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Alcoholic Cardiomyopathy: Clinical and Molecular Findings
M Correale,I Laonigro,F Altomare,MDi Biase
Iranian Cardiovascular Research Journal , 2008,
Abstract: It has been known for some decades that chronic alcoholism can lead to dilated cardiomyopathy. Although excessivedrinking is known to result in alcoholic cardiomyopathy and light-to-moderate drinking may confer somecardiovascular benefits, recent studies suggest that it is not only the quantity, but also drinking patterns and genetic factors, that may influence the relation between alcohol consumption and cardiovascular disease. Alcoholicpatients consuming > 90g of alcohol a day for > 5 years are at risk for the development of asymptomatic alcoholiccardiomyopathy. Those who continue to drink may become symptomatic and develop signs and symptoms ofheart failure. We summarize the experimental and clinical evidence regarding the role of alcohol in pathophysiologyof alcoholic cardiomyopathy.
Acetaldehyde Adducts in Alcoholic Liver Disease  [PDF]
Mashiko Setshedi,Jack R. Wands,Suzanne M. de la Monte
Oxidative Medicine and Cellular Longevity , 2010, DOI: 10.4161/oxim.3.3.12288
Abstract: Chronic alcohol abuse causes liver disease that progresses from simple steatosis through stages of steatohepatitis, fibrosis, cirrhosis, and eventually hepatic failure. In addition, chronic alcoholic liver disease (ALD), with or without cirrhosis, increases risk for hepatocellular carcinoma (HCC). Acetaldehyde, a major toxic metabolite, is one of the principal culprits mediating fibrogenic and mutagenic effects of alcohol in the liver. Mechanistically, acetaldehyde promotes adduct formation, leading to functional impairments of key proteins, including enzymes, as well as DNA damage, which promotes mutagenesis. Why certain individuals who heavily abuse alcohol, develop HCC (7.2–15%) versus cirrhosis (15–20%) is not known, but genetics and co-existing viral infection are considered pathogenic factors. Moreover, adverse effects of acetaldehyde on the cardiovascular and hematologic systems leading to ischemia, heart failure, and coagulation disorders, can exacerbate hepatic injury and increase risk for liver failure. Herein, we review the role of acetaldehyde adducts in the pathogenesis of chronic ALD and HCC.
Acetaldehyde Adducts in Alcoholic Liver Disease  [PDF]
Mashiko Setshedi,Jack R. Wands,Suzanne M. de la Monte
Oxidative Medicine and Cellular Longevity , 2010, DOI: 10.4161/oxim.3.3.12288
Abstract: Chronic alcohol abuse causes liver disease that progresses from simple steatosis through stages of steatohepatitis, fibrosis, cirrhosis, and eventually hepatic failure. In addition, chronic alcoholic liver disease (ALD), with or without cirrhosis, increases risk for hepatocellular carcinoma (HCC). Acetaldehyde, a major toxic metabolite, is one of the principal culprits mediating fibrogenic and mutagenic effects of alcohol in the liver. Mechanistically, acetaldehyde promotes adduct formation, leading to functional impairments of key proteins, including enzymes, as well as DNA damage, which promotes mutagenesis. Why certain individuals who heavily abuse alcohol, develop HCC (7.2–15%) versus cirrhosis (15–20%) is not known, but genetics and co-existing viral infection are considered pathogenic factors. Moreover, adverse effects of acetaldehyde on the cardiovascular and hematologic systems leading to ischemia, heart failure, and coagulation disorders, can exacerbate hepatic injury and increase risk for liver failure. Herein, we review the role of acetaldehyde adducts in the pathogenesis of chronic ALD and HCC.
Short-term salivary acetaldehyde increase due to direct exposure to alcoholic beverages as an additional cancer risk factor beyond ethanol metabolism
Dirk W Lachenmeier, Yulia B Monakhova
Journal of Experimental & Clinical Cancer Research , 2011, DOI: 10.1186/1756-9966-30-3
Abstract: Salivary acetaldehyde levels were determined in the context of sensory analysis of different alcoholic beverages (beer, cider, wine, sherry, vodka, calvados, grape marc spirit, tequila, cherry spirit), without swallowing, to exclude systemic ethanol metabolism.The rinsing of the mouth for 30 seconds with an alcoholic beverage is able to increase salivary acetaldehyde above levels previously judged to be carcinogenic in vitro, with levels up to 1000 μM in cases of beverages with extreme acetaldehyde content. In general, the highest salivary acetaldehyde concentration was found in all cases in the saliva 30 sec after using the beverages (average 353 μM). The average concentration then decreased at the 2-min (156 μM), 5-min (76 μM) and 10-min (40 μM) sampling points. The salivary acetaldehyde concentration depends primarily on the direct ingestion of acetaldehyde contained in the beverages at the 30-sec sampling, while the influence of the metabolic formation from ethanol becomes the major factor at the 2-min sampling point.This study offers a plausible mechanism to explain the increased risk for oral cancer associated with high acetaldehyde concentrations in certain beverages.Acetaldehyde (ethanal, CH3CHO) is a potent volatile flavouring compound found in many beverages and foods [1-3]. In alcoholic beverages, acetaldehyde may be formed by yeast, acetic acid bacteria, and by coupled auto-oxidation of ethanol and phenolic compounds [3]. In a recent study, a large collective of different alcoholic beverages (n > 1500) was evaluated. Beer (9 ± 7 mg/l, range 0-63 mg/l) contained significantly lower amounts of acetaldehyde than wine (34 ± 34 mg/l, range 0-211 mg/l), or spirits (66 ± 101 mg/l, range 0-1159 mg/l) [4].According to the International Agency for Research on Cancer (IARC), acetaldehyde associated with alcohol consumption is regarded as 'carcinogenic to humans' (IARC Group 1) [5]. Evidence points to the oesophagus, head and neck as principal sites of carcinogenici
CASE REPORT A 42-year-old patient with alcoholic cardiomyopathy
Robert Irzmański,Ewa Serwa-St?pień,Marcin Barylski,Maciej Banach
Archives of Medical Science , 2005,
Abstract: Introduction: Alcoholic cardiomyopathy represents about 3.8% of all cardiomyopathy cases and it is a result of long-term (>5 years) alcohol consumption (>90 g of alcohol per day). It occurs twice as frequently in men as in women. Case report: We present the case of a 42-year-old patient, not treated for chronic diseases so far, with positive incriminating familiar anamnesis for ischemic heart disease, who was hospitalized in our Department because of progressive reduction of effort tolerance for 2 weeks with squeezing in the chest and dyspnea ("asthma cardiale" type). Basing on the clinical course, anamnesis from family members and additional tests performed, alcoholic cardiomyopathy was diagnosed. Conclusions: Alcoholism is one of the main causes of myocardial damage. Treatment of patients with alcoholic cardiomyopathy should include alcohol abstinence and recommended heart failure pharmacotherapy.
Collagen content, but not the ratios of collagen type III/I mRNAs, differs among hypertensive, alcoholic, and idiopathic dilated cardiomyopathy
Soufen, H.N.;Salemi, V.M.C.;Aneas, I.M.S.;Ramires, F.J.A.;Benício, A.M.D.;Benvenuti, L.A.;Krieger, J.E.;Mady, C.;
Brazilian Journal of Medical and Biological Research , 2008, DOI: 10.1590/S0100-879X2008001200009
Abstract: cardiac interstitial fibrosis may contribute to ventricular dysfunction and the prognosis of patients with dilated cardiomyopathy. the objective of the present study was to determine if total myocardial collagen content and collagen type iii/i (iii/i ratio) mrnas differ in hypertensive, alcoholic, and idiopathic dilated cardiomyopathy subjects. echocardiography and exercise cardiopulmonary testing were performed in patients with idiopathic (n = 22), hypertensive (n = 12), and alcoholic (n = 11) dilated cardiomyopathy. morphometric analysis of collagen was performed in fragments obtained by endomyocardial biopsy with picrosirius red staining. the collagen iii/i ratio was determined by reverse transcription polymerase chain reaction. samples of controls (n = 10) were obtained from autopsy. echocardiographic variables and maximal oxygen uptake were not different among dilated cardiomyopathy groups. collagen was higher in all dilated cardiomyopathy groups (idiopathic, hypertensive and alcoholic, 7.36 ± 1.09%) versus controls (1.12 ± 0.18%), p < 0.05. collagen was lower in idiopathic dilated cardiomyopathy (4.97 ± 0.83%) than hypertensive (8.50 ± 1.11%) and alcoholic (10.77 ± 2.09%) samples (p < 0.005 for both). the collagen iii/i ratio in all samples from dilated cardiomyopathy patients was higher compared to that in controls (0.29 ± 0.04, p < 0.05) but was the same in the samples from idiopathic (0.77 ± 0.07), hypertensive (0.75 ± 0.07), and alcoholic (0.81 ± 0.16) dilated cardiomyopathy groups. because of the different physical properties of the types of collagen, the higher iii/i ratio may contribute to progressive ventricular dilation and dysfunction in dilated cardiomyopathy patients.
Acetaldehyde-Derived Advanced Glycation End-Products Promote Alcoholic Liver Disease  [PDF]
Nobuhiko Hayashi, Joseph George, Masayoshi Takeuchi, Atsushi Fukumura, Nobuyuki Toshikuni, Tomiyasu Arisawa, Mikihiro Tsutsumi
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0070034
Abstract: Background Chronic ingestion of ethanol increases acetaldehyde and leads to the production of acetaldehyde-derived advanced glycation end-products (AA-AGE). We evaluated the toxicity of AA-AGE on hepatocytes and studied the role of AA-AGE in the pathogenesis of alcoholic liver disease (ALD). Methods Rat hepatocyte cultures were treated with N-ethyllysine (NEL) or AA-AGE and the cell viability was evaluated using MTT assay. Male Wistar rats were fed with liquid diet containing 5% ethanol for 8 weeks following normal diet for another 12 weeks. A group of animals was sacrificed at 4th, 6th, and 8th week and the remaining animals at 12th, 14th, 16th, 18th, and 20th week. The liver sections were stained for AA-AGE and 4-hydroxy-2-nonenal (4-HNE). Liver biopsy obtained from ALD patients was also stained for AA-AGE and 4-HNE. Results Hepatocyte viability was significantly reduced in cultures treated with AA-AGE compared to NEL treated or control cultures. Severe fatty degeneration was observed during chronic administration of ethanol increasing from 4–8 weeks. The staining of AA-AGE and 4-HNE was correlated with the degree of ALD in both rat and human. In rats, hepatic fatty degeneration was completely disappeared and the staining for both AA-AGE and 4-HNE returned to normal at 12th week of abstinence. Staining for AA-AGE and 4-HNE was completely absent in normal human liver. Conclusions The data demonstrated that AA-AGE is toxic to hepatocytes, but not NEL. Chronic ethanol ingestion produces AA-AGE and reactive oxygen species that contribute to the pathogenesis of ALD. Abstinence of alcohol results in complete disappearance of both AA-AGE and 4-HNE along with fatty degeneration suggesting that AA-AGE plays a significant role in the pathogenesis of ALD.
Quantitative Determination of Acetaldehyde in Foods Using Automated Digestion with Simulated Gastric Fluid Followed by Headspace Gas Chromatography  [PDF]
Michael Uebelacker,Dirk W. Lachenmeier
Journal of Analytical Methods in Chemistry , 2011, DOI: 10.1155/2011/907317
Abstract: Acetaldehyde (ethanal) is a genotoxic carcinogen, which may occur naturally or as an added flavour in foods. We have developed an efficient method to analyze the compound in a wide variety of food matrices. The analysis is conducted using headspace (HS) gas chromatography (GC) with flame ionization detector. Using a robot autosampler, the samples are digested in full automation with simulated gastric fluid (1?h at 37°C) under shaking, which frees acetaldehyde loosely bound to matrix compounds. Afterwards, an aliquot of the HS is injected into the GC system. Standard addition was applied for quantification to compensate for matrix effects. The precision of the method was sufficient (<3% coefficient of variation). The limit of detection was 0.01?mg/L and the limit of quantification was 0.04?mg/L. 140 authentic samples were analyzed. The acetaldehyde content in apples was 0 . 9 7 ± 0 . 8 0 ?mg/kg, orange juice contained 3 . 8 6 ± 2 . 8 8 ?mg/kg. The highest concentration was determined in a yoghurt (17?mg/kg). A first-exposure estimation resulted in a daily acetaldehyde intake of less than 0.1?mg/kg bodyweight from food, which is considerably lower than the exposures from alcohol consumption or tobacco smoking. 1. Introduction Acetaldehyde (ethanal) is carcinogenic in animal experiments [1, 2] and was classified by the International Agency for Research on Cancer (IARC) in 1999 as “possibly carcinogenic to humans” (group 2B) [3]. Only recently, acetaldehyde in association with alcohol consumption has been upgraded by IARC into group 1 (i.e., the highest level of evidence) as “carcinogenic to humans” [4]. The carcinogenicity is considered to be caused by a genotoxic mechanism as several acetaldehyde-DNA adducts were found in vitro and in vivo [5–9]. For this reason, it is currently not possible to suggest a clear threshold or maximum tolerable limit for foods, but the margin of exposure model has to be used for risk assessment [10–13]. This requires to have robust occurrence data for exposure assessment. In foods, acetaldehyde may occur either naturally or because of intentional addition as flavour compound [14]. Other sources of human exposure to acetaldehyde may be cosmetic products or environmental exposure from burning fossil fuels, but the major sources are tobacco smoke and exposure from ethanol oxidation following alcoholic beverage consumption [11, 13, 15]. In vivo, acetaldehyde may also be formed endogenously, but especially in the gastrointestinal tract by bacteria that metabolize ethanol or carbohydrates. In foods, the highest concentrations of
Immunopathology of cardiomyopathy in the experimental Chagas disease
Soares, Milena BP;Santos, Ricardo Ribeiro dos;
Memórias do Instituto Oswaldo Cruz , 1999, DOI: 10.1590/S0074-02761999000700043
Abstract: the mechanisms by which trypanosoma cruzi causes cardiomyopathy and induces neuronal destruction are discussed in this paper. the results suggest that autoimmunity in the chronic phase is the main cause of the progressive cardiac destruction, and that autoreactivity is restricted to the cd4+ t cell compartment. during the acute phase, the neuronal and cardiac fiber destruction occurs when ruptured parasite nests release t. cruzi antigens that bind to the cell surface in the vicinity which become targets for the cellular and humoral immune response against t. cruzi. the various factors involved in the genesis of autoimmunity in chronic t. cruzi infection include molecular mimicry, presentation of self-antigens and imbalance of immune regulation.
Immunopathology of cardiomyopathy in the experimental Chagas disease
Soares Milena BP,Santos Ricardo Ribeiro dos
Memórias do Instituto Oswaldo Cruz , 1999,
Abstract: The mechanisms by which Trypanosoma cruzi causes cardiomyopathy and induces neuronal destruction are discussed in this paper. The results suggest that autoimmunity in the chronic phase is the main cause of the progressive cardiac destruction, and that autoreactivity is restricted to the CD4+ T cell compartment. During the acute phase, the neuronal and cardiac fiber destruction occurs when ruptured parasite nests release T. cruzi antigens that bind to the cell surface in the vicinity which become targets for the cellular and humoral immune response against T. cruzi. The various factors involved in the genesis of autoimmunity in chronic T. cruzi infection include molecular mimicry, presentation of self-antigens and imbalance of immune regulation.
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