Evidence map›Paper›PMID 42203211›Full record

ArticleCardiovascular research2026

Ventricular fibrillation dynamics reveal regional asymmetry in resilience to cardiac arrest and predict clinical outcome.

Andrés Redondo-Rodríguez, Jorge G Quintanilla, Álvaro Macías, Peter Lee, David Calvo, Marinela Couselo-Seijas, Manuel Marina-Breysse, Ana Simón-Chica, Alba García-Escolano, Alba Ramos-Prada and 19 more

Abstract read
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Article in Cardiovascular research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

What it found

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

29 authors.

Andrés Redondo-RodríguezCentro Nacional de Investigaciones Cardiovasculares (CNIC), Advanced Development in Arrhythmia Mechanisms and Therapy Laboratory, Novel Arrhythmogenic Mechanisms Program, Madrid, Spain.ORCID 0000-0001-7018-0711
Jorge G QuintanillaCentro Nacional de Investigaciones Cardiovasculares (CNIC), Advanced Development in Arrhythmia Mechanisms and Therapy Laboratory, Novel Arrhythmogenic Mechanisms Program, Madrid, Spain.ORCID 0000-0002-2227-3507
Álvaro MacíasCentro Nacional de Investigaciones Cardiovasculares (CNIC), Cardiac Arrhythmia Laboratory, Cardiovascular Regeneration Program, Madrid, Spain.
Peter LeeEssel Research and Development Inc., Toronto, Canada.
David CalvoCentro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.
Marinela Couselo-SeijasCentro Nacional de Investigaciones Cardiovasculares (CNIC), Advanced Development in Arrhythmia Mechanisms and Therapy Laboratory, Novel Arrhythmogenic Mechanisms Program, Madrid, Spain.
Manuel Marina-BreysseCentro Nacional de Investigaciones Cardiovasculares (CNIC), Advanced Development in Arrhythmia Mechanisms and Therapy Laboratory, Novel Arrhythmogenic Mechanisms Program, Madrid, Spain.ORCID 0000-0002-2047-1868
Ana Simón-ChicaCentro Nacional de Investigaciones Cardiovasculares (CNIC), Advanced Development in Arrhythmia Mechanisms and Therapy Laboratory, Novel Arrhythmogenic Mechanisms Program, Madrid, Spain.ORCID 0000-0002-0664-0397
Alba García-EscolanoCentro Nacional de Investigaciones Cardiovasculares (CNIC), Advanced Development in Arrhythmia Mechanisms and Therapy Laboratory, Novel Arrhythmogenic Mechanisms Program, Madrid, Spain.
Alba Ramos-PradaCentro Nacional de Investigaciones Cardiovasculares (CNIC), Advanced Development in Arrhythmia Mechanisms and Therapy Laboratory, Novel Arrhythmogenic Mechanisms Program, Madrid, Spain.
José Manuel Alfonso-AlmazánCentro Nacional de Investigaciones Cardiovasculares (CNIC), Advanced Development in Arrhythmia Mechanisms and Therapy Laboratory, Novel Arrhythmogenic Mechanisms Program, Madrid, Spain.
Jesús Diz-DíazCentro Nacional de Investigaciones Cardiovasculares (CNIC), Advanced Development in Arrhythmia Mechanisms and Therapy Laboratory, Novel Arrhythmogenic Mechanisms Program, Madrid, Spain.
Laura Gil-MartínezCentro de Investigación e Innovación en Bioingeniería (Ci2B), Universitat Politècnica de València, Valencia, Spain.
Sergio Muñoz-RomeroDepartamento de Teoría de la Señal y Comunicaciones y Sistemas Telemáticos y Computación, Universidad Rey Juan Carlos, Madrid, Spain.
Carlos Galán-ArriolaCentro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.
Javier Sánchez-GonzálezClinical Science, Philips Healthcare Iberia, Madrid, Spain.
Juan José González-FerrerCentro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.
Victoria Cañadas-GodoyCentro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.
Ricardo Salgado-ArandaInstituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Cardiovascular Institute, Madrid, Spain.ORCID 0000-0002-2627-8436
Alba Cruz-GalbánInstituto de Investigación Sanitaria del Hospital Clínico San Carlos (IdISSC), Cardiovascular Institute, Madrid, Spain.
María Jesús García-TorrentCentro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.
José Luis Rojo-ÁlvarezDepartamento de Teoría de la Señal y Comunicaciones y Sistemas Telemáticos y Computación, Universidad Rey Juan Carlos, Madrid, Spain.
Javier SaizCentro de Investigación e Innovación en Bioingeniería (Ci2B), Universitat Politècnica de València, Valencia, Spain.
Borja IbañezCentro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.
Julián Pérez-VillacastínCentro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.
Nicasio Pérez-CastellanoCentro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.
José JalifeCentro de Investigación Biomédica en Red de Enfermedades Cardiovasculares (CIBERCV), Madrid, Spain.
José M FerreroCentro de Investigación e Innovación en Bioingeniería (Ci2B), Universitat Politècnica de València, Valencia, Spain.
David Filgueiras-RamaCentro Nacional de Investigaciones Cardiovasculares (CNIC), Advanced Development in Arrhythmia Mechanisms and Therapy Laboratory, Novel Arrhythmogenic Mechanisms Program, Madrid, Spain.ORCID 0000-0001-5909-2454

Funding

Centro Nacional de InvestigacionesComunidad de Madrid (S2022/BMD-7229European Union NextGeneration PMP22/00185Fundación Interhospitalaria para la Investigación CardiovascularHeart Rhythm AssociationInstituto de Salud Carlos III ISCIIIMinistry of Science and Innovation MCIN/AEI/10.13039/501100011033Ministry of Science and Innovation PID2023-150456OB-I00Pro CNIC FoundationSevero Ochoa Center of Excellence CEX2020- 001041-SSevero Ochoa Center of Excellence #JDC2023-050723-ISevero Ochoa Center of Excellence LCF/BQ/DR19/11740029Severo Ochoa Center of Excellence MICIN/AEI/10.13039/501100011033Severo Ochoa Center of Excellence MICIU/AEI/10.13039/501100011033Spanish Society of Cardiology
6 · The paper itself

Abstract

aimsVentricular fibrillation (VF) is the leading cause of sudden cardiac death. Nevertheless, the mechanisms underlying VF dynamics in structurally normal hearts and infarct-related substrates remain incompletely understood. We aimed to characterize the electrophysiological, structural and molecular properties that explain VF dynamics during early phases (seconds) and long-duration episodes (minutes) in experimental pig models. Additionally, we assessed the clinical impact of VF dynamics on neurological prognosis following resuscitated cardiac arrest. METHODS AND

resultsA total of 72 pigs were included in the study. In vivo multipolar-catheter recordings revealed that early VF dynamics are independent of the infarct-related substrate. Healthy and infarcted animals consistently showed higher activation rates (AR) in the right ventricle (RV) than in the left ventricle (LV), and this gradient further increased during long-duration VF. Ex vivo panoramic optical mapping of long-duration VF episodes resembling cardiac arrest conditions confirmed in vivo findings and revealed earlier electrical depression in the LV. AR gradients during VF were primarily driven by an asymmetric response to the global ischaemia conditions intrinsically associated with VF, during which the RV exhibited greater resilience than the LV. Computational simulations, incorporating experimentally derived electrophysiological properties and region-specific metabolic parameters during ischaemia, demonstrated that the fibrillating RV preserves higher excitability than the LV, creating RV-to-LV AR gradients during VF. The translational relevance of these findings was evaluated in patients with VF events, in whom long-term (>2 min) ECG-derived AR patterns (N = 3) resembled those documented in pigs. Moreover, in 60 patients with out-of-hospital cardiac arrest, ECG-derived ARs prior to the first defibrillation shock for VF were associated with favourable neurological outcome.

conclusionVF dynamics are modulated by asymmetric myocardial tolerance to global ischaemia. Among patients admitted after a VF-related cardiac arrest event, higher ARs prior to the first defibrillation shock are predictive of a favourable neurological outcome.

Indexed as

Action PotentialsHeart ArrestHeart RateMyocardial InfarctionVentricular FibrillationAnimalsComputer SimulationDisease Models, AnimalFemaleModels, CardiovascularSus scrofaTime FactorsCardiac arrestGlobal ischemiaMyocardial infarctionVentricular fibrillation

Identifiers

PMID42203211
PMCPMC13307562

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.