COVID-19 Interference with Renin-Angiotensin System in the Context of Heart Failure

Novel coronavirus severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) (coronavirus disease 2019 [COVID-19] pandemic) attacks the host cells modulating the local renin-angiotensin (RAS) system. Pending a definitive antivirus therapy, Fedson and colleagues propose in their recent article (1) a combination of generic drugs such as statins and angiotensin receptor blockers (ARBs) to prevent catastrophic cellular damage. The proposal could be applicable in a model of heart failure (HF) patients infected by coronavirus. These patients belong to the most vulnerable groups while concentrating in their RAS all the parameters sustained by Fedson and colleagues. First, most HF patients are treated with angiotensin-converting enzyme (ACE) inhibitors (ACEis) or ARBs, recently enriched with the novel compound sacubitril to form the prototype of ARBs/neprilysin (NEP) inhibitors (ARNIs) (2). Furthermore, a minority of HF patients receive statins which, however, are not an established treatment despite their immunomodulatory properties (3). All the aforementioned drugs aim at preventing the formation of deleterious angiotensins by deviating local RAS to the formation of innocuous products. To achieve this, two RAS components are needed, namely, ACE2 and NEP (4, 5). Both these proteases cleave angiotensin I and II into angiotensin (1–7) which is indispensable for cellular homeostasis (6). In fact, angiotensin (1–7) exerts antioxidant, anti-inflammatory, and antiproliferative effects, protecting target organs.