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Electrical Ventricular Remodeling in Dilated Cardiomyopathy

Ventricular arrhythmias contribute significantly to morbidity and mortality in patients with heart failure (HF). Pathomechanisms underlying arrhythmogenicity in patients with structural heart disease and impaired cardiac function include myocardial fibrosis and the remodeling of ion channels, affect...

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Autores principales: Mages, Christine, Gampp, Heike, Syren, Pascal, Rahm, Ann-Kathrin, André, Florian, Frey, Norbert, Lugenbiel, Patrick, Thomas, Dierk
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8534398/
https://www.ncbi.nlm.nih.gov/pubmed/34685747
http://dx.doi.org/10.3390/cells10102767
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author Mages, Christine
Gampp, Heike
Syren, Pascal
Rahm, Ann-Kathrin
André, Florian
Frey, Norbert
Lugenbiel, Patrick
Thomas, Dierk
author_facet Mages, Christine
Gampp, Heike
Syren, Pascal
Rahm, Ann-Kathrin
André, Florian
Frey, Norbert
Lugenbiel, Patrick
Thomas, Dierk
author_sort Mages, Christine
collection PubMed
description Ventricular arrhythmias contribute significantly to morbidity and mortality in patients with heart failure (HF). Pathomechanisms underlying arrhythmogenicity in patients with structural heart disease and impaired cardiac function include myocardial fibrosis and the remodeling of ion channels, affecting electrophysiologic properties of ventricular cardiomyocytes. The dysregulation of ion channel expression has been associated with cardiomyopathy and with the development of arrhythmias. However, the underlying molecular signaling pathways are increasingly recognized. This review summarizes clinical and cellular electrophysiologic characteristics observed in dilated cardiomyopathy (DCM) with ionic and structural alterations at the ventricular level. Furthermore, potential translational strategies and therapeutic options are highlighted.
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spelling pubmed-85343982021-10-23 Electrical Ventricular Remodeling in Dilated Cardiomyopathy Mages, Christine Gampp, Heike Syren, Pascal Rahm, Ann-Kathrin André, Florian Frey, Norbert Lugenbiel, Patrick Thomas, Dierk Cells Review Ventricular arrhythmias contribute significantly to morbidity and mortality in patients with heart failure (HF). Pathomechanisms underlying arrhythmogenicity in patients with structural heart disease and impaired cardiac function include myocardial fibrosis and the remodeling of ion channels, affecting electrophysiologic properties of ventricular cardiomyocytes. The dysregulation of ion channel expression has been associated with cardiomyopathy and with the development of arrhythmias. However, the underlying molecular signaling pathways are increasingly recognized. This review summarizes clinical and cellular electrophysiologic characteristics observed in dilated cardiomyopathy (DCM) with ionic and structural alterations at the ventricular level. Furthermore, potential translational strategies and therapeutic options are highlighted. MDPI 2021-10-15 /pmc/articles/PMC8534398/ /pubmed/34685747 http://dx.doi.org/10.3390/cells10102767 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/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 (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Mages, Christine
Gampp, Heike
Syren, Pascal
Rahm, Ann-Kathrin
André, Florian
Frey, Norbert
Lugenbiel, Patrick
Thomas, Dierk
Electrical Ventricular Remodeling in Dilated Cardiomyopathy
title Electrical Ventricular Remodeling in Dilated Cardiomyopathy
title_full Electrical Ventricular Remodeling in Dilated Cardiomyopathy
title_fullStr Electrical Ventricular Remodeling in Dilated Cardiomyopathy
title_full_unstemmed Electrical Ventricular Remodeling in Dilated Cardiomyopathy
title_short Electrical Ventricular Remodeling in Dilated Cardiomyopathy
title_sort electrical ventricular remodeling in dilated cardiomyopathy
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8534398/
https://www.ncbi.nlm.nih.gov/pubmed/34685747
http://dx.doi.org/10.3390/cells10102767
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