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<p>Endovascular thrombectomy (EVT) is the standard reperfusion therapy for emergent large-vessel occlusion; however, nearly 20% of EVT-treated patients still die within one year. Although early clinical indicators can help stratify post-EVT prognosis, the baseline neuroinflammatory biology associated with fatal outcomes after EVT remains incompletely characterized. In this prospective study of 148 EVT-treated patients, including 30 patients who died within 1 year, we profiled pre-procedure serum proteins using the Olink 384 Inflammation panel and applied an exploratory clinical-proteomic framework. A clinical-only model was used to define higher-risk and lower-risk clinical strata. We then mapped these strata to baseline proteomic patterns through differential expression and annotation-supported candidate mapping. Higher-risk phenotypes were associated with a candidate inflammation- and immune-receptor-related baseline protein pattern. Lower-risk phenotypes were associated with a candidate adhesion/extracellular-matrix-related baseline protein pattern. These internally derived findings suggest that poor outcomes after EVT are associated with candidate baseline inflammatory and tissue-structure-related proteomic patterns. This study provides a neuroinflammation-focused framework for hypothesis generation and candidate prioritization, but the findings require external validation.</p>

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An interpretable clinical-proteomic framework identifies baseline neuroinflammatory proteomic patterns associated with post-thrombectomy mortality

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月20日

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  • Min Xiao,
  • Niu Qiao,
  • Ruihong Zhang,
  • Rong Xi,
  • Xiaojun Ma,
  • Huanyin Li,
  • Hai-Qian Zhou,
  • Yang Liu,
  • Jixian Lin

摘要

Endovascular thrombectomy (EVT) is the standard reperfusion therapy for emergent large-vessel occlusion; however, nearly 20% of EVT-treated patients still die within one year. Although early clinical indicators can help stratify post-EVT prognosis, the baseline neuroinflammatory biology associated with fatal outcomes after EVT remains incompletely characterized. In this prospective study of 148 EVT-treated patients, including 30 patients who died within 1 year, we profiled pre-procedure serum proteins using the Olink 384 Inflammation panel and applied an exploratory clinical-proteomic framework. A clinical-only model was used to define higher-risk and lower-risk clinical strata. We then mapped these strata to baseline proteomic patterns through differential expression and annotation-supported candidate mapping. Higher-risk phenotypes were associated with a candidate inflammation- and immune-receptor-related baseline protein pattern. Lower-risk phenotypes were associated with a candidate adhesion/extracellular-matrix-related baseline protein pattern. These internally derived findings suggest that poor outcomes after EVT are associated with candidate baseline inflammatory and tissue-structure-related proteomic patterns. This study provides a neuroinflammation-focused framework for hypothesis generation and candidate prioritization, but the findings require external validation.