Arginine vasopressin as a target in the treatment of acute heart failure

Abstract

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.

Keywords: Heart failure; Arginine vasopressin antagonist; Vaptan; Hyponatremia; Aquaresis; Vasopressin

Core tip: Beneficial therapies in the setting of acute decompensated heart failure are limited. When bound to the V1a and/or V2 receptors, vasopressin, which is upregulated in heart failure, causes vasoconstriction, left ventricular remodeling and free water reabsorption. Over recent years, vasopressin antagonists such as conivaptan and tolvaptan have been investigated and approved for use in the appropriate setting. We review the evidence and implications behind use of vaptans in the setting of heart failure.