Abstract DP241: Hypoperfusion on Early MRI Despite Successful Thrombectomy: a Prospective Imaging and Inflammatory Biomarkers Study.

Background and Purpose: Persistent hypoperfusion despite successful endovascular treatment (EVT) for acute ischemic stroke (AIS) due to large-vessel occlusion (LVO), which results from either residual distal macrovascular occlusion or microvascular dysfunction ("no-reflow"), is increasingly recognized as a potential contributor to poor outcome. We aimed to characterize early post-EVT perfusion abnormalities on MRI and assessed their relationship with a panel of inflammatory biomarkers. Methods: We prospectively included patients with LVO-related AIS and successful (modified Thrombolysis in Cerebral Infarction [mTICI] ≥2b) recanalization who underwent MRI perfusion (MRP) as early as feasible after EVT and blood sampling before, during, immediately after and 24 hours after EVT. mTICI was assessed by an independent reader. Hypoperfusion within the affected vascular territory was assessed using three complementary approaches: (1) significant macrovascular hypoperfusion (Tmax>6s) in any location; (2) wedge-shaped perfusion deficits on Tmax maps, indicative of distal emboli; and (3) visual microvascular hypoperfusion within the infarct core on cerebral blood volume (CBV) and/or flow (CBF) maps (two-rater assessment). Associations between macrovascular hypoperfusion and 37 inflammatory biomarkers, measured using multiplex immunoassays, were analyzed using Mann–Whitney U tests with false discovery rate (FDR) correction. Results: Seventy-one patients were included. Median time from recanalization to MRP was 45 (19-118) min. Tmax>6s hypoperfusions were found in 21% of all patients; percentages decreased with better mTICI grades: 45%, 13% and 0% in mTICI 2b, 2c, and 3, respectively. Wedge-shaped hypoperfusion deficits were observed in 97% of mTICI2b, 44% of mTICI2c, and 8% mTICI3 cases (see Figure 1 for examples). Microvascular hypoperfusion was rare (6%, see Figure 2 for examples). Several inflammatory markers showed uncorrected associations with Tmax>6s hypoperfusion, but none survived FDR correction (Figure 3). Conclusions: Early perfusion deficits after EVT most often reflect residual distal emboli. Hypoperfusion on Tmax>6s maps was not associated with inflammatory biomarkers. Nevertheless, our integrated imaging and biomarker strategy—including samples collected immediately distal to the clot during EVT—lays the foundation for future mechanistic and therapeutic studies targeting microvascular reperfusion failure.