Endothelial dysfunction in the mother–placenta–fetus system after a new coronavirus infection SARS-CoV-2: An open prospective cross-sectional study

Background. Generalized endotheliopathy in SARS-CoV-2 is associated with the release of the vasoactive peptide endothelin-1, which stimulates the activation of both the plasma and platelet clotting pathways. It is believed that endothelin-1 is one of the most potent vasopressors of the human cardiovascular system and has a strong pressor and thrombogenic effect on many vessels, including in the motherplacentafetus system. Aim. To study endothelial dysfunction in pregnant women with new coronavirus infection SARS-CoV-2. Materials and methods. An open-label prospective continuous cross-sectional study enrolled 96 patients who survived COVID-19 at various gestational ages. Depending on the severity of the underlying disease, patients were divided into groups: Group 1 (n=18) included patients with mild SARS-CoV-2 coronavirus infection, Group 2 (n=56) included women with moderate severity, Group 3 (n=22) included patients with severe COVID-19. The control group consisted of 100 pregnant women who had no COVID-19 or signs of acute respiratory viral infection. In all groups, endothelin-1 levels were determined by enzyme-linked immunosorbent assay. Results. In pregnant women with no COVID-19 and patients after mild COVID-19, the level of endothelin-1 corresponds to the reference values; in pregnant women with moderate and severe underlying disease, the level of endothelin-1 was 2.04.0 pmol/L. It reflects the increased activity of the endothelium in the uterine bloodstream and blood vessels in the motherplacentafetus system. Placental insufficiency in women after COVID-19 is caused by endothelial dysfunction that triggers vasospasm and increased vascular resistance in the uterine arteries (r=0.8; p0.01). Conclusion. The diagnosis of endothelial dysfunction in the motherplacentafetus system after COVID-19 can be helpful in the prediction and prevention of vascular complications, both placental, associated with great obstetrical syndromes (premature birth, intrauterine growth retardation, preeclampsia, antenatal fetal death), and extraplacental ones (arterial and venous thrombosis).