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].
