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most of the evidence related to NPs in HF is from these two NPs, which are the gold standard diagnostic and prognostic biomarkers in HF patients.1 The pathophysiological mechanism of NP elevation in the setting of HF is well understood: BNP is produced primarily and secreted in the cardiac ventricles as a pro-hormone in response to myocardial stretch, to later be cleaved into vasoactive BNP and inactive NT-proBNP.3,4 These NPs have been directly correlated with several haemodynamic measures including left ventricular (LV) end-diastolic pressure, LV end-systolic and end-diastolic volumes and pulmonary capillary wedge pressure.5,6 The use of NPs has been rigorously studied as a diagnostic tool in HFpEF ( Figure 2 )

The mechanisms differ entirely

Lo Faro, M

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