Poststroke c-reactive protein is a powerful prognostic tool among candidates for thrombolysis

• Published in: Stroke (1970) Vol. 37; no. 5; pp. 1205 - 1210
• Main Authors: MONTANER, Joan, FERNANDEZ-CADENAS, Israel, MOLINA, Carlos A, RIBO, Marc, HUERTAS, Rafael, ROSELL, Anna, PENALBA, Anna, ORTEGA, Laura, CHACON, Pilar, ALVAREZ-SABIN, José
• Format: Journal Article
• Language: English
• Published: Hagerstown, MD Lippincott Williams & Wilkins 01-05-2006
• Subjects: Aged; Aged, 80 and over; Biological and medical sciences; Biomarkers; Blood. Blood coagulation. Reticuloendothelial system; C-Reactive Protein - analysis; C-Reactive Protein - genetics; Female; Follow-Up Studies; Humans; Male; Medical sciences; Middle Cerebral Artery - diagnostic imaging; Middle Cerebral Artery - pathology; Neurology; Neuropharmacology; Pharmacology. Drug treatments; Polymorphism, Genetic; Predictive Value of Tests; Prognosis; Psychoanaleptics: cns stimulant, antidepressant agent, nootropic agent, mood stabilizer..., (alzheimer disease); Psychology. Psychoanalysis. Psychiatry; Psychopharmacology; Severity of Illness Index; Stroke - blood; Stroke - drug therapy; Stroke - mortality; Stroke - pathology; Stroke - physiopathology; Tissue Plasminogen Activator - administration & dosage; Ultrasonography, Doppler; Vascular diseases and vascular malformations of the nervous system; Stroke; Nervous system diseases; Prognosis; C-reactive protein; tissue plasminogen activator; Cardiovascular disease; polymorphism; Cerebral disorder; Vascular disease; inflammation; Central nervous system disease; C reactive protein; Cerebrovascular disease
• ISSN: 0039-2499; 1524-4628
• DOI: 10.1161/01.STR.0000217744.89208.4e

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