Molecular Mechanisms and Pathophysiology of Myocardial Disease: Insights from Pediatric Inflammatory Multisystem Syndrome (PIMS) Associated with SARS-CoV-2
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Identificadores
URI: https://hdl.handle.net/10902/37497DOI: 10.3390/ijms26083580
ISSN: 1661-6596
ISSN: 1422-0067
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Viadero Ubierna, María Teresa
; Caldeiro Diaz, María Jesús; Fernández Suárez, Natalia; Garde Basas, Jesús; Cabero Pérez, María Jesús
; González-Lamuño Leguina, Domingo
Fecha
2025Derechos
© 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
Publicado en
International Journal of Molecular Sciences, 2025, 26(8), 3580
Editorial
MDPI
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Palabras clave
Pediatric inflammatory multisystem syndrome (PIMS)
Multisystem inflammatory syndrome in children (MIS-C)
Myocardial dysfunction
Cytokine storm
Endothelial dysfunction
SARS-CoV-2
Kawasaki disease
Biomarkers
IVIG
Corticosteroids
Resumen/Abstract
Abstract: 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.
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