虚血性脳卒中における時間的イメージングダイナミクス：強度指標 vs. 体積指標

The fate of ischemic tissue following a thromboembolic occlusion depends on the degree of hypoperfusion and the time from stroke onset to reperfusion. Little is known about the temporal dynamics of hypoperfusion and tissue damage. In this cross-sectional study, we compared how onset-to-imaging time is associated with volumetric versus intensity-based imaging markers.

We retrospectively analyzed acute stroke imaging from 288 CT and 275 MR examinations. Hypoperfusion and infarct core were estimated using the VEOcore software based on standard thresholds (Tmax > 6s, CBF < 30% or ADC < 620 × 10^-6 mm²/s). Tissue damage was quantified on NCCT using software-assisted ASPECTS, and contralaterally normalized signal intensities (NCCT HU, ADC, DWI-b0, DWI-b1000, CBF, Tmax) within the estimated infarct core. Associations with onset-to-imaging time were evaluated using multivariable linear regression adjusting for age, sex, occlusion site and MR field strength.

CT patients were older (77 [65-83] vs. 72 [63-80] years, p<0.001) and imaged earlier (86 [64-149] vs. 102 [97-193] min, p<0.001) than MRI patients. Hypoperfusion and infarct core volumes were larger on CT (143 [96-189] vs 90 [40-156] mL; 24 [12-48] vs 17 [8-35] mL; both p<0.001). After adjustment, volumetric measures showed limited time-dependence: ASPECTS decreased by -0.33 points/h (p < 0.001) and ADC-core volume increased by +1.8 mL/h (p = 0.01), while perfusion volumes (CBF<30%, Tmax>6s, Tmax>10s) showed no significant change. Intensity measures changed markedly with time: NCCT intensity decreased by -1.1%/h (p < 0.001), ADC intensity by -0.69%/h (p = 0.001), whereas DWI-b0 increased by +2.3%/h and DWI-b1000 by +4.9%/h (both p < 0.001). Perfusion-based intensities were not significantly associated with time in either modality.

In this cross-sectional analysis of multimodal data in acute ischemic stroke, tissue signal intensities showed stronger time-dependence than volumetric measures, supporting the view that infarct evolution reflects progressive tissue injury rather than consistent volumetric expansion. This suggests that "infarct growth rate" concepts may be more applicable to NCCT and DWI as parameters of tissue demise rather than to perfusion-based metrics.