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 54 year-old Japanese female with cardiac insufficiency was found to have a left atrial mass and smaller masses on the mitral valve. Excisional surgery of the masses and mitral valve replacement were carried out. In spite of intensive post-operative radiation therapy, the patient died of intra-atrial recurrence and brain metastases after 8 months. Tumour cells were spindled to oval, were positive for vimentin, S100 protein and neurone specific enolase. Laminin and fibronectin were also demonstrated. Bone formation and myxoid areas were present. An ultrastructurally identifiable stromal component, possibly responsible for laminin and fibronectin staining, was also present. The merits of the two main diagnostic possibilities - a mesenchymal/fibroblastic sarcoma showing bone and aberrant S100 protein, and a malignant peripheral nerve sheath tumour with bone - were discussed. In practical terms, the tumour was given the diagnosis of unclassifiable sarcoma of the left atrium. Atrial sarcomas showing neural markers and bone formation are exceedingly rare, and this report adds a further exceptionally uncommon case to the literature.
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PMID:Cardiac sarcoma showing bone formation and neurogenic markers: report of a case. 1198 51

The metabolic phenotype of the failing heart includes a decrease in phosphocreatine and total creatine concentration [Cr], potentially contributing to contractile dysfunction. Surprisingly, in 32- week-old mice over-expressing the myocardial creatine transporter (CrT-OE), we previously demonstrated that elevated [Cr] correlates with left ventricular (LV) hypertrophy and failure. The aim of this study was to determine the temporal relationship between elevated [Cr] and the onset of cardiac dysfunction and to screen for potential molecular mechanisms. CrT-OE mice were compared with wild-type (WT) littermate controls longitudinally using cine-MRI to measure cardiac function and single-voxel (1)H-MRS to measure [Cr] in vivo at 6, 16, 32, and 52 weeks of age. CrT-OE mice had elevated [Cr] at 6 weeks (mean 1.9-fold), which remained constant throughout life. Despite this increased [Cr], LV dysfunction was not apparent until 16 weeks and became more pronounced with age. Additionally, LV tissue from 12 to 14 week old CrT-OE mice was compared to WT using 2D difference in-gel electrophoresis (DIGE). These analyses detected a majority of the heart's metabolic enzymes and identified seven proteins that were differentially expressed between groups. The most pronounced protein changes were related to energy metabolism: alpha- and beta-enolase were selectively decreased (p<0.05), while the remaining enzymes of glycolysis were unchanged. Consistent with a decrease in enolase content, its activity was significantly lower in CrT-OE hearts (in WT, 0.59+/-0.02 micromol ATP produced/microg protein/min; CrT-OE, 0.31+/-0.06; p<0.01). Additionally, anaerobic lactate production was decreased in CrT-OE mice (in WT, 102+/-3 micromol/g wet myocardium; CrT-OE, 78+/-13; p=0.02), consistent with decreased glycolytic capacity. Finally, we found that enolase may be regulated by increased expression of the beta-enolase repressor transcription factor, which was significantly increased in CrT-OE hearts. This study demonstrates that chronically increased myocardial [Cr] in the CrT-OE model leads to the development of progressive hypertrophy and heart failure, which may be mediated by a compromise in glycolytic capacity at the level of enolase.
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PMID:Mice over-expressing the myocardial creatine transporter develop progressive heart failure and show decreased glycolytic capacity. 1991 46

Heart failure (HF) is a prothrombotic state with increased rate of thromboembolic events. Magnetic resonance imaging studies demonstrated increased rate of silent cerebral infarcts (SCI) in this patient group and SCIs were shown lead to dementia, cognitive decline, and depression. We aimed to show acute decompensated phase is associated with increased rate of recent SCI in reduced ejection fraction HF patients. HF patients with sinus rhythm hospitalized for acute decompensation were studied. Neuron specific enolase (NSE), a sensitive neuronal ischemia marker, was used to detect recent SCI. Decompensated and compensated phase blood samples for NSE were collected on the day of admission and on the third day of compensation, respectively. One hundred and forty seven patients with mean age of 72 were studied. There were significantly more patients with positive NSE levels at decompensated state (29% vs 4%, p <0.001). Multivariate predictors for recent SCI were smoking, new onset atrial fibrillation, spontaneous echo contrast of left ventricle, and aneurysmatic apex. Statin use was found to be protective against NSE elevation. In conclusion, our data reveal that decompensated HF is significantly associated with increased levels of NSE suggestive for silent neuronal injury.
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PMID:Relation of Acute Decompensated Heart Failure to Silent Cerebral Infarcts in Patients With Reduced Left Ventricular Ejection Fraction. 3092 47