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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To compare the prevalence and cardiac status of male and female alcoholics with alcoholic cardiomyopathy during a 5-year period, all chronic alcoholics with dilated cardiomyopathy who had clinical symptoms of heart failure were included. Alcoholic cardiomyopathy was diagnosed in 10 chronic alcoholic women and in 26 men; the prevalence of alcoholic cardiomyopathy was similar in both sexes. No significant differences were observed in age, nutritional parameters, and clinical and radiologic data of heart failure between the 2 groups. Alcoholic women reported a significantly lower daily dose of ethanol (p = 0.002), a shorter duration of alcoholism (p = 0.017), and a lower total lifetime dose of ethanol consumption (p = 0.001), and had a lower New York Heart Association functional class than men. Women also had lesser ventricular dysfunction than men. In a multivariate analysis, left ventricular systolic dysfunction was related to the total lifetime dose of ethanol consumption (p <0.04), but not to gender. Finally, when patients were matched for left ventricular ejection fraction, women had consumed a lower total lifetime dose of ethanol than men (p <0.001). The prevalence of alcoholic women with dilated cardiomyopathy was found to be similar to that of alcoholic men, although women required a lower total lifetime dose of ethanol to develop the disease.
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PMID:Comparison of alcoholic cardiomyopathy in women versus men. 928 62

Forensic medical diagnosis of death from coronary heart disease, acute ethanol poisoning, alcoholic cardiomyopathy, closed cardiac injuries, mechanical injuries incompatible with life which may be directly caused by acute cardiac failure, requires identification and evaluation of diagnostic complexes of acute myocardial changes. The diagnostic significance of such complexes of myocardial changes is characterized for the first time. A method for evaluation of such changes, addressed to expert histologists, is presented.
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PMID:[Diagnostic role of acute microscopic changes in myocardium]. 1070 78

In most large scale trials the prognosis of ischemic heart failure is worse than in patients with non-ischemic etiology. The therapeutic effect of essential drugs such as ACE-inhibitors, betablockers and diuretics is similar, but response to some other drugs (amiodarone, amlodipine, digoxin, growth hormone) is better in non-ischemic heart failure. Of great practical importance is the recognition of hibernating myocardium in coronary artery disease, since revascularisation may significantly improve left ventricular function. Specific therapeutic interventions are possible in hypertensive heart disease, alcoholic cardiomyopathy and LV-dysfunction to tachyarrhythmias. The etiology of heart failure should therefore be cleared in all patients.
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PMID:[Ischemic vs nonischemic heart failure--does etiology matter?]. 1085 92

Apoptosis of cardiac muscle cells may contribute to the development of cardiomyopathy and heart failure. Alcohol (ethanol) abuse is a major cause of cardiomyopathy, but its underlying mechanism remains unknown. To determine whether ethanol causes apoptosis in cardiac muscle and whether insulin-like growth factor I (IGF 1) improves cardiac muscle survival upon ethanol exposure, we have defined the effects of ethanol and IGF I in primary cardiomyocytes. Ethanol decreased cell viability in dose-response manner from 0.2% to 1%. In contrast, ethanol (0.2-1%) did not alter viability of cardiac fibroblasts. To assess the occurrence of apoptosis, DNA fragmentation was determined with quantitation of nucleosomes. Nucleosomes were increased in ethanol-treated cells, thus confirming the apoptotic effects of ethanol. The pro-apoptotic Bax protein and Caspase 3 are important proteins of apoptotic signaling. The content of Bax and the activities of Caspase 3 were increased upon ethanol exposure. IGF I partially suppressed Bax induction, Caspase 3 activation, DNA fragmentation, and increased cardiomyocyte survival. The effects of IGF I on ethanol-induced apoptosis can be inhibited with a chemical inhibitor of PI 3 Kinase (LY-294002), suggesting that anti-apoptotic actions of IGF I involves PI 3 Kinase. These results may have important implications on further understanding the pathogenesis of alcoholic heart disease and the development of new strategies to treat alcoholic cardiomyopathy.
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PMID:Insulin-like growth factor I retards apoptotic signaling induced by ethanol in cardiomyocytes. 1102 53

The energy needed by cardiac muscle to maintain proper function is supplied by adenosine Ariphosphate primarily (ATP) production through breakdown of fatty acids. Metabolic cardiomyopathies can be caused by disturbances in metabolism, for example diabetes mellitus, hypertrophy and heart failure or alcoholic cardiomyopathy. Deficiency in enzymes of the mitochondrial beta-oxidation show a varying degree of cardiac manifestation. Aberrations of mitochondrial DNA lead to a wide variety of cardiac disorders, without any obvious correlation between genotype and phenotype. A completely different pathogenetic model comprises cardiac manifestation of systemic metabolic diseases caused by deficiencies of various enzymes in a variety of metabolic pathways. Examples of these disorders are glycogen storage diseases (e.g. glycogenosis type II and III), lysosomal storage diseases (e.g. Niemann-Pick disease, Gaucher disease, I-cell disease, various types of mucopolysaccharidoses, GM1 gangliosidosis, galactosialidosis, carbohydrate-deficient glycoprotein syndromes and Sandhoff's disease). There are some systemic diseases which can also affect the heart, for example triosephosphate isomerase deficiency, hereditary haemochromatosis, CD 36 defect or propionic acidaemia.
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PMID:Metabolic cardiomyopathies. 1129 85

The systemic circulation in patients with cirrhosis is hyperdynamic with an increased cardiac output and heart rate and a reduced systemic vascular resistance as the most pronounced alterations. The concomitant cardiac dysfunction has recently been termed "cirrhotic cardiomyopathy", which is an entity different from that seen in alcoholic heart muscle disease. Clinically, these patients present with sodium fluid retention and strain often unmasks the presence of latent heart failure. No specific treatment can yet be recommended but caution should be used with respect to procedures that may stress the heart such as shunt implantation and liver transplantation.
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PMID:Cirrhotic cardiomyopathy: a pathophysiological review of circulatory dysfunction in liver disease. 1175 53

OBJECTIVE - To describe clinical observations of marked improvement in ventricular dysfunction in a medical office environment under circumstances differing from those in study protocols and multicenter studies performed in hospital or with outpatient cohorts. METHODS - Eleven cardiac failure patients with marked ventricular dysfunction receiving treatment at a doctors office between 1994 and 1999 were studied. Their ages ranged from 20 and 66 years (mean 39.42+/-14.05 years); 7 patients were men, 4 were women. Cardiopathic etiologies were arterial hypertension in 5 patients, peripartum cardiomyopathy in 2, nondefined myocarditis in 2, and alcoholic cardiomyopathy in 4. Initial echocardiograms revealed left ventricular dilatation (average diastolic diameter, 69.45+/-8.15mm), reduced left ventricular ejection fraction (0.38+/-0.08) and left atrial dilatation (43.36+/-5.16mm). The therapeutic approach followed consisted of patient orientation, elimination of etiological or causal factors of cardiac failure, and prescription of digitalis, diuretics, and angiotensinconverting enzyme inhibitors. RESULTS - Following treatment, left ventricular ejection fraction changed to 0.63+/-0.09; left ventricular diameters changed to 57.18+/-8.13mm, and left atrium diameters changed to 37.27+/-8.05mm. Maximum improvement was noted after 16.9+/-8.63 (6 to 36) months. CONCLUSION - Patients with serious cardiac failure and ventricular dysfunction caused by hypertension, alcoholism, or myocarditis can experience marked improvement in ventricular dysfunction after undergoing appropriate therapy within the venue of the doctor's office.
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PMID:Reversibility of ventricular dysfunction. Clinical experience in a medical office. 1179 29

Some evidence suggests that light to moderate alcohol consumption protects against cardiovascular diseases. However, this cardioprotective effect of alcohol consumption in adults is absent at the population level. Approximately 20 to 30% of patients admitted to a hospital are alcohol abusers. In medical practice, it is essential that patients' levels of consumption are known because of the many adverse effects that might result in the course of routine care. Ethanol damage to the heart is evident if alcohol consumption exceeds 90 to 100 g/d. Heavy ethanol consumption leads to increased risk for sudden cardiac death and cardiac arrhythmias. In patients with coronary heart disease, alcohol use was associated with increased mortality. An early response to drinking was an increased ventricular wall thickness to diameter ratio, possibly proceeding with continuous drinking to alcoholic cardiomyopathy, which had a worse outcome compared with idiopathic dilative cardiomyopathy if drinking was not stopped or at least reduced (< 60 g/d). In the ICU, patients with chronic alcoholism have more cardiac complications postoperatively. These complications probably are caused by biventricular dysfunction, particularly with the occurrence of severe infections or septic shock, events that are three to four times more frequent among chronic alcoholics than occasional drinkers or nondrinkers. To prevent further complications from drinking and for long-term management of drinking, patients with alcohol abuse and heart failure should be treated in brief intervention and follow-up programs. Prognosis is good even in patients with New York Heart Association class IV heart failure caused by cardiomyopathy if complete abstinence is accomplished. Noncompliance to smoking and alcohol restrictions, which are amenable to change, dramatically increases the risk for hospital readmissions among patients with heart failure.
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PMID:Effects of alcohol on the heart. 1180 30

In the United States, in both sexes and all races, long-term heavy alcohol consumption (of any beverage type) is the leading cause of a nonischemic, dilated cardiomyopathy, herein referred to as alcoholic cardiomyopathy (ACM). ACM is a specific heart muscle disease of a known cause that occurs in two stages: an asymptomatic stage and a symptomatic stage. In general, alcoholic patients consuming > 90 g of alcohol a day (approximately seven to eight standard drinks per day) for > 5 years are at risk for the development of asymptomatic ACM. Those who continue to drink may become symptomatic and develop signs and symptoms of heart failure. ACM is characterized by an increase in myocardial mass, dilation of the ventricles, and wall thinning. Changes in ventricular function may depend on the stage, in that asymptomatic ACM is associated with diastolic dysfunction, whereas systolic dysfunction is a common finding in symptomatic ACM patients. The pathophysiology of ACM is complex and may involve cell death (possibly due to apoptosis) and changes in many aspects of myocyte function. ACM remains an important cause of a dilated cardiomyopathy, and in latter stages can lead to heart failure. Alcohol abstinence, as well as the use of specific heart failure pharmacotherapies, is critical in improving ventricular function and outcomes in these patients.
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PMID:Alcoholic cardiomyopathy: incidence, clinical characteristics, and pathophysiology. 1268 36

Multiple pathways are responsible for transducing mechanical and hormonal stimuli into changes in gene expression during heart failure. In this study our goals were (i) to develop a sound statistical method to establish a comprehensive cutoff point for identification of differentially expressed genes, (ii) to identify a gene expression fingerprint for heart failure, (iii) to attempt to distinguish different etiologies of heart failure by their gene expression fingerprint, and (iv) to identify gene clusters that show coordinated up- or down-regulation in human heart failure. We used oligonucleotide microarrays to profile seven nonfailing (NF) and eight failing (F) human hearts with a diagnosis of end-stage dilated cardiomyopathy. Biological and experimental variability of the hybridization data were analyzed, and then a statistical analysis procedure was developed, including Student's t test after log-transformation and Wilcoxon Mann-Whitney test. A comprehensive cutoff point composed of fold change, average difference, and absolute call was then established and validated by TaqMan PCR. Of 6,606 genes on the GeneChip, 103 genes in 10 functional groups were differentially expressed between F and NF hearts. A dendrogram identified a gene expression fingerprint of F and NF hearts and also distinguished two F hearts with distinct etiologies (familial and alcoholic cardiomyopathy, respectively) with different expression patterns. K means clustering also revealed two potentially novel pathways associated with up-regulation of atrial natriuretic factor and brain natriuretic peptide and with increased expression of extracellular matrix proteins. Gene expression fingerprints may be useful indicators of heart failure etiologies.
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PMID:The gene expression fingerprint of human heart failure. 1217 26


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