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Stroke. 2006;37:2283-2287
Published online before print August 3, 2006, doi: 10.1161/01.STR.0000236638.75591.61
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(Stroke. 2006;37:2283.)
© 2006 American Heart Association, Inc.


Original Contributions

Course of Platelet Activation and Platelet-Leukocyte Interaction in Cerebrovascular Ischemia

Patrik Htun, MD; Suzanne Fateh-Moghadam, MD; Bernd Tomandl, MD; René Handschu, MD; Kathrin Klinger, MD; Konstantinos Stellos, MD; Christoph Garlichs, MD; Werner Daniel, MD Meinrad Gawaz, MD

From the Medizinische Klinik mit Schwerpunkt Nephrologie und Intensivmedizin (P.H.), Medizinische Klinik mit Schwerpunkt Kardiologie (S.F.-M.), Charité-Campus Virchow-Klinikum, Universitätsmedizin Berlin, Humboldt-Universität zu Berlin und Freie Universität Berlin, Berlin; Klinik für Neuroradiologie (B.T.), Klinikum Bremen Mitte, Bremen; Neurologische Klinik (R.H.), Friedrich Alexander Universität, Erlangen-Nürnberg; Medizinische Klinik mit Schwerpunkt Nephrologie IV (K.K.), Friedrich Alexander Universität, Erlangen Nürnberg; Medizinische Klinik III (K.S., M.G.), Universitätsklinikum, Tübingen; and Medizinische Klinik mit Schwerpunkt Kardiologie (C.G., W.D.), Friedrich Alexander Universität, Erlangen-Nürnberg, Germany.

Correspondence to Meinrad Gawaz, MD, Medizinische Klinik III, Universitätsklinikum Tübingen, Otfried-Müller-Strasse 10, D-72076 Tübingen, Germany. E-mail meinrad.gawaz{at}med.uni-tuebingen.de or Patrik Htun, MD, Medizinsche Klinik mit Schwerpunkt Nephrologie und Intensivmedizin, Universitätsmedizin Charité-Campus Virchow, Humboldt-Universität zu Berlin, Augustenburgerplatz 1, 13353 Berlin, Germany. E-mail p.htun@web.de

Background and Purpose— Platelet activation plays a crucial role in the pathophysiology of cerebral ischemia. The aim of this study was to investigate the contribution of platelet activation and leukocyte-platelet interactions to the disease.

Methods— One hundred thirty-five patients with transient ischemic attack (TIA) or stroke were enrolled in this single-center study. They underwent cranial computer tomography within 24 hours of clinical onset and after 3 months, and systemic venous blood samples were drawn. Platelet activation (CD62P expression), leukocyte activation (L-selectin expression), and the appearance of platelet-specific antigens on leukocytes as an index of platelet-leukocyte aggregation were measured by flow cytometric techniques in the acute state and at 3-month follow-up.

Results— Patients with a completed stroke or TIA had significantly increased circulating platelet-leukocyte aggregates, increased P-selectin expression on platelets, and decreased L-selectin expression in the acute state compared with the control group (healthy volunteers). No differences in regard to the tested activation markers could be detected between patients with stroke or TIA in the acute phase of the disease. However, platelet and leukocyte activations were normalized after 3 months in patients with TIA, whereas leukocyte activation (reduced L-selectin expression) remained in stroke patients.

Conclusions— In patients with TIA and completed stroke, platelet and leukocyte activation is substantially enhanced in the acute phase of the disease. The sustained leukocyte activation observed in stroke but not in TIA patients at 3-month follow up might play a pathophysiological role in the course of the disease.


Key Words: cerebral ischemia, transient • leukocytes • platelet activation • platelets • stroke




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