The role of the renin-angiotensin-aldosterone system in the development of cardiovascular complications in COVID-19

Abstract

During the pandemic caused by SARS-CoV-2, cardiovascular disease has been found to be an important risk factor for COVID-19. At the same time, it turned out that patients who did not suffer from cardiovascular pathology before infection with SARS-CoV-2 often had cardiovascular complications in the form of myocarditis, arrhythmias, and heart failure. It is extremely important to elucidate the pathogenetic mechanisms that determine the relationship between COVID-19 and cardiovascular pathology. Analysis of the data of the scientific literature suggests that an imbalance in the renin-angiotensin-aldosterone system (RAAS), expressed in the hyperproduction of angiotensin II and the deficiency of angiotensin 1-7, is an important factor in the pathogenetic link that causes comorbidity of COVID-19 and cardiovascular pathology. According to modern concepts, the RAAS is a complex, multicomponent, multi-level, two-axis system that has, both cardio- and vasoprotective (ACE2/Ang1-7/MasR axis) and damaging effects on the heart and blood vessels (ACE/Ang II/AT1R axis). Patients with cardiovascular diseases, as a rule, already have an imbalance of the RAAS, characterized by hyperproduction of cardiotoxic angiotensin II. Coronavirus, interacting with ACE2 an important component of the cardioprotective axis of RAAS, and reducing its quantity and activity, increases this imbalance, which aggravates the damage to the cardiovascular system. In addition, an imbalance of RAAS can lead to an imbalance in the kallikrein-kinin system with the accumulation of vascular permeability-increasing des-Arg9-bradykinin, potentiate inflammation, create prerequisites for the development of COVID-19 associated coagulopathy and acute respiratory distress syndrome. In the pathogenetic therapy of coronavirus infection, complicated by lesions of the cardiovascular system, it may be advisable to use drugs that correct changes in the renin-angiotensin-aldosterone system.