TISSUE-PLASMINOGEN ACTIVATOR AND PLASMINOGEN-ACTIVATOR INHIBITOR-1 INSTROKE PATIENTS

Background and Purpose Abnormal endogenous fibrinolytic activity may b e a risk factor for stroke. Since the possible variation of tissue-typ e plasminogen activator (TPA) antigen and plasminogen activator inhibi tor-1 (PAI-1) antigen concentrations over time after stroke has been r arely studied, it was examined in plasma from stroke patients in the a cute and convalescent phases of the disease and in a control group. Me thods Plasma concentrations of TPA and PAI-1 were determined in 135 st roke patients and in 77 control subjects. All but 4 patients were exam ined within 7 days after stroke onset, and 32 patients and 18 control subjects were reexamined 2 to 4 years later. Results In the acute phas e, stroke patients had significantly higher TPA (median, 10 mu g/L) an d PAI-1 (median, 14 mu g/L) antigen concentrations, compared with cont rol subjects (median values, 6 mu g/L [P=.0001] and 8 mu g/L [P<.01], respectively); TPA levels were higher in both the cerebral infarction (n=122) and cerebral hemorrhage (n=12) subgroups, whereas PAI-I levels were higher in the cerebral infarction subgroup only. Stepwise logist ic regression analysis (with correction for age, sex, history of hyper tension, diabetes mellitus, and heart disease) showed TPA antigen leve l to be an independent discriminator between the cerebral infarction s ubgroup and control subjects (P=.0001), whereas the corresponding diff erence for PAI-1 antigen levels just: failed to reach significance (P= .05). TPA antigen levels were correlated with concentrations of serum cholesterol (Spearman's rho=0.15; P<.05), serum triglyceride (rho=0.33 ; P=.0001), and plasma homocysteine (rho=0.19; P<.01). PAI-I antigen l evels were correlated with serum triglyceride levels only (rho=0.41; P =.0001). At reexamination after 2 to 4 years, neither TPA nor PAI-1 le vels had changed significantly from the baseline values. Conclusions I n stroke patients, high TPA antigen concentrations may indicate an act ivation of the fibrinolytic system or may be due to a delayed clearanc e of TPA complexed with inhibitors. High PAI-1 antigen concentrations in patients with cerebral infarction represent increased fibrinolytic inhibition. The findings in this longitudinal study suggest that TPA a nd PAI-1 antigen concentrations both differ little between the acute a nd convalescent phases after stroke.