Urodilatin (ularitide), a natriuretic peptide, is produced within the kidneys. The aim of this study was to define the role of 24-hour intravenous infusions of urodilatin in the treatment of decompensated chronic heart failure (DHF).

In this randomized, double-blind, ascending-dose safety study, 24 patients with DHF (cardiac index 1.91 ± 0.34 L/min per square meter, pulmonary capillary wedge pressure 26 ± 6 mm Hg, right atrial pressure 11 ± 4 mm Hg) received urodilatin (7.5, 15, or 30 ng/(kg · min)) or placebo infusions over 24 hours.

Compared with baseline, urodilatin decreased pulmonary capillary wedge pressure by 10 mm Hg in the 15 ng/(kg · min) group (P < .05) and by 15 mm Hg in the 30 ng/(kg · min) group (P < .05) at 6 hours. In the same dose groups, right atrial pressure decreased, and dyspnea as reported by patients tended to improve. At 24 hours, 15 and 30 ng/(kg · min) urodilatin infusions decreased N-terminal–pro–brain natriuretic peptide levels by 40% and 45%, respectively, compared with baseline. Between 1 to 12 hours, plasma cyclic guanosine monophosphate levels at 15 and 30 ng/(kg · min) urodilatin were significantly higher than both placebo and the respective baseline after infusion start (P < .05 and .01). Among the different groups, there was no obvious difference regarding total number of patients with adverse events and total number of adverse events. During infusion, 3 transient asymptomatic hypotensions occurred in the urodilatin groups.

Our findings show that urodilatin may be a new agent for the therapy for DHF.