W Taylor Kimberly1, Bruce C V Campbell2, Felix C Ng2,3, Nawaf Yassi2,4, Gagan Sharma2, Scott B Brown5, Mayank Goyal6, Charles B L M Majoie7, Tudor G Jovin8, Michael D Hill9, Keith W Muir10, Jeffrey L Saver11,12, Francis Guillemin13, Andrew M Demchuk9, Bijoy K Menon9, Luis San Roman14, David S Liebeskind15, Philip White16, Diederik W J Dippel17, Antoni Davalos18, Serge Bracard19, Peter J Mitchell20, Michael J Wald21, Stephen M Davis2, Kevin N Sheth22. 1. Centre for Genomic Medicine, Department of Neurology, Massachusetts General Hospital, Boston (W.T.K.). 2. Department of Medicine and Neurology, Melbourne Brain Centre (F.C.N., N.Y., G.S., S.M.D., B.C.V.C.), Royal Melbourne Hospital, University of Melbourne, Parkville, Australia. 3. Department of Neurology, Austin Health, Heidelberg, Australia (F.C.N.). 4. Population Health and Immunity Division, The Walter and Eliza Hall Institute of Medical Research. Parkville, Australia (N.Y.). 5. Altair Biostatistics, St Louis Park, MN (S.B.B.). 6. Department of Radiology (M.G.), University of Calgary, Foothills Hospital, AB, Canada. 7. Department of Radiology and Nuclear Medicine, Amsterdam University Medical Centers, location AMC, the Netherlands (C.B.L.M.M.). 8. Cooper Neurological Institute, Cooper University Health Care, Camden, NJ (T.G.J.). 9. Department of Clinical Neurosciences, Hotchkiss Brain Institute, Cumming School of Medicine (M.D.H., A.M.D., B.K.M.), University of Calgary, Foothills Hospital, AB, Canada. 10. Institute of Neuroscience and Psychology, University of Glasgow, Queen Elizabeth University Hospital, United Kingdom (K.W.M.). 11. Department of Neurology and Comprehensive Stroke Center, David Geffen School of Medicine (J.L.S.), University of California, Los Angeles. 12. Stanford Stroke Center, Stanford University, CA (J.L.S.). 13. Clinical Investigation Centre-Clinical Epidemiology INSERM 1433, University of Lorraine, University Hospital of Nancy, France (F.G.). 14. Department of Radiology, Hospital Clínic, Barcelona, Spain (L.S.R.). 15. Neurovascular Imaging Research Core, Department of Neurology (D.S.L.), University of California, Los Angeles. 16. Institute of Neuroscience, Newcastle University, Newcastle upon Tyne, United Kingdom (P.W.). 17. Department of Neurology, Erasmus MC University Medical Center, Rotterdam, the Netherlands (D.W.J.D.). 18. Department of Neuroscience, Hospital Germans Trias i Pujol, Universitat Autònoma de Barcelona, Spain (A.D.). 19. Department of Diagnostic and Interventional Neuroradiology, INSERM U 947, University of Lorraine and University Hospital of Nancy, France (S.B.). 20. Department of Radiology (P.J.M.), Royal Melbourne Hospital, University of Melbourne, Parkville, Australia. 21. Biogen, Cambridge, MA (M.J.W.). 22. Department of Neurology, Yale-New Haven Hospital, CT (K.N.S.).
Abstract
Background and Purpose: Whether reperfusion into infarcted tissue exacerbates cerebral edema has treatment implications in patients presenting with extensive irreversible injury. We investigated the effects of endovascular thrombectomy and reperfusion on cerebral edema in patients presenting with radiological evidence of large hemispheric infarction at baseline. Methods: In a systematic review and individual patient-level meta-analysis of 7 randomized controlled trials comparing thrombectomy versus medical therapy in anterior circulation ischemic stroke published between January 1, 2010, and May 31, 2017 (Highly Effective Reperfusion Using Multiple Endovascular Devices collaboration), we analyzed the association between thrombectomy and reperfusion with maximal midline shift (MLS) on follow-up imaging as a measure of the space-occupying effect of cerebral edema in patients with large hemispheric infarction on pretreatment imaging, defined as diffusion-magnetic resonance imaging or computed tomography (CT)-perfusion ischemic core 80 to 300 mL or noncontrast CT-Alberta Stroke Program Early CT Score ≤5. Risk of bias was assessed using the Cochrane tool. Results: Among 1764 patients, 177 presented with large hemispheric infarction. Thrombectomy and reperfusion were associated with functional improvement (thrombectomy common odds ratio =2.30 [95% CI, 1.32–4.00]; reperfusion common odds ratio =4.73 [95% CI, 1.66–13.52]) but not MLS (thrombectomy β=−0.27 [95% CI, −1.52 to 0.98]; reperfusion β=−0.78 [95% CI, −3.07 to 1.50]) when adjusting for age, National Institutes of Health Stroke Score, glucose, and time-to-follow-up imaging. In an exploratory analysis of patients presenting with core volume >130 mL or CT-Alberta Stroke Program Early CT Score ≤3 (n=76), thrombectomy was associated with greater MLS after adjusting for age and National Institutes of Health Stroke Score (β=2.76 [95% CI, 0.33–5.20]) but not functional improvement (odds ratio, 1.71 [95% CI, 0.24–12.08]). Conclusions: In patients presenting with large hemispheric infarction, thrombectomy and reperfusion were not associated with MLS, except in the subgroup with very large core volume (>130 mL) in whom thrombectomy was associated with increased MLS due to space-occupying ischemic edema. Mitigating cerebral edema-mediated secondary injury in patients with very large infarcts may further improve outcomes after reperfusion therapies.
Background and Purpose: Whether reperfusion into infarcted tissue exacerbates cerebral edema has treatment implications in patients presenting with extensive irreversible injury. We investigated the effects of endovascular thrombectomy and reperfusion on cerebral edema in patients presenting with radiological evidence of large hemispheric infarction at baseline. Methods: In a systematic review and individual patient-level meta-analysis of 7 randomized controlled trials comparing thrombectomy versus medical therapy in anterior circulation ischemic stroke published between January 1, 2010, and May 31, 2017 (Highly Effective Reperfusion Using Multiple Endovascular Devices collaboration), we analyzed the association between thrombectomy and reperfusion with maximal midline shift (MLS) on follow-up imaging as a measure of the space-occupying effect of cerebral edema in patients with large hemispheric infarction on pretreatment imaging, defined as diffusion-magnetic resonance imaging or computed tomography (CT)-perfusion ischemic core 80 to 300 mL or noncontrast CT-Alberta Stroke Program Early CT Score ≤5. Risk of bias was assessed using the Cochrane tool. Results: Among 1764 patients, 177 presented with large hemispheric infarction. Thrombectomy and reperfusion were associated with functional improvement (thrombectomy common odds ratio =2.30 [95% CI, 1.32–4.00]; reperfusion common odds ratio =4.73 [95% CI, 1.66–13.52]) but not MLS (thrombectomy β=−0.27 [95% CI, −1.52 to 0.98]; reperfusion β=−0.78 [95% CI, −3.07 to 1.50]) when adjusting for age, National Institutes of Health Stroke Score, glucose, and time-to-follow-up imaging. In an exploratory analysis of patients presenting with core volume >130 mL or CT-Alberta Stroke Program Early CT Score ≤3 (n=76), thrombectomy was associated with greater MLS after adjusting for age and National Institutes of Health Stroke Score (β=2.76 [95% CI, 0.33–5.20]) but not functional improvement (odds ratio, 1.71 [95% CI, 0.24–12.08]). Conclusions: In patients presenting with large hemispheric infarction, thrombectomy and reperfusion were not associated with MLS, except in the subgroup with very large core volume (>130 mL) in whom thrombectomy was associated with increased MLS due to space-occupying ischemic edema. Mitigating cerebral edema-mediated secondary injury in patients with very large infarcts may further improve outcomes after reperfusion therapies.
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