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Thrombin generation in non-cardioembolic stroke subtypes

The Hemostatic System Activation Study^*

From Massachusetts General Hospital (Drs. Furie and Kistler, and B. Thornell) and Beth Israel Deaconess Medical Center (Dr. Bauer and S. Barzegar), Harvard Medical School (Dr. Rosner), Boston; Massachusetts Institute of Technology (Dr. Rosenberg), Cambridge; and Columbia Presbyterian Hospital (Dr. Mohr), Columbia University (Drs. Thompson and Sciacca, and T. Costigan), New York, NY.

Address correspondence and reprint requests to Dr. Karen L. Furie, V.B.K. 802, Stroke Service, Massachusetts General Hospital, 55 Fruit St., Boston, MA 02114; e-mail: kfurie{at}partners.org

Background: The association between hemostatic activation, stroke mechanism, and outcome is poorly defined. The Hemostatic System Activation Study (HAS) investigators measured serial levels of prothrombin fragment F1.2, a marker of thrombin generation, in patients enrolled in the Warfarin Aspirin Recurrent Stroke Study (WARSS).

Methods: HAS enrolled 631 of the 2,206 patients in WARSS. Strokes were subtyped according to inferred mechanism. Plasma was collected for F1.2 at randomization (within 30 days of stroke), 3 months, 12 months, and 18 months. The 3 to 6 month samples in aspirin-treated patients were used for the primary analysis.

Results: The authors analyzed 3 to 6 month samples on 320 patients. Higher F1.2 levels were associated with older age, female sex, and hypertension. There was no difference between mean F1.2 levels in 56 cryptogenic (0.9 ± 0.32 nmol/L) and 114 non-cryptogenic (1.13 ± 0.74 nmol/L) patients or across specific stroke subtypes. There was an 8.8%/year (p = 0.006) increase in mean F1.2 levels. There was a trend toward higher risk of recurrent stroke or death as F1.2 levels increased in aspirin (RR: 1.30, 95% CI: 0.57 to 2.94, p = 0.53) and warfarin treated patients (RR: 1.68, 95% CI: 0.48 to 5.94, p = 0.42). F1.2 levels were reduced on average 70% in warfarin-treated patients in a dose-dependent fashion.

Conclusion: F1.2 levels did not appear to differ by stroke subtype, suggesting that factors other than underlying stroke pathophysiology influence thrombin generation in the post-acute stroke period. F1.2 levels were suppressed by warfarin in a dose-dependent fashion. Additional research is needed to determine the predictive value of F1.2 after stroke.

Received February 18, 2004. Accepted in final form May 5, 2004.

See also page 768

*See the Appendix on page 783 for a list of HAS participants.

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