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 beta-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.
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 beta-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.
Authors: Xiping Gong; Xinying Zou; Liping Liu; Yuehua Pu; Yilong Wang; Yuesong Pan; Yannie O Y Soo; Thomas W H Leung; Xingquan Zhao; Yongjun Wang; Ka Sing Wong Journal: Mediators Inflamm Date: 2013-08-19 Impact factor: 4.711