Despite high recanalization rates achieved by endovascular therapy (EVT) in cases of acute ischemic stroke (AIS) related to a large‐vessel occlusion, ≈50% of the treated patients do not reach functional independence at 3 months.

A potential explanation for this finding is the occurrence of both local¹ and systemic² inflammation triggered by the AIS, which appears to be driven by neutrophils, a hypothesis supported by the identification of neutrophil count³ as a prognostic marker of unfavorable clinical outcome (CO) after an AIS.

Myeloperoxidase is predominantly, but not exclusively, secreted by activated neutrophils after an AIS and serves both as a biomarker of neutrophil activation (NA) and an effector of inflammation, partly through its association with neutrophil extracellular traps (NETs),⁴ playing a role in local and systemic inflammation after an AIS.