Remodeling of cardiac passive electrical properties and susceptibility to ventricular and atrial arrhythmias

The effective management of cardiac arrhythmias, either of atrial or of ventricular origin, remains a major challenge. Sudden cardiac death due to ventricular tachyarrhythmias remains the leading cause of death in industrialized countries while atrial fibrillation is the most common rhythm disorder;...

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Auteur principal: George E. Billman
Format: Online
Langue:anglais
Publié: Frontiers Media SA 2021
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Accès en ligne:19550
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author George E. Billman
author_browse George E. Billman
author_facet George E. Billman
author_sort George E. Billman
collection Directory of Open Access Books
description The effective management of cardiac arrhythmias, either of atrial or of ventricular origin, remains a major challenge. Sudden cardiac death due to ventricular tachyarrhythmias remains the leading cause of death in industrialized countries while atrial fibrillation is the most common rhythm disorder; an arrhythmia that’s prevalence is increasing and accounts for nearly one quarter of ischemic stokes the elderly population. Yet, despite the enormity of the problem, effective therapeutic interventions remain elusive. In fact, several initially promising antiarrhythmic agents were found to increase rather than decrease mortality in patients recovering from myocardial infarction. The question then is what went wrong, why have these interventions proven to be so ineffective? An obvious answer is the drugs were designed to attack the wrong therapeutic target. Clearly, targeting single ion channels (using either isolated ion channels or single myocytes preparations) has proven to be less than effective. What then is the appropriate target? It is well established that cardiac electrical properties can vary substantially between single cells and intact preparations. One obvious example is the observation that action potential duration is much longer in isolated cells as compared to multi-cellular preparations or intact hearts. Due to the low electrical resistance between adjacent myocytes, the cells act in coordinated fashion producing “electrotonic interdependence” between neighboring cells. Myocardial infarction and/or acute ischemia provoke profound changes in the passive electrical properties of cardiac muscle. In particular, electrotonic uncoupling of the myocytes disrupts the coordinated activation and repolarization of cardiac tissue. The resulting compensatory changes in ionic currents decrease cardiac electrical stability increasing the risk for life-threatening changes in the cardiac rhythm. Thus, the electrical properties of myocardial cells must be considered as a unit rather than in isolation. It is the purpose of this Research Topic to evaluate the largely neglected relationship between changes in passive electrical properties of cardiac muscle and arrhythmia formation.
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spelling doab-20.500.12854ir-581632024-03-31T22:45:09Z Remodeling of cardiac passive electrical properties and susceptibility to ventricular and atrial arrhythmias George E. Billman QP1-981 Q1-390 Gap Junctions Myocardial Infarction computer modeling arrhythmias Fibrosis electrotonic coupling cable theory sino-atrial node Ventricular Fibrillation Atrial Fibrillation thema EDItEUR::M Medicine and Nursing::MF Pre-clinical medicine: basic sciences::MFG Physiology The effective management of cardiac arrhythmias, either of atrial or of ventricular origin, remains a major challenge. Sudden cardiac death due to ventricular tachyarrhythmias remains the leading cause of death in industrialized countries while atrial fibrillation is the most common rhythm disorder; an arrhythmia that’s prevalence is increasing and accounts for nearly one quarter of ischemic stokes the elderly population. Yet, despite the enormity of the problem, effective therapeutic interventions remain elusive. In fact, several initially promising antiarrhythmic agents were found to increase rather than decrease mortality in patients recovering from myocardial infarction. The question then is what went wrong, why have these interventions proven to be so ineffective? An obvious answer is the drugs were designed to attack the wrong therapeutic target. Clearly, targeting single ion channels (using either isolated ion channels or single myocytes preparations) has proven to be less than effective. What then is the appropriate target? It is well established that cardiac electrical properties can vary substantially between single cells and intact preparations. One obvious example is the observation that action potential duration is much longer in isolated cells as compared to multi-cellular preparations or intact hearts. Due to the low electrical resistance between adjacent myocytes, the cells act in coordinated fashion producing “electrotonic interdependence” between neighboring cells. Myocardial infarction and/or acute ischemia provoke profound changes in the passive electrical properties of cardiac muscle. In particular, electrotonic uncoupling of the myocytes disrupts the coordinated activation and repolarization of cardiac tissue. The resulting compensatory changes in ionic currents decrease cardiac electrical stability increasing the risk for life-threatening changes in the cardiac rhythm. Thus, the electrical properties of myocardial cells must be considered as a unit rather than in isolation. It is the purpose of this Research Topic to evaluate the largely neglected relationship between changes in passive electrical properties of cardiac muscle and arrhythmia formation. 2021-02-12T01:47:08Z 2021-02-12T01:47:08Z 2016-08-16 10:34:25 2015 book 19550 16648714 9782889196470 https://directory.doabooks.org/handle/20.500.12854/58163 eng Frontiers Research Topics image/jpeg Attribution 4.0 International http://www.frontiersin.org/books/Remodeling_of_cardiac_passive_electrical_properties_and_susceptibility_to_ventricular_and_atrial_ar/690#nogo http://journal.frontiersin.org/researchtopic/2057/remodeling-of-cardiac-passive-electrical-properties-and-susceptibility-to-ventricular-and-atrial-arr Frontiers Media SA 10.3389/978-2-88919-647-0 10.3389/978-2-88919-647-0 bf5ce210-e72e-4860-ba9b-c305640ff3ae 9782889196470 141 open access
spellingShingle QP1-981
Q1-390
Gap Junctions
Myocardial Infarction
computer modeling
arrhythmias
Fibrosis
electrotonic coupling
cable theory
sino-atrial node
Ventricular Fibrillation
Atrial Fibrillation
thema EDItEUR::M Medicine and Nursing::MF Pre-clinical medicine: basic sciences::MFG Physiology
George E. Billman
Remodeling of cardiac passive electrical properties and susceptibility to ventricular and atrial arrhythmias
title Remodeling of cardiac passive electrical properties and susceptibility to ventricular and atrial arrhythmias
title_full Remodeling of cardiac passive electrical properties and susceptibility to ventricular and atrial arrhythmias
title_fullStr Remodeling of cardiac passive electrical properties and susceptibility to ventricular and atrial arrhythmias
title_full_unstemmed Remodeling of cardiac passive electrical properties and susceptibility to ventricular and atrial arrhythmias
title_short Remodeling of cardiac passive electrical properties and susceptibility to ventricular and atrial arrhythmias
title_sort remodeling of cardiac passive electrical properties and susceptibility to ventricular and atrial arrhythmias
topic QP1-981
Q1-390
Gap Junctions
Myocardial Infarction
computer modeling
arrhythmias
Fibrosis
electrotonic coupling
cable theory
sino-atrial node
Ventricular Fibrillation
Atrial Fibrillation
thema EDItEUR::M Medicine and Nursing::MF Pre-clinical medicine: basic sciences::MFG Physiology
topic_facet QP1-981
Q1-390
Gap Junctions
Myocardial Infarction
computer modeling
arrhythmias
Fibrosis
electrotonic coupling
cable theory
sino-atrial node
Ventricular Fibrillation
Atrial Fibrillation
thema EDItEUR::M Medicine and Nursing::MF Pre-clinical medicine: basic sciences::MFG Physiology
url 19550
work_keys_str_mv AT georgeebillman remodelingofcardiacpassiveelectricalpropertiesandsusceptibilitytoventricularandatrialarrhythmias