Clinical Significance

BNP (B-type natriuretic peptide, brain natriuretic peptide,) is secreted and synthesized by ventricular cells. Following transcription and translation of the BNP gene, the initial gene product is produced, which is a 134 amino acid pre-BNP precursor (pre-proBNP). The amino acid signal peptide of pre-proBNP was immediately removed, resulting in proBNP of 108 amino acids. Next, proBNP is broken down in blood by proteolytic enzymes into two parts: a biologically inactive, amino-terminal part containing 76 amino acids (NT-proBNP) and a biologically active 32 amino acid BNP.
The application of BNP (B-type natriuretic peptide) and NT-proBNP monitoring in the diagnosis, risk stratification, efficacy evaluation, prognosis, and in-hospital management of acute and chronic heart failure provides an important basis for the diagnosis and treatment of heart failure, and is helpful for the diagnosis and treatment of heart failure. Clinicians make correct decisions, help patients with early diagnosis and early treatment, and effectively improve the survival rate.
BNP is a biologically active protein with a half-life of 20 minutes, its in vitro stability time is only 1 hour, and its level is easily affected by the drug of choice. For example, when a patient is treated with recombinant human brain BNP (rh-BNP), it can cause an increase in BNP levels in the blood. It is difficult for clinicians to determine whether the increase in BNP levels is due to drug therapy or cardiac dysfunction. As an inactive NT-proBNP, the half-life is 60-120 minutes, and the in vitro stability time is as long as 24 hours. It has higher sensitivity and is not affected by rh-BNP, which is convenient for clinicians to accurately detect early and mild heart failure.

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