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dc.contributor.authorViadero Ubierna, María Teresa 
dc.contributor.authorCaldeiro Diaz, María Jesús
dc.contributor.authorFernández Suárez, Natalia
dc.contributor.authorGarde Basas, Jesús
dc.contributor.authorCabero Pérez, María Jesús 
dc.contributor.authorGonzález-Lamuño Leguina, Domingo 
dc.contributor.otherUniversidad de Cantabriaes_ES
dc.date.accessioned2025-09-29T08:17:49Z
dc.date.available2025-09-29T08:17:49Z
dc.date.issued2025
dc.identifier.issn1661-6596
dc.identifier.issn1422-0067
dc.identifier.urihttps://hdl.handle.net/10902/37497
dc.description.abstractAbstract: Multisystem inflammatory syndrome in children (MIS-C), also known as pediatric inflammatory multisystem syndrome (PIMS), presents significant challenges in pediatric cardiology, due to its complex molecular pathophysiology. In this retrospective analysis of 15 cases that were managed at a single tertiary care center, we investigated the molecular contributors to myocardial dysfunction, including cytokine storms, hyperinflammation markers, and hypercoagulable states. Transient myocardial involvement was identified in 46.6% of patients, with complete recovery achieved within 2?4 weeks following treatment. Ferritin, NT-ProBNP, and troponin levels were significantly elevated in patients with ventricular dysfunction compared to those without. The neutrophil-to-lymphocyte ratio (NLR), which was previously identified as a severity marker in acute COVID-19, was also significantly higher in patients with ventricular dysfunction, suggesting its potential as a prognostic indicator in MIS-C. Notably, no coronary artery aneurysms were detected in the cohort. These findings underscore the importance of early, standardized therapeutic interventions in mitigating severe outcomes, and they provide valuable insights into the molecular mechanisms driving myocardial dysfunction in MIS-C. Incorporating NLR and ferritin into the initial diagnostic workup may improve the early triage and identification of high-risk MIS-C patients.es_ES
dc.format.extent16 p.es_ES
dc.language.isoenges_ES
dc.publisherMDPIes_ES
dc.rights© 2025 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) licensees_ES
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/*
dc.sourceInternational Journal of Molecular Sciences, 2025, 26(8), 3580es_ES
dc.subject.otherPediatric inflammatory multisystem syndrome (PIMS)es_ES
dc.subject.otherMultisystem inflammatory syndrome in children (MIS-C)es_ES
dc.subject.otherMyocardial dysfunctiones_ES
dc.subject.otherCytokine stormes_ES
dc.subject.otherEndothelial dysfunctiones_ES
dc.subject.otherSARS-CoV-2es_ES
dc.subject.otherKawasaki diseasees_ES
dc.subject.otherBiomarkerses_ES
dc.subject.otherIVIGes_ES
dc.subject.otherCorticosteroidses_ES
dc.titleMolecular Mechanisms and Pathophysiology of Myocardial Disease: Insights from Pediatric Inflammatory Multisystem Syndrome (PIMS) Associated with SARS-CoV-2es_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.relation.publisherVersionhttps://doi.org/10.3390/ijms26083580es_ES
dc.rights.accessRightsopenAccesses_ES
dc.identifier.DOI10.3390/ijms26083580
dc.type.versionpublishedVersiones_ES


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© 2025 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) licenseExcepto si se señala otra cosa, la licencia del ítem se describe como © 2025 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license