Carolyn A Lomahan, Georgios Kalarakis, Marie Luby, Staffan Holmin, Johan Lundberg, Michael V Mazya, Lawrence L Latour, Fabian Arnberg-Sandor
{"title":"EXPRESS: Cerebral blood flow-oxygen metabolism uncoupling at 24 hours after stroke thrombectomy.","authors":"Carolyn A Lomahan, Georgios Kalarakis, Marie Luby, Staffan Holmin, Johan Lundberg, Michael V Mazya, Lawrence L Latour, Fabian Arnberg-Sandor","doi":"10.1177/0271678X261501263","DOIUrl":null,"url":null,"abstract":"<p><p>BackgroundFollowing successful endovascular therapy (EVT) for acute ischemic stroke, tissue with abnormal perfusion may have impaired oxygen extraction and metabolism. MRI model-based oxygen extraction fraction (OEFmax) and cerebral metabolic rate of oxygen (CMRO2) were characterized in hypoperfusion and hyperemia regions 24 hours post-EVT.MethodsEighty-four patients were included with anterior circulation vessel occlusion, successful recanalization, and an MRI at 24 hours post-EVT. Time-to-maximum (Tmax) and cerebral blood flow (CBF) were evaluated for hypoperfusion and hyperemia. CBF, OEFmax, and CMRO2 were quantified using i) segmentation-based and ii) single slice region of interest (ROI) analyses. Normalized CBF, OEFmax, and CMRO2 were calculated by dividing the segmentation or ROI value by the contralateral value.ResultsSixty-seven (80%) patients had abnormal perfusion; hypoperfusion in 22 (26%), hyperemia in 36 (43%), and both in 9 (11%). Compared to control, hypoperfused regions demonstrated a 62% CBF decrease, 52% CMRO2 decrease, and 68% OEFmax increase (p<0.01). Hyperemic regions demonstrated a 58% CBF increase, 26% CMRO2 increase, and 25% OEFmax decrease (p<0.01). Hyperemia had no significant correlation between normalized CBF and CMRO2 (p=0.14).ConclusionHyperemia regions demonstrated cerebral blood flow-oxygen metabolism uncoupling, suggesting the underlying mechanism as loss of cerebrovascular autoregulation rather than hypermetabolic demand.</p>","PeriodicalId":520660,"journal":{"name":"Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism","volume":" ","pages":"271678X261501263"},"PeriodicalIF":4.5000,"publicationDate":"2026-10-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1177/0271678X261501263","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
BackgroundFollowing successful endovascular therapy (EVT) for acute ischemic stroke, tissue with abnormal perfusion may have impaired oxygen extraction and metabolism. MRI model-based oxygen extraction fraction (OEFmax) and cerebral metabolic rate of oxygen (CMRO2) were characterized in hypoperfusion and hyperemia regions 24 hours post-EVT.MethodsEighty-four patients were included with anterior circulation vessel occlusion, successful recanalization, and an MRI at 24 hours post-EVT. Time-to-maximum (Tmax) and cerebral blood flow (CBF) were evaluated for hypoperfusion and hyperemia. CBF, OEFmax, and CMRO2 were quantified using i) segmentation-based and ii) single slice region of interest (ROI) analyses. Normalized CBF, OEFmax, and CMRO2 were calculated by dividing the segmentation or ROI value by the contralateral value.ResultsSixty-seven (80%) patients had abnormal perfusion; hypoperfusion in 22 (26%), hyperemia in 36 (43%), and both in 9 (11%). Compared to control, hypoperfused regions demonstrated a 62% CBF decrease, 52% CMRO2 decrease, and 68% OEFmax increase (p<0.01). Hyperemic regions demonstrated a 58% CBF increase, 26% CMRO2 increase, and 25% OEFmax decrease (p<0.01). Hyperemia had no significant correlation between normalized CBF and CMRO2 (p=0.14).ConclusionHyperemia regions demonstrated cerebral blood flow-oxygen metabolism uncoupling, suggesting the underlying mechanism as loss of cerebrovascular autoregulation rather than hypermetabolic demand.