Existing literature suggests that anemia may be a poor prognostic marker in stroke patients.^{Reference Barlas, Honney and Loke1,Reference Desai, Oh and Rao2} In their meta-analysis, Najdawi et al. investigated the association between periprocedural hemoglobin levels and functional outcomes in acute ischemic stroke patients with large vessel occlusion treated with endovascular thrombectomy (EVT).^{Reference Nadawi3} Patients with good functional outcomes (mRS 0–2) had hemoglobin levels approximately 0.5 g/L higher than those with poor outcomes. Each 1 g/L increase in hemoglobin was associated with a 22% increased probability of achieving a good outcome, though it remains uncertain whether this relationship is linear and within which hemoglobin ranges it applies. Using WHO-specified cutoffs, anemic patients were more than twice as likely to experience poor outcomes compared to non-anemic patients.

Several mechanisms could explain the association between hemoglobin levels and functional outcomes in EVT-treated stroke patients. First, while cerebral perfusion is the most critical determinant of infarct growth, low hemoglobin levels may exacerbate the mismatch between energy demand and supply. However, a recent study found no such association,^{Reference Pensato, Bosshart and Stebner4} likely because only severely low hemoglobin levels significantly alter the oxygen-hemoglobin dissociation curve. Additionally, a preconditioning effect of chronic anemia could also mitigate its impact on infarct growth. Second, hemoglobin levels might affect stroke etiology or thrombus characteristics, influencing response rates to recanalization.^{Reference Joundi and Menon5} Third, anemia, similar to other blood biomarkers (e.g., neutrophil-to-lymphocyte ratio and mean platelet volume), may reflect broader patient characteristics, such as comorbidities, frailty or inflammation, rather than directly driving poor outcomes. Fourth, lower post-procedural hemoglobin levels could indicate longer and more complex EVT procedures, which themselves are associated with poorer outcomes.

This study adds to the growing body of evidence linking anemia to poor outcomes in stroke patients. However, its causal role remains unclear. Understanding these mechanisms is crucial before considering anemia correction strategies different from those used in non-stroke populations.

Future studies could provide more insight into the role of hemoglobin in outcomes of EVT-treated stroke patients by focusing on three key issues: (i) the timing of hemoglobin measurement (pre- vs. post-EVT), (ii) adjusting for additional confounding factors (e.g., comorbidities and stroke severity) and (iii) further differentiating between chronic and acute anemia. Addressing these gaps could clarify whether anemia is a modifiable risk factor or simply a marker of underlying patient vulnerability.