Please use this identifier to cite or link to this item: https://repository.southwesthealthcare.com.au/swhealthcarejspui/handle/1/3849
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dc.contributor.authorNg, Felix C.-
dc.contributor.authorChurilov, Leonid-
dc.contributor.authorYassi, Nawaf-
dc.contributor.authorKleinig, Timothy J.-
dc.contributor.authorThijs, Vincent-
dc.contributor.authorWu, Teddy Y.-
dc.contributor.authorShah, Darshan G..-
dc.contributor.authorDewey, Helen M.-
dc.contributor.authorSharma, Gagan-
dc.contributor.authorDesmond, Patricia M.-
dc.contributor.authorYan, Bernard-
dc.contributor.authorParsons, Mark W.-
dc.contributor.authorDonnan, Geoffrey A.-
dc.contributor.authorDavis, Stephen M.-
dc.contributor.authorMitchell, Peter J.-
dc.contributor.authorLeigh, Richard-
dc.contributor.authorCampbell, Bruce C. V.-
dc.contributor.authorPart, EXTEND-IA TNK-
dc.contributor.authorInvestigators-
dc.date.accessioned2023-04-24T02:44:21Z-
dc.date.available2023-04-24T02:44:21Z-
dc.date.issued2022-05-
dc.identifier.urihttps://repository.southwesthealthcare.com.au/swhealthcarejspui/handle/1/3849-
dc.description.abstractBACKGROUND: Factors contributing to cerebral edema in the post-hyperacute period of ischemic stroke (first 24-72 hours) are poorly understood. Blood-brain barrier (BBB) disruption and postischemic hyperperfusion reflect microvascular dysfunction and are associated with hemorrhagic transformation. We investigated the relationships between BBB integrity, cerebral blood flow, and space-occupying cerebral edema in patients who received acute reperfusion therapy. METHODS: We performed a pooled analysis of patients treated for anterior circulation large vessel occlusion in the EXTEND-IA TNK and EXTEND-IA TNK part 2 trials who had MRI with dynamic susceptibility contrast-enhanced perfusion-weighted imaging 24 hours after treatment. We investigated the associations between BBB disruption and cerebral blood flow within the infarct with cerebral edema assessed using 2 metrics: first midline shift (MLS) trichotomized as an ordinal scale of negligible (<1 mm), mild (>/=1 to <5 mm), or severe (>/=5 mm), and second relative hemispheric volume (rHV), defined as the ratio of the 3-dimensional volume of the ischemic hemisphere relative to the contralateral hemisphere. RESULTS: Of 238 patients analyzed, 133 (55.9%) had negligible, 93 (39.1%) mild, and 12 (5.0%) severe MLS at 24 hours. The associated median rHV was 1.01 (IQR, 1.00-1.028), 1.03 (IQR, 1.01-1.077), and 1.15 (IQR, 1.08-1.22), respectively. MLS and rHV were associated with poor functional outcome at 90 days (P<0.002). Increased BBB permeability was independently associated with more edema after adjusting for age, occlusion location, reperfusion, parenchymal hematoma, and thrombolytic agent used (MLS cOR, 1.12 [95% CI, 1.03-1.20], P=0.005; rHV beta, 0.39 [95% CI, 0.24-0.55], P<0.0001), as was reduced cerebral blood flow (MLS cOR, 0.25 [95% CI, 0.10-0.58], P=0.001; rHV beta, -2.95 [95% CI, -4.61 to -11.29], P=0.0006). In subgroup analysis of patients with successful reperfusion (extended Treatment in Cerebral Ischemia 2b-3, n=200), reduced cerebral blood flow remained significantly associated with edema (MLS cOR, 0.37 [95% CI, 0.14-0.98], P=0.045; rHV beta, -2.59 [95% CI, -4.32 to -0.86], P=0.004). CONCLUSIONS: BBB disruption and persistent hypoperfusion in the infarct after reperfusion treatment is associated with space-occupying cerebral edema. Further studies evaluating microvascular dysfunction during the post-hyperacute period as biomarkers of poststroke edema and potential therapeutic targets are warranted.-
dc.relation.isversionof20211223-
dc.subjectBlood-Brain Barrier-
dc.subjectBrain Edema-
dc.subjectBrain Ischemia-
dc.subjectCerebral Infarction-
dc.subjectCerebrovascular Circulation-
dc.subjectHumans-
dc.subjectBlood-Brain Barrier-
dc.subjectHematoma-
dc.subjectMagnetic Resonance Imaging-
dc.subjectPerfusion-
dc.subjectPermeability-
dc.titleMicrovascular Dysfunction in Blood-Brain Barrier Disruption and Hypoperfusion Within the Infarct Posttreatment Are Associated With Cerebral Edema-
dc.typeJournal Article-
dc.identifier.journaltitleStroke-
dc.accession.number34937423-
dc.identifier.urlhttps://www.ncbi.nlm.nih.gov/pubmed/34937423-
dc.description.affiliationDepartment of Medicine and Neurology, Melbourne Brain Centre at the Royal Melbourne Hospital, University of Melbourne, Parkville, Australia (F.C.N., L.C., N.Y., G.S., B.Y., M.W.P., G.A.D., S.M.D., B.C.V.C.).-
dc.description.affiliationThe Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Australia (F.C.N., V.T.).-
dc.description.affiliationDepartment of Neurology, Austin Hospital, Austin Health, Heidelberg, Australia (L.C., V.T., B.C.V.C.).-
dc.description.affiliationMelbourne Medical School, The University of Melbourne, Heidelberg, Australia (L.C.).-
dc.description.affiliationPopulation Health and Immunity Division. The Walter and Eliza Hall Institute of Medical Research. Parkville, Australia (N.Y.).-
dc.description.affiliationDepartment of Neurology, Royal Adelaide Hospital, Australia (T.J.K.).-
dc.description.affiliationDepartment of Neurology, Christchurch Hospital, New Zealand (T.Y.W.).-
dc.description.affiliationDepartment of Neurology, Princess Alexandra Hospital, Brisbane, Australia (D.G.S.).-
dc.description.affiliationEastern Health and Eastern Health Clinical School, Department of Neurosciences, Monash University, Clayton, Australia (H.M.D.).-
dc.description.affiliationDepartment of Radiology, Royal Melbourne Hospital, University of Melbourne, Parkville, Australia (P.M.D., B.Y., P.J.M.).-
dc.description.affiliationDepartment of Neurology, John Hopkins University, Baltimore, MD (R.L.).-
dc.format.startpage1597-1605-
dc.source.volume53-
local.issue.number5-
dc.identifier.notesMeta-Analysis-
dc.identifier.importdoi10.1161/STROKEAHA.121.036104-
dc.identifier.dateMay-
dc.identifier.date2022-
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