Laboratory markers of endothelial destruction and hemostasis activation in patients with acute cerebrovascular accident and 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.