N-terminal pro-B-type natriuretic peptide (NT-proBNP) is the N-terminal part of a 108 amino acids prohormone called proBNP, and its gene is located on chromosome 1. It is produced when cardiac disease occurs especially in patients with heart failure (HF). Cardiac wall stress is the main stimulus for proBNP production and secretion. Once in the circulation, the prohormone is split into BNP (32 amino acids) and NT-proBNP (76 amino acids) [1]. Natriuretic pepetide constitutes an endogenous compensatory system that acts to counter excess cardiac load and volume expansion and its actions include natriuresis, diuresis, vasodilatation, and lusitropism, plus direct suppression of volume-retaining, vasoconstricting system including the renin-angiotensin-aldosterone and sympathetic nervous system. Natriuretic peptide also has trophic actions opposing cardiac hypertrophy and fibrosis [2]. Thus, the main effect of natriuretic pepetide is on the cardio-renal axis, and its actions are targeted in order to treat HF as in the case of sacubitril-valsartan [3]. In clinical practice, this peptide is used to identify people who require further cardiac investigation because HF is suspected [4]. In acute setting of HF, NT-proBNP cutoff point should be set at 300 pg/ml whilst in chronic HF instead, the optimal cutoff is below 125 pg/ml. The clinical strength of natriuretic peptide is to permit a rule out diagnosis of HF [4]. If low concentrations are detected, negative predictive values is high (0.94-0.98) in both acute and non-acute setting. Moreover, the positive predictive values are lower both in the acute setting (0.66-0.67) and in the non-acute setting (0.44-0.57) [4]. It should be underlined that natriuretic peptides plasma