Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with heart failure frequently exhibit abnormal skeletal muscle metabolic responses to exercise, as assessed with 31P NMR. To investigate whether these metabolic abnormalities are due to intrinsic skeletal muscle changes, we performed gastrocnemius muscle biopsies on 22 patients with heart failure (peak VO2, 15.4 +/- 4.7 ml/kg/min; ejection fraction, 20 +/- 7%) and on eight normal subjects. Biopsies were analyzed for fiber type and area, capillarity, citrate synthase, phosphofructokinase, lactate dehydrogenase, and beta-hydroxyacyl CoA dehydrogenase activity. All patients with heart failure also underwent 31P NMR studies of their calf muscle during plantarflexion at three workloads. Muscle pH responses and the relation of the ratio of inorganic phosphate to phosphocreatine (Pi/PCr) to systemic VO2 were then evaluated. Compared with normal subjects, patients with heart failure exhibited a shift in fiber distribution with increased percentage of the fast twitch, glycolytic, easily fatigable type IIb fibers (normal subjects, 22.7 +/- 10.1; heart failure, 33.1 +/- 11.1%; p less than 0.05), atrophy of type IIa (normal subjects, 5,477 +/- 1,109; heart failure, 4,239 +/- 1,247 microns 2; p less than 0.05) and type IIb fibers (normal subjects, 5,957 +/- 1,388; heart failure, 4,144 +/- 945 microns 2; p less than 0.01), and decreased activity of beta-hydroxyacyl CoA dehydrogenase (normal subjects, 5.17 +/- 1.44; heart failure, 3.67 +/- 1.68 mol/kg protein/hr; p less than 0.05). No significant linear correlation could be identified between the slope of the Pi/PCr to VO2 relation and muscle histochemistry or enzyme activities. Similarly, no linear relation was found between intracellular pH at peak exercise and any muscle variable.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Contribution of intrinsic skeletal muscle changes to 31P NMR skeletal muscle metabolic abnormalities in patients with chronic heart failure. 280 70

A 15-year-old girl with a four-month history of cardiac failure from undetermined cause was admitted to the hospital with weakness, fatigue, and weight loss. During her hospitalization she was found to have abused diet aids, laxatives, and cathartics. Although an electrocardiogram revealed nonspecific T-wave abnormalities and laboratory studies showed supranormal enzyme test results for creatine kinase and lactate dehydrogenase, no definite explanation of the cardiomyopathy was forthcoming. Ipecac abuse leading to cardiomyopathy was suspected early in the hospitalization. HPLC analysis of a urine sample showed emetine, a principle component of ipecac, the presence of which was later confirmed by more-specific HPLC analysis with photodiode array detection.
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PMID:Emetine identified in urine by HPLC, with fluorescence and ultraviolet/diode array detection, in a patient with cardiomyopathy. 292 Apr 26

Experimental hyperthyroidism induced in rats by daily injections of 3,3',5,5'-tetraiode-L-thyroxine (0.5 mg/kg i.p.) for 14 days resulted in a significant increase in heart weight and heart weight/body weight ratio. Hemodynamic and morphological studies were performed in one group. Thyroxine-treated rats showed a characteristic cardiovascular hyperdynamic state, such as tachycardia and augmented rate of contraction, but no evidence of heart failure such as elevated end-diastolic pressures. The cardiac cells in hyperthyroid rats had a significantly larger diameter and more mitochondria than did those of the control rats. In another group the activities of cardiac enzymes involved in energy utilization and liberation were measured biochemically and compared with those of normal controls. Hyperthyroidism resulted in increased specific activity of cytochrome C oxidase and actomyosin ATPase in the myocardium. The specific activity of long-chain acyl-CoA synthetase, carnitine palmityl-transferase, carnitine acetyltransferase, malate dehydrogenase and citrate synthase showed a moderate to marked increment, whereas the specific activity of lactate dehydrogenase and pyruvate kinase remained at the control values. These results suggest that in hyperthyroid rat hearts the functions of both energy liberation and utilization systems are enhanced to meet the added workload. Moreover, the increased activity of the enzymes participating in fatty acid metabolism suggest that in thyroxine-induced hypertrophic and hyperdynamic rat hearts, fatty acids contribute more to the energy supply than do carbohydrates.
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PMID:Biochemical and morphological study of cardiac hypertrophy. Effects of thyroxine on enzyme activities in the rat myocardium. 315 81

The serum-ascites albumin difference is reported to be superior to ascitic total protein, ascitic-to-serum total protein ratio, lactic dehydrogenase, and ascitic-to-serum lactic dehydrogenase ratio in differentiating between ascites from liver disease and malignant ascites, S-A greater than 1.1 reflecting portal hypertension. We analyzed ascitic fluid from 46 consecutive patients with chronic liver disease, 28 patients with ascites associated with malignancy, 10 patients with right-sided heart failure, 4 patients with hypothyroidism, and 6 patients with miscellaneous causes of ascites to determine if this albumin difference is indeed a more valuable parameter. Analysis of our data confirms with a larger number of patients that the serum-ascites albumin difference is a more reliable indicator of transudative ascites, better termed portal hypertensive ascites. Malignant ascites without liver metastases had features of nonportal hypertensive ascites, and the serum-ascites albumin difference confirms this. The characteristics of malignant ascites associated with liver metastases, however, resemble those of the portal hypertensive ascites complicating liver disease. This new parameter is also helpful in distinguishing congestive heart failure with high protein ascites and portal hypertensive ascitic features from malignant ascites without liver metastases. Of particular note, myxedematous ascitic fluid, classically categorized as exudative, had an S-A greater than 1.1, indicating the possible role of portal hypertension in the development of ascites in these patients.
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PMID:Usefulness of serum-ascites albumin difference in separating transudative from exudative ascites. Another look. 316 91

In a prospective study, there were 13 patients with cardiac ascites among a group of 262 ascites patients (5% of the total). I compared the characteristics of 20 ascitic fluid samples from these patients with heart failure to those of 20 patients with cirrhotic ascites. The serum-ascites albumin concentration gradient was greater than or equal to 1.1 g/dl in all patients in both groups. The ascitic fluid total protein concentration was greater than or equal to 2.5 g/dl in all patients with cardiac ascites whereas only 10% of patients with cirrhotic ascites had such high values. The ascitic fluid lactate dehydrogenase and red cell counts were significantly higher in cardiac ascites than in cirrhotic ascites--although cardiac ascites was not visibly bloody. The peripheral hematocrit of patients with cardiac ascites was also significantly higher than that of patients with cirrhotic ascites. The ascitic fluid analysis in patients with cardiac ascites is characteristic and may assist in the differential diagnosis of ascites.
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PMID:Cardiac ascites: a characterization. 341 89

To characterize the incidence and severity of liver function abnormalities in patients with congestive heart failure, we analyzed systemic hemodynamics and biochemical profiles in 133 patients with stable chronic congestive heart failure, secondary to a dilated cardiomyopathy. The patients were divided into three groups, based on the severity of the reduction in cardiac index (CI). The mean values of all liver function tests in groups 1 (n = 43; CI greater than or equal to 2.0 L/min/m2) and 2 (n = 48; CI greater than 1.5 and less than 2.0 L/min/m2) were essentially normal, except for minimally elevated alkaline phosphatase levels and slightly decreased albumin levels in both groups, and slight increases in levels of gamma-glutamyl transpeptidase and total bilirubin in group 2. In contrast, group 3 patients (n = 42; CI less than or equal to 1.5 L/min/m2) had the most severe heart failure, as assessed by the lowest CI and highest cardiac filling pressures, and significantly higher levels of aspartate aminotransferase (65 +/- 82 U/L), alanine aminotransferase (77 +/- 102 U/L), lactate dehydrogenase (282 +/- 91 U/L), and total bilirubin (29 +/- 14 mumol/L [1.7 +/- 0.8 mg/dL]). The percentage of patients in group 3 with these abnormalities ranged between 27% and 80%. Although linear regression analysis showed that the elevations in right atrial and pulmonary wedge pressures, and the decreases in CI, were significantly correlated with liver function abnormalities, the correlation coefficients were small. Thus, liver function abnormalities remain common in patients with congestive heart failure but are generally small in magnitude and not associated with clinically apparent hepatic disease. It is likely that reduced forward flow and passive backward congestion are both contributing factors in the pathogenesis of these biochemical abnormalities, although nonhemodynamic factors may also be important.
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PMID:Liver function abnormalities in chronic heart failure. Influence of systemic hemodynamics. 360 80

I confirmed the existence of an additional isozyme band of lactate dehydrogenase (LD) (EC 1.1.1.27) cathodic to LD-5 utilizing agarose gel isozyme electrophoresis in seven patients. Three of the patients died of circulatory failure within three weeks after the isozyme was identified. Four patients survived after successful therapy for heart failure. The under-lying clinical condition was arteriosclerotic cardiovascular disease causing congestive heart failure with passive congestion of the major viscera. I performed biochemical analysis on the isozyme and found that it was extremely heat stable, was not immunoglobulin bound, and contained only M, not H, subunits. It may represent a posttranslationally modified LD-5 or alcohol dehydrogenase.
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PMID:Lactate dehydrogenase-6. A biochemical sign of serious hepatic circulatory disturbance. 402 70

Rabbits receiving adriamycin (ADR) on a chronic schedule developed significant histopathologic, ultrastructural and tissue electrolyte alterations of the ventricular myocardium. Rabbits that developed clinicopathologic evidence of cardiomyopathy with ADR had histologic lesions of the myocardium, including perivascular fibrosis, interstitial fibrosis and edema and myocytolysis. Ultrastructurally, large vacuoles resembling distended sarcoplasmic reticulum displaced the contractile elements and mitochondria, which were diminished in number within affected myocytes. Frequently, mitochondria appeared as electron-dense structures surrounded by layers of membranes resembling myelin figures. In addition, rabbits with cardiomyopathy had marked elevations in ventricular Ca, Na and H(2)O concentrations. Serum electrolytes were not significantly elevated, but lactic dehydrogenase (LDH) and creatine phosphokinase (CPK) were significantly increased, indicative of a cardiomyopathy. Rabbits receiving ADR but not developing clinicopathologic evidence of heart failure also had significant elevations in ventricular Ca, Na and H(2)O. Rabbits with no cardiomyopathy had no increases either in serum electrolyte concentrations or CPK and LDH levels. These studies indicate that marked increases in ventricular tissue Ca precede and accompany morphologic evidence of chronic myocardial degeneration and may be instrumental in the development of the ADR-induced cardiomyopathy.
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PMID:Electrolyte and morphologic alterations of myocardium in adriamycin-treated rabbits. 443 14

Measurement of lactate dehydrogenase (LDH), glucose and protein was performed in ascites fluid of 44 patients in addition to bacteriological and cytological examinations. In patients with cirrhosis of the liver protein content of ascites was low, LDH normal, and the ascites/serum ratio of glucose concentration was higher than 1. These values were statistically significant different from the values in patients with tumorous or inflammatory disease of the peritoneum - protein and LDH in the ascites fluid being high and the ascites/serum ratio of glucose concentration being below 1. Cirrhosis however and tumors of the liver could not be differentiated by this method. Ascites from patients with cardiac failure had high protein content. In patients with liver cirrhosis high concentrations of protein in ascitic fluid may mean possibly a better survival time.
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PMID:[Diagnostic value of laboratory examination of ascites fluid (author's transl)]. 616 37

Among 2175 patients seen over the last three years in a non-specialized department of internal medicine with no intensive care unit, 100 had supranormal serum lactic dehydrogenase activities. These patients' case-reports have been analyzed. Nearly half the patients (47/100) had a malignant disease (cancer or hemopathy). Among the remaining patients, 19 had a hepatic disorder (alcohol hepatitis in 10, viral hepatitis in 8, and isoniazide hepatitis in 1), 7 had a heart disease (heart failure with hepatomegaly in 5, myocardial infarction in 2), and 27 had various other conditions (including hemolysis in 6 and polymyositis en 3). The value of serum LDH assay is obvious in situations other than acute conditions such as myocardial infarction of pulmonary embolism; these are better known and have not been studied here as their prevalence was low among the patients enlisted in our study. In comparison to other enzymes (alkaline phosphatase (AP), gamma-glutamyl transpeptidase (GGT), transaminases (GOT, GPT) that were also routinely assayed in our patients, abnormal serum LDH activities are much less common and their significance is quite different. An increase in serum and their significance is quite different. An increase in serum LDH activity indicates a serious condition, often with a fatal outcome. The "various other conditions" group includes patients with hemolysis, hepatitis and myositis; the other patients in this group either had severe infectious diseases or died suddenly in the first few days of their hospitalization before diagnosis had been established. Each etiologic group has been analyzed to asses the characteristics of patients with increased LDH activity according to each etiology. Analysis of coincident abnormalities of the other enzymes listed above shows marked differences between etiologic groups; diagnostic accuracy can thus be enhanced in certain conditions. Most patients with malignancies had poorly differentiated tumors, with metastases: 28 had an epithelial tumor, with hepatic and/or bone metastases in 23 cases, 5 had cancer of the liver, 10 had a malignant hemopathy (2 lymphomas, 5 myeloproliferative syndromes, 3 acute leukemias), and 4 had a sarcoma. Cancer of the lung is the most common malignancy (10 cases) and may be responsible for increased serum LDH activity even in patients without metastases. Serum LDH assay is of value for monitoring the course in patients with initially increased activities as it falls under effective therapy and rises during exacerbations.
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PMID:[Value and diagnostic significance of serum lactic dehydrogenase in internal medicine (author's transl)]. 628 24


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