Abstract DP036: Intracranial and Peripheral Inflammatory Biomarkers Associated with Futile Recanalization After Thrombectomy

Background and Purpose: Futile recanalization, defined as the absence of functional independence despite successful recanalization, remains a significant limitation of endovascular treatment (EVT) for large vessel occlusion (LVO) stroke. Inflammation has emerged as a key contributor to brain reperfusion injury. We investigated whether intracranial and peripheral blood-based inflammatory biomarkers are associated with futile recanalization. Methods: We prospectively included patients with anterior circulation LVO achieving successful EVT (modified Thrombolysis in Cerebral infarction, mTICI ≥2b) for anterior LVO and without intracranial reocclusion. Peripheral blood samples were collected immediately before and after EVT and at 24 hours, and intracranial arterial blood samples were retrieved distal to the clot during EVT before recanalization. Thirty-seven major biomarkers related to inflammation and vascular activation were measured using multiplex immunoassays. Associations with futile recanalization were first assessed using non-parametric tests with false discovery rate (FDR) correction and by calculating effect sizes (Cohen’d) on rank-transformed data. For biomarkers with an effect size ≥0.5, univariable and multivariable logistic regression models were used, adjusting for predefined confounders (age, baseline NIHSS and ASPECTS, intravenous thrombolysis use, and time from last-known-well to groin puncture). Results: Among 139 included patients (median age 77 [IQR, 70–83]; 41% women), 64 (46%) had futile recanalization. Six biomarkers showed at least a medium effect size at one or more timepoints: interleukin-6, interleukin-10, interleukin-15, vascular endothelial growth factor receptor 1 (VEGFR1), vascular cell adhesion molecule-1(VCAM-1), and serum amyloid A (SAA) (Figures 1-2). In adjusted multivariable models, VCAM-1 (intracranial and post-EVT), interleukin-10 (intracranial and pre-EVT), interleukin-15 (pre-EVT), and SAA (post-EVT) remained independently associated with futile recanalization (Figure 3). Discussion: Among all biomarkers assessed, VCAM-1 and IL-10 levels when measured intracranially immediately before, or peripherally early after, recanalization, were the most robust predictors of futile recanalization. Our findings provide novel evidence that early neuroinflammation may negatively impacts post-EVT outcome, and highlight the potential for biomarker-guided risk stratification and targeted anti-inflammatory therapies.

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Journal
Stroke
Published
2026-01-29
DOI
https://doi.org/10.1161/str.57.suppl_1.dp036
Primary Topic
Neuroinflammation and Neurodegeneration Mechanisms
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article
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article

Abstract DP036: Intracranial and Peripheral Inflammatory Biomarkers Associated with Futile Recanalization After Thrombectomy

Isabelle Mourand, Quentin Varnier, Pierre-Henri Lefèvre, C Jorgensen et al.
Stroke
Neuroinflammation and Neurodegeneration Mechanisms
article

Abstract DP036: Intracranial and Peripheral Inflammatory Biomarkers Associated with Futile Recanalization After Thrombectomy

Isabelle Mourand, Quentin Varnier, Pierre-Henri Lefèvre, C Jorgensen, Nicola Andrea Marchi, Federico Cagnazzo, Julien Labreuche, Emmanuelle Le Bars, Marine Blaquière, Vincent Costalat, Xavier Ayrignac, Lucas Corti, Marinette MOYNIER, Thibaut Roux, Cyril Dargazanli, Maarten G. Lansberg, Jeremy J. Heit, Thomas Checkouri, Adrien ter Schiphorst, Christophe Hirtz, Francois Louis collemiche, Farida Djouad, Jean-Claude Baron, Gregory W. Albers, JEAN MARC OLIVOT, Caroline Arquizan
article en

Abstract

Background and Purpose: Futile recanalization, defined as the absence of functional independence despite successful recanalization, remains a significant limitation of endovascular treatment (EVT) for large vessel occlusion (LVO) stroke. Inflammation has emerged as a key contributor to brain reperfusion injury. We investigated whether intracranial and peripheral blood-based inflammatory biomarkers are associated with futile recanalization. Methods: We prospectively included patients with anterior circulation LVO achieving successful EVT (modified Thrombolysis in Cerebral infarction, mTICI ≥2b) for anterior LVO and without intracranial reocclusion. Peripheral blood samples were collected immediately before and after EVT and at 24 hours, and intracranial arterial blood samples were retrieved distal to the clot during EVT before recanalization. Thirty-seven major biomarkers related to inflammation and vascular activation were measured using multiplex immunoassays. Associations with futile recanalization were first assessed using non-parametric tests with false discovery rate (FDR) correction and by calculating effect sizes (Cohen’d) on rank-transformed data. For biomarkers with an effect size ≥0.5, univariable and multivariable logistic regression models were used, adjusting for predefined confounders (age, baseline NIHSS and ASPECTS, intravenous thrombolysis use, and time from last-known-well to groin puncture). Results: Among 139 included patients (median age 77 [IQR, 70–83]; 41% women), 64 (46%) had futile recanalization. Six biomarkers showed at least a medium effect size at one or more timepoints: interleukin-6, interleukin-10, interleukin-15, vascular endothelial growth factor receptor 1 (VEGFR1), vascular cell adhesion molecule-1(VCAM-1), and serum amyloid A (SAA) (Figures 1-2). In adjusted multivariable models, VCAM-1 (intracranial and post-EVT), interleukin-10 (intracranial and pre-EVT), interleukin-15 (pre-EVT), and SAA (post-EVT) remained independently associated with futile recanalization (Figure 3). Discussion: Among all biomarkers assessed, VCAM-1 and IL-10 levels when measured intracranially immediately before, or peripherally early after, recanalization, were the most robust predictors of futile recanalization. Our findings provide novel evidence that early neuroinflammation may negatively impacts post-EVT outcome, and highlight the potential for biomarker-guided risk stratification and targeted anti-inflammatory therapies.

StrokeVol. 57(Suppl_1)
Centre National de la Recherche Scientifique (FR), Inserm (FR), Palo Alto University (US), Université de Montpellier (FR), Université Paris Cité (FR), Centre Hospitalier Universitaire de Lille (FR), Centre Hospitalier Universitaire de Montpellier (FR), Institut de Psychiatrie et Neurosciences de Paris (FR), Stanford Medicine (US), Hôpital Paule de Viguier (FR), Institut de Génomique Fonctionnelle (FR), Stanford University (US)
Good health and well-being
Openalex Percentile: Top 79%
Neuroinflammation and Neurodegeneration Mechanisms
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