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Mark Fisher, MD; Robert Francis, MD

Arch Neurol. 1990;47(10):1075-1079.

Abstract
• We investigated hemostatic function in patients with cerebral ischemia by evaluating platelet activation, fibrin generation, and fibrinolysis. Plasma β-thromboglobulin, an index of platelet activation, was significantly increased both acutely (14.9 ± 9.2 ng/mL; n = 85) and approximately 2 months later (17.3 ± 10.1 ng/mL; n = 57). Thrombin activity was measured using assays for fibrinopeptide A and fibrin D-dimer. Increased fibrinopeptide A was found in 9 (11.5%) of 78 patients acutely and 6 (10.7%) of 56 at follow-up; fibrin D-dimer levels were significantly increased acutely (166 ± 188 ng/mL; n = 66) but not at follow-up. Fibrinolytic activity was measured using assays for fibrinopeptide B-β 1-42 and plasminogen activator inhibitor 1. Fibrinopeptide B-β 1-42 was significantly reduced acutely (6.3 ± 2.2 pmol/mL; n = 35) and at follow-up (4.8 ± 1.5pmol/mL; n = 21). Plasminogen activator inhibitor 1 was normal acutely (20.1 ± 12.0 ng/mL; n = 73) but increased at follow-up (27.8 ± 20.1 ng/mL; n = 45). These results demonstrate that patients with cerebral ischemia have abnormal hemostatic function that is not explained by the acute phase reaction, and that components of the prethrombotic state are present in some of these patients.

Author Affiliations
From the Departments of Neurology (Dr Fisher) and Internal Medicine (Dr Francis), University of Southern California School of Medicine, Los Angeles.

Footnotes
Accepted for publication November 22, 1989.

Reprint requests to the Department of Neurology, University of Southern California School of Medicine, 2025 Zonal Ave, Los Angeles, CA 90033 (Dr Fisher).

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