(Stroke. 1996;27:1066-1071.)
© 1996 American Heart Association, Inc.
Articles |
Tissue Plasminogen Activator and Plasminogen Activator Inhibitor-1 in Stroke Patients
Presented in part at the 4th International Symposium on Thrombolytic Therapy in Acute Ischemic Stroke, Copenhagen, Denmark, May 30-June 1, 1996.
From the Department of Neurology (A.L., B.N., B.B.J.) and the Research Laboratory of the Department of Obstetrics and Gynecology (C.L., B.Å.), University Hospital, Lund, Sweden.
Correspondence to Arne Lindgren, MD, Department of Neurology, University Hospital, S-221 85 Lund, Sweden.
Background and Purpose Abnormal endogenous fibrinolytic activity may be a risk factor for stroke. Since the possible variation of tissue-type plasminogen activator (TPA) antigen and plasminogen activator inhibitor-1 (PAI-1) antigen concentrations over time after stroke has been rarely studied, it was examined in plasma from stroke patients in the acute and convalescent phases of the disease and in a control group.
Methods Plasma concentrations of TPA and PAI-1 were determined in 135 stroke patients and in 77 control subjects. All but 4 patients were examined within 7 days after stroke onset, and 32 patients and 18 control subjects were reexamined 2 to 4 years later.
Results In the acute phase, stroke patients had
significantly higher TPA (median, 10 µg/L) and PAI-1 (median, 14
µg/L) antigen concentrations, compared with control subjects (median
values, 6 µg/L [P=.0001] and 8 µg/L
[P<.01], respectively); TPA levels were higher in both
the cerebral infarction (n=122) and cerebral hemorrhage (n=12)
subgroups, whereas PAI-1 levels were higher in the cerebral infarction
subgroup only. Stepwise logistic regression analysis (with
correction for age, sex, history of hypertension, diabetes mellitus,
and heart disease) showed TPA antigen level to be an independent
discriminator between the cerebral infarction subgroup and control
subjects (P=.0001), whereas the corresponding difference for
PAI-1 antigen levels just failed to reach significance
(P=.05). TPA antigen levels were correlated with
concentrations of serum cholesterol (Spearman's 
=0.15;
P<.05), serum triglyceride (=0.33;
P=.0001), and plasma homocysteine (=0.19;
P<.01). PAI-1 antigen levels were correlated with serum
triglyceride levels only (=0.41; P=.0001). At
reexamination after 2 to 4 years, neither TPA nor PAI-1 levels had
changed significantly from the baseline values.
Conclusions In stroke patients, high TPA antigen concentrations may indicate an activation of the fibrinolytic system or may be due to a delayed clearance 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 and PAI-1 antigen concentrations both differ little between the acute and convalescent phases after stroke.
Key Words: cerebral hemorrhage • cerebral infarction • fibrinolysis • plasminogen activator, tissue-type
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