# Association of the Stress Hyperglycemia Ratio and Prognosis After Endovascular Treatment: A Systematic Review and Meta‐Analysis

**Authors:** Jiayu You, Qianshuo Liu, Xingqiang Li

PMC · DOI: 10.1002/brb3.71245 · Brain and Behavior · 2026-02-05

## TL;DR

This study finds that higher stress hyperglycemia ratio (SHR) is linked to worse outcomes in stroke patients after endovascular treatment.

## Contribution

The study introduces SHR as a novel prognostic indicator for large vessel occlusion stroke patients undergoing endovascular treatment.

## Key findings

- Higher SHR is associated with increased risk of poor functional outcomes at 90 days.
- Elevated SHR correlates with higher mortality and intracranial hemorrhage risks after treatment.
- SHR serves as a reliable indicator for risk stratification in stroke patients post-EVT.

## Abstract

Stress hyperglycemia (SH) is prevalent in patients with acute ischemic stroke (AIS). The stress hyperglycemia ratio (SHR), calculated as the fasting blood glucose (FBG)/glycosylated hemoglobin (HbA1c) ratio, has been widely used to evaluate SH. However, the correlation between SHR and clinical outcomes in AIS patients with large vessel occlusion (LVO) following endovascular treatment (EVT, including mechanical thrombectomy, contact aspiration, intra‐arterial thrombolysis, excluding intravenous thrombolysis) remains unclear. This study aimed to perform a meta‐analysis to investigate the association between SHR and clinical outcomes in EVT‐treated AIS patients with LVO.

A comprehensive literature search was conducted across multiple databases, including PubMed, Web of Science, Embase, and the Cochrane Library, to identify studies investigating the association between SHR and clinical outcomes. The entire study was executed in strict adherence to the Preferred Reporting Items for Systematic Reviews and Meta‐Analysis (PRISMA) guidelines. References were screened based on pre‐specified inclusion and exclusion criteria, and the Newcastle–Ottawa Scale (NOS) was rigorously applied to assess potential bias risks in the selected studies. RevMan 5.3 software was utilized for performing meta‐analyses on the included literature.

A total of 10 studies met the inclusion criteria, and 3646 AIS patients who underwent EVT were included in this analysis. The meta‐analysis results demonstrated a higher SHR was associated with an increased risk of poor outcomes (modified Rankin Scale [mRS] 3–6) at 90 days (odds ratio [OR] = 2.65, 95% CI: 2.30–3.06, p < 0.001), mortality (OR = 2.62, 95% CI: 1.81–3.79, p < 0.001), intracranial hemorrhage (ICH) (OR = 1.53, 95% confidence interval [CI]: 1.27–1.85, p < 0.001), symptomatic intracranial hemorrhage (sICH) (OR = 2.05, 95% CI: 1.27–3.30, p < 0.003) after EVT.

A higher SHR may increase the occurrence of poor outcomes, mortality, ICH, and sICH in AIS patients caused by LVO after EVT. SHR is associated with poor prognosis in AIS patients caused by LVO after EVT.

A comprehensive electronic literature search was performed in PubMed, Web of Science, Embase, and the Cochrane Library following the PRISMA guidelines. After screening by pre‐defined inclusion/exclusion criteria and methodological quality assessment using the Newcastle–Ottawa Scale (NOS), 10 eligible studies involving 3646 LVO‐AIS patients who received EVT were included. Meta‐analysis via RevMan 5.3 software revealed that elevated SHR was significantly associated with increased risks of 90‐day poor functional outcomes (modified Rankin Scale [mRS] 3‐6, odds ratio [OR] = 2.65, 95% confidence interval [CI]:2.30‐3.06, p < 0.001), all‐cause mortality (OR = 2.62, 95% CI: 1.81‐3.79, p < 0.001), intracranial hemorrhage (ICH, OR = 1.53, 95% CI: 1.27‐1.85, p < 0.001), and symptomatic intracranial hemorrhage (sICH, OR = 2.05, 95% CI: 1.27‐3.30, p = 0.003). Collectively, SHR can serve as a reliable prognostic indicator for LVO‐AIS patients after EVT, providing valuable reference for clinical risk stratification and management.

## Full-text entities

- **Genes:** GH1 (growth hormone 1) [NCBI Gene 2688] {aka GH, GH-N, GHB5, GHN, IGHD1A, IGHD1B}
- **Diseases:** retriever"[all (MESH:C536496), intracerebral hemorrhage (MESH:D002543), hemorrhage (MESH:D006470), critical illness (MESH:D016638), LVO (MESH:C536223), neurological deterioration (MESH:D009422), Hyperglycemia (MESH:D006943), ischemic stroke (MESH:D002544), hemorrhagic stroke (MESH:D000083302), Stroke (MESH:D020521), hematoma (MESH:D006406), neurovascular injury (MESH:D013901), inflammation (MESH:D007249), AIS (MESH:D000083242), transient ischemic attack (MESH:D002546), ICH (MESH:D020300), death (MESH:D003643), functional disability (MESH:D003291), dysregulation (MESH:D021081), diabetes (MESH:D003920), insulin resistance (MESH:D007333), neurological deficits (MESH:D009461)
- **Chemicals:** catecholamines (MESH:D002395), EVT (-), glucose (MESH:D005947)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

44 references — full list in the complete paper: https://tomesphere.com/paper/PMC12876047/full.md

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Source: https://tomesphere.com/paper/PMC12876047