B-Type Natriuretic Peptide (BNP) and N-Terminal proBNP in Patients with End-Stage Heart Failure Supported by a Left Ventricular Assist Device

B-Type natriuretic peptide (BNP) is a cardiac neurohormone synthesized in the cardiac ventricles. It is released as a preproBNP peptide of 134 amino acids and is cleaved into proBNP (108 amino acids) and a signal peptide of 26 amino acids. ProBNP is subsequently cleaved into BNP (32 amino acids) and the inactive N-terminal proBNP peptide (NT-proBNP; 76 amino acids). The release of BNP into the circulation is directly proportional to the ventricular expansion and volume overload of the ventricles and therefore reflects the decompensated state of the ventricles (1). The effects of BNP—vasodilatation, natriuresis, and diuresis—lead to some improvement of the loading conditions of the failing heart. Although BNP is the active neurohormone, both BNP and NT-proBNP have been described as useful markers for the diagnosis and exclusion of congestive heart failure (2)(3), and plasma concentrations correlate with the functional classification of patients according to the New York Heart Association (NYHA) (2)(4). Therapy guided by BNP leads to a reduction of total cardiovascular events and delayed time to a new event when compared with clinically guided treatment (5).