alcoholic cardiomyopathy is especially dangerous because

In contrast, chronic and excessive alcohol consumption could lead to progressive cardiac dysfunction and heart failure (HF)[3]. New strategies to improve the natural course of ACM have been proposed as promising agents in this field [112,147]. Since ethanol has multiple cell targets with different pathological mechanisms implicated, those different strategies to directly target alcohol-induced heart damage are only partially effective and can only be used as support medication in a multidisciplinary approach [112]. They try to control myocardial remodeling to avoid the progression of myocyte hypertrophy [39,148] or fibrosis [149] and ventricle dysfunction and dilatation, as well as to increase the degree of myocyte regeneration [150]. Recently, new cardiomyokines (FGF21, Metrnl) and several growth factors (myostatin, IGF-1, leptin, ghrelin, miRNA, and ROCKs inhibitors) have been described as being able to regulate cardiac plasticity and decrease cardiac damage, improving cardiac repair mechanisms [112,119].

Is there an immediate risk of alcohol intake?

If you are a heavy drinker, talking to a primary care provider can help keep this condition from becoming even more severe in the future, or even prevent it from happening. Your provider is the best source of information and guidance, and they can connect you to other resources that can help and experts who can assist. Alcohol has toxic effects, alcoholic cardiomyopathy is especially dangerous because but your body can limit the damage and break alcohol down into non-toxic forms if you don’t drink too much too quickly. However, consistent heavy drinking strains those protective processes — especially in your liver — making them less effective. Ultimately, your body can’t keep up with the damage to multiple organ systems, including your heart.

  • In ACM, protein degradation with sarcomere disarray and contractile protein loss has been suggested to be a key point of autophagy induction [18].
  • The exact mechanism by which an increased adherence to the traditional Mediterranean diet exerts its favorable effects is not known.
  • In spite of numerous studies, the sequence of events that occur in alcohol-induced myocardial damage is still highly controversial.
  • Because hypertension may directly contribute to left ventricular (LV) dysfunction, this may be a confounding comorbidity in persons who abuse alcohol, and it should be differentiated from pure forms of alcoholic cardiomyopathy.
  • It is a type of dilated cardiomyopathy since it involves dilation or enlargement of one of the heart’s chambers.

4. The dose-Related Effect of Ethanol and Beverage Types on the Heart

  • Once the damage is considered irreversible, it’s difficult for the heart and rest of the body to recover.
  • Although there is beneficial potential in some patients, the coexistence of increased risk of cancer, neurological brain damage, and the high risk of ethanol addiction makes it necessary to discourage this low-dose consumption in the general population [19,41,45].
  • In addition, there is a relevant role on each organ, particularly on defense and adaptive mechanisms, with a clear induction of anti-oxidant, metabolic, and anti-inflammatory protective responses as a result of ethanol aggression [18,25,26].
  • In chronic alcoholics, arrhythmia may frequently appear in relation to episodes of ethanol abstinence because of the increased release of catecholamines and electrolyte deficiencies [19].

Certain microscopic features may suggest damage secondary to alcohol causing cardiomyopathy. Commonly seen cellular structural alterations include changes in the mitochondrial reticulum, cluster formation of mitochondria and disappearance of inter-mitochondrial junctions. Biomarkers of heart failure such as NT-proBNP and of myocardial necrosis such as the troponins and CKMB indicate heart failure or myocytolysis.

Is this condition only a chronic (long-term) problem?

  • Ethanol may induce changes in nuclear regulation of transcription with a dose-dependent translocation of NFkB into the nucleus [106].
  • Jugular venous distention, peripheral edema, and hepatomegaly are evidence of elevated right heart pressures and right ventricular dysfunction.
  • Ethyl alcohol has detrimental effects on myocardial metabolism; nevertheless, the pathogenetic mechanisms of alcoholic cardiomyopathy remain uncertain.
  • This altogether supports a causal relationship between alcohol consumption and a hypertensive state.
  • In fact, ACM is related to systemic damage induced by ethanol misuse and its global biological response [10,11,31].

Finally, only Urbano-Márquez et al[24] found a clear decrease in the ejection fraction, in a cohort of 52 alcoholics, which was directly proportional to the accumulated alcohol intake throughout the patients’ lives. Askanas et al[21] 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, https://ecosoberhouse.com/article/do-you-genuinely-like-the-feeling-of-being-drunk/ 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 al[22] 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.

alcoholic cardiomyopathy is especially dangerous because

alcoholic cardiomyopathy is especially dangerous because

A person can speak with a doctor about any concerns regarding lifestyle changes. ACM can also induce a feeling of fatigue or a decrease in exercise tolerance. A person may not be able to withstand the amount of exercise or activity as they had previously. Electrolyte abnormalities, including hypokalemia, hypomagnesemia, and hypophosphatemia, should be corrected promptly because of the risk of arrhythmia and sudden death.

Organ-Specific Toxicologic Pathology

  • This causes a decrease in sarcolemmal contraction and also disturbance in other intercellular organelles dependent of i.c.
  • Abstaining from alcohol may help some people recover, but others will need medication or even surgery.
  • 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].

Risk factors

alcoholic cardiomyopathy is especially dangerous because

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