MRI-Derived Patterns of Post-Cardiac Arrest Brain Injury: Linking Anatomical Injury and Cerebrovascular Physiology
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Introduction
Post-cardiac arrest brain injury (PCABI) patterns across patients are heterogeneous, and conventional clinical variables incompletely capture in vivo injury severity. Here, we evaluated whether anatomically resolved diffusion-weighted MRI (DWI) lesion patterns identify biologically distinct PCABI phenotypes.
Methods
We conducted a retrospective study of patients with PCABI who underwent brain MRI and intraparenchymal brain tissue oxygen tension (PbtO 2 ) monitoring (n = 24). Ischemic lesion burden was quantified using an MNI atlas-based apparent diffusion coefficient pipeline with a voxel intensity threshold of <650×10 -6 mm²/s and was summarized at whole-brain, hemispheric, tissue-class, and segment-levels. Principal component analysis (PCA) and k-means clustering were used to identify MRI- derived injury patterns for downstream physiological analysis.
Results
Greater whole-brain lesion burden was associated with lower mean PbtO 2 (r = -0.49, p = 0.014), with concurrent associations in the left hemisphere (r = -0.50, p = 0.012), right hemisphere (r = -0.48, p = 0.019), grey matter (r = -0.48, p = 0.018), and white matter (r = -0.49, p = 0.016). PCA identified a dominant lesion-pattern axis associated with PbtO 2 (r = 0.48, p = 0.0169). K-means clustering in PC1- PC2 space identified three MRI-derived injury patterns with distinct regional signatures and progressively greater whole-brain lesion burden (p < 0.001).
Discussion
Greater MRI-defined lesion burden was associated with lower PbtO 2 post-cardiac arrest. Anatomically resolved DWI/ADC lesion mapping identified three MRI-derived injury patterns that differed in cerebrovascular physiology, lesion patterning and whole-brain injury burden. Integrating quantitative MRI, intraparenchymal neuromonitoring, and blood biomarkers improved the characterization of the heterogeneity observed in PCABI patients.
HIGHLIGHTS
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Atlas DWI/ADC mapping identified three MRI-derived injury patterns.
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MRI-derived patterns captured regional injury beyond whole-brain burden.
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Greater ischemic lesion burden was associated with lower PbtO 2 .
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MRI-derived patterns differed in PbtO 2 and selected biomarkers.
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Brain injury patterns were not explained by admission physiology nor time to ROSC.
