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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

With no intention of belittling the importance of chronic ischemic heart disease (CIHD) in modern cardiology, the article focuses the attention on primary alcoholic heart disease--alcoholic cardiomyopathy (ACMP)--which arouses a far from causal interest due to the prevalence of alcoholism. It is suggested to distinguish three main clinical forms of ACMP: valence of alcoholism. It is suggested to distinguish three main clinical forms of ACMP: (1) "classical", manifested by dilatation of the heart and signs of its failure; (2) "quasi-ischemic" manifested by cardialgia and changes in the ECG, resembling those in CIHD; (3) "arrythmic", characterized by variants of disorders of myocardial excitability and conduction. The ACMP diagnostic criteria, methods for its identification and differential diagnosis from CIHD, modern conceptions of ACMP pathogenesis, and the main principles of treatment are discussed.
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PMID:[Alcoholic heart disease (alcoholic cardiomyopathy)]. 14 8

Two patients had cardiac disease and serological evidence for respiratory syncytial virus (RSV) infection. The first patient had myocarditis and complete atrioventricular heart block with repeated syncopal episodes two weeks following infection. The second patient had alcoholic cardiomyopathy and worsening congestive heart failure associated with RSV infection. The significance of RSV infection in these two patients may bear a significant relationship to sudden infant death syndrome, chronic cardiomyopathy, and alcohol-related heart disease. Cardiac disease secondary to RSV infection may be more prevalent than is presently recognized.
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PMID:Respiratory syncytial virus and heart disease. A report of two cases. 18 2

The widespread use of ethyl alcohol suggests its potential importance in clinical medicine. There is no proven therapeutic effect in cardiac patients and its role as an etiologic factor in heart disease has been disputed over the years and attributed to coexistent malnutrition. The latter factor, however, has been dissociated from ethanol use in many patients with the cardiomyopathic form of heart failure. Major support for the role of ethanol as a toxic agent when used in large amounts for a prolonged period has been obtained in various species of animals, including the subhuman primate. Abnormalities include depression of ventricular function, and metabolic and morphologic changes that parallel the changes in humans with preclinical malfunction of the heart. While the mechanism of progression to heart failure or arrhythmias is not known, several factors may be associated. These include, particularly in males, the cumulative effects of ethanol alone or after intensified drinking episodes, simultaneous exposure to trace metals in excess, and occasional specific nutritional deficiency or superimposed infection. The low prevalence of clinical nutritional deficiency in patients with alcoholic cardiomyopathy and the infrequency of heart disease in patients with cirrhosis or neuropathy supports the view that the cardiac abnormality is commonly not dependent on malnutrition. Clinical data indicate that the cessation of alcohol intake may reverse the disease or interrupt its progression in many patients. However, the pathogenic process may continue unabated in some patients who become abstinent.
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PMID:The role of ethanol in cardiac disease. 32 69

Fifty patients with the following suspected diseases were examined: examined: congenital heart disease (25), rheumatic heart disease (7), infectious-allergic myocarditis (12), fibroelastosis of the endocardium (3), alcoholic cardiomyopathy (2), drug cardiomyopathy (1). Catheterization biopsy of the endo- and myocardium was accomplished with a special bioptome after catheterization of the heart. No complications occurred during or after biopsy. The results of histologic and histochemical examination of the bioptates of the cardiac muscle are discussed. On the basis of the data in the literature and personal experience, it is concluded that biopsy of the endo- and myocardium may be undertaken to specify the etiology and pathogenesis of cardiomyopathy. The method is comparatively safe.
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PMID:[Endomyocardial biopsy in the diagnosis of myocarditis and cardiomyopathies]. 67 90

Systolic left ventricular dysfunction is relatively common in even asymptomatic alcoholics, but whether diastolic function is also altered is much less well-studied. We used M-mode and Doppler echocardiography to study left ventricular size, mass, systolic function and diastolic filling in 32 alcoholics free of clinically detectable heart disease and in 15 healthy control subjects. Left ventricular mass index and posterior wall thickness were higher in alcoholics than in controls, but there was no statistically significant difference either in end-diastolic size or in systolic ventricular function. More abnormalities were found in the Doppler indexes of diastolic function, however. The alcoholics had a prolonged relaxation time (200 +/- 6 vs 184 +/- 5 ms [mean +/- standard error], p less than 0.05), a decreased peak early diastolic velocity (52 +/- 2 vs 60 +/- 3 cm/s, p less than 0.05), a slower acceleration of the early flow (410 +/- 18 vs 552 +/- 43 cm/s2, p less than 0.01), and a higher atrial-to-early peak velocity ratio (0.74 +/- 0.04 vs 0.60 +/- 0.05, p less than 0.05). This pattern of changes suggests a primary abnormality in the relaxation of the left ventricle. In multivariate analyses, the abnormalities in the Doppler indexes were independent of the duration of alcoholism, the quantity of the most recent ethanol exposure and the increased mass of the left ventricle. Impaired early filling of the left ventricle due to delayed relaxation is common in asymptomatic alcoholics and may in fact be the earliest functional sign of preclinical alcoholic cardiomyopathy.
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PMID:Left ventricular filling impairment in asymptomatic chronic alcoholics. 225 94

The ability to induce alcoholic cardiomyopathy has been tested in a variety of animal species. Myocardial alterations consistent with subclinical heart disease have been produced in many of these studies through a direct effect of ethanol or its metabolites upon the heart or a neurohumoral mechanism. In the rat most studies have, however, failed to finding diminished contractility in the basal state. In long-term animals the acute left ventricular responses to isoproterenol and calcium as well as pacing were reduced. Long-term studies in mongrel dogs fed 36 per cent of calories as ethanol produced an early decrease in left ventricular diastolic compliance related to interstitial collagen accumulation. Diminished contractility developed by four years. In addition to the morphologic evidence of distorted sarcoplasmic reticulum, in vitro experiments suggest important acute effects. Each mole of ethanol is bound tightly to each mole of protein comprising the Ca-ATPase pump, which is inhibited. Impaired uptake and binding of calcium by the sarcoplasmic reticulum has been observed in chronic alcohol models at one to two day intervals following the last exposure to ethanol. In addition, the flux of calcium ion does not appear normal in terms of access to contractile protein, where the calcium regulated inhibition of the troponin interaction with myosin is impaired. Experimental studies in a canine model of alcoholism revealed that the ventricular fibrillation threshold was moderately reduced in the basal state after 18 months and was diminished further after acute exposure.
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PMID:Experimental models for studying the effects of ethanol on the myocardium. 331 64

Prolonged QT interval and arrhythmias have been reported to occur in chronic alcoholics. To investigate the role of chronic alcohol consumption in the onset of arrhythmias and the development of the preclinical left ventricular dysfunction, in a group of 12 asymptomatic chronic alcoholics with no clinical evidence of heart disease, with histologically proven hepatic damage, after a week of abstinence from alcohol, the following investigations were performed: measurements of the corrected QT interval (QTc), 24-hours Holter monitoring, systolic time intervals, M-mode echocardiograms. The results were compared to those of 10 normal subjects. Our data suggested no difference in QTc interval between chronic alcoholics and normal persons. The distribution of arrhythmias was not statistically different in the two groups, particularly frequent and complicated arrhythmias occurred in only one subject in each group. Preejection period corrected for heart rate (PEPI) was significantly longer in alcoholics (132 +/- 16 vs 119 +/- 11, p less than 0.05). All echocardiographic parameters examined were not significantly different in the two groups. On the basis of our results, our impression is that the arrhythmogenic role of alcohol, not under acute ingestion, is relatively unimportant and further studies are needed to become a definitive conclusion about subclinical alcoholic cardiomyopathy.
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PMID:[Correlation between QT interval, ventricular arrhythmias and left ventricular function in chronic alcoholics]. 374 31

With the number of chronic heavy users of ethanol in the United States estimated to be 15 to 20 million and the evidence increasing that ethanol causes serious cardiac metabolic disturbances, ethanol abuse is obviously a serious problem and most likely is an important contributing factor to cardiac morbidity and mortality. However, a direct cause-and-effect relationship between the biochemical dysfunctions produced by ethanol and the clinical entity of alcoholic cardiomyopathy has not been clearly established. What is lacking is a method to differentiate the damage secondary to ethanol abuse from that secondary to other causes. Sorely needed is a biochemical or anatomic marker (perhaps evaluated by serial myocardial biopsy) for alcoholic cardiomyopathy and a study to detect which cases of dilated cardiomyopathy indeed are due to ethanol-induced damage. Further longterm studies are also needed to demonstrate the benefits of abstinence upon large groups of patients, the effects of abstinence upon sudden death, and the effects of discontinuance of ethanol use for patients in the early stages of alcoholic cardiomyopathy. Ethanol is probably an underestimated contributing factor to cardiac disease. The importance of determining ethanol's impact on cardiovascular morbidity and mortality is underscored by the facts that alcoholic heart disease is completely avoidable and is largely reversible by abstinence.
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PMID:Ethanol and heart disease. An underestimated contributing factor. 394 21

Beri-beri heart disease is a distinctive clinical entity which must be distinguished from alcoholic cardiomyopathy and other forms of heart disease in chronic alcoholics. A 27-year-old man is described who for six months before the onset of symptoms of right heart failure-admitted to hospital with dyspnea and pitting edema in the lower limbs and over the sacrum-had lived over a tavern and consumed 24 pints of beer daily.The pathophysiology of beri-beri heart disease includes right heart failure, edema and peripheral vasodilatation in the muscular bed. These features were described by Wenckebach and others as early as 1928. Within the main entity, beri-beri heart disease, a number of sub-groups with special features and prognosis such as acute pernicious beri-beri have been described. Beri-beri heart disease is due to vitamin B(1) deficiency and is curable if this deficiency is corrected in time.
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PMID:Beri-Beri heart disease. 594 Jul 85

Systolic time intervals corrected for heart rate were measured non invasively in 12 male patients (32 to 59 years) with chronic calcifying pancreatitis of alcoholic origin and compared with 24 normal subjects without evidence for chronic alcoholism or heart disease. Systolic time intervals (in detail: the time from the beginning of QRS to the first heart sound (QS1), the isovolumic contraction time (IVCT), the total electromechanical systolic interval (QS2c), the pre-ejection period (PEPc), the left ventricular ejection time (LVETc) and the ratio PEPc/LVETc) in patients with chronic calcifying pancreatitis were not different when compared with healthy man. Therefore we conclude, that the amount of alcohol that induced a chronic calcifying pancreatitis was not able to alter systolic time intervals as seen in an alcoholic cardiomyopathy.
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PMID:[Systolic time intervals in chronic calcifying pancreatitis caused by alcohol abuse]. 686 22


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