Evaluation of endothelial function patient infected with SARS-CoV-2 virus

Background and Aim: Vascular endothelium is an active organ with paracrine, autocrine, and endocrine functions that is vital for regulation of vascular tone and the maintenance of vascular homoeostasis Endothelial dysfunction is the primary factor of microvascular dysfunction characterized by vasoconstriction and subsequent organ ischemia, inflammation associated with tissue edema, and pro-coagulant state SARS-CoV-2 infects the host using the angiotensin converting enzyme 2 (ACE2) receptor, which is expressed in several organs, including the lung, heart, kidney, and intestine ACE2 receptors are also expressed by endothelial cells Endothelial cell infection and endotheliitis were currently demonstrated histologically in COVID-19 patients Whether vascular derangements in COVID-19 are due to endothelial cell involvement by the virus is currently unknown In this study we investigated early-mid term effect of SARS-CoV-2 viruse on endothelial functions in patient with COVID-19 infection Methods: We included 51 COVID-19 patient (27 symptomatic, 24 asymptomatic) and 54 healthy controle in this study Endothelial function was assessed by measuring endothelial-dependent flow-mediated vasodilatation (FMD %) and nitroglycerin-mediated dilatation (NMD %) in the brachial artery We enrolled COVID-19 patients in the study after three negative PCR test and median duration from PCR negativity was 40 4±13 4 days Results: Age and gender distribution were well matched between groups (38 2±8 4 vs 38 1±11 4;p=0 95) Although controle patient have higher BMI than COVID patients, BSA was similar in both groups Whilst hyperlipidemia and smoking habitus were similar between the groups, there were more hypertensive patient in controle group Plasma CRP (2 19±1 83 vs 0 63±1 17 p=0 001), Total cholesterol (206 9±38 8 vs 181 1±49 2 p=0 005) and LDL cholesterol (127 9±37 7 vs 109 2±40 9, p=0 015) levels were found significantly high in patient with COVID-19 infection In patients who have had COVID-19 infection, FMD% was significantly impaired compared to patients with controle (8 5±3 27 vs 10 4±2 77, p=0 002), however no significant difference was observed in NMD% (11 7±2 36 vs 12 0±2 52, p=0 55) Conclusions: In this study we found that endothelial function assessed by endothelium-dependent vasodilation was significantly impaired in patients who have had COVID-19 infection before average 40 days ago We determined that abnormalities in arterial function may persist for at least 6 weeks after COVID-19 infection These could help to explain in part the earlier reported increase in cardiovascular risk during the first weeks after COVID-19 incfection In the current situation because of little known about long term residual adverse effect of COVID-19 on arterial endothelial function and cardiovascular system, more comprehensive and long-term studies are needed in this area