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)

A syndrome on four dairy farms in which calves up to two months of age died suddenly during a period of excitement usually precipitated by feeding was investigated. The description given by owners was that during, or shortly after milk feeding, the calves grunted, fell and died within one minute. Post mortem examinations revealed patchy myocardial pallor but no other lesions or evidence of infectious disease. Histopathological studies revealed peracute myocardial degeneration. Biochemical examinations have shown a selenium deficiency in in-contact calves and since this was corrected, no further cases have occurred. It is suggested that this is an additional manifestation of the selenium deficiency syndrome and that in certain circumstances, a deficiency of available selenium renders cardiac muscle vulnerable to stresses which induce severe peracute damage and leads to cardiac failure and sudden death.
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PMID:Sudden death in calves associated with acute myocardial degeneration and selenium deficiency. 71 69

Five horses with histories of colic developed signs of myocardial failure and skeletal muscle disease. Necropsy revealed pale areas in the cervical, pectoral, pelvic, and cardiac musculature; histologically, the lesions were indicative of dystrophic myodegeneration. Serum vitamin E concentrations were normal in 2 of the horses but serum selenium concentrations were normal in 2 of the horses, but serum selenium concentrations were low when compared with values obtained from clinically normal horses.
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PMID:Dystrophic myodegeneration in adult horses. 89 19

A specific selenium deficiency is a risk factor for Keshan disease, an endemic cardiomyopathy observed in China. In a Sahelian area of Niger, plasma selenium concentration was measured by neutronic activation and particle induced X-ray emission in 35 black African women with peripartum cardiomyopathy and 36 breast-feeding women without cardiac failure as controls. The plasma selenium concentration in patients was lower (48 +/- 25 ng/ml, mean +/- standard deviation) than in controls (77 +/- 16 ng/ml) (P less than 0.0001). Moreover, 40% (14/35) patients with peripartum cardiomyopathy had very low plasma selenium concentrations, below 45 ng/ml, versus none in controls. A low plasma selenium concentration is a risk factor for the Sahelian peripartum cardiomyopathy.
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PMID:A low plasma selenium is a risk factor for peripartum cardiomyopathy. A comparative study in Sahelian Africa. 142 53

We describe a girl aged 17 y who died after a cardiac arrest secondary to septic shock. At autopsy, the enlarged, soft, and flabby heart showed microscopic evidence of acute myocardial infarction, myocardial edema, myocardiocyte loss, replacement fibrosis in the interventricular septum, and right and left ventricular hypertrophic nucleomegaly. The pathological diagnosis was that of cardiomyopathy due to prolonged selenium deficiency. The patient had been on total parenteral nutrition for 17 mo, following extensive bowel resection for intractable pain, nausea, and vomiting caused by chronic idiopathic intestinal pseudoobstruction. Seven months before death, when severe biochemical selenium deficiency was diagnosed, supplemental selenium was added to the infusion, and plasma selenium concentrations increased. In long-standing selenium deficiency, sepsis may contribute the final insult to a damaged myocardium, triggering symptomatic cardiac failure and sudden death.
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PMID:Cardiomyopathy associated with nonendemic selenium deficiency in a Caucasian adolescent. 216 25

We studied the relationship between serum selenium (Se) and left ventricular performance in 33 patients on maintenance haemodialysis. Low serum Se was frequent. However, there were no significant differences in echocardiographic indices of left ventricular function between patients with serum Se less than 0.9 umol/l and those with serum Se greater than 0.9 umol/l. We conclude that Se deficiency is not an important cause of cardiac failure in uraemia.
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PMID:Is selenium deficiency the cause of uraemic cardiomyopathy? 344 30

Between November 1979 and July 1982, 7 captive gelada baboons (Theropithecus gelada) died; 5 of them died unexpectedly, 1 died after a 4-month history of heart failure, and 1 was anemic and dyspneic for 2 days before death. Of those that died unexpectedly, 1 was anemic and 4 were clinically normal. At necropsy, all baboons had white or pale patches of myocardium. Histologically, fibrosis and acute myocytolysis were observed in the myocardium. Three affected baboons were tested for plasma alpha-tocopherol content and were found deficient. Four unaffected baboons were given vitamin E for 24 months, and plasma alpha-tocopherol content returned to normal. Blood selenium content was determined in 1 affected baboon and was normal.
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PMID:Cardiomyopathy associated with vitamin E deficiency in seven gelada baboons. 651 80

We encountered three patients with chronic respiratory failure who had heart failure of cardiac arrhythmias and low levels of serum selenium. All three had tracheostomies and had received long-term parenteral nutrition that had not included selenium. All three also had refractory cardiac dysfunction, which was manifested in edema, heart failure, and various tachycardias. We suspected that selenium deficiency had caused their cardiac dysfunction. Serum selenium concentrations were found to be much lower than normal in all three, so 100 micrograms/day of selenium was administered in addition to their tube feedings. Cardiac function improved after replacement of selenium. These cases show the need for preventing selenium deficiency in patients with chronic respiratory failure during long-term administration of parenteral nutrition.
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PMID:[Selenium deficiency associated with cardiac dysfunction in three patients with chronic respiratory failure]. 902 29

Peripartum cardiomyopathy is a classic but uncommon entity in African women about which there is little etiologic understanding. From January 1990 to March 1996 a series of 30 cases of peripartum cardiomyopathy was collected at the Principal Hospital in Dakar, Senegal. Peripartum cardiomyopathy was defined as the occurrence of cardiac insufficiency in a woman with no previous history of heart disease, during the period between the second and twentieth weeks after delivery confirmed by ultrasound evidence of dilated cardiomyopathy. The overall incidence of peripartum cardiomyopathy during the study period was 30 out of 1200 deliveries. The mean age of the women in the study was 34 years and mean parity was 5.2. In 13.3% of cases births involved twins. There were no predisposing socio-economic or climatic factors. The clinical picture was severe cardiac failure in 80.3% of cases and left ventricular insufficiency in 16.6%. In all cases ultrasound findings were typical of dilated cardiomyopathy. Serum selenium and vitamin B1 levels were normal. Measurements of T CD4 and CD8 in eight patients were normal. Conversion enzyme inhibitors were administered to twenty patients. Complete remission was achieved in 14 patients, three patients died, and thirteen patients presented ultrasonic evidence of persistent dilated cardiomyopathy. One patient relapsed after a subsequent delivery. These findings are in agreement with previous reports concerning the clinical and prognostic features of peripartum cardiomyopathy in Africa.
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PMID:[Etiopathogenic, ultrasonographic and prognostic features of postpartum cardiomyopathy]. 913 97

Lesions of heart failure, specifically cardiac dilation or hypertrophy along with a nodular liver (chronic passive congestion) and ascites, have been found in 4-5% of aborted bovine fetuses. In this study, a group of 22 such fetuses was compared with groups of aborted fetuses without lesions of heart failure and with nonaborted fetuses obtained from a slaughterhouse. The fetuses were necropsied, tissues were taken for histopathology, and samples were collected for routine bacteriologic and virologic examinations. Liver and kidney tissue was saved for selenium analysis. Histopathologic examinations of myocardium of fetuses with cardiac failure revealed myocardial necrosis and mineralization in 7 fetuses, lymphocytic myocarditis in 5 fetuses, myocardial fibrosis in 5 fetuses, or no microscopic lesions in 5 fetuses. Mean liver selenium levels were 5.5 mumol/kg in the fetuses with heart lesions, 6.5 mumol/kg in the fetuses without heart lesions and 7.5 mumol/kg in fetuses from the slaughterhouse; these differences were statistically significant. The results suggest that selenium deficiency in bovine fetuses may cause myocardial necrosis and heart failure. This study also provides data on normal liver and kidney selenium levels in bovine fetuses from the analyses of 19 nonaborted fetuses.
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PMID:Investigation of the selenium status of aborted calves with cardiac failure and myocardial necrosis. 921 Dec 37

Normal ageing is associated with different changes in the cardiovascular system that lead to an increase in pathological processes such as hypertension and heart failure. Therefore the importance of glutathione peroxidase and catalase for protection against peroxidation was studied in the rat heart. Each of the these enzymes was regulated by feeding rats a low selenium diet either unsupplemented or supplemented with 0.4 parts per million of selenium, with or without the catalase inhibitor, sodium fluoride, in their drinking water. After 2 months, selenium deficient rats had 87% reductions in mitochondrial and cytosolic glutathione peroxidase activities. These reductions were accompanied by increased peroxidation in heart homogenates and mitochondrial suspensions. Since increased mitochondrial peroxidation only occurred when both the cytosolic and mitochondrial glutathione peroxidase activities were involved, these selenoenzymes appear to work in tandem and reductions in both are a prerequisite for increased peroxidation in the heart. Peroxidation did not occur in sodium fluoride treated rats even though cytosolic catalase activity was inhibited by 70%. Moreover, inhibition of catalase activity did not exacerbate the level of peroxidation in selenium deficient rats depleted of glutathione peroxidase activity. Because increased peroxidation was only associated with reductions in glutathione peroxidase activity irrespective of catalase activity, the selenoenzyme appears to be more important for detoxification of hydrogen peroxide in the heart.
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PMID:Enzymatic defenses of the rat heart against lipid peroxidation. 922 21


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