Assessment of hemostatic changes in patients with chronic cerebral ischemia after recovery from COVID-19

Background. COVID-19 is associated with disorders in the blood coagulation system that may persist beyond the acute phase of the disease, particularly in individuals with pre-existing cerebrovascular conditions. This research purposed to evaluate changes in key parameters of the procoagulant, anticoagulant, and fibrinolytic links of the hemostatic system in patients with chronic cerebral ischemia (CCI) following recovery from COVID-19. Materials and methods. The study involved 100 patients aged 43 to 74 years diagnosed with CCI and divided into two experimental groups: the CCI + COVID-19 group, which included 60 patients with a history of COVID-19, and the CCI group, consisted of 40 patients without SARS-CoV-2 infection in the past. Plasma levels of hemostatic markers, such as prothrombin, protein C, thrombomodulin, plasminogen, tissue plasminogen activator, plasminogen activator inhibitor-1, and von Willebrand factor, were measured using enzyme-linked immunosorbent assay. Results. The study did not observe significant differences in prothrombin or protein C levels between CCI patients with and without a history of COVID-19. However, there was a 20.9 % increase in plasma thrombomodulin levels in participants with CCI who had recovered from COVID-19 compared to those without prior infection. An increase in plasminogen activator inhibitor-1 content by 19.4 % was found in the CCI + COVID-19 group compared to the CCI group, while no significant differences in the levels of plasminogen and its tissue activator were established. Notably, von Willebrand factor levels did not show statistically significant differences between the groups, which could indicate a gradual correction of endothelial disturbances in post-COVID-19 over time. Conclusions. The data obtained indicate the complexity of post-COVID-19 hemostatic changes in patients with CCI, characterized by persistent low-grade inflammation and possible fibrinolysis inhibition. At the same time, the results suggest that endothelial dysfunction may not be a pronounced feature in the late post-COVID-19 period.