June 1, 2008Open Access
Tolvaptan: the evidence for its therapeutic value in acute heart failure syndrome.
Key Result
Tolvaptan reduces bodyweight, improves serum sodium, and lowers pulmonary capillary wedge pressure compared with placebo in acute heart failure syndrome, but does not improve long-term mortality.
Structured PICO
Does tolvaptan improve clinical outcomes in patients with acute heart failure syndrome?
P
Population
Patients with acute heart failure syndrome (AHFS)
I
Intervention
Tolvaptan
C
Comparator
Placebo
Tolvaptan is a safe and effective adjunct to standard diuretic therapy for treating congestion and improving serum sodium in acute heart failure syndrome, though it does not improve long-term mortality.
Limitations
- Has yet to demonstrate reversal of cardiac remodeling
- No differences in long-term mortality rates between tolvaptan and placebo
Abstract
INTRODUCTION: Acute heart failure syndrome (AHFS) is one of the leading causes of hospital admission in the US. Tolvaptan is a vasopressin V(2) receptor antagonist that blocks the effect of arginine vasopressin (AVP) in reabsorbing water from the collecting ducts of the nephrons in congestive heart failure. AIMS: To review the evidence for utilizing tolvaptan in the treatment of AHFS. EVIDENCE REVIEW: Several clinical trials have sought to assess the clinical effects of tolvaptan in heart failure. Compared with placebo, tolvaptan has been shown to reduce bodyweight and improve serum sodium in patients with AHFS without worsening renal function. Tolvaptan appeared to be well tolerated with a good safety profile. It caused a significant reduction in pulmonary capillary wedge pressure compared with placebo, but has yet to demonstrate reversal of cardiac remodeling. A large-scale mortality trial showed no differences in long-term mortality rates between tolvaptan and placebo, although early symptom relief was apparent with tolvaptan and lower diuretic use. PLACE IN THERAPY: Tolvaptan has shown to be safe and effective in treating congestion in AHFS. Free water excretion in fluid-overloaded patients vulnerable to cardiorenal compromise with standard diuretic therapy makes V(2) vasopressin receptor blockade an attractive adjunct to standard medical therapy aimed at reducing congestion in AHFS.