# Association of the neutrophil percentage-to-albumin ratio after endovascular treatment and 3-month clinical outcomes

**Authors:** Chang Cui, Liang Liu, Hui-Sheng Chen

PMC · DOI: 10.3389/fneur.2026.1768949 · Frontiers in Neurology · 2026-02-12

## TL;DR

This study shows that higher neutrophil percentage-to-albumin ratio after stroke treatment is linked to worse recovery outcomes.

## Contribution

The study identifies NPAR as a novel predictor of poor outcomes after endovascular stroke treatment.

## Key findings

- Higher 48-hour NPAR levels predict worse 3-month outcomes (adjusted OR 15.09).
- An increase in NPAR from admission to 48 hours also predicts poor outcomes (adjusted OR 7.69).
- The optimal cutoff for 48-hour NPAR is 2.312, with 66% sensitivity and 79% specificity.

## Abstract

Neutrophil percentage-to-albumin ratio (NPAR) is associated with clinical outcomes in malignancy, cardiovascular disease, and stroke. This study aimed to evaluate whether NPAR levels are associated with clinical outcomes in patients with acute ischemic stroke (AIS) due to large vessel occlusion (LVO) who underwent endovascular treatment (EVT).

From a prospective cohort, we consecutively enrolled patients with anterior circulation LVO-AIS who underwent EVT and had available admission and 48-h post-EVT NPAR data. Three-month clinical outcome was assessed using the modified Rankin Scale (mRS). Poor functional outcome was defined as functional dependence or death (mRS 3–6). Multivariable logistic regression analyses were performed to explore the relationship between NPAR levels and clinical outcomes.

A total of 121 eligible patients were included in the final analysis. Multivariable logistic regression models showed that a higher 48-h NPAR level (Model 1: adjusted OR = 15.09, 95% CI 3.72–61.22, p < 0.001) and an increase in NPAR from admission to 48 h (Model 2: adjusted OR = 7.69, 95% CI 2.06–28.70, p = 0.002) were independently associated with poorer functional outcome. The optimal cutoff value of 48-h NPAR level for predicting poor functional outcome was 2.312, with a sensitivity of 66% and a specificity of 79%.

Higher 48-h follow-up NPAR levels and increases in NPAR from admission to 48 h were independent predictors of poor 3-month functional outcomes in patients with large vessel occlusion treated with endovascular therapy.

https://www.clinicaltrials.gov, identifier (NCT05092139).

## Full-text entities

- **Genes:** GPT (glutamic--pyruvic transaminase) [NCBI Gene 2875] {aka AAT1, ALT, ALT1, GPT1, SGPT}, SLC17A5 (solute carrier family 17 member 5) [NCBI Gene 26503] {aka AST, ISSD, NSD, SD, SIALIN, SIASD}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}
- **Diseases:** cerebral edema (MESH:D001929), intracranial hemorrhage (MESH:D020300), Post-stroke (MESH:D020521), Hypoalbuminemia (MESH:D034141), acute hemodilution (MESH:D000208), AIS (MESH:D000083242), damage (MESH:D020263), platelet aggregation (MESH:D001791), trauma (MESH:D014947), inflammation (MESH:D007249), ischemic (MESH:D002545), diabetes (MESH:D003920), LVO (MESH:C536223), cancer (MESH:D009369), ischemic brain (MESH:D020520), cardioembolism (MESH:D000083262), infarct (MESH:D007238), hepatic or renal disease (MESH:D007674), TIA (MESH:D002546), sepsis (MESH:D018805), tissue injury (MESH:D017695), reperfusion injury (MESH:D015427), intracerebral hemorrhage (MESH:D002543), intracranial haemorrhage (MESH:D013345), large artery atherosclerosis (MESH:D050197), hematological disease (MESH:D006402), brain injury (MESH:D001930), hypertension (MESH:D006973), death (MESH:D003643), cerebral infarction (MESH:D002544), EVT (MESH:D016609), cardiovascular disease (MESH:D002318), infection (MESH:D007239)
- **Chemicals:** EVT (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

37 references — full list in the complete paper: https://tomesphere.com/paper/PMC12935595/full.md

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Source: https://tomesphere.com/paper/PMC12935595