Tolvaptan for the treatment of heart failure: a review of the literature.

Link to article at PubMed

Tolvaptan for the treatment of heart failure: a review of the literature.

Expert Opin Pharmacother. 2011 Mar 15;

Authors: Ambrosy A, Goldsmith SR, Gheorghiade M

Introduction: It has been > 25 years since it was first discovered that arginine vasopressin levels are elevated in heart failure and this elevation is proportional to the severity of heart failure. Tolvaptan is an oral nonpeptide V(2)-selective antagonist and has been shown to induce free water excretion without increasing urine sodium, an effect termed 'aquaresis'. Areas covered: This paper aims to review the physiology, chemistry, pharmacokinetics, clinical efficacy and safety of tolvaptan in HF. A PubMed literature search was performed using 'tolvaptan' and the MeSH term 'heart failure', yielding 89 references. Expert opinion: Clinical trials conducted in ambulatory and hospitalized patients with HF have found treatment with tolvaptan causes rapid and sustained body weight reductions concurrent with increases in urine output, improves and/or normalizes serum sodium in hyponatremic patients, reduces signs and symptoms of congestion and increases thirst. However, tolvaptan has not been shown to decrease HF re-hospitalization or mortality. As an adjunct to standard therapy, tolvaptan is unique in that it is virtually the only novel agent tested in patients hospitalized for acute heart failure syndrome (AHFS) to reach its primary end point for short-term efficacy without causing deleterious side effects. There is theoretical concern that chronic V(2) receptor blockade may cause harmful long-term side effects via enhanced V(1a) receptor activation, potentially offsetting any favorable effects on congestion and hyponatremia. The 'vaptan' class of drugs is an active and promising area for clinical investigation and future research is necessary to clarify the therapeutic role of selective and nonselective vasopressin inhibition in chronic HF and AHFS.

PMID: 21401442 [PubMed - as supplied by publisher]

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