What is the clinical evidence from this study?

Study design: RCT. Population: Chronic Heart Failure (n=50). Intervention: Torasemide vs. Furosemide. Primary outcome: Left ventricular end-diastolic diameter (LVDd) at 6 months (p=<0.05).

January 1, 2003Open Access

Effects of Torasemide on Left Ventricular Function and Neurohumoral Factors in Patients With Chronic Heart Failure

Q: What are the key findings of this study?

Switching from furosemide to torasemide significantly reduced left ventricular end-diastolic diameter and left ventricular mass index, and decreased plasma B-type natriuretic peptide concentration in patients with chronic heart failure.

Key Result

Switching from furosemide to torasemide significantly reduced left ventricular end-diastolic diameter and left ventricular mass index, and decreased plasma B-type natriuretic peptide concentration in patients with chronic heart failure.

Study Design

Type

RCT (n=50)

Blinding

Open-label

Randomization

Randomized

Multicenter

Structured PICO

Does switching from furosemide to torasemide improve left ventricular function and neurohumoral factors in patients with chronic heart failure?

Population

50 outpatients with chronic, stable, moderate heart failure (NYHA class II-III) and left ventricular ejection fraction ≤45% on long-term ACE inhibitors and furosemide, followed for 6 months.

Intervention

Torasemide 4-8 mg/day oral for 6 months (in place of furosemide).

Comparator

Continued oral furosemide at the same dose of 20-40 mg/day for 6 months.

Outcome

Echocardiographic parameters (left ventricular end-diastolic diameter, left ventricular mass index, Doppler filling parameters) and neurohumoral assays (B-type natriuretic peptide, active renin, aldosterone) at 6 months.surrogate

Switching from furosemide to torasemide in patients with chronic heart failure improves left ventricular remodeling and neurohumoral profiles, potentially due to aldosterone receptor blockade.

Main Result

Absolute Event Rate: 63.2% vs 65.5%

p-value: p=<0.05

Limitations

Patients allocated to the torasemide group stopped their potassium supplementation, which may affect aldosterone production.
Did not measure the plasma concentration of procollagen type III aminoterminal peptide, a biochemical marker of LV fibrosis.
Open-label study involving a relatively small number of patients.
Did not determine whether torasemide improves LV function in patients with 'restrictive filling' or 'pseudonormalization' patterns.

Abstract

The effect of torasemide and furosemide therapy was compared in 50 patients who had chronic heart failure and symptoms NYHA class II-III despite long-term therapy with both low-dose furosemide and angiotensin-converting enzyme inhibitors. In this randomized 6-month, open-label trial, baseline and follow-up echocardiograms and neurohumoral assays were obtained in 25 group F patients (continued same dose of oral furosemide at 20-40 mg/day) and in 25 group T patients (received torasemide at 4-8 mg/day in place of furosemide). At 6 months, parameters were unchanged in group F whereas the group T patients had a lower left ventricular end-diastolic diameter (p<0.005) and left ventricular mass index (p<0.005) with improved Doppler filling parameters, decreased plasma B-type natriuretic concentration (p<0.001) and increased plasma concentrations of active renin (p<0.005) and aldosterone (p<0.001). The magnitude of these changes appeared dose dependent and it is suggested these favorable effects of switching from furosemide to torasemide may be related to aldosterone receptor blockade.

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