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(Stroke. 2009;40:977.)
© 2009 American Heart Association, Inc.

Research Letters

Elevated C-Reactive Protein and Long-Term Mortality After Ischaemic Stroke

Relationship With Markers of Endothelial Cell and Platelet Activation

Saran Shantikumar, MBChB; Peter J. Grant, MD; Andrew J. Catto, PhD; John M. Bamford, MD Angela M. Carter, PhD

From the Division of Cardiovascular and Diabetes Research (S.S., P.J.G., A.J.C., A.M.C.), The LIGHT Institute, University of Leeds, Leeds, UK; Department of Neurology (J.M.B.), Leeds General Infirmary, Leeds, UK.

Correspondence to Dr Angela M. Carter, Division of Cardiovascular and Diabetes Research, The LIGHT Laboratories, Clarendon Way, University of Leeds, LS2 9JT, UK. E-mail a.carter{at}leeds.ac.uk

Background and Purpose— Inflammatory biomarkers predict development of atherothrombotic events. In the present study we examined the relationships between C-reactive protein (CRP), complement C3, and long-term mortality after acute ischemic stroke.

Methods— CRP and C3 were analyzed by in-house enzyme-linked immunosorbent assay in 394 subjects with acute ischemic stroke who survived for >30 days, followed-up for a median of 7.4 years.

Results— CRP was higher in subjects who died (10.8 mg/L; 95% CI, 9.1–12.8) compared with survivors (3.8 mg/L; 95% CI, 3.1–4.7), whereas C3 was similar in both groups (P=0.26). CRP remained predictive for mortality after adjusting for conventional clinical and demographic risk factors (the adjusted hazard ratio for those with CRP in the highest compared with the lowest quartile was 2.0; 95% CI, 1.3–3.1). However, CRP was no longer independently predictive of mortality after additionally adjusting for β-thromboglobulin or von Willebrand factor.

Conclusions— Our data suggest that the relationship between CRP and poststroke mortality may in part reflect inflammation-induced endothelial cell dysfunction and platelet activation.

Key Words: C-reactive protein • cerebral infarction • endothelial cell dysfunction • mortality • platelet activation

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