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Cardiac Conduction Velocity, Remodeling and Arrhythmogenesis

Cardiac electrophysiological disorders, in particular arrhythmias, are a key cause of morbidity and mortality throughout the world. There are two basic requirements for arrhythmogenesis: an underlying substrate and a trigger. Altered conduction velocity (CV) provides a key substrate for arrhythmogen...

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Autores principales: Han, Bo, Trew, Mark L., Zgierski-Johnston, Callum M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8616078/
https://www.ncbi.nlm.nih.gov/pubmed/34831145
http://dx.doi.org/10.3390/cells10112923
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author Han, Bo
Trew, Mark L.
Zgierski-Johnston, Callum M.
author_facet Han, Bo
Trew, Mark L.
Zgierski-Johnston, Callum M.
author_sort Han, Bo
collection PubMed
description Cardiac electrophysiological disorders, in particular arrhythmias, are a key cause of morbidity and mortality throughout the world. There are two basic requirements for arrhythmogenesis: an underlying substrate and a trigger. Altered conduction velocity (CV) provides a key substrate for arrhythmogenesis, with slowed CV increasing the probability of re-entrant arrhythmias by reducing the length scale over which re-entry can occur. In this review, we examine methods to measure cardiac CV in vivo and ex vivo, discuss underlying determinants of CV, and address how pathological variations alter CV, potentially increasing arrhythmogenic risk. Finally, we will highlight future directions both for methodologies to measure CV and for possible treatments to restore normal CV.
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spelling pubmed-86160782021-11-26 Cardiac Conduction Velocity, Remodeling and Arrhythmogenesis Han, Bo Trew, Mark L. Zgierski-Johnston, Callum M. Cells Review Cardiac electrophysiological disorders, in particular arrhythmias, are a key cause of morbidity and mortality throughout the world. There are two basic requirements for arrhythmogenesis: an underlying substrate and a trigger. Altered conduction velocity (CV) provides a key substrate for arrhythmogenesis, with slowed CV increasing the probability of re-entrant arrhythmias by reducing the length scale over which re-entry can occur. In this review, we examine methods to measure cardiac CV in vivo and ex vivo, discuss underlying determinants of CV, and address how pathological variations alter CV, potentially increasing arrhythmogenic risk. Finally, we will highlight future directions both for methodologies to measure CV and for possible treatments to restore normal CV. MDPI 2021-10-28 /pmc/articles/PMC8616078/ /pubmed/34831145 http://dx.doi.org/10.3390/cells10112923 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
Han, Bo
Trew, Mark L.
Zgierski-Johnston, Callum M.
Cardiac Conduction Velocity, Remodeling and Arrhythmogenesis
title Cardiac Conduction Velocity, Remodeling and Arrhythmogenesis
title_full Cardiac Conduction Velocity, Remodeling and Arrhythmogenesis
title_fullStr Cardiac Conduction Velocity, Remodeling and Arrhythmogenesis
title_full_unstemmed Cardiac Conduction Velocity, Remodeling and Arrhythmogenesis
title_short Cardiac Conduction Velocity, Remodeling and Arrhythmogenesis
title_sort cardiac conduction velocity, remodeling and arrhythmogenesis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8616078/
https://www.ncbi.nlm.nih.gov/pubmed/34831145
http://dx.doi.org/10.3390/cells10112923
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