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Coagulation-fibrinolysis system in poststroke patients receiving antiplatelet medication
H Tohgi1, H Takahashi, K Chiba
1Department of Neurology, Iwate Medical University, Japan.
Insights
In chronic poststroke patients, coagulation-fibrinolysis markers are mildly elevated. Antiplatelet medications effectively reduce elevated plasminogen activator inhibitor-1 levels, a key marker in stroke recovery.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Neurology
Background:
- Poststroke patients often exhibit altered coagulation-fibrinolysis system activity.
- Chronic phase alterations in hemostasis may influence stroke recurrence and outcomes.
Purpose of the Study:
- To investigate coagulation-fibrinolysis system activity in chronic poststroke patients.
- To evaluate the impact of antiplatelet medication on these hemostatic markers.
Main Methods:
- Plasma levels of fibrinogen, antithrombin III, thrombin-antithrombin III complex, tissue plasminogen activator antigen, plasminogen activator inhibitor-1, plasmin-alpha 2 plasmin inhibitor complex, and D-dimer were measured.
- 153 chronic poststroke patients were analyzed: 33 untreated, 78 on ticlopidine, and 42 on aspirin.
- Results were compared to control subjects and among treatment groups.
Main Results:
- Fibrinogen, thrombin-antithrombin III complex, antithrombin III, plasmin-alpha 2 plasmin inhibitor complex, and tissue plasminogen activator were mildly elevated in all patient groups versus controls.
- Plasminogen activator inhibitor-1 (PAI-1) was significantly elevated in untreated patients but normalized with ticlopidine or aspirin.
- Lower PAI-1 levels correlated with inhibited platelet aggregation due to antiplatelet therapy.
Conclusions:
- Coagulation-fibrinolysis markers show mild increases in chronic poststroke patients.
- Antiplatelet therapy, including ticlopidine and aspirin, effectively reduces elevated PAI-1 levels.
- These findings highlight a potential therapeutic target for managing hemostasis poststroke.
Background And Purpose:
We studied the activities of the coagulation-fibrinolysis system in the chronic stage of poststroke patients and the effect of antiplatelet medication on the system.
Methods:
We determined fibrinogen, antithrombin III, thrombin-antithrombin III complex, tissue plasminogen activator antigen, plasminogen activator inhibitor-1, plasmin-alpha 2 plasmin inhibitor complex, and D-dimer in plasma from 153 poststroke patients in the chronic phase (ie, 33 patients not receiving antiplatelet medication, 78 patients receiving 200 mg/d ticlopidine, and 42 patients receiving 40 mg/d aspirin), and compared the results in control subjects and among the treatment groups.
Results:
The concentrations of fibrinogen, thrombin-antithrombin III complex, antithrombin III, plasmin-alpha 2 plasmin inhibitor complex, and tissue plasminogen activator were slightly but significantly increased in all treatment groups compared with control subjects (P < .01) but did not differ among the treatment groups. The plasminogen activator inhibitor-1 levels were significantly elevated in patients not receiving antiplatelet medication compared with control subjects (P < .01), whereas they were in the normal range and significantly lower in patients receiving ticlopidine or aspirin than in patients not receiving antiplatelet medication (P < .01). The plasminogen activator inhibitor-1 levels were significantly lower in patients whose platelet aggregation was inhibited by antiplatelet medication than in patients with uninhibited platelet aggregability (P < .05).
Conclusions:
These findings suggest that coagulation-fibrinolysis markers are mildly increased in poststroke patients in the chronic phase and that antiplatelet medication is effective in reducing the elevated plasminogen activator inhibitor-1 levels.