Beneficial effects of torasemide on systolic wall stress and sympathetic nervous activity in asymptomatic or mildly symptomatic patients with heart failure: comparison with azosemide.
Loop diuretics could adversely influence prognosis due to activation of neurohumoral mechanism in the long term. Previous study showed torasemide, a loop diuretic with anti-aldosteronergic properties, was associated with lower mortality in patients with chronic heart failure (CHF). We evaluated the effects of torasemide, in comparison with azosemide, in patients with CHF. Patients received oral diuretic therapy with torasemide (8 mg/d, n = 15) or azosemide (60 mg/d, n = 15) for 3 months. Torasemide and azosemide were then switched, and the patients were treated for another 3 months. Torasemide treatment induced significant decreases in left ventricular (LV) systolic wall stress (from 259 +/- 95 to 232 +/- 80 kdyn/cm2) and the plasma level of aldosterone (from 133 +/- 61 to 95 +/- 50 pg/mL) and was not associated with a change in the plasma level of norepinephrine. In contrast, the plasma level of norepinephrine was significantly increased (from 370 +/- 170 to 481 +/- 247 pg/mL), whereas LV systolic wall stress was unchanged after azosemide treatment. This study indicates that torasemide treatment reduced LV systolic wall stress without activation of the sympathetic nervous system in patients with CHF. The anti-aldosteronergic properties of torasemide may contribute to its favorable effects.
Harada
Ken
K
Department of Cardiology, Nagoya University Graduate School of Medicine, Nagoya, Japan. haraken@med.nagoya-u.ac.jp
Izawa
Hideo
H
Nishizawa
Takao
T
Hirashiki
Akihiro
A
Murase
Yosuke
Y
Kobayashi
Masakazu
M
Isobe
Satoshi
S
Cheng
Xian Wu
XW
Noda
Akiko
A
Nagata
Kohzo
K
Yokota
Mitsuhiro
M
Murohara
Toyoaki
T
D000284:Administration, Oral; D000450:Aldosterone / Q000097:blood; D018592:Cross-Over Studies; D003692:Delayed-Action Preparations; D004334:Drug Administration Schedule; D005260:Female; D006333:Heart Failure / Q000188:drug therapy / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use*; D009638:Norepinephrine / Q000097:blood; D049994:Sodium Potassium Chloride Symporter Inhibitors / Q000627:therapeutic use*; D013424:Sulfanilamides / Q000627:therapeutic use*; D013449:Sulfonamides / Q000627:therapeutic use*; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000503:physiopathology; D013599:Systole; D000077786:Torsemide; D018487:Ventricular Dysfunction, Left / Q000188:drug therapy* / Q000503:physiopathology; D013777:Tetrazoles; D013876:Thiophenes; D000096926:Benzenesulfonamides
D000450:Aldosterone; D003692:Delayed-Action Preparations; D000451:Mineralocorticoid Receptor Antagonists; D009638:Norepinephrine; D049994:Sodium Potassium Chloride Symporter Inhibitors; D013424:Sulfanilamides; D013449:Sulfonamides; D000077786:Torsemide; C018222:azosemide; D013777:Tetrazoles; D013876:Thiophenes; D000096926:Benzenesulfonamides