Nesiritide for Acute Decompensated Heart Failure

2002 ◽  
Vol 18 (6) ◽  
pp. 295-304
Author(s):  
Teresa S Barclay ◽  
Joanne J Kim ◽  
Audrey J Lee

Objective: To evaluate nesiritide for the treatment of acute decompensated heart failure (HF) with respect to its pharmacology, pharmacokinetics, clinical efficacy, adverse effect profile, and outcomes. Data Source: Primary and review articles were identified by MEDLINE search (1966–March 2001). Data from the PRECEDENT trial and additional dosing/administration and safety information were obtained from Scios, Inc. Study Selection: All of the articles identified from the data sources were evaluated and all information deemed relevant was included in this review. Data Synthesis: Research into the cardiac natriuretic peptides has revealed that brain natriuretic peptide (BNP) is elevated in patients with HF and may counterregulate the pathophysiologic mechanisms involved in progression of the disease. Nesiritide (Natrecor), recombinant human BNP, is the first natriuretic peptide to be approved by the FDA for treatment of acute decompensated HF. Nesiritide is a potent venous and arterial vasodilator that reduces pulmonary capillary wedge pressure and systemic vascular resistance in a dose-dependent manner with minimal effect on heart rate. It improves signs and symptoms of HF; however, its effect on patient outcomes is unclear because of limited data. The most commonly reported adverse effects in clinical trials were dose-related hypotension and nausea. Conclusions: Nesiritide is an intravenous arterial and venous vasodilator that may be particularly useful in patients who may not tolerate the arrhythmogenic effects of dobutamine and milrinone or who cannot tolerate nitroglycerin and nitroprusside. Further well-designed comparative studies are needed to define nesiritide's place in management of acute decompensated HF.

Author(s):  
Benedetta De Berardinis ◽  
Hanna K. Gaggin ◽  
Laura Magrini ◽  
Arianna Belcher ◽  
Benedetta Zancla ◽  
...  

AbstractIn order to predict the occurrence of worsening renal function (WRF) and of WRF plus in-hospital death, 101 emergency department (ED) patients with acute decompensated heart failure (ADHF) were evaluated with testing for amino-terminal pro-B-type natriuretic peptide (NT-proBNP), BNP, sST2, and neutrophil gelatinase associated lipocalin (NGAL).In a prospective international study, biomarkers were collected at the time of admission; the occurrence of subsequent in hospital WRF was evaluated.In total 26% of patients developed WRF. Compared to patients without WRF, those with WRF had a longer in-hospital length of stay (LOS) (mean LOS 13.1±13.4 days vs. 4.8±3.7 days, p<0.001) and higher in-hospital mortality [6/26 (23%) vs. 2/75 (2.6%), p<0.001]. Among the biomarkers assessed, baseline NT-proBNP (4846 vs. 3024 pg/mL; p=0.04), BNP (609 vs. 435 pg/mL; p=0.05) and NGAL (234 vs. 174 pg/mL; p=0.05) were each higher in those who developed WRF. In logistic regression, the combination of elevated natriuretic peptide and NGAL were additively predictive for WRF (OR: In ED patients with ADHF, the combination of NT-proBNP or BNP plus NGAL at presentation may be useful to predict impending WRF (Clinicaltrials.gov NCT#0150153).


2020 ◽  
Author(s):  
Miriam T Rademaker ◽  
Nicola J A Scott ◽  
Cho Yeow Koh ◽  
R Manjunatha Kini ◽  
A Mark Richards

Abstract Aims Management of acute decompensated heart failure (ADHF) requires disparate treatments depending on the state of systemic/peripheral perfusion and the presence/absence of expanded body–fluid volumes. There is an unmet need for therapeutics that differentially treat each aspect. Atrial natriuretic peptide (ANP) plays an important role in blood pressure and volume regulation. We investigate for the first time the integrated haemodynamic, endocrine and renal effects of human ANP analogues, modified for exclusive vasodilatory (ANP-DRD) or diuretic (ANP-DGD) activities, in normal health and experimental ADHF. Methods and results We compared the effects of incremental infusions of ANP analogues ANP-DRD and ANP-DGD with native ANP, in normal (n = 8) and ADHF (n = 8) sheep. ANP-DRD administration increased plasma cyclic guanosine monophosphate (cGMP) in association with dose-dependent reductions in arterial pressure in normal and heart failure (HF) sheep similarly to ANP responses. In contrast to ANP, which in HF produced a diuresis/natriuresis, this analogue was without significant renal effect. Conversely, ANP-DGD induced marked stepwise increases in urinary cGMP, urine volume, and sodium excretion in HF comparable to ANP, but without accompanying vasodilatory effects. All peptides increased packed cell volume relative to control in both states, and in HF, decreased left atrial pressure. In response to ANP-DRD-induced blood pressure reductions, plasma renin activity rose compared to control only during the high dose in normals, and not at all in HF—suggesting relative renin inhibition, with no increase in aldosterone in either state, whereas renin and aldosterone were both significantly reduced by ANP-DGD in HF. Conclusion These ANP analogues exhibit distinct vasodilatory (ANP-DRD) and diuretic/natriuretic (ANP-DGD) activities, and therefore have the potential to provide precision therapy for ADHF patients with differing pathophysiological derangement of pressure–volume homeostasis.


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