Longting Lin1,2, Jianhong Yang1, Chushuang Chen2, Huiqiao Tian2, Andrew Bivard3, Neil J Spratt2, Christopher R Levi2,4, Mark W Parsons5,3. 1. Department of Neurology, Ningbo First Hospital, Ningbo, China. 2. School of Medicine and Public Health, University of Newcastle, Newcastle, Australia. 3. Melbourne Brain Centre@Royal Melbourne Hospital, University of Melbourne, Melbourne, Australia. 4. The Sydney Partnership for Health, Education, Research and Enterprise, Sydney, Australia. 5. School of Medicine and Public Health, University of Newcastle, Newcastle, Australia markp@unimelb.edu.au.
Abstract
OBJECTIVE: To test the hypothesis that acute ischemic patients with poorer collaterals would have faster ischemic core growth, we included 2 cohorts in the study, cohort 1 of 342 patients for derivation and cohort 2 of 414 patients for validation purpose. METHODS: Acute ischemic stroke patients with large vessel occlusion were included. Core growth rate was calculated by the following equation: Core growth rate = Acute core volume on CTP/Time from stroke onset to CTP. Collateral status was assessed by the ratio of severe hypoperfusion volume within the hypoperfusion region of CTP. The CTP collateral index was categorized in tertiles; for each tertile, core growth rate was summarized as median and inter-quartile range. Simple linear regressions were then performed to measure the predictive power of CTP collateral index in core growth rate. RESULTS: For patients allocated to good collateral on CT perfusion (tertile 1 of collateral index), moderate collateral (tertile 2), and poor collateral (tertile 3), the median core growth rate was 2.93 mL/h (1.10-7.94), 8.65 mL/h (4.53-18.13), and 25.41 mL/h (12.83-45.07) respectively. Increments in the collateral index by 1% resulted in an increase of core growth by 0.57 mL/h (coefficient = 0.57, 95% confidence interval = [0.46, 0.68], p < 0.001). The relationship of core growth and CTP collateral index was validated in cohort 2. An increment in collateral index by 1% resulted in an increase of core growth by 0.59 mL/h (coefficient = 0.59 [0.48-0.71], p < 0.001) in cohort 2. CONCLUSION: Collateral status is a major determinant of ischemic core growth.
OBJECTIVE: To test the hypothesis that acute ischemicpatients with poorer collaterals would have faster ischemic core growth, we included 2 cohorts in the study, cohort 1 of 342 patients for derivation and cohort 2 of 414 patients for validation purpose. METHODS: Acute ischemic strokepatients with large vessel occlusion were included. Core growth rate was calculated by the following equation: Core growth rate = Acute core volume on CTP/Time from stroke onset to CTP. Collateral status was assessed by the ratio of severe hypoperfusion volume within the hypoperfusion region of CTP. The CTP collateral index was categorized in tertiles; for each tertile, core growth rate was summarized as median and inter-quartile range. Simple linear regressions were then performed to measure the predictive power of CTP collateral index in core growth rate. RESULTS: For patients allocated to good collateral on CT perfusion (tertile 1 of collateral index), moderate collateral (tertile 2), and poor collateral (tertile 3), the median core growth rate was 2.93 mL/h (1.10-7.94), 8.65 mL/h (4.53-18.13), and 25.41 mL/h (12.83-45.07) respectively. Increments in the collateral index by 1% resulted in an increase of core growth by 0.57 mL/h (coefficient = 0.57, 95% confidence interval = [0.46, 0.68], p < 0.001). The relationship of core growth and CTP collateral index was validated in cohort 2. An increment in collateral index by 1% resulted in an increase of core growth by 0.59 mL/h (coefficient = 0.59 [0.48-0.71], p < 0.001) in cohort 2. CONCLUSION: Collateral status is a major determinant of ischemic core growth.
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