223 How can the role of N terminal pro B natriuretic peptide (NT-proBNP) be optimised in heart failure screening? A prospective observational comparative study

Introduction: Although many predictive tools have already been developed, efforts are still proceeding to identify a reliable biomarker to predict the prognosis of the patients with acute heart disorders. Objectives: The aim was to evaluate the role of renal injury biomarkers (serum cystatin C, serum and urine interleukin-18, IL-18) and heart failure biomarkers (plasma B-type natriuretic peptide, BNP) in the prediction of the postdischarge requirement of renal replacement therapy (RRT) and/or 6-month mortality in patients with acute heart disorders. Patients and Methods: In patients diagnosed with acute heart disorders (acute heart failure [AHF] and/or acute coronary syndrome [ACS]) and admitted to the intensive care units, baseline clinical parameters, renal and cardiac biomarkers were determined. Patients were followed up for 6 months. The composite outcome was the postdischarge requirement of RRT and/or 6-month mortality. Results: Of 120 patients, 5.8% continued RRT after discharge. The 6-month mortality was 20%. Cox logistic regression analysis showed that urine IL-18 (P=0.021), plasma BNP (P=0.046), Acute Physiology and Chronic Health Evaluation (APACHE) II score (P=0.002), and left ventricular diastolic dysfunction (P=0.045) were independent predictors of the postdischarge requirement of RRT and/or 6-month mortality. For predicting RRT and/or 6-month mortality, using urine IL-18 cutoff value of 29.1 pg/mL showed 66.7% sensitivity and 67.7% specificity (area under the curve, AUC 0.70, P=0.003), while using plasma BNP cutoff value of 881.6 pg/mL showed 66.7% sensitivity and 70.8% specificity (AUC 0.76, P<0.001). Conclusion: Urine IL-18 and plasma BNP are independently predictive for the postdischarge requirement of RRT and/or 6-month mortality in patients with acute heart disorders.

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Authors’ reply: role of natriuretic peptide receptor C signalling in obesity-induced heart failure with preserved ejection fraction with pulmonary hypertension

Pulmonary Circulation ◽

10.1177/2045894020910979 ◽

2020 ◽

Vol 10 (1) ◽

pp. 204589402091097

Author(s):

Vineet Agrawal ◽

Anna R. Hemnes

Keyword(s):

Heart Failure ◽

Pulmonary Hypertension ◽

Ejection Fraction ◽

Natriuretic Peptide ◽

Natriuretic Peptide Receptor ◽

Preserved Ejection Fraction ◽

Peptide Receptor

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Role of endogenous atrial natriuretic peptide on systemic and renal hemodynamics in heart failure rats

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1994.267.1.h182 ◽

1994 ◽

Vol 267 (1) ◽

pp. H182-H186 ◽

Cited By ~ 3

Author(s):

T. Nishikimi ◽

K. Miura ◽

N. Minamino ◽

K. Takeuchi ◽

T. Takeda

Keyword(s):

Heart Failure ◽

Atrial Natriuretic Peptide ◽

Natriuretic Peptide ◽

Diastolic Pressure ◽

Urinary Sodium Excretion ◽

Left Ventricular ◽

Renal Hemodynamics ◽

Renal Tubular ◽

Atrial Natriuretic

To investigate the role of endogenous atrial natriuretic peptide (ANP) in rats with heart failure (HF), we administered HS-142-1 (HS; 3 mg/kg body wt iv), a novel nonpeptide ANP-receptor antagonist, to rats with surgically induced myocardial infarction and sham-operated rats. HF was characterized by a higher left ventricular end-diastolic pressure and higher plasma ANP concentration vs. controls. HS administration significantly reduced the plasma and urinary levels of guanosine 3',5'-cyclic monophosphate in rats with HF [plasma concentration 10.6 +/- 2.6 vs. 2.7 +/- 0.4 nM (P < 0.05); urinary excretion 48 +/- 8 vs. 12 +/- 2 pmol/min (P < 0.05)]. Systemic and renal hemodynamics were unaffected by HS administration. Urine flow (-35%) and urinary sodium excretion (-50%) were significantly decreased after HS only in those rats with HF that had no changes in systemic and renal hemodynamics. These results suggest that the elevated ANP levels in HF do not contribute directly to the maintenance of systemic hemodynamics but rather compensate for the HF mainly via diuresis and natriuresis, achieved by the inhibition of renal tubular reabsorption rather than by renal vasodilatation.

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The role of natriuretic peptide testing in guiding chronic heart failure management: Review of available data and recommendations for use

Archives of Cardiovascular Diseases ◽

10.1016/j.acvd.2011.10.007 ◽

2012 ◽

Vol 105 (1) ◽

pp. 40-50 ◽

Cited By ~ 38

Author(s):

James L. Januzzi

Keyword(s):

Heart Failure ◽

Chronic Heart Failure ◽

Natriuretic Peptide ◽

Heart Failure Management ◽

Management Review

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The Importance of Natriuretic Peptides in Cardiometabolic Diseases

Journal of the Endocrine Society ◽

10.1210/jendso/bvaa052 ◽

2020 ◽

Vol 4 (6) ◽

Cited By ~ 2

Author(s):

Shravya Vinnakota ◽

Horng H Chen

Keyword(s):

Heart Failure ◽

Natriuretic Peptide ◽

Defense Mechanisms ◽

Pressure Overload ◽

Natriuretic Peptide Receptor ◽

Therapeutic Role ◽

Peptide Receptor ◽

Genes Encoding ◽

Natriuretic Peptide Receptor A

Abstract The natriuretic peptide (NP) system is composed of 3 distinct peptides (atrial natriuretic peptide or ANP, B-type natriuretic peptide or BNP, and C-type natriuretic peptide or CNP) and 3 receptors (natriuretic peptide receptor-A or NPR-A or particulate guanynyl cyclase-A natriuretic peptide receptor-B or NPR-B or particulate guanynyl cyclase-B, and natriuretic peptide receptor-C or NPR-C or clearance receptor). ANP and BNP function as defense mechanisms against ventricular stress and the deleterious effects of volume and pressure overload on the heart. Although the role of NPs in cardiovascular homeostasis has been extensively studied and well established, much remains uncertain about the signaling pathways in pathological states like heart failure, a state of impaired natriuretic peptide function. Elevated levels of ANP and BNP in heart failure correlate with disease severity and have a prognostic value. Synthetic ANP and BNP have been studied for their therapeutic role in hypertension and heart failure, and promising trials are under way. In recent years, the expression of ANP and BNP in human adipocytes has come to light. Through their role in promotion of adipocyte browning, lipolysis, lipid oxidation, and modulation of adipokine secretion, they have emerged as key regulators of energy consumption and metabolism. NPR-A signaling in skeletal muscles and adipocytes is emerging as pivotal to the maintenance of long-term insulin sensitivity, which is disrupted in obesity and reduced glucose-tolerance states. Genetic variants in the genes encoding for ANP and BNP have been associated with a favorable cardiometabolic profile. In this review, we discuss several pathways that have been proposed to explain the role of NPs as endocrine networkers. There is much to be explored about the therapeutic role of NPs in improving metabolic milieu.

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