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<p>Neutrophil extracellular traps (NETs) are implicated in thrombosis and inflammation during acute myocardial infarction (AMI), but their kinetics, local distribution, and clinical relevance remain unclear. We conducted a prospective study in 144 patients with ST-segment elevation (STEMI) and non–ST-segment elevation AMI (NSTEMI) undergoing coronary angioplasty (PCI), quantifying double-stranded DNA (dsDNA), myeloperoxidase (MPO), and neutrophil elastase (NE) in the infarct-related artery (IRA), contralateral coronary artery (CCA), and peripheral blood. Coronary thrombi and DNASE1 Q222R were also analysed. NET markers were elevated in the IRA, and NE and dsDNA increased peripherally after PCI. IRA NE levels independently predicted cardiovascular events (HR, 1.76; 95%CI: 1.24 – 2.51). Thrombi with higher NE and citrullinated histone H3 content were associated with suboptimal PCI results. dsDNA levels were significantly higher in patients with the GG DNASE1 genotype. These findings indicate a compartmentalized NET response in AMI and support a potential prognostic impact of NETs.</p> Graphical Abstract <p>Neutrophil extracellular traps in acute myocardial infarction. Schematic representation of the study design and main findings. Blood samples were collected from patients with acute myocardial infarction (92 STEMI and 52 NSTEMI) undergoing percutaneous coronary intervention (PCI) via radial access. Sampling was performed from of the infarct-related artery (IRA), the contralateral coronary artery (CCA), and the arterial sheath. Neutrophil extracellular trap (NET) markers—including double-stranded DNA (dsDNA), neutrophil elastase (NE), and myeloperoxidase (MPO)—were quantified at baseline and up 96&#xa0;h after PCI. Coronary thrombi were analysed histologically for NET content using immunostaining for citrullinated histone H3 (CitH3) and NE. DNASE1 genotyping was performed to explore its influence on NET burden.</p> <p></p>

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Characterization of Neutrophil Extracellular Traps in Acute Myocardial Infarction: A Translational Study

  • 期刊论文

  • 发表日期：

    2025年9月3日

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  • Sergio Huertas-Nieto,
  • Ana Moraga-Yébenes,
  • Lydia Zamora-Pérez,
  • Guillermo Moreno,
  • Nicolás Maneiro-Melón,
  • Fernando Sarnago-Cebada,
  • Berk Feyzi Kadir,
  • Aitana Medina,
  • Rosa María García-Martín,
  • Ignacio Lizasoain,
  • Héctor Bueno

摘要

Neutrophil extracellular traps (NETs) are implicated in thrombosis and inflammation during acute myocardial infarction (AMI), but their kinetics, local distribution, and clinical relevance remain unclear. We conducted a prospective study in 144 patients with ST-segment elevation (STEMI) and non–ST-segment elevation AMI (NSTEMI) undergoing coronary angioplasty (PCI), quantifying double-stranded DNA (dsDNA), myeloperoxidase (MPO), and neutrophil elastase (NE) in the infarct-related artery (IRA), contralateral coronary artery (CCA), and peripheral blood. Coronary thrombi and DNASE1 Q222R were also analysed. NET markers were elevated in the IRA, and NE and dsDNA increased peripherally after PCI. IRA NE levels independently predicted cardiovascular events (HR, 1.76; 95%CI: 1.24 – 2.51). Thrombi with higher NE and citrullinated histone H3 content were associated with suboptimal PCI results. dsDNA levels were significantly higher in patients with the GG DNASE1 genotype. These findings indicate a compartmentalized NET response in AMI and support a potential prognostic impact of NETs.

Graphical Abstract

Neutrophil extracellular traps in acute myocardial infarction. Schematic representation of the study design and main findings. Blood samples were collected from patients with acute myocardial infarction (92 STEMI and 52 NSTEMI) undergoing percutaneous coronary intervention (PCI) via radial access. Sampling was performed from of the infarct-related artery (IRA), the contralateral coronary artery (CCA), and the arterial sheath. Neutrophil extracellular trap (NET) markers—including double-stranded DNA (dsDNA), neutrophil elastase (NE), and myeloperoxidase (MPO)—were quantified at baseline and up 96 h after PCI. Coronary thrombi were analysed histologically for NET content using immunostaining for citrullinated histone H3 (CitH3) and NE. DNASE1 genotyping was performed to explore its influence on NET burden.