
Arginine vasopressin as a target in the treatment of acute heart failure
Author(s) -
Nisha A. Gilotra,
Stuart D. Russell
Publication year - 2014
Publication title -
world journal of cardiology
Language(s) - English
Resource type - Journals
ISSN - 1949-8462
DOI - 10.4330/wjc.v6.i12.1252
Subject(s) - medicine , heart failure , tolvaptan , vasopressin , inotrope , hyponatremia , vasopressin antagonists , cardiology , arginine vasopressin receptor 2 , intensive care medicine , acute decompensated heart failure , arginine , nesiritide , pharmacology , receptor , natriuretic peptide , antagonist , biochemistry , chemistry , amino acid
Congestive heart failure (CHF) is one of the most common reasons for hospitalization in the United States. Despite multiple different beneficial medications for the treatment of chronic CHF, there are no therapies with a demonstrated mortality benefit in the treatment of acute decompensated heart failure. In fact, studies of inotropes used in this setting have demonstrated more harm than good. Arginine vasopressin has been shown to be up regulated in CHF. When bound to the V1a and/or V2 receptors, vasopressin causes vasoconstriction, left ventricular remodeling and free water reabsorption. Recently, two drugs have been approved for use that antagonize these receptors. Studies thus far have indicated that these medications, while effective at aquaresis (free water removal), are safe and not associated with increased morbidity such as renal failure and arrhythmias. Both conivaptan and tolvaptan have been approved for the treatment of euvolemic and hypervolemic hyponatremia. We review the results of these studies in patients with heart failure.