Richard Leigh1, Shyian S Jen2, Argye E Hillis2, John W Krakauer2, Peter B Barker2. 1. From the Departments of Neurology and Radiology (R.L.), Neurology, Physical Medicine and Rehabilitation and Cognitive Science (A.E.H.), Neurology and Neuroscience (J.W.K.), and Radiology (P.B.B.), Johns Hopkins University, Baltimore, MD; and Department of Radiology, Emory University, Atlanta, GA (S.S.J.). rleigh4@jhu.edu. 2. From the Departments of Neurology and Radiology (R.L.), Neurology, Physical Medicine and Rehabilitation and Cognitive Science (A.E.H.), Neurology and Neuroscience (J.W.K.), and Radiology (P.B.B.), Johns Hopkins University, Baltimore, MD; and Department of Radiology, Emory University, Atlanta, GA (S.S.J.).
Abstract
BACKGROUND AND PURPOSE: Early blood-brain barrier damage after acute ischemic stroke has previously been qualitatively linked to subsequent intracranial hemorrhage (ICH). In this quantitative study, it was investigated whether the amount of blood-brain barrier damage evident on pre-tissue-type plasminogen activator MRI scans was related to the degree of post-tissue-type plasminogen activator ICH in patients with acute ischemic stroke. METHODS: Analysis was performed on a database of patients with acute ischemic stroke provided by the Stroke Imaging Repository (STIR) and Virtual International Stroke Trials Archive (VISTA) Imaging Investigators. Patients with perfusion-weighted imaging lesions>10 mL and negative gradient-recalled echo imaging before intravenous tissue-type plasminogen activator were included. Postprocessing of the perfusion-weighted imaging source images was performed to estimate changes in blood-brain barrier permeability within the perfusion deficit relative to the unaffected hemisphere. Follow-up gradient-recalled echo images were reviewed for evidence of ICH and divided into 3 groups according to European Cooperative Acute Stroke Study (ECASS) criteria: no hemorrhage, hemorrhagic infarction, and parenchymal hematoma. RESULTS: Seventy-five patients from the database met the inclusion criteria, 28 of whom experienced ICH, of which 19 were classified as hemorrhagic infarction and 9 were classified as parenchymal hematoma. The mean permeability (±SDs), expressed as an index of contrast leakage, was 17.0±8.8% in the no hemorrhage group, 19.4±4.0% in the hemorrhagic infarction group, and 24.6±4.5% in the parenchymal hematoma group. Permeability was significantly correlated with ICH grade in univariate (P=0.007) and multivariate (P=0.008) linear regression modeling. CONCLUSIONS: A perfusion-weighted imaging-derived index of blood-brain barrier damage measured before intravenous tissue-type plasminogen activator is given is associated with the severity of ICH after treatment in patients with acute ischemic stroke.
BACKGROUND AND PURPOSE: Early blood-brain barrier damage after acute ischemic stroke has previously been qualitatively linked to subsequent intracranial hemorrhage (ICH). In this quantitative study, it was investigated whether the amount of blood-brain barrier damage evident on pre-tissue-type plasminogen activator MRI scans was related to the degree of post-tissue-type plasminogen activatorICH in patients with acute ischemic stroke. METHODS: Analysis was performed on a database of patients with acute ischemic stroke provided by the Stroke Imaging Repository (STIR) and Virtual International Stroke Trials Archive (VISTA) Imaging Investigators. Patients with perfusion-weighted imaging lesions>10 mL and negative gradient-recalled echo imaging before intravenous tissue-type plasminogen activator were included. Postprocessing of the perfusion-weighted imaging source images was performed to estimate changes in blood-brain barrier permeability within the perfusion deficit relative to the unaffected hemisphere. Follow-up gradient-recalled echo images were reviewed for evidence of ICH and divided into 3 groups according to European Cooperative Acute Stroke Study (ECASS) criteria: no hemorrhage, hemorrhagic infarction, and parenchymal hematoma. RESULTS: Seventy-five patients from the database met the inclusion criteria, 28 of whom experienced ICH, of which 19 were classified as hemorrhagic infarction and 9 were classified as parenchymal hematoma. The mean permeability (±SDs), expressed as an index of contrast leakage, was 17.0±8.8% in the no hemorrhage group, 19.4±4.0% in the hemorrhagic infarction group, and 24.6±4.5% in the parenchymal hematoma group. Permeability was significantly correlated with ICH grade in univariate (P=0.007) and multivariate (P=0.008) linear regression modeling. CONCLUSIONS: A perfusion-weighted imaging-derived index of blood-brain barrier damage measured before intravenous tissue-type plasminogen activator is given is associated with the severity of ICH after treatment in patients with acute ischemic stroke.
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