A newer assay measuring N-terminal pro-BNP, or 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; for example, BNP level of 300 — which is high, but not quite definite heart failure, which would be > 400.
NT-proBNP levels are also higher in patients with atrial fibrillation and acute coronary syndrome. The level of NT-proBNP may be helpful not only to evaluate heart failure, but also to detect acute coronary syndromes in patients with chest pain presenting to the emergency department where it has been found to be elevated, although further investigation is underway.
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 (> 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 — such as 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.
Measuring the NT-proBNP level can help distinguish these two entities which have historically been quite difficult to diagnose.
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 prohibits 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.