Changes in the concentration of physiological anticoagulants in the peripheral venous blood during the acute phase of ischemic stroke before and after thrombolytic therapy
S.A. Ikonnikova, A.N. Yasamanova, I.E. Solnyshkova, E.V. Izmailova, M.Kh. Shurdumova, D.Yu. Timofeev, A.V. Kubenko, P.R. KamchatnovObjective. To investigate the activity of physiological anticoagulants in patients during the acute phase of ischemic stroke (IS) before and after thrombolytic therapy (TLT). Material and methods. The study included 29 patients (16 males and 13 females), aged 42 to 88 years, diagnosed with acute IS and undergoing TLT. Evaluations of neurological deficit severity were conducted using the National Institutes of Health Stroke Scale (NIHSS). The assessments of antithrombin III (ATIII) and protein C (PC) levels were performed prior to TLT, 1 hour and 24 hours post-TLT, and on days 3 to 5 following the onset of IS. Results. In Group 1, ATIII activity demonstrated a significant increase 1 hour after TLT (p=0.02), reaching a peak by days 3 to 5. Group 2 showed no significant changes in ATIII levels at 1 hour (p=0.09), with a notable increase observed at 24 hours (p<0.005) and peak levels by days 3 to 5. In both groups, PC activity increased markedly 1 hour after TLT (p<0.005), peaking at 24 hours, then declining by days 3 to 5. The increase in PC activity was recorded by 23.5% in Group 1 and 3.0% in Group 2 (p<0.05). No significant differences were observed in the activities of ATIII and PC with respect to the severity of IS during the follow-up period. There were also no differences in ATIII and PC activity based on the type of thrombolytic agent administered. Conclusion. The increased activity of endogenous anticoagulants following TLT is associated with a favorable progression of fibrinolysis, particularly in patients exhibiting less pronounced neurological deficits. Monitoring the levels of endogenous anticoagulants in the acute phase of ischemic stroke may facilitate the prediction of the risk associated with ischemic/reperfusion injury and the potential recurrence of thrombosis.