B-type natriuretic peptide


B-type natriuretic peptide is released by cardiac myocytes in response to wall stretch. There are many hemodynamic effects of BNP which are beneficial in the setting of decompensated congestive heart failure including arterial and venous vasodilation and increased excretion of sodium (natriuresis). BNP is similar to atrial natriuretic peptide (ANP), however ANP is not as easily measured.

B-type natriuretic peptide measurement

The initial primary use of measuring b-type natriuretic peptide (BNP) is to determine the etiology of dyspnea in patients presenting to the emergency department. If the BNP level is significantly elevated (greater than 400 pg/mL), heart failure is the likely diagnosis. Note that the degree of BNP elevation does not correlate with the severity of symptoms.

BNP levels are elevated in patients with atrial fibrillation and acute coronary syndromes as well, however it is not used to diagnose these conditions.

BNP levels play an important prognostic role in other cardiac conditions. Patients with high BNP levels during acute coronary syndromes or in the setting of severe valvular heart disease (aortic stenosis and/or mitral regurgitation) have a worse prognosis. Also, BNP levels are low in patients with heart failure from constrictive pericarditis which differentiates it from restrictive cardiomyopathy where the BNP levels are high.

A newer assay measuring NT-terminal pro-BNP (NT-proBNP) is more sensitive to detect heart failure and used in many institutions. The levels of BNP and NT-proBNP are essentially the same in normal individuals, but in the presence of heart failure the NT-proBNP is approximately four times higher than the corresponding BNP level, thus reducing the likelihood of a result in the ambiguous range (i.e. BNP level of 300 which is high, but not quite definite heart failure which would be > 400).

Measuring the BNP level (b-type natriuretic peptide) can help distinguish between constrictive pericarditis and restrictive cardiomyopathy. In constrictive pericarditis the BNP level is normal to very minimally elevated while in restrictive cardiomyopathy the BNP level is significantly elevated. This was initially described by Leya et. al. in 2005. BNP is released in response to myocardial wall stretch. In constrictive pericarditis, the scarred pericardium probits wall stretch and thus the levels are low. In restrictive cardiomyopathy, the walls indeed do stretch from the increased cardiac pressures resulting in high serum levels of BNP.


Nesiritide is a recombinant form of B-type natriuretic peptide and is used for the treatment of acute decompensated heart failure. Nesiritide has potent vasodilatory properties and reduces pulmonary capillary wedge pressure effectively. This results in improvement of dyspnea.

Once large trial (ASCEND-HF) randomized 7141 patients to nesiritide versus placebo. While nesiritide did improve the symptom of dyspnea better than placebo, there was no reduction in 30 day rehospitalization and no mortality benefit. Hypotension was significant in the nesiritide group.

Nesiritide is not recommended for routine use during decompensated heart failure. If patients with normal blood pressures are not responding well to typical management with loop diuretics, then nesiritide can be considered.