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:	Sander Verheule, Ulrich Schotten
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	fibrosis conduction arrhythmias tissue structure heart Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/5cf7b3733fc34b5daa801b81eb39769f
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spelling	oai:doaj.org-article:5cf7b3733fc34b5daa801b81eb39769f2021-11-25T17:13:00ZElectrophysiological Consequences of Cardiac Fibrosis10.3390/cells101132202073-4409https://doaj.org/article/5cf7b3733fc34b5daa801b81eb39769f2021-11-01T00:00:00Zhttps://www.mdpi.com/2073-4409/10/11/3220https://doaj.org/toc/2073-4409For 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.Sander VerheuleUlrich SchottenMDPI AGarticlefibrosisconductionarrhythmiastissue structureheartBiology (General)QH301-705.5ENCells, Vol 10, Iss 3220, p 3220 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	fibrosis conduction arrhythmias tissue structure heart Biology (General) QH301-705.5
spellingShingle	fibrosis conduction arrhythmias tissue structure heart Biology (General) QH301-705.5 Sander Verheule Ulrich Schotten Electrophysiological Consequences of Cardiac Fibrosis
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.
format	article
author	Sander Verheule Ulrich Schotten
author_facet	Sander Verheule Ulrich Schotten
author_sort	Sander Verheule
title	Electrophysiological Consequences of Cardiac Fibrosis
title_short	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_sort	electrophysiological consequences of cardiac fibrosis
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/5cf7b3733fc34b5daa801b81eb39769f
work_keys_str_mv	AT sanderverheule electrophysiologicalconsequencesofcardiacfibrosis AT ulrichschotten electrophysiologicalconsequencesofcardiacfibrosis
_version_	1718412589515407360

Electrophysiological Consequences of Cardiac Fibrosis

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