LABORATORY MARKERS OF ENDOTHELIAL DESTRUCTION AND HEMOSTASIS ACTIVATION IN PATIENTS WITH ACUTE CEREBROVASCULAR ACCIDENT AND COVID-19; ЛАБОРАТОРНЫЕ МАРКЕРЫ ЭНДОТЕЛИАЛЬНОЙ ДЕСТРУКЦИИ И АКТИВАЦИИ ГЕМОСТАЗА У ПАЦИЕНТОВ С ИНСУЛЬТОМ И COVID-19

Introduction. The severity of endothelial destruction in patients with the new COVID-19 new coronavirus infection may be correlated with the risk of developing acute cerebrovascular accident (ACVA). Objective. To study the role of hemostasis system activation markers and vascular wall damage markers in the development of stroke in patients with the new coronavirus infection. Materials and methods. The study included 38 patients with the new coronavirus infection and ACVA and 40 patients with the new coronavirus infection without ACVA. All patients were tested for antibodies to β2-glycoprotein, antibodies to cardiolipin, plasminogen activator inhibitor type 1 (PAI-1), α2-antiplasmin, intercellular adhesion molecule type 1 (ICAM-1), von Willebrand factor, and homocysteine. Results. No statistically significant differences were found between the groups in terms of antiphospholipid antibody levels; however, increased antibodies to β2-glycoprotein relative to the reference interval were more frequent in the group without ACVA. Significant differences in PAI-1 levels were found between the group with ACVA and the comparison group (p < 0.001), with the PAI-1 concentration being 1.6 times higher in the comparison group. No significant differences were observed between the groups in terms of α2-antiplasmin, ICAM-1, and von Willebrand factor levels. Significant differences for homocysteine were found between the ACVA group and the comparison group (p < 0.001), with the concentration in the comparison group being 1.8 times higher. Conclusions. The development of acute cerebrovascular accident in patients with lower concentrations of homocysteine and PAI-1 may be explained by weaker compensatory mechanisms aimed at repairing of the vascular wall and harmonization of interaction of hemostasis system links, which eventually led to vascular wall damage. © 2025 Elsevier B.V., All rights reserved.