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(Stroke. 2006;37:1205.)
© 2006 American Heart Association, Inc.

Original Contributions

Poststroke C-Reactive Protein Is a Powerful Prognostic Tool Among Candidates for Thrombolysis

Joan Montaner, MD, PhD; Israel Fernandez-Cadenas, MSc; Carlos A. Molina, MD, PhD; Marc Ribó, MD, PhD; Rafael Huertas, MD; Anna Rosell, PhD; Anna Penalba; Laura Ortega; Pilar Chacón, MD, PhD José Alvarez-Sabín, MD, PhD

From the Neurovascular Research Laboratory, Neurovascular Unit (J.M., I.F.-C., C.A.M., M.R., R.H., A.R., A.P., L.O., J.A.-S.), and Lipid Research Unit (P.C.), Departament de Medicina Interna, Vall d’Hebron Hospital, Universitat Autonoma de Barcelona, Barcelona, Spain.

Correspondence to Dr Joan Montaner, Laboratorio de Investigación Neurovascular, Unidad Neurovascular, Institut de Recerca, Hospital Vall d’Hebron, Pg Vall d’Hebron 119-129, 08035 Barcelona, Spain. E-mail 31862jmv{at}comb.es

Background and Purpose— After acute stroke, an increased level of C-reactive protein (CRP) measured at discharge predicts unfavorable outcome. We sought to investigate whether CRP measured before tissue plasminogen activator (tPA) treatments may add prognostic information to guide stroke thrombolysis.

Methods— Our target was 151 consecutive patients with an ischemic stroke involving the middle cerebral artery territory who received tPA within 3 hours of symptom onset. High-sensitivity CRP was measured before tPA administration, and CRP gene polymorphisms were determined (G1059C and C1444T). Functional outcome was evaluated by 3-month modified Rankin Scale (mRS).

Results— A total of 143 tPA-treated patients were valid for analyses after exclusion of those with inflammatory diseases and those probably infected (CRP >6 mg/dL). Patients with history of previous stroke, hypertension, or atrial fibrillation had higher levels of CRP (P<0.05). CRP was higher in patients who died after thrombolysis (n=19) than in survivors (0.85 versus 0.53 mg/dL; P=0.002). Among the 94 patients with proximal middle cerebral artery occlusions, CRP level was 0.53 for 81 survivors versus 0.81 mg/dL for 13 who died (P=0.001). CRP-survival association was found even among patients who recanalized by the end of tPA infusion (P=0.007). A correlation between CRP and mRS was found (r=0.36, P=0.02), although CRP polymorphisms were not related to neurological outcome. In a logistic regression model, CRP (odds ratio=8.51; 95% CI, 2.16 to 33.5; P=0.002) and age (odds ratio=6.25; 95% CI, 1.44 to 27.19; P=0.015) were the only baseline mortality predictors.

Conclusions— Admission CRP predicts mortality among tPA-treated stroke patients. Very early recanalization does not ameliorate the negative prognostic impact of elevated CRP.

Key Words: C-reactive protein • inflammation • polymorphism • stroke • tissue plasminogen activator

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