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Highly trabeculated structure of the human endocardium underlies asymmetrical response to low-energy monophasic shocks
Novel low-energy defibrillation therapies are thought to be driven by virtual-electrodes (VEs), due to the interaction of applied monophasic electric shocks with fine-scale anatomical structures within the heart. Significant inter-species differences in the cardiac (micro)-anatomy exist, however, pa...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
AIP Publishing LLC
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5570597/ https://www.ncbi.nlm.nih.gov/pubmed/28964115 http://dx.doi.org/10.1063/1.4999609 |
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author | Connolly, Adam Robson, Matthew D. Schneider, Jürgen Burton, Rebecca Plank, Gernot Bishop, Martin J. |
author_facet | Connolly, Adam Robson, Matthew D. Schneider, Jürgen Burton, Rebecca Plank, Gernot Bishop, Martin J. |
author_sort | Connolly, Adam |
collection | PubMed |
description | Novel low-energy defibrillation therapies are thought to be driven by virtual-electrodes (VEs), due to the interaction of applied monophasic electric shocks with fine-scale anatomical structures within the heart. Significant inter-species differences in the cardiac (micro)-anatomy exist, however, particularly with respect to the degree of endocardial trabeculations, which may underlie important differences in response to low-energy defibrillation protocols. Understanding the interaction of monophasic electric fields with the specific human micro-anatomy is therefore imperative in facilitating the translation and optimisation of these promising experimental therapies to the clinic. In this study, we sought to investigate how electric fields from implanted devices interact with the highly trabeculated human endocardial surface to better understand shock success in order to help optimise future clinical protocols. A bi-ventricular human computational model was constructed from high resolution (350 μm) ex-vivo MR data, including anatomically accurate endocardial structures. Monophasic shocks were applied between a basal right ventricular catheter and an exterior ground. Shocks of varying strengths were applied with both anodal [positive right ventricle (RV) electrode] and cathodal (negative RV electrode) polarities at different states of tissue refractoriness and during induced arrhythmias. Anodal shocks induced isolated positive VEs at the distal side of “detached” trabeculations, which rapidly spread into hyperpolarised tissue on the surrounding endocardial surfaces following the shock. Anodal shocks thus depolarised more tissue 10 ms after the shock than cathodal shocks where the propagation of activation from VEs induced on the proximal side of “detached” trabeculations was prevented due to refractory endocardium. Anodal shocks increased arrhythmia complexity more than cathodal shocks during failed anti-arrhythmia shocks. In conclusion, multiple detached trabeculations in the human ventricle interact with anodal stimuli to induce multiple secondary sources from VEs, facilitating more rapid shock-induced ventricular excitation compared to cathodal shocks. Such a mechanism may help explain inter-species differences in response to shocks and help to develop novel defibrillation strategies. |
format | Online Article Text |
id | pubmed-5570597 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | AIP Publishing LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-55705972017-09-01 Highly trabeculated structure of the human endocardium underlies asymmetrical response to low-energy monophasic shocks Connolly, Adam Robson, Matthew D. Schneider, Jürgen Burton, Rebecca Plank, Gernot Bishop, Martin J. Chaos Focus Issue: Complex Cardiac Dynamics Novel low-energy defibrillation therapies are thought to be driven by virtual-electrodes (VEs), due to the interaction of applied monophasic electric shocks with fine-scale anatomical structures within the heart. Significant inter-species differences in the cardiac (micro)-anatomy exist, however, particularly with respect to the degree of endocardial trabeculations, which may underlie important differences in response to low-energy defibrillation protocols. Understanding the interaction of monophasic electric fields with the specific human micro-anatomy is therefore imperative in facilitating the translation and optimisation of these promising experimental therapies to the clinic. In this study, we sought to investigate how electric fields from implanted devices interact with the highly trabeculated human endocardial surface to better understand shock success in order to help optimise future clinical protocols. A bi-ventricular human computational model was constructed from high resolution (350 μm) ex-vivo MR data, including anatomically accurate endocardial structures. Monophasic shocks were applied between a basal right ventricular catheter and an exterior ground. Shocks of varying strengths were applied with both anodal [positive right ventricle (RV) electrode] and cathodal (negative RV electrode) polarities at different states of tissue refractoriness and during induced arrhythmias. Anodal shocks induced isolated positive VEs at the distal side of “detached” trabeculations, which rapidly spread into hyperpolarised tissue on the surrounding endocardial surfaces following the shock. Anodal shocks thus depolarised more tissue 10 ms after the shock than cathodal shocks where the propagation of activation from VEs induced on the proximal side of “detached” trabeculations was prevented due to refractory endocardium. Anodal shocks increased arrhythmia complexity more than cathodal shocks during failed anti-arrhythmia shocks. In conclusion, multiple detached trabeculations in the human ventricle interact with anodal stimuli to induce multiple secondary sources from VEs, facilitating more rapid shock-induced ventricular excitation compared to cathodal shocks. Such a mechanism may help explain inter-species differences in response to shocks and help to develop novel defibrillation strategies. AIP Publishing LLC 2017-09 2017-08-24 /pmc/articles/PMC5570597/ /pubmed/28964115 http://dx.doi.org/10.1063/1.4999609 Text en © 2017 Author(s). 1054-1500/2017/27(9)/093913/15 All article content, except where otherwise noted, is licensed under a Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Focus Issue: Complex Cardiac Dynamics Connolly, Adam Robson, Matthew D. Schneider, Jürgen Burton, Rebecca Plank, Gernot Bishop, Martin J. Highly trabeculated structure of the human endocardium underlies asymmetrical response to low-energy monophasic shocks |
title | Highly trabeculated structure of the human endocardium underlies asymmetrical response to low-energy monophasic shocks |
title_full | Highly trabeculated structure of the human endocardium underlies asymmetrical response to low-energy monophasic shocks |
title_fullStr | Highly trabeculated structure of the human endocardium underlies asymmetrical response to low-energy monophasic shocks |
title_full_unstemmed | Highly trabeculated structure of the human endocardium underlies asymmetrical response to low-energy monophasic shocks |
title_short | Highly trabeculated structure of the human endocardium underlies asymmetrical response to low-energy monophasic shocks |
title_sort | highly trabeculated structure of the human endocardium underlies asymmetrical response to low-energy monophasic shocks |
topic | Focus Issue: Complex Cardiac Dynamics |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5570597/ https://www.ncbi.nlm.nih.gov/pubmed/28964115 http://dx.doi.org/10.1063/1.4999609 |
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