{
  "abstract": "Pulsed field ablation (PFA) is increasingly used for atrial fibrillation, but the mechanisms of PFA-induced cell death remain incompletely understood. This study aimed to elucidate the early mechanisms and temporal dynamics of cell death induced by PFA as acute indicators of ablation effectiveness in pre-clinical models. Epicardial left ventricular ablations were performed using the AblaView® System, with lesions created at predefined locations. Hearts were harvested for histopathological and immunohistochemical analysis at 10, 40, and 100 minutes, as well as at 1-month post-ablation, while a separate survival cohort was also examined at 1 month. Structural damage and lesion borders were assessed using routine histology and desmin staining, and regulated cell death pathways, inflammation, and metabolic stress were evaluated via immunohistochemistry. PFA produced lesions with comparable biophysical parameters across all time points. Within minutes, structural markers revealed loss of cardiomyocyte striation, increased intercellular spacing, and disappearance of myocardial anisotropy. RIPK3 and Gasdermin increased significantly over time (both p=0.01), indicating activation of necroptotic and pyroptotic pathways, while caspase-8 showed transient elevation consistent with extrinsic apoptotic signaling. Myeloperoxidase staining increased over time (p<0.05), reflecting neutrophil-driven inflammation, and GLUT1 inhibition at 100 minutes suggested hypoxia and metabolic stress. At 1-month, ablated regions were replaced by fibrotic scar tissue. Overall, PFA induces multiple regulated cell death pathways—including apoptosis, necroptosis, and pyroptosis—alongside inflammation and hypoxia-associated stress, ultimately leading to chronic scar formation; these acute markers may support the development of new tools to better characterize PFA lesions and assess ablation effectiveness.",
  "abstract_shown": true,
  "affiliations": [],
  "article_type": null,
  "arxiv": null,
  "author_total": 10,
  "authors": [
    {
      "name": "David Herranz"
    },
    {
      "name": "Eduardo Caleiras"
    },
    {
      "name": "Quim Castellví"
    },
    {
      "name": "Christian Jay Vera"
    },
    {
      "name": "Fernando Peláez"
    },
    {
      "name": "Antoni Ivorra"
    },
    {
      "name": "Carlota Largo Aramburu"
    },
    {
      "name": "Christophe Bailleul"
    },
    {
      "name": "Raphaël P Martins"
    },
    {
      "name": "Atul Verma"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/9x28mntmwnj3t.bib",
  "cited_by": 0,
  "doi": "10.1038/s41598-026-70530-5",
  "fulltext_url": null,
  "id": "9x28mntmwnj3t",
  "issns": [
    "2045-2322"
  ],
  "landing_url": "https://hal.science/hal-05785918v1",
  "language": "en",
  "licence": "CC-BY-NC-ND",
  "licence_label": "CC BY-NC-ND",
  "licence_source": "journal",
  "licence_url": "https://creativecommons.org/licenses/by-nc-nd/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "hal",
      "0.sdv"
    ],
    [
      "hal",
      "1.sdv.ib"
    ],
    [
      "openalex",
      "2705|Cardiac Arrhythmias and Treatments"
    ]
  ],
  "openalex": "W7214351556",
  "pdf_url": "https://www.nature.com/articles/s41598-026-70530-5_reference.pdf",
  "pmcid": null,
  "pmid": null,
  "published": "2026-10-08",
  "publisher": "Nature Publishing Group",
  "ris": "https://research.draconitic.com/paper/9x28mntmwnj3t.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T12:17:50Z",
      "native_id": "hal-05785918",
      "source": "hal",
      "url": "https://hal.science/hal-05785918v1"
    }
  ],
  "subjects": [
    {
      "field": "biology",
      "origin": "hal:1.sdv.ib",
      "subfield": "systems-synthetic"
    }
  ],
  "title": "Mechanisms and time course of cell death in pulsed field ablation",
  "title_text": "Mechanisms and time course of cell death in pulsed field ablation",
  "type": "peer-reviewed",
  "updated_at": "2026-10-30T12:17:50Z",
  "url": "https://research.draconitic.com/paper/9x28mntmwnj3t",
  "venue": "Scientific Reports",
  "versions": []
}