BNP as a biomarker in heart disease

Abstract

Heart ventricles produce B-type natriuretic peptide (BNP) in response to increased mechanical load and wall stretch. BNP protects the heart from adverse consequences of overload by increasing natriuresis and diuresis, relaxing vascular smooth muscle, inhibiting the renin-angiotensin-aldosterone system, and by counteracting cardiac hypertrophy and fibrosis. BNP is synthesized by human cardiac myocytes as a 108-amino acid prohormone (proBNP), which is cleaved to the 32-residue BNP and the 76-residue N-terminal fragment of proBNP (NT-proBNP). Both can be used as sensitive biomarkers of cardiac dysfunction and well-characterized commercial assays have recently become available. In acute coronary syndromes increased concentrations are strong predictors of recurring myocardial infarction, heart failure, and death. In acute dyspnea, high BNP and NT-proBNP point to a cardiac rather than a pulmonary origin of the symptoms. BNP and NT-proBNP help in the assessment of the severity of ventricular dysfunction and heart failure and as a prognostic predictor, regardless of the primary cause of the condition. They can be used to guide the therapy of heart failure and left ventricular dysfunction. BNP and NT-proBNP work better when they are used for specific clinical purposes, rather than for screening in the general population. Their main strength is the excellent negative predictive value with regard to left ventricular dysfunction and heart failure. BNP and NT-proBNP are nonspecific biomarkers of cardiac dysfunction. Specific diagnostic tools, such as echocardiography, are required to define the actual abnormality.