases (GOT, GPT), especially a ratio of GOT/GPT higher than 2 might be indicative of alcoholic liver disease instead of liver disease from other etiologies 120, 121.
• Patients may notice improvements in energy levels and well-being within a few weeks.

Doctors may ask about your alcohol history and perform blood tests, including liver function tests, to detect alcohol-related damage. Genetic testing may be recommended if there’s a family history of dilated cardiomyopathy. An echocardiogram can reveal enlarged heart chambers in both conditions, but alcohol-related liver damage or a history of heavy drinking points more toward alcoholic cardiomyopathy. Dizziness is reported what is alcoholic cardiomyopathy in about 20-30% of patients with alcoholic cardiomyopathy. It can occur when the heart is unable to pump enough blood to the brain, leading to lightheadedness or a sensation of spinning. Dizziness may also be related to arrhythmias or low blood pressure, both common in patients with weakened heart function.

Even just one night of excessive drinking can interfere with your heart’s electrical signals. If you want to avoid alcohol altogether and alcohol is a major temptation for you, you may wish to look for social settings where alcohol will not be served. If you have to go to events where alcohol is served, consider telling people close to you to help you drug addiction with your goal.

• 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.
• With his innovative approach and unwavering commitment to providing evidence-based solutions, he is a highly sought-after speaker and a leader in his field.
• If you experience any of the following effects of heart problems, seek medical attention.
• After a person with AUD completes a rehab program, they may need aftercare support.

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. Post-mortem biopsies from the hearts of human alcoholics revealed that the myocardial mitochondria is enlarged and damaged 1-9. Along with signs of heart failure such as increased N-terminal pro-B-type natriuretic peptide, blood tests can provide hints suggesting chronic alcohol abuse.

• Although all of the studies reported an increase in left ventricular mass and volume, it cannot generally be stated that they provided the alcohol consumption dosage required to cause ACM.
• The trace amounts of arsenic have not been comparable to the arsenic-in-beer endemic in Manchester but may still reach up to 10-times the amount admitted for arsenic in drinking water in the European Union and the US.
• Furthermore, Fernández-Solá et al30, when analysing a population of alcoholics, found a higher prevalence of DCM in alcoholics than among the general population.
• Atrial fibrillation and supraventricular tachyarrhythmias are common findings in 15–20 % of patients 111, whereas ventricular tachycardias are rare 112.

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It took almost 60 years before further attention was paid to the complex interaction between the heart and the peripheral vasculature in various cross-sectional and prospective epidemiologic studies, which have empirically confirmed this early report. One is aware today that alcohol may cause an acute but transient vasodilation, which may lead to an initial fall in blood pressure probably mediated by the atrial natriuretic peptide (ANP) 46. But also short- and long-term pressor effects mediated by the renin–aldosterone system and plasma vasopressin have been described 47, 48.