Thromb Haemost 2012; 107(02): 346-355
DOI: 10.1160/TH11-05-0345
Cardiovascular Biology and Cell Signalling
Schattauer GmbH

Upregulation of CD40 ligand and enhanced monocyte-platelet aggregate formation are associated with worse clinical outcome after ischaemic stroke

Maria Lukasik
1   Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland
,
Grzegorz Dworacki
2   Department of Clinical Immunology, Poznan University of Medical Sciences, Poznan, Poland
,
Joanna Kufel-Grabowska
1   Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland
,
Cezary Watala
3   Department of Haemostatic Disorders, Medical University of Lodz, Lodz, Poland
,
Wojciech Kozubski
1   Department of Neurology, Poznan University of Medical Sciences, Poznan, Poland
› Author Affiliations
Financial support: This study was supported financially by the governmental research grant NN 402366233.
Further Information

Publication History

Received: 23 May 2011

Accepted after major revision: 01 January 2011

Publication Date:
29 November 2017 (online)

Summary

The white blood cell count and mean platelet volume determined shortly after the symptom onset are known as independent predictors for clinical outcome after stroke. In the present study we sought to evaluate the prognostic value of platelet-derived inflammatory biomarkers measured prospectively after an ischaemic event. Using five-colour flow cytometry, the platelet surface expression of CD40L, CD62P and subpopulations of leukocyte-platelet aggregates were assessed in 93 stroke patients on the first (V0), 10th (V1) and 90th (V2) day after stroke, and once in 65 disease controls. The clinical outcome was evaluated using the Scandinavian Stroke Scale (SSS) and modified Rankin Scale (mRS) at the same time points as blood sampling and 24 months after the event. Patients with either CD40L surface expression or the percentage of monocyte-platelet aggregates (M-plt) in the third tertile (T3) at V0 had a significantly lower score on the SSS at V1. Patients with the percentage M-plt at V0 higher than the median value of M-plt in controls were at increased risk of SSS < 40 at V1 (odds ratio: 2.6; 95% confidence interval [CI]: 1.4 – 8.7; p=0.006). Patients with the percentage of M-plt in T3 at V0 showed progressive decline in survival (hazard ratio [HR]: 1.6; 95% CI: 1.1–1.9; p=0.02) and a significantly higher number of recurrent vascular events (HR: 2.64; 95% CI: 1.3–3.2; p=0.02) when compared to the first tertile. In conclusion, increased levels of M-plt could be a predictive marker for both early outcome and long-term prognosis while increased CD40L was correlated with worse clinical outcome.

The preliminary results of this study were presented in part during a poster session at the 62nd Annual Meeting of the American Academy of Neurology in Toronto, 7–17 April 2010.

 
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