BACKGROUND AND OBJECTIVE: We aimed to investigate the relation between values of C-reactive protein (CRP) and carotid artery intima-media thickness (IMT) in patients with atherothrombotic ischemic stroke. PATIENTS AND METHOD: One hundred and thirty five patients within 48h after index ischemic stroke were included. CRP levels were obtained at this time and a carotid ultrasonography was performed. Neurological and functional disability were evaluated, and all patients underwent a cardiovascular risk stratification. Patients were divided in three groups according to the tertiles of they IMT distribution. We adjusted for the possible confounding effect using a multivariate logistic model. RESULTS: Forty three in-patients were classified into group 1 (IMT between 0.7 and 1.1 millimetres), 43 into group 2 (IMT between 1.2 and 1.5 millimetres) and 49 into group 3 (IMT higher of 1.6 millimetres). We found a significant elevation of CRP levels at different groups (p<0.0008), with medians by group of 0.3, 0.4 and 1.5mg/dl respectively. Likewise, we found significant differences by group in functional disability (p<0.03) and in vascular risk stratification (p<0.02). CONCLUSIONS: CRP is a marker of increased IMT in patients with atherothrombotic ischemic stroke. A cutoff point of 1.5mg/dl for CRP provided a greater IMT and a worse outcome in functional disability as cardiovascular risk. Therefore, this group requires a more intensive treatment in secondary prevention.
BACKGROUND AND OBJECTIVE: We aimed to investigate the relation between values of C-reactive protein (CRP) and carotid artery intima-media thickness (IMT) in patients with atherothrombotic ischemic stroke. PATIENTS AND METHOD: One hundred and thirty five patients within 48h after index ischemic stroke were included. CRP levels were obtained at this time and a carotid ultrasonography was performed. Neurological and functional disability were evaluated, and all patients underwent a cardiovascular risk stratification. Patients were divided in three groups according to the tertiles of they IMT distribution. We adjusted for the possible confounding effect using a multivariate logistic model. RESULTS: Forty three in-patients were classified into group 1 (IMT between 0.7 and 1.1 millimetres), 43 into group 2 (IMT between 1.2 and 1.5 millimetres) and 49 into group 3 (IMT higher of 1.6 millimetres). We found a significant elevation of CRP levels at different groups (p<0.0008), with medians by group of 0.3, 0.4 and 1.5mg/dl respectively. Likewise, we found significant differences by group in functional disability (p<0.03) and in vascular risk stratification (p<0.02). CONCLUSIONS:CRP is a marker of increased IMT in patients with atherothrombotic ischemic stroke. A cutoff point of 1.5mg/dl for CRP provided a greater IMT and a worse outcome in functional disability as cardiovascular risk. Therefore, this group requires a more intensive treatment in secondary prevention.