The Alcoholic Cardiomyopathies – Genuine and Pseudo

Constant, Jules

doi:10.1159/000006886

Cited by 9 publications

(4 citation statements)

References 31 publications

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“…Data from our group also suggested that acetaldehyde-induced cardiac mechanical dysfunction may be ablated by folate or thiamine supplementation [Aberle et al 2004[Aberle et al , 2003, suggesting a possible interaction between acetaldehydeinduced cardiac toxicity and nutritional status. This is somewhat consistent with the favorable response of patients with alcoholic cardiomyopathy to thiamine and nutrition treatment [Constant, 1999].…”

Section: Nonacetaldehyde-related Mechanism In Alcoholic Cardiomyopathysupporting

confidence: 81%

Mechanisms of alcoholic heart disease

Ren

Wold

2008

Therapeutic Advances in Cardiovascular Disease

103

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Compromised heart function is regularly seen in patients with chronic alcohol ingestion and is often manifested as cardiomegaly, reduced myocardial contractility (with concomitant reductions in ejection fraction and stroke volume), myocardial fibrosis, enhanced risk of stroke and hypertension, and disruptions in the myofibrillary structure. A number of mechanisms including oxidative damage, deposition of triglycerides, altered fatty acid extraction, decreased myofilament Ca(2+) sensitivity, and impaired protein synthesis have been proposed for the development of alcoholic cardiomyopathy. Nonetheless, the underlying mechanism(s) has not been delineated. Several alcohol metabolites have been identified as specific toxins of myocardial tissue, including ethanol, its first and major metabolic product--acetaldehyde--and fatty acid ethyl esters. Acetaldehyde directly impairs cardiac contractile function, disrupts cardiac excitation-contraction coupling and promotes oxidative damage and lipid peroxidation. Unfortunately, the most direct approach to studying this (direct administration of acetaldehyde) is impossible, since direct intake of acetaldehyde is highly toxic and unsuitable for chronic studies. In order to overcome this obstacle, transgenic mice have recently been produced to artificially alter ethanol/acetaldehyde metabolism, resulting in elevated acetaldehyde levels after ethanol ingestion. This review will summarize some of the postulated mechanisms for alcoholic cardiomyopathy, with special emphasis on animal models.

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Section: Nonacetaldehyde-related Mechanism In Alcoholic Cardiomyopathysupporting

confidence: 81%

Mechanisms of alcoholic heart disease

Ren

Wold

2008

Therapeutic Advances in Cardiovascular Disease

103

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“…Data from our group also suggested that acetaldehyde-induced cardiac mechanical dysfunction may be ablated by folate or thiamine supplementation [116,117], suggesting a possible interaction between acetaldehyde-induced cardiac toxicity and nutritional status. This is somewhat consistent with the favorable response of patients with alcoholic cardiomyopathy to thiamine and nutrition treatment [118]. …”

Section: Mechanisms Of Alcoholic Diseasessupporting

confidence: 82%

Alcohol and Acetaldehyde in Public Health: From Marvel to Menace

Guo

Ren

2010

IJERPH

136

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Alcohol abuse is a serious medical and social problem. Although light to moderate alcohol consumption is beneficial to cardiovascular health, heavy drinking often results in organ damage and social problems. In addition, genetic susceptibility to the effect of alcohol on cancer and coronary heart disease differs across the population. A number of mechanisms including direct the toxicity of ethanol, its metabolites [e.g., acetaldehyde and fatty acid ethyl esters (FAEEs)] and oxidative stress may mediate alcoholic complications. Acetaldehyde, the primary metabolic product of ethanol, is an important candidate toxin in developing alcoholic diseases. Meanwhile, free radicals produced during ethanol metabolism and FAEEs are also important triggers for alcoholic damages.

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“…In accordance with Bryson`s data (26), alcohol consumption appears to have a more complex relationship with episodes of heart failure, there is no linear dependence. Nonetheless, a strong contribution of hypertension and atrial fi brillation as risk factors for strokes must be considered, especially in the background of heavy drinking (23,27).…”

Section: Discussionmentioning

confidence: 99%

Alcoholic cardiomyopathy and cardiovascular events – an insight from the Liptov region

Kycina¹,

Murı́n²

2013

BLL

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Abstract:Aim: This study was conducted to study the association between alcohol consumption and cardiovascular events and echocardiographical parameters in 100 consumers with the average daily dose <120 g and ≥120 g of alcohol per day during a 4-year follow-up. Methods: 100 patients/heavy alcohol consumers (on average ≥ 80 g daily), with no cardiovascular disease, divided into 2 groups, underwent a baseline echocardiographic and clinical evaluation and were followed-up for cardiovascular events, biochemical analysis and rhythm disorder for 4 years. Results: Data regarding the dose and duration of alcohol consumption showed a low correlation and nonlinear character between the duration of alcohol consumption and monitored parameters. There were no differences between the groups in the echo-parameters ejection fraction EF (p=0.43), in the diameter of left atrium LA (p=0.51). Left chamber -LVEDD -was slightly bigger in the group with a heavier drinking pattern (p=0.09). There were no differences in biochemical parameters between the groups. When comparing these two groups of consumers the percentage of diabetes mellitus (p=0.283), episodes of heart failure (p=0.308), atrial fi brillation (p=0.652), cerebral vascular accident (p=0.722) and delirium (p=0.559) were not signifi cantly different; only 2 subjects suffered from myocardial infarction during the follow-up. Conclusion: We conclude, that no signifi cant differences (p<0.05) between the two groups of heavy alcohol consumers were observed in echo parameters, biochemical values and cardiovascular events (Tab. 4, Ref. 28). Full Text in PDF www.elis.sk. Key words: alcoholic cardiomyopathy, echocardiography, heart failure, atrial fi brillation, delirium. Alcohol abuse is unquestionably harmful. Compelling epidemiological evidence suggests that long lasting (strong) alcohol consumption (on average ≥80-100 g per day) is associated with the risk of development of alcoholic cardiomyopathy. Alcoholic cardiomyopathy (ACMP) is a common cause of cardiomyopathies (CMP) and the most common form of the secondary CMP (1, 2). Phenotypically and clinically it closely resembles the idiopathic dilated cardiomyopathy (DCMP). The disorder is linked to ongoing excessive alcohol consumption and appears to be both dose-related and responsive to cessation of alcohol exposure. Alcohol exposure also increases the risk of comorbidities that can contribute to cardiovascular disease, such as hypertension, stroke, arrhythmia and also sudden cardiac death. Liptov region in Northern Slovakia is known for heavy alcohol consumption -estimated consumption 13.3 litres/100 % of ethanol (attributable to a higher consumption of spirits, not wine or beer) per year (3) and many of these patients frequently use healthcare system facilities for that reason. In Slovakia, the estimated consumption of alcohol is on average 10.3 litres/100 % of ethanol per year (4, 5). In our fi rst smaller survey from 2004 (47 male consumers, 16 abstainers in the comparative group, 54 years mean age, no medical treatment, n...

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The Alcoholic Cardiomyopathies – Genuine and Pseudo

Cited by 9 publications

References 31 publications

Mechanisms of alcoholic heart disease

Mechanisms of alcoholic heart disease

Alcohol and Acetaldehyde in Public Health: From Marvel to Menace

Alcoholic cardiomyopathy and cardiovascular events – an insight from the Liptov region

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