RESUMO
BACKGROUND: Attempts have been made to use the signal changes of fluid-attenuated inversion recovery (FLAIR) MRI as "a tissue clock," defined as a surrogate marker of the tissue damage resulting from acute ischemic stroke. The evolution of FLAIR signals after stroke onset has never been fully explained solely by time. The aim of this study was to determine whether cerebral small-vessel disease (SVD) affects FLAIR changes following acute ischemic stroke. METHODS: Based on data from a prospective stroke registry, consecutive patients who were hospitalized to the stroke center within 12 hours of stroke onset between January 2004 and May 2011 and had occlusion of the major cerebral arteries in the anterior circulation, as evidenced by MR angiography, were enrolled. Cases with FLAIR changes and controls without FLAIR changes were matched according to the time elapsed from stroke onset to MR study. RESULTS: Among the 130 patients who met the eligibility criteria, 62 (47.7%) had FLAIR changes. The time interval between stroke onset and MR study differed significantly between those with and without FLAIR changes (5.2 hours vs. 3.0 hours). FLAIR changes were more common among males and smokers. Comparisons between cases and controls matched on a one-to-one basis did not reveal any difference in the three signs of cerebral SVD: white-matter hyperintensities, lacunae, and cerebral microbleeds. CONCLUSIONS: This study failed to find any data supporting the hypothesis that cerebral SVD affects FLAIR changes after acute ischemic stroke.
Assuntos
Humanos , Masculino , Angiografia , Biomarcadores , Estudos de Casos e Controles , Artérias Cerebrais , Glicosaminoglicanos , Estudos Prospectivos , Acidente Vascular CerebralRESUMO
No abstract available.
Assuntos
Humanos , Artéria Retiniana , Oclusão da Artéria Retiniana , Fatores de Risco , Acidente Vascular CerebralRESUMO
BACKGROUND AND PURPOSE: The CHADS2 (an acronym for congestive heart failure, hypertension, age > or =75 years, diabetes mellitus, and prior stroke or transient ischemic attack or thromboembolism) score is a widely used system for estimating the risk of stroke in patients with atrial fibrillation. However, how the CHADS2 score is related to stroke severity and outcome in patients with strokes due to atrial fibrillation has not yet been elucidated. METHODS: We enrolled patients with atrial fibrillation who visited our stroke center within 7 days after the onset of acute ischemic stroke between October 2002 and September 2008. CHADS2 scores were categorized into three groups: 0 points, low risk; 1 or 2 points, intermediate risk; and 3-6 points, high risk. Poor neurological state was defined as follows: a National Institutes of Health Stroke Scale (NIHSS) score of > or =2, and a modified Rankin Scale (mRS) score of > or =3 at discharge. Mortality information was ascertained as at December 2008. RESULTS: A cohort of 298 patients with atrial-fibrillation-related stroke was included in this study. A high-risk CHADS2 score at admission was a powerful predictor of poor neurological outcome [for NIHSS: odds ratio (OR), 4.17; 95% confidence interval (CI), 1.76-9.87; for mRS: OR, 2.97; 95% CI, 1.23-7.16] after controlling for all possible confounders. In addition, a high-risk CHADS2 score was an independent predictor of all causes of death during the follow-up [hazard ratio (HR), 3.01; 95% CI, 1.18-7.65] and vascular death (HR, 12.25; 95% CI, 1.50-99.90). CONCLUSIONS: Although the CHADS2 score was originally designed to distinguish patients with a future risk of stroke, our study shows that it may also be used to predict poor neurological outcome after atrial-fibrillation-related stroke.