Identifying the ischaemic penumbra using pH-weighted magnetic resonance imaging.
Identifying the ischaemic penumbra using pH-weighted magnetic resonance imaging.
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DOI：
10.1093/brain/awu374
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发表时间：
2015-01
期刊：
影响因子：
--
通讯作者：
Kennedy J
中科院分区：
文献类型：
--
作者：
Harston GW;Tee YK;Blockley N;Okell TW;Thandeswaran S;Shaya G;Sheerin F;Cellerini M;Payne S;Jezzard P;Chappell M;Kennedy J
Harston等人建立了急性缺血性卒中患者临床使用pH加权MRI的原则证据。详细的组织水平的分析表明，脑细胞内的pH值，代谢应激的标志物，与最终的组织结果，并补充建立成像模式。缺血半暗带的最初概念表明，需要对局部脑血流和代谢进行成像，以识别可能受益于干预的组织。酰胺质子转移磁共振成像是一种化学交换饱和转移技术，已被用于推导临床前卒中模型中的脑细胞内pH值，并已被提议作为缺血半暗带的代谢标志物。在这项原理性临床研究中，我们探索了这种pH加权磁共振成像技术在组织水平上的潜力。对来自12例急性缺血性卒中患者的前瞻性队列数据进行了详细的体素分析。缺血核心内的体素比最终梗死的低灌注组织具有更严重的细胞内酸中毒（P < 0.0001），而后者又比存活的低灌注组织具有更严重的酸中毒（P < 0.0001）。此外，当局限于灰质灌注不足时，梗死组织和存活组织的细胞内pH值（P < 0.0001）不同，而脑血流量（P = 0.31）无差异。在呈现的表观扩散系数病变中，具有早期表观扩散病变正常化的组织和具有真正放射学恢复的组织之间的细胞内pH不同。这些发现支持需要进一步研究急性缺血性卒中患者的pH加权成像。
Harston et al. establish proof of principle for clinical use of pH-weighted MRI in patients with acute ischaemic stroke. Detailed tissue-level analysis reveals that cerebral intracellular pH, a marker of metabolic stress, is associated with eventual tissue outcome, and complements established imaging modalities. The original concept of the ischaemic penumbra suggested imaging of regional cerebral blood flow and metabolism would be required to identify tissue that may benefit from intervention. Amide proton transfer magnetic resonance imaging, a chemical exchange saturation transfer technique, has been used to derive cerebral intracellular pH in preclinical stroke models and has been proposed as a metabolic marker of ischaemic penumbra. In this proof of principle clinical study, we explored the potential of this pH-weighted magnetic resonance imaging technique at tissue-level. Detailed voxel-wise analysis was performed on data from a prospective cohort of 12 patients with acute ischaemic stroke. Voxels within ischaemic core had a more severe intracellular acidosis than hypoperfused tissue recruited to the final infarct (P < 0.0001), which in turn was more acidotic than hypoperfused tissue that survived (P < 0.0001). In addition, when confined to the grey matter perfusion deficit, intracellular pH (P < 0.0001), but not cerebral blood flow (P = 0.31), differed between tissue that infarcted and tissue that survived. Within the presenting apparent diffusion coefficient lesion, intracellular pH differed between tissue with early apparent diffusion lesion pseudonormalization and tissue with true radiographic recovery. These findings support the need for further investigation of pH-weighted imaging in patients with acute ischaemic stroke.
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