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Thromb Haemost 1995; 74(04): 1050-1054
DOI: 10.1055/s-0038-1649880
Original Article
Clinical Studies
Schattauer GmbH Stuttgart

Decreased Plasma Tissue Factor Pathway Inhibitor Activity in Ischemic Stroke Patients

Takeo Abumiya
1   The Research Institute Suita, Department of Medicine, National Cardiovascular Center, Suita, Osaka
,
Takenori Yamaguchi
2   The Cerebrovascular Division, Department of Medicine, National Cardiovascular Center, Suita, Osaka
,
Tadashi Terasaki
2   The Cerebrovascular Division, Department of Medicine, National Cardiovascular Center, Suita, Osaka
,
Toshinori Kokawa
1   The Research Institute Suita, Department of Medicine, National Cardiovascular Center, Suita, Osaka
,
Kazuomi Kario
3   The Department of Internal Medicine, Awaji-Hokudan Public Clinic, Hokudan, Hyogo, Japan
,
Hisao Kato
1   The Research Institute Suita, Department of Medicine, National Cardiovascular Center, Suita, Osaka
› Author Affiliations
Further Information

Publication History

Received 13 March 1994

Accepted 26 June 1995

Publication Date:
09 July 2018 (online)

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Summary

Although tissue factor pathway inhibitor (TFPI) plays an essential role in the regulation of blood coagulation, the quantitative changes in its levels in thrombotic disease are still undefined. We compared TFPI activity in ischemic stroke patients and control subjects matched for age and cholesterol level to determine whether TFPI activity is changed in the disease. TFPI activity was significantly lower in the stroke patients (1.01 ± 0.24 U/ml) than in the control subjects (1.10 ± 0.16 U/ml). In relation to clinical subtypes of stroke, TFPI activity in atherothrombotic infarction (0.93 ± 0.19 U/ml) and lacunar infarction (0.99 ± 0.23 U/ml) was significantly lower than in the control subjects, whereas the level in cardioembolic infarction (1.16 ± 0.31 U/ml) was not. No relationship could be established between TFPI activity and other haemostatic parameters reflecting the production of thrombin/fibrin and the activation of fibrinolysis. These results may suggest that the moderately lower TFPI activity in stroke patients could be due to atherosclerotic changes rather than to consumptive coagulopathy.

 

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