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|Identification of a potential cardiac antifibrotic mechanism of torasemide in patients with chronic heart failure|
|Authors: ||Lopez, B. (Begoña)|
Gonzalez, A. (Arantxa)
Beaumont, J. (Javier)
Querejeta, R. (Ramón)
Larman, M. (Mariano)
Diez, J. (Javier)
|Keywords: ||Antihypertensive Agents/pharmacology|
Heart Failure/drug therapy
|Issue Date: ||2007|
|Publisher version: ||http://www.sciencedirect.com/science/article/pii/S0735109707018220|
|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.|
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.
|Permanent link: ||http://hdl.handle.net/10171/21862|
|Appears in Collections:||DA - CIMA - Cardiovasculares - Cardiopatía hipertensiva - Artículos de Revista|
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