COVID -19 cardiovascular view and brief therapy overview

SARS-CoV-2 virus binds to transmembrane angiotensin-converting enzyme 2 (ACE2), homologue of ACE to enter different cell types, through following mechanism: direct cytotoxic effect, dysregulation of the RAAS, endothelial cell damage with thromboinflammation and dysregulated immune response. Consistent RAAS activation results in imbalance of Ang II hyper-production and inhibition of Ang-(1-7) formation, which increases inflammation, vascular hiperpermeability, prothrombogenesis and decreases anti-inflammatory and antithrombogenic properties. This endotheliopathy begins with impaired endothelium starting coagulation, platelet and fibrinolytic cascade. COVID-19 affect cardiovascular system by ischemic components (myocardial damage, endothelial dysfunction, microvascular dysfunction, plaque instability, ACS ), non-ischemic components ( cytokines storm, stress cardiomyopathy, metabolic dysfunction, sympathetic neuronal activation, electricity imbalance) and comorbidites ( age, hypertension, diabetes, obesity, CAD, COPD, cancer). Consequently CV complications are arrhythmias, cardiac injury (20–40% of hospitalized cases, including MINOCA), myocarditis, heart failure, cardiogenic shock (multiorgan failure), pericardial effusion, pulmonary embolism, disseminated intravascular coagulation. STEMI in COVID-19 had higher rates of stent and multi-vessel thrombosis, higher thrombus burden, use of glycoprotein IIb/IIIa inhibitors. Standard cardiovascular therapies should be used as appropriate (including ACE inhibitors/ARBs). No convincing evidence was found for the use of reconvalescent plasma, colchicine, hydroxychloroquine, hloroquine, azithromycin and strong evidence in reduced mortality for using corticosteroids, tocilizumab ( anti-IL-6R Ab) in severe COVID-19 forms and bamlanivimab (SARS-CoV-2 neutralizing Ab) for the treatment of mild to moderate forms who are at risk for severe progression.