PLATELET ACTIVATION IS NOT INVOLVED IN ACCELERATION OF THE COAGULATION SYSTEM IN ACUTE CARDIOEMBOLIC STROKE WITH NONVALVULAR ATRIAL-FIBRILLATION

Citation
T. Nagao et al., PLATELET ACTIVATION IS NOT INVOLVED IN ACCELERATION OF THE COAGULATION SYSTEM IN ACUTE CARDIOEMBOLIC STROKE WITH NONVALVULAR ATRIAL-FIBRILLATION, Stroke, 26(8), 1995, pp. 1365-1368
Citations number
31
Categorie Soggetti
Neurosciences,"Cardiac & Cardiovascular System","Peripheal Vascular Diseas","Clinical Neurology
Journal title
StrokeACNP
ISSN journal
00392499
Volume
26
Issue
8
Year of publication
1995
Pages
1365 - 1368
Database
ISI
SICI code
0039-2499(1995)26:8<1365:PAINII>2.0.ZU;2-Y
Abstract
Background and Purpose It is generally accepted that the coagulation s ystem is activated in ischemic stroke and that platelet activation is involved in the pathogenesis of this disease. However, little is known about how and to what extent platelet activity participates in coagul ation system enhancement. We evaluated the hemostatic condition, espec ially with regard to platelet function and the coagulation system, wit hin 3 days of onset of acute stroke. The study participants were limit ed to elderly patients with cardioembolic stroke due to nonvalvular at rial fibrillation. Methods Seventeen elderly patients with acute cardi oembolic stroke due to nonvalvular atrial fibrillation were investigat ed, Within 3 days of stroke onset, beta-thromboglobulin (BTG), platele t factor 4 (PF4), thrombin-antithrombin III complex (TAT), and D-dimer from arterial blood were carefully evaluated in these patients. Blood samples from 19 healthy age-and sex-matched control subjects were als o examined. Results The two studied markers of platelet activity did n ot change in the patients or the control subjects, and the between-gro up differences between the stroke and control groups were not statisti cally significant (BTG, 43.8 versus 31.9 ng/mL; PF4, 9.06 versus 5.78 ng/mL; respectively). In contrast, the two studied coagulation-system indicators were markedly elevated in the patients compared with the co ntrol subjects (TAT, 13.8 versus 3.5 ng/mL, P < .01 D-dimer, 366.3 ver sus 147.2 ng/mL, P < .01; respectively). Conclusions Platelet function was not enhanced in the acute stage of cardioembolic stroke with nonv alvular atrial fibrillation. This result indicates that enhancement of the coagulation system in cardioembolic stroke is not the result of p latelet hyperfunction, ie, ''platelet-fibrin'' thrombi, but rather of ''stasis-related'' thrombi formation.