Coagulation-fibrinolysis system in poststroke patients receiving antiplatelet medication.
OBJECTIVE
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.
Tohgi
H
H
Department of Neurology, Iwate Medical University, Japan.
Takahashi
H
H
Chiba
K
K
Tamura
K
K
D000368:Aged; D000933:Antifibrinolytic Agents / Q000032:analysis; D000990:Antithrombin III / Q000032:analysis; D001241:Aspirin / Q000627:therapeutic use*; D001777:Blood Coagulation / Q000187:drug effects*; D002561:Cerebrovascular Disorders / Q000097:blood* / Q000188:drug therapy; D005260:Female; D005340:Fibrinogen / Q000032:analysis; D005341:Fibrinolysin / Q000032:analysis; D005342:Fibrinolysis / Q000187:drug effects*; D006801:Humans; D008297:Male; D008875:Middle Aged; D010447:Peptide Hydrolases / Q000032:analysis; D017395:Plasminogen Activator Inhibitor 1 / Q000032:analysis*; D010974:Platelet Aggregation / Q000187:drug effects; D013988:Ticlopidine / Q000627:therapeutic use*; D010959:Tissue Plasminogen Activator / Q000032:analysis; D000979:alpha-2-Antiplasmin
D000933:Antifibrinolytic Agents; D017395:Plasminogen Activator Inhibitor 1; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; C037742:plasmin-plasmin inhibitor complex; D000990:Antithrombin III; D005340:Fibrinogen; D010447:Peptide Hydrolases; D010959:Tissue Plasminogen Activator; D005341:Fibrinolysin; D013988:Ticlopidine; D001241:Aspirin