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Electrophysiological Consequences of Cardiac Fibrosis

For both the atria and ventricles, fibrosis is generally recognized as one of the key determinants of conduction disturbances. By definition, fibrosis refers to an increased amount of fibrous tissue. However, fibrosis is not a singular entity. Various forms can be distinguished, that differ in distr...

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Autores principales: Verheule, Sander, Schotten, Ulrich
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8625398/
https://www.ncbi.nlm.nih.gov/pubmed/34831442
http://dx.doi.org/10.3390/cells10113220
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author Verheule, Sander
Schotten, Ulrich
author_facet Verheule, Sander
Schotten, Ulrich
author_sort Verheule, Sander
collection PubMed
description For both the atria and ventricles, fibrosis is generally recognized as one of the key determinants of conduction disturbances. By definition, fibrosis refers to an increased amount of fibrous tissue. However, fibrosis is not a singular entity. Various forms can be distinguished, that differ in distribution: replacement fibrosis, endomysial and perimysial fibrosis, and perivascular, endocardial, and epicardial fibrosis. These different forms typically result from diverging pathophysiological mechanisms and can have different consequences for conduction. The impact of fibrosis on propagation depends on exactly how the patterns of electrical connections between myocytes are altered. We will therefore first consider the normal patterns of electrical connections and their regional diversity as determinants of propagation. Subsequently, we will summarize current knowledge on how different forms of fibrosis lead to a loss of electrical connectivity in order to explain their effects on propagation and mechanisms of arrhythmogenesis, including ectopy, reentry, and alternans. Finally, we will discuss a histological quantification of fibrosis. Because of the different forms of fibrosis and their diverging effects on electrical propagation, the total amount of fibrosis is a poor indicator for the effect on conduction. Ideally, an assessment of cardiac fibrosis should exclude fibrous tissue that does not affect conduction and differentiate between the various types that do; in this article, we highlight practical solutions for histological analysis that meet these requirements.
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spelling pubmed-86253982021-11-27 Electrophysiological Consequences of Cardiac Fibrosis Verheule, Sander Schotten, Ulrich Cells Review For both the atria and ventricles, fibrosis is generally recognized as one of the key determinants of conduction disturbances. By definition, fibrosis refers to an increased amount of fibrous tissue. However, fibrosis is not a singular entity. Various forms can be distinguished, that differ in distribution: replacement fibrosis, endomysial and perimysial fibrosis, and perivascular, endocardial, and epicardial fibrosis. These different forms typically result from diverging pathophysiological mechanisms and can have different consequences for conduction. The impact of fibrosis on propagation depends on exactly how the patterns of electrical connections between myocytes are altered. We will therefore first consider the normal patterns of electrical connections and their regional diversity as determinants of propagation. Subsequently, we will summarize current knowledge on how different forms of fibrosis lead to a loss of electrical connectivity in order to explain their effects on propagation and mechanisms of arrhythmogenesis, including ectopy, reentry, and alternans. Finally, we will discuss a histological quantification of fibrosis. Because of the different forms of fibrosis and their diverging effects on electrical propagation, the total amount of fibrosis is a poor indicator for the effect on conduction. Ideally, an assessment of cardiac fibrosis should exclude fibrous tissue that does not affect conduction and differentiate between the various types that do; in this article, we highlight practical solutions for histological analysis that meet these requirements. MDPI 2021-11-18 /pmc/articles/PMC8625398/ /pubmed/34831442 http://dx.doi.org/10.3390/cells10113220 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
Verheule, Sander
Schotten, Ulrich
Electrophysiological Consequences of Cardiac Fibrosis
title Electrophysiological Consequences of Cardiac Fibrosis
title_full Electrophysiological Consequences of Cardiac Fibrosis
title_fullStr Electrophysiological Consequences of Cardiac Fibrosis
title_full_unstemmed Electrophysiological Consequences of Cardiac Fibrosis
title_short Electrophysiological Consequences of Cardiac Fibrosis
title_sort electrophysiological consequences of cardiac fibrosis
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8625398/
https://www.ncbi.nlm.nih.gov/pubmed/34831442
http://dx.doi.org/10.3390/cells10113220
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