[Plasminogen activator inhibitor-1 in the evolution of stroke]

Fibrinolytic activity in the acute stroke was examined by monitoring the level of plasminogen activator inhibitor-1 (PAI-1), as one of the indicators of fibrinolytic activity. Given the role of PAI-1 in the processes of atherogenesis and thrombogenesis, plasma PAI-1 level was measured in 59 patients (up to 50 years of age) with atherothrombotic stroke (verified by computed tomography scanning or magnetic resonance imaging of brain) in the period from 12 to 24 hours (I analysis) and 30 days after the onset of stroke (II analysis); then, it was correlated with plasma PAI-1 level in the control group (57 healthy subjects), which was 2.86 +/- 0.70 U/ml. It was found that PAI-1 level was significantly higher in the acute stroke (I analysis: PAI-1 = 4.10 +/- 1.40 U/ml, p < 0.001; II analysis: PAI-1 = 3.64 +/- 0.90 U/ml, p < 0.001), while fibrinolytic activity was lower, especially on the first day from the stroke that was not completely increased even after 30 days. There was no difference in PAI-1 levels between the subgroups of patients with infarction and lacunar cerebral ischemia (p > 0.05), as well as between females and males (p > 0.05). Along with significantly increased fibrinogen level (4.65 +/- 1 g/l, in the controls--2.83 +/- 0.64 g/l, p < 0.001), significantly higher triglycerides (2.04 +/- 0.76 mmol/l, in the controls--1.38 +/- 0.54 mmol/l, p < 0.001) and lipoproteins(a) (0.405 +/- 0.29 g/l, in the controls--0.172 +/- 0.14 g/l, p < 0.001) were found, correlating with higher plasma PAI-1 level in these patients. The increased plasma level of PAI-1 pointed to possibility of decreased fibrinolytic activity in pathogenesis of ischemic stroke, as well as, risk of reinsult, which had been the greatest after the onset of stroke and declined gradually within several weeks.