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At least 19 recordsLinked to original sources
PubMed2003

Experimental Assessment of the Role of Acetaldehyde in Alcoholic Cardiomyopathy.

Alcoholism is one of the major causes of non-ischemic heart damage. The myopathic state of the heart due to alcohol consumption, namely alcoholic cardiomyopathy, is manifested by cardiac hypertrophy, compromised ventricular contractility and cardiac output. Several mechanisms have been postulated for alcoholic cardiomyopathy including oxidative damage, accumulation of triglycerides, altered fatty acid extraction, decreased myofilament Ca(2+ )sensitivity, and impaired protein synthesis. Despite intensive efforts to unveil the mechanism and ultimate toxin responsible for alcohol-induced cardiac toxicity, neither has been clarified thus far. Primary candidates for the specific toxins are ethanol, its first and major metabolic product - acetaldehyde (ACA) and fatty acid ethyl esters. Evidence from our lab suggests that ACA directly impairs cardiac function and promotes lipid peroxidation resulting in oxidative damage. The ACA-induced cardiac contractile depression may be reconciled with inhibitors of Cytochrome P-450 oxidase, xanthine oxidase and lipid peroxidation Unfortunately, the common methods to investigate the toxicity of ACA have been hampered by the fact that direct intake of ACA is toxic and unsuitable for chronic study, which is unable to provide direct evidence of direct cardiac toxicity for ACA. In order to overcome this obstacle associated with the chemical properties of ACA, our laboratory has used the chronic ethanol feeding model in transgenic mice with cardiac over-expression of alcohol dehydrogenase (ADH) and an in vitro ventricular myocyte culture model. The combination of both in vivo and in vitro approaches allows us to evaluate the role of ACA in ethanol-induced cardiac toxicity and certain cellular signaling pathways leading to alcoholic cardiomyopathy.

Journal Article↗
PubMedDate not supplied

[Enzymatic markers in the alcoholic cardiomyopathy].

Alcoholic cardiomyopathy can ensue from heavy consumption of alcohol over a long period of time. The clinical features include dilatation of the left ventricle, poor myocardial contractility with reduced left ventricular ejection volume, raised tissue enzymes. In numerous experimental data has been observed increased generation of oxygen and ethanol free radicals, indicate that free radicals are implied in myocardial and hepatic damage. Ethanol administration also elicits hepatic disturbances in the availability of antioxidant defense. The resulting antioxidative stress leads to enhanced lipid peroxidation and can also affect other important cellular component.

Adult↗
PubMed1984

Effect of chronic ethanol ingestion on the metabolism of copper, iron, manganese, selenium, and zinc in an animal model of alcoholic cardiomyopathy.

Alcoholic cardiomyopathy (AC) is one of the diseases caused by alcohol abuse, and there has been considerable debate about the possibility that nutritional factors may be important in the etiology of AC. In addition, there is evidence that ethanol may affect the metabolism of trace elements. The purpose of this investigation was to determine if chronic ethanol administration produces changes in the metabolism of the essential metals copper, iron, manganese, zinc, and selenium using an animal model of AC. Eighteen male Sprague-Dawley rats were divided into three groups: an ad libitum control group (AL), a pair-fed control group (PF), and an ethanol-dosed group (ETOH). The latter group received gradually increasing concentrations (5-25%) of ethanol in the drinking water for 15 wk. Food intake was monitored and urine and feces collected for a 4-d period during the study to determine ethanol effects on trace-element balance. Growth of both the PF and ETOH animals was inhibited. Ethanol produced substantial increases in liver manganese and decreases in liver copper and zinc. Metal concentrations in heart and concentrations in other tissues studied (spleen, testes, brain, bone, kidney, and muscle) did not differ significantly among the groups, except for testes selenium and kidney zinc. Reduced food intake and ethanol ingestion were associated with a reduced percentage of ingested selenium excreted in the urine. Deficiencies of copper, iron, manganese, selenium, and zinc in myocardial tissue are not likely to be involved in the pathogenesis of AC in the rat.

Animals↗
PubMed1990

Relationship between morbidity and mortality due to alcoholic cardiomyopathy and alcohol consumption in Australia.

The study was undertaken to determine whether morbidity and mortality rates for alcoholic cardiomyopathy vary with community alcohol consumption levels. The cardiomyopathy mortality comparisons for Australia from 1968 to 1978 showed a positive relationship for both males and females aged 30 to 59 years, and 60 years and over. From 1979 to 1986 a decrease in consumption was associated with a decrease in alcoholic cardiomyopathy mortality for females, and to a lesser extent males, aged 30 to 59 years. The morbidity comparisons for Western Australia from 1971 to 1984 gave similar results to the Australian mortality findings for the males aged 30 to 59 years. It appears that the prevention of alcoholic cardiomyopathy will be facilitated by lowering the overall level of alcohol consumption in the community.

Adult↗
PubMed1991

Rarity of preclinical alcoholic cardiomyopathy in chronic alcoholics less than 40 years of age.

Preclinical alcoholic cardiomyopathy, myocardial damage in the absence of overt congestive heart failure in chronic alcoholics, is well characterized at necropsy, but attempts to identify such a clinical entity before death have produced conflicting results. Studying subjects only at rest, the inclusion of older alcoholics and limitations of noninvasive techniques may explain some of the disagreement. To determine if preclinical alcoholic cardiomyopathy could be identified independent of the aforementioned limitations, 25 asymptomatic chronic alcoholics aged less than 40 years (mean 34), each of whom had consumed a minimum of 1 pint of whiskey or one 6-pack of beer greater than or equal to 5 days per week for greater than or equal to 5 years, underwent radionuclide ventriculography for measurements of systolic and diastolic function at rest, peak supine exercise and during recovery, and echocardiography for assessment of chamber size, wall thickness and left ventricular mass. Red blood cell levels of selenium and thiamine were measured to determine whether abnormalities were present in these 2 potential mediators of alcoholic cardiomyopathy. For comparison, an age-matched group of healthy control subjects was also studied. For alcoholics and control subjects at rest, mean ejection fraction (67 +/- 7% vs 71 +/- 6%) and diastolic peak filling rate (3.4 +/- 0.6 vs 3.3 +/- 0.6 end-diastolic volumes per second [EDV/s]) were similar.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

[Ultrastructure of the human heart sinus node in alcoholic cardiomyopathy under acute alcohol intoxication and without it].

An electron-microscopic study of the sinus nodes (SN) was conducted in the hearts of 8 males aged 32-60 who had suddenly died of alcoholic cardiomyopathy in the background of acute alcohol intoxication (4 cases) or without it (4 cases). The hearts of matched-for-age 7 males and 1 female whose cause of sudden death was other than cardiac served as control. It appeared that all the components of the sinus nodes from hearts of the study group underwent chronic or acute destructive changes. The latter were seen both in dark and clear SN conducting myocytes. There were also defects in neurohumoral regulation of the myocytic function due to nervous and microcirculatory SN disturbances. SN connective tissue was affected too. Relevance of the elicited SN changes to cardiac rhythm derangement and to the mechanism of sudden cardiac death is discussed.

Adult↗
PubMed1996

Changes in cardiac signal transduction systems in chronic ethanol treatment preceding the development of alcoholic cardiomyopathy.

Chronic alcohol consumption has been postulated as an important pathogenetic mechanism for the development of alcoholic cardiomyopathy. This form of chronic heart failure shares with other forms of cardiomyopathy the pronounced alterations of the adrenergic signal transduction systems. These alterations include a significant reduction of beta-adrenergic receptors and a reduced responsiveness of the adenylyl cyclase. Changes of other receptor systems such as alpha-adrenergic and muscarinic receptors have not been studied extensively so far. To address the question if changes of the adrenergic signal transduction systems may occur early in the development of alcoholic cardiomyopathy and if alpha 1-adrenergic receptors and muscarinic receptors may be subjected to an altered expression even before severe impairment of the left ventricular function becomes obvious, rats were chronically fed with an alcohol diet containing 35% of total calorie intake as ethanol. In cardiac plasma membranes beta-adrenergic receptors, alpha 1-adrenergic receptors, muscarinic receptors and adenylyl cyclase activities were determined after 4 and 8 weeks of chronic alcohol treatment. After these periods of chronic alcohol diet no signs of overt heart failure such as pleural effusion or increased lung wet weight as parameters for congestion were present. Body weight gain was comparable in the controls and under chronic alcohol treatment in these adolescent rats. Both after 4 and 8 weeks of chronic alcohol treatment the density of cardiac beta-adrenergic receptors remained unchanged and all adenylyl cyclase activities remained fully responsive. In contrast, after 8 weeks of alcohol treatment the developmental increase of cardiac muscarinic receptors in the adolescent rats was greatly impaired resulting in a significantly reduced expression of these receptors even before clinical signs of heart failure. In contrast the density of cardiac alpha 1-adrenergic receptors were significantly reduced already after 4 weeks of chronic alcohol treatment with an additional impairment of the developmental increase after 8 weeks of alcohol treatment. These data characterize for the first time early changes of cardiac receptor system in chronic alcohol treatment which precede the development of overt heart failure. These changes include alpha 1-adrenergic and muscarinic receptors, but in contrast to severe heart failure, leave the beta 1-adrenergic system and the responsiveness of the adenylyl cyclase intact. Additionally these data show the developmentally increased expression of cardiac alpha 1-adrenergic and muscarinic receptors in rat heart.

Adenylyl Cyclases↗
PubMed1988

[Association of myopathies and alcoholic cardiomyopathy: clinical, electroneuromyographic and histopathologic study of the skeletal muscle in 10 cases of alcoholic cardiomyopathy].

Myocardial and skeletal muscle impairment caused by alcohol has been thoroughly studied. Nevertheless, the simultaneous involvement of those tissues by ethanol has not been broached in medical literature. We have studied ten patients undergoing alcoholic cardiomyopathy. They were subjected to a detailed neurological examination, muscle enzymes serum level determinations, electromyography, and muscle biopsy with analysis of the tissue by usual histological techniques and by electron microscopy. Only one of ten patients exhibited proximal weakness and atrophy of the lower limbs, the electromyographic and histological findings correlating with the clinical feature of the chronic muscle disease due to alcohol consumption. The electromyographic findings included muscle disease in eight patients, neuron disease in one patient and no changes at all in the tenth patient. In one patient only, the skeletal muscle proved normal when examined by conventional histological techniques. In the other nine patients there were several minimal changes, such as the proliferation of nuclei beneath the sarcolemma, atrophy of fibers, hyalinization, vacuolation, loss of muscle fiber striae, and atrophy of groups of fibers. Electron microscopy demonstrated the following changes in nine patients: intracellular edema, dissociation of myofilaments, alteration of the Z line, changing in the shape and increase in the number of mitochondria, thickening of sarcolemma, and vacuolation and increase of the glycogen granules. Since all patients exhibited skeletal muscle injury, we concluded that there is a close relation between alcoholic cardiomyopathy and skeletal muscle disease.

Adult↗
PubMed1987

Normalization of variables of left ventricular function in patients with alcoholic cardiomyopathy after cessation of excessive alcohol intake: an echocardiographic study.

An excessive alcohol intake has been reported as one of the possible causes or risk factors of 'alcoholic cardiomyopathy'. The possibility that this cardiomyopathy may improve or even reverse if the alcohol abuse has been terminated has been suggested, but unequivocal echocardiographic documentation of this improvement has never been described. This study reports the normalization of cardiac chamber dimensions and of variables of left ventricular function documented by M-mode and cross-sectional echocardiographic follow-up studies, after cessation of excessive consumption of alcohol, in three cases of alcoholic cardiomyopathy.

Adult↗
PubMed1986

Ultrastructural and histochemical observations in human and experimental alcoholic cardiomyopathy.

The morphologic features of alcoholic cardiomyopathy in human sudden death compared with those of experimental alcoholic cardiomyopathy (6 weeks of alcohol administration and simultaneous inhibition of catalase activity) proved to be nearly identical. Regular and similar alterations in alcoholic cardiomyopathy in both human victims of sudden death and experimental rats are described as a complex of alterations characteristic of alcoholic cardiomyopathy. This complex of changes was used as the basis for morphologic diagnosis of endomyocardial biopsy in two groups of patients: I) chronic alcoholics (second to third stages), and II) patients with clinically diagnosed congestive cardiomyopathy. Typical signs of alcoholic cardiomyopathy were found in 9 of the 11 patients in the first group and in 6 of 18 in the second group. The fact that the features of alcoholic cardiomyopathy were not found in all cases of chronic alcoholism supports the hypothesis that the administration of alcohol itself is not sufficient for the development of this disease. The level of enzyme activity in the metabolism of alcohol appears to be of great importance. This hypothesis is confirmed by experiments with rats in which this disease developed only when there was simultaneous alcohol administration and inhibition of catalase activity. Histochemical study showed that the alterations of enzyme (both energetic and alcohol metabolism) in rats were similar to those found in the biopsy specimens from patients with alcoholic cardiomyopathy. Certain questions regarding the pathogenesis of alcoholic cardiomyopathy are discussed.

Adult↗
PubMed2002

Angiotensin-converting enzyme gene polymorphism is associated with vulnerability to alcoholic cardiomyopathy.

BACKGROUND: Chronic alcohol abuse has a dose-dependent toxic effect on the myocardium, leading to alcoholic cardiomyopathy. The fact that only a minority of persons with chronic alcoholism have this condition suggests the possibility of a genetic vulnerability. In this context, polymorphism of the angiotensin-converting enzyme (ACE) gene has been implicated in cardiac dysfunction. OBJECTIVE: To compare the ACE genotypes of alcoholic persons who have cardiomyopathy with those of comparable alcohol abusers who have normal cardiac function. DESIGN: Case-control study over a 2-year period. SETTING: An academic tertiary referral hospital in Barcelona, Spain. PATIENTS: 30 alcoholic men with symptomatic cardiomyopathy and 27 alcoholic men with normal cardiac function. MEASUREMENTS: Ethanol intake, cardiac status, left ventricular ejection fraction (LVEF), and ACE gene polymorphism. RESULTS: The DD ACE genotype was present in 57% of alcoholic persons with an LVEF less than 0.50 and in 7% of those with normal cardiac function. Compared with persons who had an I allele, the odds ratio for development of left ventricular dysfunction in alcoholic persons with the DD genotype was 16.4. CONCLUSIONS: Vulnerability to cardiomyopathy among chronic alcohol abusers is partially genetic and is related to presence of the ACE DD genotype. This finding demonstrates genetic susceptibility to alcohol-induced myocardial damage.

Adult↗
PubMed1999

A transgenic model of acetaldehyde overproduction accelerates alcohol cardiomyopathy.

Chronic alcohol consumption produces alcoholic heart muscle disease (AHMD), a prevalent form of congestive heart failure. Several hypotheses have been proposed to explain the damaging effects of alcohol on the heart, but neither the mechanism nor the ultimate toxin has been established. In this study, we use transgenic overexpression of alcohol dehydrogenase to elevate cardiac exposure to acetaldehyde, the major and most reactive metabolite of alcohol. Overexpression of alcohol dehydrogenase by 40-fold produced no detectable deleterious effects to the heart in the absence of alcohol. In the presence of alcohol, transgenic hearts contained 4-fold higher acetaldehyde than control hearts. Chronic alcohol exposure produced many changes similar to AHMD in transgenic hearts. Compared with control hearts, these pathological changes occurred more rapidly and to a greater extent: alcohol-exposed transgenic hearts were almost twice as large as control hearts. They demonstrated ultrastructural damage consistent with AHMD and had much lower contractility than alcohol-exposed control hearts. In addition, the transgenic hearts showed greater changes in mRNA expression for alpha-skeletal actin and atrial natriuretic factor than alcohol-exposed control hearts. Alterations in NAD(+)/NADH levels were insufficient to account for such severe damage in cardiomyopathic hearts. The increased damage produced in transgenic hearts suggests an important role for acetaldehyde in AHMD.

Acetaldehyde↗
PubMed1994

Alcoholic cardiomyopathy.

Chronic alcoholism is one of the most important causes of dilated cardiomyopathy, and a large proportion of chronic alcoholics demonstrate impairment of cardiac function. The development of cardiac dysfunction is apparently related to the total lifetime dose of ethanol. Studies in experimental animals have demonstrated that both acute and chronic ethanol administration impair cardiac contractility. However, the relationship, if any, between the acute effects of alcohol and the development of irreversible cardiomyopathy remain to be elucidated.

Alcohol Drinking↗