Thromb Haemost 2010; 103(03): 644-650
DOI: 10.1160/TH09-08-0599
Platelets and Blood Cells
Schattauer GmbH

Platelet activation and reactivity in the convalescent phase of ischaemic stroke

Maria Lukasik
1   Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland
,
Marcin Rozalski
2   Department of Haemostatic Disorders, Medical University Lodz, Lodz, Poland
,
Boguslawa Luzak
2   Department of Haemostatic Disorders, Medical University Lodz, Lodz, Poland
,
Slawomir Michalak
1   Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland
,
Wojciech Kozubski
1   Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland
,
Cezary Watala
2   Department of Haemostatic Disorders, Medical University Lodz, Lodz, Poland
› Author Affiliations
Financial support:This study was supported financially by the governmental research grant NN 402366233.
Further Information

Publication History

Received: 26 August 2009

Accepted after major revision: 12 January 2009

Publication Date:
22 November 2017 (online)

Summary

The study was aimed at the evaluation of blood platelet activation and reactivity in patients in the convalescent phase of stroke (n=58) and controls matched in respect to risk factors of vascular pathology (n=55). Both groups were treated daily with acetylsalicylic acid (ASA), 150 mg/day. Using flow cytometry, the expressions of P-selectin and the active GP IIb/IIIa receptor, as well as the fraction of platelet-derived microparticles (PMPs) and total platelet aggregates (Ag), were evaluated in non-stimulated platelets and in platelets stimulated in vitro by thrombin, thrombin receptor activating peptide (TRAP) or ADP. The expression of P-selectin in non-stimulated platelets was found to be significantly (p=0.04) lower in stroke patients. In parallel, these patients manifested a significantly (p=0.0008) higher proportion of PMPs and a lowered (p=0.003) proportion of Ag, as compared to the controls. In the stroke patients the increased expressions of P-selectin and active GP IIb/IIIa in TRAP- or ADP-activated cells were less pronounced (p<0.01), while the increments in PMP fraction remained higher (p<0.05). Our results may indicate that chronic platelet activation develops in patients in the convalescent phase of stroke and the process of PMP generation prevails over blood platelet degranulation and aggregation. This shift may be particularly unfavourable due to the procoagulative and proatherosclerotic properties of PMPs, accompanied by their decreased sensitivity to the action of antiplatelet drugs.

Note: The results of this study were presented in part during a poster session at the XVIII European Stroke Conference in Stockholm, 26–29 May 2009.

 
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