Hyperoxia-Induced ¥ÄR1: MRI Biomarker of Histological Infarction in Acute Cerebral Stroke

Korean Journal of Radiology 2022³â 23±Ç 4È£ p.446 ~ p.454

¹Ú°èÁø(Park Kye-Jin) - University of Ulsan College of Medicine Asan Medical Center Department of Radiology
¼­Áö¿¬(Suh Ji-Yeon) - University of Ulsan College of Medicine Asan Medical Center Asan Institute for Medical Sciences
Çãâȸ(Heo Chang-Hoe) - University of Ulsan College of Medicine Asan Medical Center Asan Institute for Medical Sciences
±è¹Ì¿¬(Kim Mi-Yeon) - University of Ulsan College of Medicine Asan Medical Center Asan Institute for Medical Sciences
¹éÁøÈñ(Baek Jin-Hee) - University of Ulsan College of Medicine Asan Medical Center Asan Institute for Medical Sciences
±èÁ¤°ï(Kim Jeong-Kon) - University of Ulsan College of Medicine Asan Medical Center Department of Radiology

Abstract

Objective: To evaluate whether hyperoxia-induced ¥ÄR1 (hyperO2¥ÄR1) can accurately identify histological infarction in an acute cerebral stroke model.

Materials and Methods: In 18 rats, MRI parameters, including hyperO2¥ÄR1, apparent diffusion coefficient (ADC), cerebral blood flow and volume, and 18F-fluorodeoxyglucose uptake on PET were measured 2.5, 4.5, and 6.5 hours after a 60-minutes occlusion of the right middle cerebral artery. Histological examination of the brain was performed immediately following the imaging studies. MRI and PET images were co-registered with digitized histological images. The ipsilateral hemisphere was divided into histological infarct (histological cell death), non-infarct ischemic (no cell death but ADC decrease), and non-ischemic (no cell death or ADC decrease) areas for comparisons of imaging parameters. The levels of hyperO2¥ÄR1 and ADC were measured voxel-wise from the infarct core to the non-ischemic region. The correlation between areas of hyperO2¥ÄR1-derived infarction and histological cell death was evaluated.

Results: HyperO2¥ÄR1 increased only in the infarct area (p ¡Â 0.046) compared to the other areas. ADC decreased stepwise from non-ischemic to infarct areas (p = 0.002 at all time points). The other parameters did not show consistent differences among the three areas across the three time points. HyperO2¥ÄR1 sharply declined from the core to the border of the infarct areas, whereas there was no change within the non-infarct areas. A hyperO2¥ÄR1 value of 0.04 s-1 was considered the criterion to identify histological infarction. ADC increased gradually from the infarct core to the periphery, without a pronounced difference at the border between the infarct and non-infarct areas. Areas of hyperO2¥ÄR1 higher than 0.04 s-1 on MRI were strongly positively correlated with histological cell death (r = 0.862; p < 0.001).

Conclusion: HyperO2¥ÄR1 may be used as an accurate and early (2.5 hours after onset) indicator of histological infarction in acute stroke.

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MRI, Acute stroke, Infarction, Biomarker, Hyperoxia-induced ¥ÄR1
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MRI-driven hyperO2¥ÄR1 above 0.04 s-1 delineated areas with histological cell death 2.5 hours after stroke onset.
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