Published: 22 April 2022
Author(s): Pasquale Perrone-Filardi, Stefania Paolillo, Piergiuseppe Agostoni, Christian Basile, Cristina Basso, Francesco Barillà, Michele Correale, Antonio Curcio, Massimo Mancone, Marco Merlo, Marco Metra, Saverio Muscoli, Savina Nodari, Alberto Palazzuoli, Roberto Pedrinelli, Roberto Pontremoli, Michele Senni, Massimo Volpe, Ciro Indolfi, Gianfranco Sinagra
Issue: August 2022
Section: Review Article

Renin-angiotensin-aldosterone system (RAAS) activation is one the main pathophysiological mechanisms involved in the development and progression of heart failure (HF) and its inhibition is a mainstay of the pharmacological treatment of HF with reduced ejection fraction (HFrEF) [1]. In the last years several trials investigated the role of RAAS modulation in HF and, recently, RAAS blockade has been further developed by the introduction of the Angiotensin Receptor-Neprilysin Inhibitor (ARNI) sacubitril/valsartan, that combines RAAS inhibition with the antagonism of neprilysin (NEP), boosting the positive effects of natriuretic peptides [2].

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