LAUSR

Natriuretic peptides (NPs) are hormones released by the heart, which have diuretic, natriuretic, and vascular smooth muscle-relaxing effects.1 Plasma concentrations of NPs are modulated by several physiological factors, such as circadian rhythm, age, gender, exercise, body posture, and sodium intake.1 Levels of NP are also increased by ventricular dysfunction, haemodynamic overload, myocardial inflammation, ischaemia, and necrosis.1 Furthermore, NP production and release are promoted by non-cardiac disorders (e.g. pulmonary embolism, chronic obstructive pulmonary disease, hyperthyroidism and hypothyroidism, Cushing syndrome, hyperaldosteronism, liver cirrhosis, renal failure), and are influenced by several drugs, including diuretics, renin–angiotensin–aldosterone system inhibitors, anti-adrenergic agents and neprilysin inhibitors.1,2 A progressive increase in NP levels with age has been reported and attributed to myocardial function decline, decrease in NP renal clearance rate,3 and age-dependent modulation of maximum binding capacity of clearance (C-type) receptors.4 Plasma concentrations of brain natriuretic peptide (BNP) and the N-terminal fragment of proBNP (NT-proBNP) may be easily determined by dedicated assays.1,2 Both B-type NP have been extensively studied for their use as diagnostic and prognostic biomarkers and to guide treatment in acute or chronic heart failure (HF) patients.5 The most recent European Society of Cardiology Guidelines strongly recommend NP testing to reject a cardiac origin of acute dyspnoea (Class I, level of evidence A), setting a 100 ng/L rule-out cut-point irrespective of age as a guide to further echocardiographic examination.6 The Guidelines also recommend NP