BACKGROUND AND OBJECTIVE: Experimental data have demonstrated controversial results regarding loop diuretics and their influence on the pulmonary vasculature. The aim of this pilot study was to compare the effect of torasemide versus furosemide on systemic and pulmonary haemodynamics in patients with secondary pulmonary hypertension. METHODS:Twenty-one patients were enrolled in this double-blind, randomized trial: the furosemide group (n = 11) received 40 mg intravenously (IV) and 80 mg orally whereas the torasemide group (n = 10) received 20 mg IV and 20 mg orally. Haemodynamic variables were documented and endothelin-1 and arterial angiotensin-II plasma levels were simultaneously analysed at baseline (T0), 5 minutes after IV administration (T1), at baseline prior to oral administration (T2), and 60 minutes after oral administration (T3). RESULTS:Cardiac output (relative treatment effect over time between groups; p = 0.03) increased significantly in the torasemide group compared with the furosemide group. In the furosemide group, a significant increase in arterial angiotensin-II (AT-II) plasma levels was observed compared with the torasemide group (relative treatment effect over time between groups; p = 0.031). CONCLUSION:Torasemide increased cardiac output (relative treatment effect over the time), whereas treatment with furosemide significantly increased arterial AT-II plasma levels. A possible explanation for these findings might be activation of the renin-angiotensin system by furosemide. However, the underlying pathomechanism remains to be established and evidence from an adequately powered trial is needed to determine if furosemide aggravates cardiac function by increasing AT-II plasma levels.
RCT Entities:
BACKGROUND AND OBJECTIVE: Experimental data have demonstrated controversial results regarding loop diuretics and their influence on the pulmonary vasculature. The aim of this pilot study was to compare the effect of torasemide versus furosemide on systemic and pulmonary haemodynamics in patients with secondary pulmonary hypertension. METHODS: Twenty-one patients were enrolled in this double-blind, randomized trial: the furosemide group (n = 11) received 40 mg intravenously (IV) and 80 mg orally whereas the torasemide group (n = 10) received 20 mg IV and 20 mg orally. Haemodynamic variables were documented and endothelin-1 and arterial angiotensin-II plasma levels were simultaneously analysed at baseline (T0), 5 minutes after IV administration (T1), at baseline prior to oral administration (T2), and 60 minutes after oral administration (T3). RESULTS: Cardiac output (relative treatment effect over time between groups; p = 0.03) increased significantly in the torasemide group compared with the furosemide group. In the furosemide group, a significant increase in arterial angiotensin-II (AT-II) plasma levels was observed compared with the torasemide group (relative treatment effect over time between groups; p = 0.031). CONCLUSION:Torasemide increased cardiac output (relative treatment effect over the time), whereas treatment with furosemide significantly increased arterial AT-II plasma levels. A possible explanation for these findings might be activation of the renin-angiotensin system by furosemide. However, the underlying pathomechanism remains to be established and evidence from an adequately powered trial is needed to determine if furosemide aggravates cardiac function by increasing AT-II plasma levels.
Authors: Grazyna Snopek; Hanna Pogorzelska; Tomasz M Rywik; Aldona Browarek; Jadwiga Janas; Jerzy Korewicki Journal: Am J Cardiol Date: 2002-07-15 Impact factor: 2.778
Authors: A M Calafiore; G Teodori; A Mezzetti; G Bosco; A M Verna; G Di Giammarco; D Lapenna Journal: Ann Thorac Surg Date: 1995-02 Impact factor: 4.330