Full metadata record
DC Field | Value | Language |
---|---|---|
dc.creator | Lopez-Salazar, M.B. (María Begoña) | - |
dc.creator | Gonzalez, A. (Arantxa) | - |
dc.creator | Beaumont, J. (Javier) | - |
dc.creator | Querejeta, R. (Ramón) | - |
dc.creator | Larman, M. (Mariano) | - |
dc.creator | Diez-Martinez, J. (Javier) | - |
dc.date.accessioned | 2012-05-02T11:24:03Z | - |
dc.date.available | 2012-05-02T11:24:03Z | - |
dc.date.issued | 2007 | - |
dc.identifier.citation | Lopez B, Gonzalez A, Beaumont J, Querejeta R, Larman M, Diez J. Identification of a potential cardiac antifibrotic mechanism of torasemide in patients with chronic heart failure. J Am Coll Cardiol 2007 Aug 28;50(9):859-867. | es_ES |
dc.identifier.issn | 1558-3597 | - |
dc.identifier.uri | https://hdl.handle.net/10171/21862 | - |
dc.description.abstract | OBJECTIVES: This study sought to investigate whether torasemide inhibits the enzyme involved in the myocardial extracellular generation of collagen type I molecules (i.e., procollagen type I carboxy-terminal proteinase [PCP]). BACKGROUND: Torasemide has been reported to reduce myocardial fibrosis in patients with chronic heart failure (HF). METHODS: Chronic HF patients received either 10 to 20 mg/day oral torasemide (n = 11) or 20 to 40 mg/day oral furosemide (n = 11) in addition to their standard HF therapy. At baseline and after 8 months from randomization, right septal endomyocardial biopsies were obtained to analyze the expression of PCP by Western blot and the deposition of collagen fibers (collagen volume fraction [CVF]) with an automated image analysis system. The carboxy-terminal propeptide of procollagen type I (PICP) released as a result of the action of PCP on procollagen type I was measured in serum by radioimmunoassay. RESULTS: The ratio of PCP active form to PCP zymogen, an index of PCP activation, decreased (p < 0.05) in torasemide-treated patients and remained unchanged in furosemide-treated patients. A reduction (p < 0.01) in both CVF and PICP was observed in torasemide-treated but not in furosemide-treated patients. Changes in PCP activation were positively correlated (p < 0.001) with changes in CVF and changes in PICP in patients receiving torasemide. CONCLUSIONS: These findings suggest the hypothesis that the ability of torasemide to reduce myocardial fibrosis in chronic HF patients is related to a decreased PCP activation. Further studies are required to ascertain whether PCP may represent a new target for antifibrotic strategies in chronic HF. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | Elsevier | es_ES |
dc.rights | info:eu-repo/semantics/closedAccess | - |
dc.subject | Antihypertensive Agents/pharmacology | es_ES |
dc.subject | Heart Failure/drug therapy | es_ES |
dc.subject | Sulfonamides/pharmacology | es_ES |
dc.title | Identification of a potential cardiac antifibrotic mechanism of torasemide in patients with chronic heart failure | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.relation.publisherversion | http://www.sciencedirect.com/science/article/pii/S0735109707018220 | es_ES |
dc.type.driver | info:eu-repo/semantics/article | es_ES |
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