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Stroke. 2002;33:2570-2574
doi: 10.1161/01.STR.0000034398.34938.20
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(Stroke. 2002;33:2570.)
© 2002 American Heart Association, Inc.


Original Contributions

Course of Platelet Activation Markers After Ischemic Stroke

Lars Marquardt, Cand Med; Andreas Ruf, MD; Ulrich Mansmann, PhD; Ralph Winter, MD; Matthias Schuler, MD; Florian Buggle, MD; Horst Mayer, MD Armin J. Grau, MD

From the Department of Neurology (L.M., F.B., A.J.G.), Institute of Medical Biometry and Informatics (U.M.), and Krankenhaus Bethanien, Geriatric Center (M.S.), University of Heidelberg; Center for Laboratory Medicine, Microbiology, Transfusion Medicine, Klinikum Karlsruhe (A.R., H.M.); and Department of Neurology, Kurpfalzkrankenhaus Heidelberg (R.W.), Heidelberg, Germany.

Correspondence to Armin J Grau, MD, Department of Neurology, University of Heidelberg, Im Neuenheimer Feld 400, 69120 Heidelberg, Germany. E-mail armin_grau{at}med.uni-heidelberg.de

Background and Purpose— The aim of this study was to evaluate the time course of platelet activation after ischemic stroke and to investigate whether platelet activation and inflammation are correlated with each other.

Methods— We serially determined expression of p-selectin (CD62p) and lysosome-associated membrane protein (CD63) by platelets using flow cytometry at 10 time points between days 1 and 90 in patients after ischemic stroke (n=50), in healthy subjects (n=30), and in risk factor control subjects (n=20). Furthermore, we correlated leukocyte count, C-reactive protein, and fibrinogen levels with platelet activation markers.

Results— CD62p and CD63 expression was higher on day 1 after stroke than in both control groups (P<0.005 for both). CD62p expression rapidly declined, whereas CD63 expression remained significantly elevated until day 90. Stroke severity and different medication for secondary stroke prevention did not influence CD62p or CD63 expression. Platelet activation markers and inflammatory parameters were not correlated with each other at any time point after stroke.

Conclusions— The initial increase in both CD62p and CD63 expression by platelets is followed by a differential regulation of both parameters after stroke. The rapid decrease in CD62p expression may be caused by shedding from the cell surface. Its persistent elevation makes CD63 a good candidate for studies on predictors for stroke recurrence. Our findings suggest that the expression of CD62p and CD63 by platelets is regulated independently from inflammatory indexes.


Key Words: flow cytometry • inflammation • platelets • stroke




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