Moreover, myofibrils showed a progressively distorted structure, resulting in a homogeneous mass. 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. Acetaldehyde is produced at a lower quantity in the heart as compared to the liver, and systemic acetaldehyde does not achieve toxic heart concentrations 77. 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.

alcoholic cardiomyopathy

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alcoholic cardiomyopathy

In contrast, European studies focusing on the prevalence of ACM included only subjects diagnosed with DCM and applied the consumption threshold of 80 g/d for ≥ 5 years, finding an ACM prevalence of 23%-47% among idiopathic DCM patients9-12 (Figure 1). Askanas et al21 found a significant increase in the myocardial mass and of the pre-ejection periods in drinkers of over 12 oz of whisky (approximately 120 g of alcohol) compared to a control group of non-drinkers. However, no differences were found in these parameters between the sub-group of individuals who had been drinking for 5 to 14 years and the sub-group of individuals who had a drinking history of over 15 years. Kino et al22 found increased ventricular thickness when consumption exceeded 75 mL/d (60 g) of ethanol, and the increase was higher among those subjects who consumed over 125 mL/d (100 g), without specifying the duration of consumption. In another study on this topic, Lazarević et al23 divided a cohort of 89 asymptomatic individuals whose consumption exceeded 80 g/d (8 standard units) into 3 groups according to the duration of their alcohol abuse.

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Although a small number relative to the more than 1000 proteins localized to amphetamine addiction treatment the mitochondria, high fidelity mtDNA is critical in the formation and stability of the complexes important for oxidative phosphorylation 69, 75-78. The consequence of the decrease in many mitochondrial proteins is poorly functioning mitochondria. Experimental studies analysing the depressive properties of alcohol on the cardiac muscle invariably use similar approaches31-39. Accordingly, a given amount of alcohol is administered to volunteers or alcoholics, followed by the measurement of a number of haemodynamic parameters and, in some cases, echocardiographic parameters.

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alcoholic cardiomyopathy

Since ethanol consumption of the global population is not currently under control 2, the incidence of alcoholic cardiomyopathy is expected to be maintained in the future, especially in specific population groups, such as adolescents and young people 3. Therefore, efforts for the prevention, early detection, and specific treatment in this relevant disease should be established 45. The direct dose-dependent effect between alcohol intake and development of ACM is clearly established 50,52, women being more sensitive than men to the toxic effects of ethanol on the heart 46. However, genetic polymorphisms, the use of other concomitant drugs (tobacco, cocaine), and the https://ecosoberhouse.com/ presence of other cardiac risk factors (hypertension, diabetes) may influence and worsen the natural course of ACM in each specific individual 27,72,98.

3. Ethanol or Acetaldehyde

Dysregulated excessive autophagy, together with other factors such as oxidative stress, neurohormonal activation, and altered fatty acid metabolism, contributes to cardiac structural and functional damage following alcoholism. This influences the maintenance of cardiac geometry and contractile function, increasing the development of ACM 121. In ACM, protein degradation with sarcomere disarray and contractile protein loss has been suggested to be a key point of autophagy induction 18. Different pathogenic hypotheses have been suggested, such as the pivotal role of acetaldehyde 122, the role of oxidative stress and stress signaling cascades 109, and the translocation alcoholic cardiomyopathy is especially dangerous because of NFkB into the nucleus 106. Apoptosis occurs mainly as a consequence of lipid peroxidation and oxidative stress in various body organs.