The Effects of Ethanol on the Heart: Alcoholic Cardiomyopathy

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). Some cardiomyokines, such as FGF21, may regulate this process of alcohol-induced cardiac fibrosis 119. Occidental Berberi is the term used for the clinical scenario caused by thiamine deficit, a situation commonly present in chronic alcohol misuse, and was attributed as the cause of ACM 68,69.

• As women typically have a lower BMI than men, a similar amount of alcohol would reach a woman’s heart after consuming smaller quantities of alcohol.
• This can cause heart inflammation, leading to an atypically fast heart rhythm, such as atrial fibrillation (AF).
• He recruited 48 patients admitted to hospital with cardiomegaly without a clear aetiology and severe alcoholism.
• Alcohol septal ablation is a commonly used procedure to treat hypertrophic cardiomyopathy — the most common type of inherited heart disease.

3. Relationship between independent predictors and all-cause mortality

The majority of the echocardiographic studies performed on asymptomatic alcoholics found only mild changes in their hearts with no clear impairment of the systolic function. For example, a slight increase in the pre-ejection period/left ventricular ejection time ratio (PEP/LVET) was found by some authors, suggesting a sub-clinical impairment of systolic function21,33. Mathews and Kino found a small, but significant increase in left ventricular mass in individuals consuming at least 12 oz of whisky during 6 years and 60 g of ethanol per day, respectively22,40. Finally, only Urbano-Márquez et al24 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. One of the relevant facts in ACM is the existence of a clear gender difference, women being more susceptible to the toxic effects of alcohol than men at the same level of lifetime ethanol consumption 93,94. This fact has been assessed with echocardiographic monitoring in women consuming high doses of ethanol both in the subclinical period of disease 46 as well as in the clinical period when congestive heart failure appears 95.

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Specifically, ethanol disturbs the ryanodine Ca2+ release, the sarcomere Ca2+sensitivity 102,103, the excitation–contraction coupling and myofibrillary structure, and protein expression, decreasing heart contraction 86. Ethanol-induced disruption of ribosomal protein synthesis also contributes to non-contractile protein depletion 104. Several aspects of mitochondrial https://mgodeloros.ru/stati/pohmele-pohozhe-ne-silno-vlijaet-na-vremja-do.html 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.

• Prompt treatment can help prevent the disease from getting worse and developing into a more serious condition, such as congestive heart failure (CHF).
• The risk of ACM significantly increases with alcohol intake exceeding 80 g per day for a minimum of five years 3.
• Dilated cardiomyopathy secondary to alcohol use does not have a pre-defined exposure time.
• Despite this clear epidemiological evidence of ethanol’s unsafe consumption and increased health risk, results of consumption policies are not effective enough.

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One of the few papers analysing genetic susceptibility in ACM was published by Fernández-Solà et al64 in 2002. He compared the prevalence of different polymorphisms of the angiotensin-converting enzyme gene in 30 ACM patients and in 27 alcoholics with normal ventricular function. 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. However, this individual susceptibility mediated by polymorphisms of the angiotensin-converting enzyme gene does not appear to be specific to ACM insofar as several diseases, including some that are not of a cardiologic origin, have been related to this genetic finding65. Unfortunately Lazarević et al23, https://www.rusmoney.com/dictionary/engrus_slovar.html?dic_tid=2494 as in most of these studies, systematically excluded patients with a history of heart disease or with HF symptoms. It is therefore possible that most of these studies may have also consistently omitted most alcohol abusers in whom alcohol had already caused significant ventricular dysfunction.

• Cobalt poisoning and alcohol together acted synergistically in these patients.
• In recent years, basic and clinical research has shed light on its pathogenesis, which includes direct toxic effects of alcohol on the myocardium, oxidative stress, mitochondrial dysfunction, and genetic susceptibility.
• It also appears that the changes emerging in ACM patients only differ from idiopathic DCM in quantitative terms, with histological changes being more striking in idiopathic DCM than in ACM44.
• Studies of alcohol and stroke are complicated by the various contributing factors to stroke.
• Growth factors and cardiomyokines are relevant molecules that may modify this process.
• Incidence of alcoholic cardiomyopathy ranges from 1-2% of all heavy alcohol users.

Natural history and prognosis of alcohol-induced cardiomyopathy

However, in this context, experimental in vitro studies using cardiomyocytes have http://modnaya.ru/shop/aliexpress/2003-1/200000532/200000663/Costumes-Accessories.htm shown that alcohol depresses the contractile capacity of the myocardium, regardless of the sympathetic tone and the haemodynamic conditions36. Alcoholic cardiomyopathy can present with signs and symptoms of congestive heart failure. Symptoms include gradual onset worsening shortness of breath, orthopnea/paroxysmal nocturnal dyspnea. Palpitations and syncopal episodes can occur due to tachyarrhythmias seen in alcoholic cardiomyopathy. In the absence of myocardial biopsy, the diagnosis of myocarditis is always questionable.

S3 gallop sound along with apical pansystolic murmur due to mitral regurgitation is often heard. Acute can be defined as large volume acute consumption of alcohol promotes myocardial inflammation leading to increased troponin concentration in serum, tachyarrhythmias including atrial fibrillation and rarely ventricular fibrillation. The association between alcohol-induced cardiomyopathy and myocarditis is controversial. In one six-patient study (12) focusing on alcoholic cardiomyopathy, the surprising histological findings on endomyocardial biopsy of two patients was found to be myocarditis with lymphocytic infiltration in association with myocyte degeneration or focal necrosis.