Abstract DP218: The Role of Immune Indices NLR, SII, PLR and SIRI in Predicting Post-Mechanical Thrombectomy (MT) Outcomes

Introduction: MT is an established treatment for acute ischemic stroke (AIS). With expanding eligibility windows and improved devices, outcome prediction and patient selection remain crucial. Increasing evidence implicates systemic and intra-/peri-thrombus inflammation in AIS prognosis. Among systemic immune indices, neutrophil (N)-to-lymphocyte (L) ratio (NLR), systemic immune-inflammation index (SII), platelet (P)-to-L ratio (PLR), and systemic inflammation response index (SIRI) predict AIS outcomes, but their role in MT remain unclear. We retrospectively reviewed MT cases at our institution to assess whether these indices predict post-MT outcomes. Methods: We studied 68 MT patients treated between 9/2023 and 12/2025 at UC Irvine. Demographics and clinical variables were summarized using means (SD) or proportions. Indices were calculated as NLR=N/L, SII = (P×N)/L, SIRI = (N×monocytes)/L, PLR=P/L. Predictive performance was tested against NIHSS, dense MCA sign, TICI, mRS, LOS, and hemorrhagic transformation (HE) using 2×2 tables. Thresholds were defined by ROC-derived Youden index or clinical cutoffs. PPV/NPV with 95% CIs were calculated; Fisher’s exact test with False Discovery Rate (FDR) correction assessed significance. Results: Several indices showed significant predictive value (FDR 7 days (PPVs 65–100%). At discharge, NLR (≥4.7), SII (≥721), and SIRI (≥1.1) predicted discharge mRS ≥3 (PPVs 86–93%), though NPVs were low; 90-day mRS results trended similarly, with SIRI showing strongest NPV (86%). Conclusions: Elevated immune indices were consistently associated with greater stroke severity, dense MCA sign, HE, and longer hospitalization, with trends toward poor reperfusion and functional outcomes, whereas lower values strongly excluded adverse events such as parenchymal hematoma. These leukocyte-based indices may improve MT candidate selection, as inflammation likely contributes substantially to AIS pathogenesis and treatment response.