From recanalization to recovery: inflammation and futile reperfusion after mechanical thrombectomy
- 1Department of Cerebrovascular Surgery, Heze Hospital Affiliated to Shandong First Medical University
Abstract
Mechanical thrombectomy (MT) has markedly improved reperfusion outcomes in patients with acute ischemic stroke caused by large-vessel occlusion. However, successful angiographic reperfusion does not invariably translate into functional independence. Poor functional outcome despite successful angiographic reperfusion is commonly described as futile reperfusion. This clinical-angiographic mismatch may reflect persistent tissue injury, including inflammatory injury, alongside pretreatment damage and other determinants of outcome. Experimental findings and clinical associations implicate persistent inflammatory activation, thrombo-inflammation, endothelial dysfunction, microvascular no-reflow, and blood–brain barrier disruption as contributors to secondary tissue injury after MT. Here, we examine potential inflammatory contributions to futile reperfusion and consider how inflammatory biomarkers might inform risk stratification after MT. Ischemia activates microglia, endothelial cells, platelets, complement pathways, and circulating immune cells. Subsequent reperfusion may amplify oxidative stress, cytokine signaling, neutrophil-endothelial interactions, neutrophil extracellular trap formation, matrix metalloproteinase activity, and barrier failure. Together, these processes can promote microvascular obstruction, cerebral edema, hemorrhagic transformation, infarct growth, and impaired neurological recovery despite successful angiographic reperfusion. Among circulating biomarkers, the neutrophil-to-lymphocyte ratio has been studied repeatedly, alongside platelet-to-lymphocyte ratio, systemic immune-inflammation index, systemic inflammation response index, interleukin-6, matrix metalloproteinase-9, and other molecular markers. Their specificity, incremental predictive value, and clinical utility require further validation in standardized thrombectomy cohorts. We therefore view inflammation as a plausible biological link between macrovascular reperfusion and persistent tissue-level injury after MT. From a translational perspective, the immediate priorities are to standardize sampling protocols, characterize dynamic inflammatory trajectories, develop multimodal prediction models, and test biomarker-guided therapeutic strategies.
Related
- Precision medicine for futile recanalization after mechanical thrombectomy in acute ischemic stroke: mechanisms, diagnostics, and tailored therapies
- Nonlinear association between platelet distribution width and futile recanalization in acute ischemic stroke patients undergoing mechanical thrombectomy
- Beyond the Rankin Scale: A Patient‐Centered Score for Meaningful Recovery After Mechanical Thrombectomy in Older Adults With Pre‐Stroke Disability
- Endothelial glycocalyx dysfunction in the setting of mechanical thrombectomy: a conceptual link between cardiometabolic vulnerability and microvascular reperfusion failure
- Passive Advancement of the Aspiration Catheter During Mechanical Thrombectomy is Independently Associated with Superior Recanalization Outcomes
BibTeX
@article{zhang2026from,
title = {{From recanalization to recovery: inflammation and futile reperfusion after mechanical thrombectomy}},
author = {Furong Zhang and Kai Wang and Xinfang Zhang and Qing Zhao},
journal = {Frontiers in Neurology},
year = {2026},
month = oct,
doi = {10.3389/fneur.2026.1950009},
url = {https://www.frontiersin.org/articles/10.3389/fneur.2026.1950009/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - From recanalization to recovery: inflammation and futile reperfusion after mechanical thrombectomy
AU - Furong Zhang
AU - Kai Wang
AU - Xinfang Zhang
AU - Qing Zhao
PY - 2026
DA - 2026/10/13
JO - Frontiers in Neurology
DO - 10.3389/fneur.2026.1950009
UR - https://www.frontiersin.org/articles/10.3389/fneur.2026.1950009/full
AB - Mechanical thrombectomy (MT) has markedly improved reperfusion outcomes in patients with acute ischemic stroke caused by large-vessel occlusion. However, successful angiographic reperfusion does not invariably translate into functional independence. Poor functional outcome despite successful angiographic reperfusion is commonly described as futile reperfusion. This clinical-angiographic mismatch may reflect persistent tissue injury, including inflammatory injury, alongside pretreatment damage and other determinants of outcome. Experimental findings and clinical associations implicate persistent inflammatory activation, thrombo-inflammation, endothelial dysfunction, microvascular no-reflow, and blood–brain barrier disruption as contributors to secondary tissue injury after MT. Here, we examine potential inflammatory contributions to futile reperfusion and consider how inflammatory biomarkers might inform risk stratification after MT. Ischemia activates microglia, endothelial cells, platelets, complement pathways, and circulating immune cells. Subsequent reperfusion may amplify oxidative stress, cytokine signaling, neutrophil-endothelial interactions, neutrophil extracellular trap formation, matrix metalloproteinase activity, and barrier failure. Together, these processes can promote microvascular obstruction, cerebral edema, hemorrhagic transformation, infarct growth, and impaired neurological recovery despite successful angiographic reperfusion. Among circulating biomarkers, the neutrophil-to-lymphocyte ratio has been studied repeatedly, alongside platelet-to-lymphocyte ratio, systemic immune-inflammation index, systemic inflammation response index, interleukin-6, matrix metalloproteinase-9, and other molecular markers. Their specificity, incremental predictive value, and clinical utility require further validation in standardized thrombectomy cohorts. We therefore view inflammation as a plausible biological link between macrovascular reperfusion and persistent tissue-level injury after MT. From a translational perspective, the immediate priorities are to standardize sampling protocols, characterize dynamic inflammatory trajectories, develop multimodal prediction models, and test biomarker-guided therapeutic strategies.
SN - 1664-2295
ER -