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A Thrombotic Stroke Model Based On Transient Cerebral Hypoxia-ischemia
Published on: August 18, 2015
Thrombin generation in non-cardioembolic stroke subtypes: the Hemostatic System Activation Study
K L Furie1, R Rosenberg, J L Thompson
1V.B.K. 802, Stroke Service, Massachusetts General Hospital, 55 Fruit St., Boston, MA 02114, USA. kfurie@partners.org
Neurology
|September 15, 2004
Summary
Thrombin generation markers (F1.2) did not differ by stroke type but increased over time. Warfarin effectively reduced F1.2 levels, suggesting its impact on hemostasis post-stroke.
Area of Science:
- Neurology
- Cardiology
- Hematology
Background:
- The relationship between hemostatic activation, stroke mechanism, and patient outcomes remains unclear.
- The Hemostatic System Activation Study (HAS) investigated prothrombin fragment F1.2 (F1.2) levels, a marker of thrombin generation, in stroke patients.
Purpose of the Study:
- To assess serial levels of prothrombin fragment F1.2 in patients from the Warfarin Aspirin Recurrent Stroke Study (WARSS).
- To explore the association between F1.2 levels, stroke subtypes, and patient outcomes.
Main Methods:
- 631 patients from the WARSS trial were enrolled in the HAS study.
- Plasma F1.2 levels were measured serially (randomization, 3, 12, 18 months); primary analysis used 3-6 month samples from aspirin-treated patients.
- Strokes were subtyped based on inferred mechanism.
Main Results:
- Higher F1.2 levels correlated with older age, female sex, and hypertension.
- No significant difference in mean F1.2 levels was observed between cryptogenic and non-cryptogenic stroke subtypes.
- A significant annual increase in mean F1.2 levels (8.8%/year) was noted, with a trend towards increased recurrent stroke or death risk as F1.2 levels rose.
Conclusions:
- F1.2 levels did not vary by stroke subtype, indicating other factors influence post-acute stroke thrombin generation.
- Warfarin treatment dose-dependently suppressed F1.2 levels.
- Further research is required to establish the predictive value of F1.2 in post-stroke patients.
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