Marcelo Marinho de Figueiredo1, Edson Amaro Júnior2, Maramélia Araújo de Miranda Alves3, Marcela Vazzoler4, Renata Carolina Acre Nunes Miranda4, Gisele Sampaio Silva5. 1. Department of Neurology and Neurosurgery, Universidade Federal de São Paulo, São Paulo, Brazil. Electronic address: marcelomarinho1@yahoo.com.br. 2. Hospital Israelita Albert Einstein, São Paulo, Brazil; Department of Radiology, University of Sao Paulo Medical School, Sao Paulo, Brazil. 3. Department of Neurology and Neurosurgery, Universidade Federal de São Paulo, São Paulo, Brazil. 4. Hospital Israelita Albert Einstein, São Paulo, Brazil. 5. Department of Neurology and Neurosurgery, Universidade Federal de São Paulo, São Paulo, Brazil; Hospital Israelita Albert Einstein, São Paulo, Brazil.
Abstract
BACKGROUND: Fluid-attenuated inversion recovery (FLAIR) vascular hyperintensities (FVHs) are common in patients with acute ischemic stroke, possibly representing impaired hemodynamics in the ischemic territory due to intracranial steno-occlusive disease. There are few reports on FVHs in patients with transient ischemic attack (TIA). AIMS: We investigated the prevalence of FVHs and its clinical correlations in patients with TIA. METHODS: We evaluated consecutive patients admitted with TIA from February 2009 to June 2012 who had undergone magnetic resonance imaging within 30 hours of symptoms onset and intracranial and extracranial vascular imaging. Two independent neuroradiologists determined the presence of FVHs. We assessed the relationship between FVHs, clinical presentation, vascular risk factors, neuroimaging characteristics, and the presence of large artery stenosis or occlusion. RESULTS: Seventy-two patients with TIA were evaluated. FVHs were present in 12 (16.7%) patients. The overall agreement between examiners was good (κ = .67). There were no differences in the frequency of intracranial or cervical arterial stenosis in patients with and without FVH. In a multivariate logistic regression analysis including atrial fibrillation (AF), congestive heart failure, and diabetes, only AF remained in the final model. CONCLUSIONS: FVH signals on FLAIR images occur in patients with TIA and might correlate with clinical variables like AF and not only with large vessel occlusion. The presence of FVH in patients with TIA and AF might be a surrogate marker for a large vessel occlusion spontaneously recanalized or for impaired autoregulation in a previously ischemic vascular territory.
BACKGROUND: Fluid-attenuated inversion recovery (FLAIR) vascular hyperintensities (FVHs) are common in patients with acute ischemic stroke, possibly representing impaired hemodynamics in the ischemic territory due to intracranial steno-occlusive disease. There are few reports on FVHs in patients with transient ischemic attack (TIA). AIMS: We investigated the prevalence of FVHs and its clinical correlations in patients with TIA. METHODS: We evaluated consecutive patients admitted with TIA from February 2009 to June 2012 who had undergone magnetic resonance imaging within 30 hours of symptoms onset and intracranial and extracranial vascular imaging. Two independent neuroradiologists determined the presence of FVHs. We assessed the relationship between FVHs, clinical presentation, vascular risk factors, neuroimaging characteristics, and the presence of large artery stenosis or occlusion. RESULTS: Seventy-two patients with TIA were evaluated. FVHs were present in 12 (16.7%) patients. The overall agreement between examiners was good (κ = .67). There were no differences in the frequency of intracranial or cervical arterial stenosis in patients with and without FVH. In a multivariate logistic regression analysis including atrial fibrillation (AF), congestive heart failure, and diabetes, only AF remained in the final model. CONCLUSIONS: FVH signals on FLAIR images occur in patients with TIA and might correlate with clinical variables like AF and not only with large vessel occlusion. The presence of FVH in patients with TIA and AF might be a surrogate marker for a large vessel occlusion spontaneously recanalized or for impaired autoregulation in a previously ischemic vascular territory.