However, no other biopsy study of patients with presumed alcohol-induced cardiomyopathy has found this. It is likely that those two patients were incorrectly labelled with alcohol-induced cardiomyopathy. A 48-year-old woman presented to the emergency department with confusion and shortness of breath. She admitted to an eight-year history of the ingestion of more than 600 mL of vodka per day. Within the month before presentation, alcoholic cardiomyopathy symptoms she had increased her alcohol intake by drinking a large glass of 70% ethanol per day.
Health Conditions
Illustrations of a typical heart, as shown on the left, and a heart with hypertrophic cardiomyopathy. Note that the heart walls are much thicker in the heart with hypertrophic cardiomyopathy. If you have the condition, your healthcare professional might recommend that your family members be checked.
- The point at which these abnormalities appear during the course of an individual’s lifetime of drinking, such that the abnormalities can be called a DCM, is not well established and is highly individualized.
- Often, when a doctor suspects cardiomyopathy, they will order an echocardiogram.
- Apoptosis may be induced by ethanol through mitochondrial membrane permeabilization and the release of pro-apoptotic factors (cytochrome c) from the mitochondrial inter-membrane space to the cytosol.
- Alcoholic cardiomyopathy (ACM) is defined by a dilated and impaired left ventricle due to chronic excess alcohol consumption.
- Abstinence is the preferred goal, although controlled drinking may still improve cardiac function.
- Therefore, the need to establish a more effective control on ethanol consumption has been repeatedly claimed 2.
- A literature review using the PubMed database with the search terms ‘alcoholic cardiomyopathy’, ‘alcoholic heart disease’, was conducted up to January 2017.
General Health
Further research is required to determine the definitive role of genetics on ACM pathophysiology. The NIAAA provides an Alcohol Treatment Navigator, where people can learn about AUD treatments and access care and support networks locally. According to the NIAAA, many people with AUD recover, although setbacks are common among those receiving treatment. Alcoholic cardiomyopathy is best managed with an interprofessional approach with the involvement of primary care physician and cardiology. Other deficiencies including nutritional such as thiamine or other toxic materials ingested may lead to additional concomitant complications.
Clinical manifestations and diagnosis of alcohol-induced cardiomyopathy
In addition, the AHA advises against starting to drink alcohol solely for potential health benefits, as the risks can outweigh the advantages. It is crucial to exercise caution and be aware of individual tolerance and personal health circumstances when making decisions about alcohol consumption. Consulting with a healthcare professional can provide personalized advice and guidance.
Cardiovascular and Skeletal Muscle Systems
The ‘Quebec beer drinkers’ cardiomyopathy’ was related to cobalt supplementation to beer that was made in the past. It was described as a form of DCM with severe pericardial effusion, low cardiac output, and purplish skin coloration. Another curious hypothesis from Germany suspected that some ethanol additives, such as anti-foam beer products with arsenic or cobalt content, produced cardiac toxicity and development of ACM 71. Therefore, it is evident that ACM may develop with normal serum thiamine and electrolyte levels 38,66. Consumption of other drugs such as cocaine or tobacco may interact with ethanol and potentiate the final ethanol-related cardiac damage 22,72.
- Furthermore, 89% of the alcoholics with a DD genotype developed ACM, whereas only 13% of those with an II or ID genotype developed this condition.
- The resulting effect in those multiple sites may be additive and synergistic, increasing the final damage 20,52 (Figure 1).
- Antioxidant, anti-inflammatory, anti-apoptotic, and antifibrogenic mechanisms try to avoid myocyte necrosis and heart fibrosis 14,30,58.
1. Study limitations
Catalase activity is significantly increased 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. They demonstrated a much higher catalase activity among rats suffering from ACM. 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. Myocyte apoptosis, based on assessment of TUNEL staining and caspase activity, has been demonstrated to be an active phenomenon leading to myocyte loss in diverse cardiomyopathies 113,114 and also in chronic high-dose ethanol consumption both in experimental 109 and clinical models 101.
