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Nesiritide in the treatment of acute decompensated heart failure

Wilson S Colucci, MD
Section Editors
Stephen S Gottlieb, MD
James Hoekstra, MD
Deputy Editor
Susan B Yeon, MD, JD, FACC


Acute decompensated heart failure (HF) is a common and potentially fatal cause of acute respiratory distress. The clinical syndrome is characterized by the development of dyspnea, which is commonly associated with the rapid accumulation of fluid within the lung's interstitial and alveolar spaces due to acutely elevated cardiac filling pressures (cardiogenic pulmonary edema) [1]. Acute decompensated HF can also present as elevated left ventricular filling pressures and dyspnea without pulmonary edema.

Multiple modalities are used in the treatment of acute decompensated HF, including oxygen, diuretics, vasodilators, and, in selected patients, inotropic agents. Nesiritide (recombinant human brain natriuretic peptide, BNP 1-32) is a vasodilator that has undergone clinical trials in patients with acute HF.

The possible role of nesiritide in the management of acute decompensated HF will be reviewed here. General issues related to the management of acute decompensated HF, the pathophysiology and evaluation of patients with this disorder, and the management of chronic systolic and diastolic HF are presented separately. (See "Treatment of acute decompensated heart failure: General considerations" and "Evaluation of acute decompensated heart failure" and "Overview of the therapy of heart failure with reduced ejection fraction" and "Treatment and prognosis of heart failure with preserved ejection fraction".)


Although plasma brain natriuretic peptide (BNP) levels are increased in patients with heart failure (HF), such patients are sodium avid and have increased systemic vascular resistance. This apparent paradox may be caused by lack of specificity of commercially available immunoreactive-BNP assays that measure inactive as well as active forms; bioactive BNP 1-32 levels may be low in patients with HF [2]. In addition, patients with HF have high levels of vasoconstrictors, particularly angiotensin II and norepinephrine, which may overcome BNP’s effects. (See "Pathophysiology of heart failure: Neurohumoral adaptations".)

The high level of vasoconstrictors and high systemic vascular resistance and possibly low levels of bioactive BNP in these patients provides the rationale for therapy with vasodilators, such as nesiritide. Infusion of nesiritide at doses of up to 0.1 mcg/kg per min in patients with HF can raise the mean plasma BNP concentration from 700 to 13,000 pg/mL with associated arterial and venous vasodilation [3].


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Literature review current through: Sep 2016. | This topic last updated: Jun 13, 2016.
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