Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is known that chronic alcoholism causes morphological changes of the myocardium before the development of a specific dilated cardiomyopathy. We studied a group of chronic alcoholics, with normal arterial pressure and without clinical evidence of liver cirrhosis, to evaluate left ventricular function, both before and after withdrawal of ethanol. A M-B mode echo recording of the left ventricle and left ventricular inflow Doppler velocimetry with carotid pulse tracing was performed in each patient within 24 hours of the last alcohol consumption and after a period of abstinence at least 3 weeks. We analysed parameters of left ventricular systolic and diastolic functions, in comparison with a group of normal subjects well matched for age, body surface area and heart rate. The results showed that, in the group of alcoholics, a cardiac hypertrophy exists with increased left ventricular mass and normal parameters of left systolic ventricular function, but with altered ratio PEP/LVET. This last result is the consequence of an abnormal left diastolic ventricular function, as demonstrated from the analysis of the Doppler indexes of left ventricular filling (lower ratio E/A). Left ventricular inflow Doppler velocimetry showed different results in alcoholics and control subjects in the early diastolic flow velocity peak (61 +/- 12 vs 84 +/- 8) and in the peak flow velocity in the atrial contraction phase (62 +/- 10 vs 40 +/- 5.6). We have not observed any change of the echocardiographic parameters after the short period of alcohol withdrawal. We advance the hypothesis that there is an altered diastolic function depending, not only on the hypertrophy of the myocardium, but also on the myocardial interstitial involvement caused by ethanol.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Noninvasive evaluation of left ventricular function in alcoholics before and after suspension of ethanol abuse]. 183 30

Chylous ascites is a well-documented sequelae of traumatic rupture of the thoracic duct and mechanical obstruction of the lymphatic system due to neoplastic, inflammatory, or congenital anomalies. Less commonly, chylous ascites results from altered hemodynamics and lymphatic flow, as seen in cirrhosis and constrictive pericarditis. Rarely, severe right-sided heart failure from a variety of causes has also resulted in chylous ascites or a protein-losing enteropathy. We report a case of chylous ascites due to dilated cardiomyopathy with autopsy findings. The pathophysiology of chylous ascites formation in right heart failure will be discussed, with a review of the literature.
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PMID:Dilated cardiomyopathy associated with chylous ascites. 259 59

Clinical studies using 31P and 1H MRS with a whole body 2.0 T MRI/MRS system are described. In most cases, techniques to quantitate absolute molar concentrations of metabolites in various organs were used. In the brain, AIDS, chronic stroke, and white matter lesions were associated with alterations of brain 31P metabolites. Epilepsy was associated with increased pH in the seizure focus. In the heart, dilated cardiomyopathy was associated with increased PDE/ATP while PCr/ATP was unchanged. In the liver, alcoholic hepatitis and cirrhosis were associated with diminished hepatic ATP while alcoholic hepatitis had increased pH and cirrhosis had decreased pH. This allowed differentiation of normal liver, alcoholic hepatitis, and alcoholic cirrhosis without biopsy. In the prostate, malignancy was associated with increased PME/ATP and decreased PCr/ATP. The PME/PCr was greatly increased in malignant prostate with no overlap in normals. Other cancers outside the brain had increased PME and effective treatment was often associated with diminished PME. 1H MRS of the brain was performed using ISIS and outer volume suppression pulses for volume localization. Excellent high resolution 1H water-suppressed spectra were obtained at echo times as short as 30 ms, showing well resolved peaks for lactate, N-acetylaspartate, glutamate, choline, creatinine, and inositol. 1H MRS demonstrated that the uptake of ethanol by the brain was slower than the rise of ethanol in blood. 31P spectroscopic imaging of the brain with resolution of 2.25 x 2.25 x 2.5 cm produced metabolic images and high resolution spectra from desired regions of interest.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Clinical magnetic resonance spectroscopy of brain, heart, liver, kidney, and cancer. A quantitative approach. 270 9

From 1969 to 1973, 68 patients were admitted to the 4th Division of Medicine of the Brescia Civil Hospital with the diagnosis of viral myocarditis. The patients were divided into two groups according to the results of the Coxsackie virus complement fixing antibodies test: Group 1 (42 patients) with a fourfold or greater rising antibody titre; Group 2 (26 patients) with a negative serum test. Both groups were examined after a follow-up period of 15 years. Ten patients from Group 1 died. The diagnoses were chronic myocarditis (three cases); chronic cardiomyopathy-pulmonary embolism (one case); chronic cardiomyopathy-liver cirrhosis (one case); dilated cardiomyopathy-sudden death (two cases); congestive cardiomyopathy (three cases). No Group 2 patients died. The 15-year mortality rate of Group 1 was significantly higher than that of Group 2 (Fisher Test: p less than 0.005). In conclusion, the natural history of Coxsackie virus heart disease is characterized by two possibilities: a complete recovery from a clinical point of view, in some cases with only minor T wave abnormalities, or evolution into a chronic disease (dilated cardiomyopathy) having a high mortality rate within 10 years of the onset of the acute disease.
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PMID:Coxsackie virus heart disease: 15 years after. 322 24

Surgical implantation of a sutureless myocardial electrode and pulse generator was performed in 18 dogs, using a ventral abdominal, transdiaphragmatic approach. Twelve dogs were greater than or equal to 10 years old. The 18 dogs weighed from 3 to 54 kg. Indications for permanent cardiac pacemaker implantation included complete (3rd degree) atrioventricular block, sick sinus syndrome, and sinus bradycardia. Few complications developed during or after surgery. One dog died during surgery from ventricular fibrillation, and hypertrophic cardiomyopathy was found at necropsy. Five dogs died 1 to 19 months after surgery (mean, 8.6 months) because of renal failure, hepatic cirrhosis, congestive cardiomyopathy, or idiopathic causes. Twelve dogs were alive 1 to 48 months after surgery (mean, 15.1 months). The surgical approach was used a second time in 3 dogs to replace the myocardial electrode wire and pulse generator 4, 16, and 26 months after surgery; technical complications were not associated with the second surgery in these 3 dogs. In 2 dogs that had initial pacemaker implantation via lateral thoracotomy, a transdiaphragmatic approach was used to replace the myocardial electrode lead and pulse generator 25.5 and 26 months after surgery. According to results of this study, the ventral abdominal, transdiaphragmatic approach for permanent pacemaker implantation in the dog is a simpler technique, with decreased surgery time, decreased time of tissue exposure, and decreased rate of infection, as compared with results described by investigators who used lateral thoracotomy or midline celiotomy and caudal one-third median sternotomy.
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PMID:Ventral abdominal, transdiaphragmatic approach for implantation of cardiac pacemakers in the dog. 379 71

Alcohol has acute and chronic cardiovascular effects. Acutely, alcohol depresses cardiac function and alters regional blood flow. Even when withdrawn from alcohol for several days, alcoholics may still manifest evidence of left ventricular dysfunction. In some alcoholics a severe muscle disorder may ensue with the clinical features of a dilated cardiomyopathy. The concomitant presence of a thiamine deficiency or cirrhosis may produce hemodynamic changes that can obscure the clinical features of alcohol-induced heart muscle disease. Alcoholics may also develop acute myocardial infarction with patent coronary arteries; some may have cardiac arrhythmias even without other evidence of heart disease. Although epidemiological studies suggest that moderate users of alcohol have fewer coronary events than teetotalers, such studies also demonstrate a relation between alcohol abuse and hypertension and an increased occurrence of coronary disease. Thus, the injurious cardiovascular effects of alcohol must be considered when establishing recommendations for its use.
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PMID:Cardiovascular effects of alcohol with particular reference to the heart. 639 13

Congestive cardiomyopathy and final stage of a liver cirrhosis due to massive overload of iron are often the cause of death in polytransfused patients with aplastic anaemia. With increasing frequency of transfusion the problem of overload of iron becomes more actual. The toxicity of abundant iron is based on various mechanisms of action, which are compiled with the help of literature. Our experiences hitherto made with the intravenous long-term infusion of desferrioxamine are reported. This regimen of therapy is not to be practiced in the long run.
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PMID:[Transfusion induced hypersiderosis in aplastic anemia--physiopathology and therapeutic aspects]. 684 80

The toxic effects of chronic ethanol abuse on cerebral and hepatic function have long been recognized. The role of ethanol abuse as an etiologic factor in heart disease is less clear and is often attributed to coexistent malnutrition. However, malnutrition has been dissociated from ethanol use in many patients with congestive cardiomyopathy. Studies in various animals provide major support for the role of ethanol as a toxic agent when used in large amounts for a prolonged period. Abnormalities that result from ethanol in test animals include depression of left ventricular performance and metabolic and morphologic changes that parallel the changes in human alcoholics with subclinical mechanical dysfunction of the heart, such as symptomatic cardiac arrhythmias, particularly during intensive alcohol ingestion. What causes the progression to heart failure or arrhythmias is not known, but several factors may be involved. These include, particularly in males, the cumulative effects of ethanol alone or after intensified drinking episodes, excessive exposure to trace metals or superimposed infection. The low prevalence of clinical nutritional deficiency in patients with alcoholic cardiomyopathy and the apparent infrequency of heart failure in patients with cirrhosis or neuropathy supports the view that the cardiac abnormality is often 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 pathogenetic process may continued unabated in some who become abstinent.
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PMID:Ethanol abuse and heart disease. 702 Sep 81

Based on anecdotal impressions, there is a common clinical perception that alcoholics with liver disease do not develop cardiomyopathy and that those with alcohol-induced cardiac disease are spared cirrhosis. To determine the relationship between alcoholic cardiomyopathy and cirrhosis, we carried out a prospective cross-sectional study that included: (1) 30 alcoholic men with cardiomyopathy; (2) 30 alcoholic men without cardiomyopathy (left ventricular ejection fraction > 55%); (3) 20 actively drinking alcoholics with cirrhosis; (4) 15 abstaining alcoholics with cirrhosis; and (5) 15 nonalcoholics with cirrhosis of other etiologies. Cirrhosis was observed in 13 of 30 patients with alcoholic cardiomyopathy (43%), compared with 2 of 30 alcoholics without cardiomyopathy (6%) (P < .001). Ten of the 20 active alcoholics with cirrhosis (50%) showed evidence of dilated cardiomyopathy. Actively drinking alcoholics with cirrhosis had a significantly lower mean ejection fraction and shortening fraction, as well as a greater mean end-diastolic diameter and left ventricular mass than abstaining alcoholics with cirrhosis. Cardiac studies of patients with nonalcoholic cirrhosis were normal. We conclude that a positive correlation exists between alcoholic cardiomyopathy and cirrhosis. Alcoholics admitted solely for cardiomyopathy have a higher prevalence of cirrhosis than unselected alcoholics without heart disease. Actively drinking alcoholics admitted only for cirrhosis show impaired cardiac performance, whereas abstaining alcoholics with liver disease tend to manifest normal cardiac function.
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PMID:Relationship between cardiomyopathy and liver disease in chronic alcoholism. 763 21

A neonate with deficiency of branching enzyme (glycogenosis type IV) presented symptoms of severe hypotonia pre- and postnatally, and dilated cardiomyopathy in early infancy. The classical clinical manifestation of liver cirrhosis was not present, although amylopectin-like inclusions were found in the hepatocytes. In contrast to a previous report, the neurons in the brain stem and spinal anterior horns contained PAS-positive, diastase-resistant deposits. The combined involvement of the muscles and motor neurones could account for the severity of hypotonia. The muscle biopsy, electromyogram and biochemical and enzyme assays were helpful in establishing the diagnosis.
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PMID:Neonatal hypotonia and cardiomyopathy secondary to type IV glycogenosis. 805 7


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