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<p>Myocardial infarction (MI) induces an inflammatory response that may be amenable to targeted therapy. This cohort study evaluated the systemic inflammatory burden across different infarct sizes using serial measurements of C-reactive protein (CRP), interleukin-6 (IL-6), and targeted inflammatory proteomics (Olink’s Target 96 Inflammation panel) during hospitalization and up to 12&#xa0;weeks post-MI. Baseline IL-6&#xa0;concentrations were progressively higher with increasing infarct size, with differential temporal trajectories observed across infarct size strata (<i>P</i> for interaction &lt; 0.001), a finding confirmed by proteomic analysis (<i>P</i><sub><i>adj</i></sub> for interaction = 0.009). Patients with small infarct size showed no significant changes in CRP or IL-6 concentrations, yet demonstrated downregulation of urokinase (uPA) and upregulation of angiogenesis-related proteins (tumor necrosis factor-related weak inducer of apoptosis [TWEAK] and hepatocyte growth factor [HGF]), similar to those observed in patients with moderate or large infarct sizes, emphasizing the biological significance of these processes. Overall, greater myocardial injury was associated with higher inflammatory burden, highlighting IL-6 as a promising therapeutic target for acute anti-inflammatory treatment after large MI.</p>

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The Immediate Impact of Infarct Size on the Systemic Inflammatory Response: IL-6 as Central Mediator Identified through Biomarker and Proteomic Profiling

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月29日

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  • Jonathan Los,
  • Frans B. Mensink,
  • Özlem Bulut,
  • Ilse H. Hol,
  • Aysun Cetinyurek-Yavuz,
  • Niels P. Riksen,
  • Saloua El Messaoudi,
  • Jan H. Cornel,
  • Robert-Jan M. van Geuns

摘要

Myocardial infarction (MI) induces an inflammatory response that may be amenable to targeted therapy. This cohort study evaluated the systemic inflammatory burden across different infarct sizes using serial measurements of C-reactive protein (CRP), interleukin-6 (IL-6), and targeted inflammatory proteomics (Olink’s Target 96 Inflammation panel) during hospitalization and up to 12 weeks post-MI. Baseline IL-6 concentrations were progressively higher with increasing infarct size, with differential temporal trajectories observed across infarct size strata (P for interaction < 0.001), a finding confirmed by proteomic analysis (Padj for interaction = 0.009). Patients with small infarct size showed no significant changes in CRP or IL-6 concentrations, yet demonstrated downregulation of urokinase (uPA) and upregulation of angiogenesis-related proteins (tumor necrosis factor-related weak inducer of apoptosis [TWEAK] and hepatocyte growth factor [HGF]), similar to those observed in patients with moderate or large infarct sizes, emphasizing the biological significance of these processes. Overall, greater myocardial injury was associated with higher inflammatory burden, highlighting IL-6 as a promising therapeutic target for acute anti-inflammatory treatment after large MI.