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Modeling diffusion-weighted imaging lesion expansion between 2 and 24 h after endovascular thrombectomy in acute ischemic stroke

  • Nathaniel Rex,
  • Karim Oueidat,
  • Johanna Ospel,
  • Rosalie McDonough,
  • Leon Rinkel,
  • Grayson L. Baird,
  • Scott Collins,
  • Gaurav Jindal,
  • Matthew D. Alvin,
  • Jerrold Boxerman,
  • Phil Barber,
  • Mahesh Jayaraman,
  • Wendy Smith,
  • Amanda Amirault-Capuano,
  • Michael Hill,
  • Mayank Goyal,
  • Ryan McTaggart

摘要

Purpose

Diffusion-weighted imaging (DWI) lesion expansion after endovascular thrombectomy (EVT) is not well characterized. We used serial diffusion-weighted magnetic resonance imaging (MRI) to measure lesion expansion between 2 and 24 h after EVT.

Methods

In this single-center observational analysis of patients with acute ischemic stroke due to large vessel occlusion, DWI was performed post-EVT (< 2 h after closure) and 24-h later. DWI lesion expansion was evaluated using multivariate generalized linear mixed modeling with various clinical moderators.

Results

We included 151 patients, of which 133 (88%) had DWI lesion expansion, defined as a positive change in lesion volume between 2 and 24 h. In an unadjusted analysis, median baseline DWI lesion volume immediately post-EVT was 15.0 mL (IQR: 6.6–36.8) and median DWI lesion volume 24 h post-EVT was 20.8 mL (IQR: 9.4–66.6), representing a median change of 6.1 mL (IQR: 1.5–17.7), or a 39% increase. There were no significant associations among univariable models of lesion expansion. Adjusted models of DWI lesion expansion demonstrated that relative lesion expansion (defined as final/initial DWI lesion volume) was consistent across eTICI scores (0–2a, 0.52%; 2b, 0.49%; 2c–3, 0.42%, p = 0.69). For every 1 mL increase in lesion volume, there was 2% odds of an increase in 90-day mRS (OR: 1.021, 95%CI [1.009, 1.034], p < 0.001).

Conclusion

We observed substantial lesion expansion post-EVT whereby relative lesion expansion was consistent across eTICI categories, and greater absolute lesion expansion was associated with worse clinical outcome. Our findings suggest that alternate endpoints for cerebroprotectant trials may be feasible.