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Blood-oxygen-level-dependent MRI allows metabolic description of tissue at risk in acute stroke patients.
BACKGROUND AND PURPOSE: The delineation of the "penumbra" is of particular interest in acute stroke imaging. The "mismatch concept" applying perfusion-weighted imaging (PWI) and diffusion-weighted imaging (DWI) appears to be an oversimplification of the underlying electrophysiological tissue status. An additional parameter reflecting the metabolic state of the threatened brain tissue would improve our ability to describe the penumbra. One candidate is deoxyhemoglobin (deoxy-Hb) as an indicator of the oxygen extraction fraction that can be visualized by T2*-based blood oxygen level-dependent (BOLD) imaging.
METHODS: We analyzed data from 32 patients with acute stroke in the territory of the middle cerebral artery. MRI included fluid-attenuated inversion recovery, DWI, PWI, time-of-flight angiography, and quantitative T2 and T2* (qT2, qT2*) imaging. Follow-up was performed on day 1 and days 5 to 8. We calculated 1/T2'=1/qT2*-1/qT2. Changes of T2', representing the deoxy-Hb effect, were analyzed by 3D regions of interest (ROIs): apparent diffusion coefficient lesion day 0 (L0), time-to-peak-lesion day 0 (T0), final infarct size days 5 to 8 (F5-8), lesion growth (LG; F5-8-L0), and surviving tissue (ST; T0-F5-8).
RESULTS: We observed a clear decrease of T2' in the infarcted hemisphere compared with the unaffected control ROIs. The mean value showed the most pronounced loss of T2' signal intensity in L0 (-15.7%), followed by LG (-10.5%) and ST (-8.0%).
CONCLUSIONS: The implementation of BOLD imaging in acute stroke MRI offers a noninvasive estimation of the O2 utilization and is able to add additional information concerning the present metabolic state of the threatened brain tissue. The changes in T2' intensity are visually noticeable in the reconstructed T2' images and provide a better estimation of the real penumbra.
METHODS: We analyzed data from 32 patients with acute stroke in the territory of the middle cerebral artery. MRI included fluid-attenuated inversion recovery, DWI, PWI, time-of-flight angiography, and quantitative T2 and T2* (qT2, qT2*) imaging. Follow-up was performed on day 1 and days 5 to 8. We calculated 1/T2'=1/qT2*-1/qT2. Changes of T2', representing the deoxy-Hb effect, were analyzed by 3D regions of interest (ROIs): apparent diffusion coefficient lesion day 0 (L0), time-to-peak-lesion day 0 (T0), final infarct size days 5 to 8 (F5-8), lesion growth (LG; F5-8-L0), and surviving tissue (ST; T0-F5-8).
RESULTS: We observed a clear decrease of T2' in the infarcted hemisphere compared with the unaffected control ROIs. The mean value showed the most pronounced loss of T2' signal intensity in L0 (-15.7%), followed by LG (-10.5%) and ST (-8.0%).
CONCLUSIONS: The implementation of BOLD imaging in acute stroke MRI offers a noninvasive estimation of the O2 utilization and is able to add additional information concerning the present metabolic state of the threatened brain tissue. The changes in T2' intensity are visually noticeable in the reconstructed T2' images and provide a better estimation of the real penumbra.
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