Key result
Torasemide reduces PCP activation and myocardial collagen volume fraction versus furosemide in chronic HF.
Why the study?
Torasemide reduces myocardial fibrosis in chronic heart failure, but whether it inhibits procollagen type I carboxy-terminal proteinase was unknown.
RCT (n=22)
Randomized
p-value: p=<0.05
Captured external expert commentary on this paper, strongest first. Original sources are linked where available.
“previous work with torsemide, a loop diuretic available for routine use across the spectrum of HF, suggests that the medication may exert favourable biochemical and molecular effects on myocardial fibrosis. Conceivably, such properties may make torsemide a particularly helpful drug in HFpEF, whereby a single agent could control congestion while simultaneously attenuating (or reversing) changes in myocardial fibrosis. Thus, confirmation of added anti-fibrotic and clinical outcome benefits of torsemide beyond its symptomatic role as a diuretic would differentiate it from other loop diuretics, highlighting it as the clear choice in HFpEF and potentially other forms of HF.”
Clinical investigation demonstrates myocardial collagen reduction from torasemide in chronic heart failure, indicating unique antifibrotic benefits beyond standard diuresis.
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.
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López et al. (2007) conducted an RCT in Chronic heart failure (n=22). Torasemide vs. Furosemide (20 to 40 mg/day oral) was evaluated on Ratio of PCP active form to PCP zymogen (index of PCP activation) (p=<0.05). In patients with chronic heart failure, torasemide significantly decreased PCP activation (p<0.05) and myocardial collagen volume fraction (p<0.01) compared to furosemide over 8 months.
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