Athinoula A. Martinos Center for Biomedical Imaging, Department of Radiology, Massachusetts General Hospital, Charlestown, MA, USA.
Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Ann Neurol. 2023 Dec;94(6):1155-1163. doi: 10.1002/ana.26785. Epub 2023 Sep 22.
Functional and morphologic changes in extracranial organs can occur after acute brain injury. The neuroanatomic correlates of such changes are not fully known. Herein, we tested the hypothesis that brain infarcts are associated with cardiac and systemic abnormalities (CSAs) in a regionally specific manner.
We generated voxelwise p value maps of brain infarcts for poststroke plasma cardiac troponin T (cTnT) elevation, QTc prolongation, in-hospital infection, and acute stress hyperglycemia (ASH) in 1,208 acute ischemic stroke patients prospectively recruited into the Heart-Brain Interactions Study. We examined the relationship between infarct location and CSAs using a permutation-based approach and identified clusters of contiguous voxels associated with p < 0.05.
cTnT elevation not attributable to a known cardiac reason was detected in 5.5%, QTc prolongation in the absence of a known provoker in 21.2%, ASH in 33.9%, and poststroke infection in 13.6%. We identified significant, spatially segregated voxel clusters for each CSA. The clusters for troponin elevation and QTc prolongation mapped to the right hemisphere. There were 3 clusters for ASH, the largest of which was in the left hemisphere. We found 2 clusters for poststroke infection, one associated with pneumonia in the left and one with urinary tract infection in the right hemisphere. The relationship between infarct location and CSAs persisted after adjusting for infarct volume.
Our results show that there are discrete regions of brain infarcts associated with CSAs. This information could be used to bootstrap toward new markers for better differentiation between neurogenic and non-neurogenic mechanisms of poststroke CSAs. ANN NEUROL 2023;94:1155-1163.
急性脑损伤后,颅外器官可能会发生功能和形态变化。这些变化的神经解剖学相关性尚不完全清楚。在此,我们假设脑梗死与心脏和全身异常(CSAs)具有区域特异性相关,并对此进行了测试。
我们对前瞻性纳入的 1208 例急性缺血性脑卒中患者的心脏-脑相互作用研究中,脑卒后血浆心肌肌钙蛋白 T(cTnT)升高、QTc 延长、住院感染和急性应激性高血糖(ASH)的脑梗死患者进行了基于体素的脑梗死 p 值图生成。我们使用基于置换的方法,研究了梗死部位与 CSAs 之间的关系,并确定了与 p<0.05 相关的连续体素簇。
5.5%的患者检测到不能归因于已知心脏原因的 cTnT 升高,21.2%的患者出现无已知诱因的 QTc 延长,33.9%的患者出现 ASH,13.6%的患者出现卒中后感染。我们确定了每个 CSA 的显著、空间分离的体素簇。cTnT 升高和 QTc 延长的簇映射到右侧半球。有 3 个与 ASH 相关的簇,其中最大的簇位于左侧半球。我们发现了 2 个卒中后感染的簇,一个与左侧肺炎有关,一个与右侧尿路感染有关。在调整了梗死体积后,梗死部位与 CSAs 之间的关系仍然存在。
我们的研究结果表明,脑梗死存在与 CSAs 相关的离散区域。这些信息可用于引导开发新的标志物,以更好地区分卒中后 CSAs 的神经源性和非神经源性机制。