Short-Term Add-On Therapy With Angiotensin Receptor Blocker for End-Stage Inotrope-Dependent Heart Failure Patients: B-Type Natriuretic Peptide Reduction in a Randomized Clinical Trial

Abstract

OBJECTIVE:We aimed to evaluate angiotensin receptor blocker add-on therapy in patients with low cardiac output during decompensated heart failure. METHODS: We selected patients with decompensated heart failure, low cardiac output, dobutamine dependence, and an ejection fraction ,0.45 who were receiving an angiotensin-converting enzyme inhibitor. The patients were randomized to losartan or placebo and underwent invasive hemodynamic and B-type natriuretic peptide measurements at baseline and on the seventh day after intervention. ClinicalTrials.gov: NCT01857999. RESULTS: We studied 10 patients in the losartan group and 11 patients in the placebo group. The patient characteristics were as follows: age 52.7 years, ejection fraction 21.3%, dobutamine infusion 8.5 mcg/kg.min, indexed systemic vascular resistance 1918.0 dynes.sec/cm 5 .m 2 , cardiac index 2.8 L/min.m 2 , and B-type natriuretic peptide 1,403 pg/mL. After 7 days of intervention, there was a 37.4% reduction in the B-type natriuretic peptide levels in the losartan group compared with an 11.9% increase in the placebo group (mean difference, -49.1%; 95% confidence interval: -88.1 to -9.8%, p = 0.018). No significant difference was observed in the hemodynamic measurements. CONCLUSION: Short-term add-on therapy with losartan reduced B-type natriuretic peptide levels in patients hospitalized for decompensated severe heart failure and low cardiac output with inotrope dependence.

Angiotensin receptor-neprilysin inhibition in patients with acute decompensated heart failure: an expert consensus position paper

“…Interestingly, only a small minority of the study patients (7.7%) required inotropes during hospitalization, possibly because of hypoperfusion or hypotension. Need for inotropes during hospitalization reflects a high-risk patient profile with an unfavorable prognosis [42][43][44][45], which may, however, benefit from neurohormonal axis inhibition [9,46]. As mentioned above, current guidelines strongly support the concept of continuation or initiation of the oral evidence-based HF-modifying therapies after hemodynamic stabilization for all the patients with AHF without any exception [10].…”