BNP (B-type Natriuretic Peptide) Research & Studies

Increased plasma levels of B-type natriuretic peptide (BNP) serve as a biomarker for heart failure (HF). This study aimed to develop a risk score to predict elevated BNP levels using traditional cardiovascular disease (CVD) risk factors.

Myocardial infarction (MI) elicits cardiac fibroblast activation and extracellular matrix (ECM) deposition to maintain the structural integrity of the heart. Recent studies demonstrate that Fap (fibroblast activation protein)-a prolyl-specific serine protease-is an important marker of activated cardiac fibroblasts after MI.

The associations of N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) with dual energy x-ray absorptiometry (DEXA)-derived measures of body mass and composition are largely unknown.

Myocardial wall stress, cytokines, hormones, and ischemia all stimulate B-type (or brain) natriuretic peptide (BNP) gene expression. Within the myocardium, ProBNP-108, a BNP precursor, undergoes glycosylation, after which a portion is cleaved by furin into mature BNP-32 and N-terminal proBNP-76, depending on the glycosylation status. As a result, active BNP, less active proBNP, and inactive N-terminal proBNP all circulate in the blood. There are three major pathways for BNP clearance: (1) cellular internalization via natriuretic peptide receptor (NPR)-A and NPR-C; (2) degradation by proteases in the blood, including neprilysin, dipeptidyl-peptidase-IV, insulin degrading enzyme, etc.; and (3) excretion in the urine. Because neprilysin has lower substrate specificity for BNP than atrial natriuretic peptide (ANP), the increase in plasma BNP after angiotensin receptor neprilysin inhibitor (ARNI) administration is much smaller than the increase in plasma ANP. Currently available BNP immunoassays react with both mature BNP and proBNP. Therefore, BNP measured with an immunoassay is mature BNP + proBNP. ARNI administration increases mature BNP but not proBNP, as the latter is not degraded by neprilysin. Consequently, measured plasma BNP initially increases with ARNI administration by the amount of the increase in mature BNP. Later, ARNI reduces myocardial wall stress, and the resultant reduction in BNP production more than offsets the increase in mature BNP mediated by inhibiting degradation by neprilysin, which lowers plasma BNP levels. These results suggest that even in the ARNI era, BNP can be used for diagnosis and assessment of the pathophysiology and prognosis of heart failure, though the mild increases early during ARNI administration should be taken into consideration.

Heart failure is a complex clinical syndrome that usually presents with breathlessness, leg edema, and fatigue. Clinically measurable natriuretic neurohormones such as B-type natriuretic peptide (BNP) and N-terminal proBNP (NT-proBNP) are elevated in people with heart failure. We conducted a health technology assessment of BNP and NT-proBNP tests for people with suspected heart failure, which included an evaluation of diagnostic accuracy, clinical impact, cost-effectiveness, the budget impact of publicly funding BNP and NT-proBNP tests, and patient preferences and values.

Obese patients have lower plasma concentrations of the cardiac natriuretic peptides (NPs) than their age- and sex-matched counterparts. This may reflect lower production and/or increased peptide clearance. It is unclear whether NP bioactivity is affected by obesity.

To study the predictive value of B-type natriuretic peptide (BNP) and soluble thrombomodulin (sTM) in the severity stratification and prognosis evaluation of sepsis.

Fluid overload is a common complication in patients with cirrhosis. B-type natriuretic peptide (BNP) is a marker of increased blood volume, commonly used in heart failure, that has been shown to be elevated in patients with liver disease. This study examined if BNP levels can be used to determine prognosis and predict worsening of ascites in patients with cirrhosis without concomitant heart disease. A retrospective study was performed at a large urban hospital in Chicago, Illinois and included 430 patients with cirrhosis who had BNP levels ordered during their hospital stay. Patients with clinical heart failure, arrhythmias or pulmonary hypertension were excluded. The primary outcome was 90-day mortality and the secondary outcome was a requirement for therapeutic paracentesis in the 90 days following BNP results. 53 patients (12%) had BNP levels ≥ 300 pg/mL. They had significantly increased serum levels of creatinine, bilirubin, and International Normalized Ratio (INR) when compared to those with BNP < 300 pg/mL. Patients with higher BNP had significantly higher mortality rates (HR 3.49; p = 0.037) and were more likely to require therapeutic paracentesis (HR 2.26; p = 0.02) in the next 90 days. A BNP ≥ 300 pg/mL had specificity of 88.2% in predicting 90-day mortality. BNP may serve as a practical and reliable marker of underlying disease severity in patients with cirrhosis, with potential to be included in prognostication tools for assessment of end-stage liver disease.

Baseline elevated B-type Natriuretic Peptide (BNP) has been found in high altitude pulmonary edema susceptible population. Exaggerated pulmonary vascular response to hypoxia may be related to endothelial dysfunction in hypoxia susceptible. We hypothesize that baseline BNP levels can predict hypoxia susceptibility in healthy individuals.

B-type natriuretic peptide (BNP) and N-terminal-pro-BNP (NTpBNP) have a major role in screening and diagnosis of cardiac disease and monitoring of the treatment response in children and adults. This review discusses the evidence underpinning the potential benefits of these natriuretic peptides in neonatology. They may serve as a useful adjunct to echocardiography in the diagnosis of patent ductus arteriosus and its response to treatment and the diagnosis of persistent pulmonary hypertension of the newborn. However, more work is needed to explore the possible roles of BNP/NTpBNP in the management of sepsis and monitoring of cardiac performance in neonates.

B-type natriuretic peptide (BNP) is synthesized in cardiac ventricles in response to volume expansion. This study evaluated BNP levels to determine trends during pregnancy, and to assess BNP as a diagnostic tool in preeclampsia.

Cardiovascular disease is the leading cause of morbidity and mortality in diabetic subjects. Diabetes, independently of the mechanism, is associated with an increased risk of left ventricular hypertrophy, left ventricular dysfunction and coronary artery disease. B-type natriuretic peptide (BNP) is a cardiac neurohormone predominantly released from the cardiac ventricles in response to left ventricular volume expansion and pressure overload. Numerous studies have shown that BNP levels are elevated in asymptomatic or symptomatic left ventricular dysfunction, hypertrophy and coronary artery disease. BNP testing plays an important role in the screening and diagnosis of left ventricular dysfunction by improving the performance of non-specialist physicians in diagnosing heart failure. In clinical practice, BNP testing is best used as a 'rule out' test targeted to patients at high risk for left-ventricular dysfunction, such as those with diabetes. Studies are needed to establish if this promising biological tool, in the next future, would assist the management of diabetic patients.

Brain natriuretic peptide (BNP) is a 32 amino acid cardiac natriuretic peptide hormone originally isolated from porcine brain tissue. The human BNP gene is located on chromosome 1 and encodes the prohormone proBNP. The biologically active BNP and the remaining part of the prohormone, NT-proBNP (76 amino acids) can be measured by immunoassay in human blood. Cardiac myocytes constitute the major source of BNP related peptides. The main stimulus for peptide synthesis and secretion is myocyte stretch. Recently, cardiac fibroblasts have also been shown to produce BNP. Other neurohormones may stimulate cardiac BNP production in different cardiac cell types. In contrast to atrial natriuretic peptides (ANP/NT-proANP), which originate mainly from atrial tissue, BNP related peptides are produced mainly from ventricular myocytes. Ventricular (NT-pro)BNP production is strongly upregulated in cardiac failure and locally in the area surrounding a myocardial infarction. In peripheral organs BNP binds to the natriuretic peptide receptor type A causing increased intracellular cGMP production. The biological effects include diuresis, vasodilatation, inhibition of renin and aldosterone production and of cardiac and vascular myocyte growth. In mice BNP gene knockout leads to cardiac fibrosis, gene over-expression to hypotension and bone malformations. BNP is cleared from plasma through binding to the natriuretic peptide clearance receptor type C, but it seems relatively resistant to proteolysis by neutral endopeptidase NEP 24.11. Clearance mechanisms for NT-proBNP await further study. While the plasma concentration of NT-proBNP and BNP is approximately equal in normal controls, NT-proBNP plasma concentration is 2-10 times higher than BNP in patients with heart failure. This relative change in peptide levels may be explained by shifts in cardiac secretion and/or clearance mechanisms.

Many claims have been made in recent years regarding the utility of plasma B-type natriuretic peptide (BNP) concentration measurements in the diagnosis, risk stratification and monitoring of patients with heart failure. This paper summarizes the current evidence and provides guidance for practising clinicians. Overall, plasma BNP testing appears to be of most value in the diagnostic arena, where it is likely to improve the performance of non-specialist physicians in diagnosing heart failure. In clinical practice, BNP testing is best used as a 'rule out' test for suspected cases of new heart failure in breathless patients presenting to either the outpatient or emergency care settings; it is not a replacement for echocardiography and full cardiological assessment, which will be required for patients with an elevated BNP concentration. Although work is ongoing in establishing the 'normal' values of BNP, heart failure appears to be highly unlikely below a plasma concentration of 100 pg/ml. However, as BNP levels rise with age and are affected by gender, comorbidity and drug therapy, the plasma BNP measurement should not be used in isolation from the clinical context.

Finding a simple blood test that would aid in the diagnosis and management of patients with CHF would clearly have a favorable impact on the staggering costs associated with the disease. B-type natriuretic peptide (BNP) may be the first potential "white count" for heart failure. The fact that a point-of-care, rapid assay for BNP has recently been approved by the FDA gives the clinician an opportunity to explore its potential usefulness. Data suggest that serial point-of-care testing of BNP will be of immense help in patients presenting to urgent care clinics with dyspnea. Additionally, BNP might serve as a screen for patients referred for echocardiography, and might also be an effective way to improve the in-hospital management of patients admitted with decompensated CHF. Finally, the role of BNP in the outpatient cardiac or primary care clinic may be one of critical importance in titration of therapies as well as assessment of the state of the patient's neurohormonal compensation.