alcoholic cardiomyopathy (ACM) is a type of heart disease that can result from chronic alcohol consumption. Experts do not know what quantity of alcohol a person needs to consume to develop ACM. They also have not identified the minimum length of time someone needs to drink alcohol before developing the condition. Alcoholic cardiomyopathy is a form of heart disease caused by alcohol abuse. Long-term alcohol abuse weakens and thins the heart muscle, affecting its ability to pump blood. When your heart can’t pump blood efficiently, the lack of blood flow disrupts all your body’s major functions.
Heartache in a Bottle: Understanding Alcoholic Cardiomyopathy
After myocyte apoptosis or necrosis, the heart tries to repair and regenerate this tissue damage [39,123], but the heart regenerative capacity is low as a result of the ethanol aggressive damage and develops ineffective repair mechanisms such as progressive fibrosis [124,125]. In fact, ethanol itself decreases the myocyte regeneration capacity https://ecosoberhouse.com/ and increases the fibrogenic process [52,126]. Subendocardial and interstitial fibrosis progressively appear in the course of ACM, usually in advanced stages [52,56]. 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).
1. The Natural Course of ACM
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Alcoholic Cardiomyopathy and Your Health
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- Experts do not know what quantity of alcohol a person needs to consume to develop ACM.
- The primary treatment for ACM involves complete abstinence from alcohol or other drugs.
- In addition, the AHA advises against starting to drink alcohol solely for potential health benefits, as the risks can outweigh the advantages.
- The percentage of apoptotic myocytes in ACM is relatively low but, in combination with a persistent decrease in myocyte proliferation, they may contribute to an absolute cell loss and decreased cardiac contractility [52,115].
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. One relevant question concerning ethanol cardiac toxicity is if ethanol itself or its active metabolite acetaldehyde causes cardiac damage [73,74]. In fact, both molecules are directly cardiotoxic, decreasing structural protein synthesis and heart contractility and increasing oxidative and metabolic damage, leading to autophagy [20,75]. In experimental studies, acetaldehyde directly impairs cardiac contractile function [76], disrupts cardiac excitation–contraction coupling, and promotes oxidative damage and lipid peroxidation [20].
Coronary artery disease and atherosclerosis
Ethanol-induced disruption of ribosomal protein synthesis also contributes to non-contractile protein depletion [104]. Several aspects of mitochondrial function, including respiratory complex activities and mitochondrial-dependent oxidative damage and apoptosis, are also induced by ethanol [26,100]. Myocyte cytoskeletal structure [21], connexin channel communication, and desmosomal contacts are affected by ethanol, causing structural cell instability [105]. Ethanol may induce changes in nuclear regulation of transcription with a dose-dependent translocation of NFkB into the nucleus [106]. The resulting effect in those multiple sites may be additive and synergistic, increasing the final damage [20,52] (Figure 1).
5. The effects of Moderate Consumption of Ethanol and Binge-drinking
- Furthermore, Fernández-Solá et al[30], when analysing a population of alcoholics, found a higher prevalence of DCM in alcoholics than among the general population.
- Depression of LV ejection fraction (EF) is the hallmark of this period that also occurs with a reduction in LV shortening fraction, increase in LV diameter, and mass indices that may be measured by echocardiography or cardiac MR spectroscopy [40,52].
- By being more susceptible to the damaging effects of alcohol, you’re more likely to develop alcoholic cardiomyopathy.
- If you see any signs of alcoholic cardiomyopathy, contact emergency medical services immediately.
- List of the 15 articles reviewed in this study, indicating the study authors, objectives, design, sample size, patient characteristics, experimental procedures, outcome measures, and main findings.
- However, it has been evidenced that ACM may develop in the absence of protein or caloric malnutrition [38].
Excessive EtOH consumption is one of the main causes of non-ischemic dilated cardiomyopathy (CMP), representing around one-third of cases [30]. More specifically, atrial fibrillation with rapid ventricular response is a cause of arrhythmia-induced cardiomyopathy,61 which can potentially worsen LVEF in AC patients, on top of the direct toxic effect of ethanol, acetaldehyde damage, or the aforementioned genetic factors. Prior studies have investigated the impact of ethanol on changes in the activity and levels of oxidative enzymes. 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.
Enhancing Healthcare Team Outcomes
This observation led to the erroneous belief that alcohol is an immediate coronary vasodilator. Symptomatic relief of angina could be through the anesthetic effect of ethanol or through peripheral vasodilation, which could transiently reduce oxygen demand of the heart. Clinical observation confirmed that several days to weeks of drinking show higher and weeks of abstinence lower pressures. Alcohol intake may also interfere with the drug and dietary treatment of hypertension.
Clinical manifestations and diagnosis of alcohol-induced cardiomyopathy
