Effects of Fibrosis Morphology on Reentrant Ventricular Tachycardia Inducibility and Simulation Fidelity in Patient-Derived Models

Myocardial fibrosis detected via delayed-enhanced magnetic resonance imaging (MRI) has been shown to be a strong indicator for ventricular tachycardia (VT) inducibility. However, little is known regarding how inducibility is affected by the details of the fibrosis extent, morphology, and border zone...

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Main Authors: Jordan Ringenberg, Makarand Deo, David Filgueiras-Rama, Gonzalo Pizarro, Borja Ibañez, Rafael Peinado, José L. Merino, Omer Berenfeld, Vijay Devabhaktuni
Format: Article
Language:English
Published: SAGE Publishing 2014-01-01
Series:Clinical Medicine Insights: Cardiology
Online Access:https://doi.org/10.4137/CMC.S15712
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spelling doaj-409483f88b9d4da3b08802355e520bed2020-11-25T02:48:08ZengSAGE PublishingClinical Medicine Insights: Cardiology1179-54682014-01-018s110.4137/CMC.S15712Effects of Fibrosis Morphology on Reentrant Ventricular Tachycardia Inducibility and Simulation Fidelity in Patient-Derived ModelsJordan Ringenberg0Makarand Deo1David Filgueiras-Rama2Gonzalo Pizarro3Borja Ibañez4Rafael Peinado5José L. Merino6Omer Berenfeld7Vijay Devabhaktuni8EECS Department, College of Engineering, University of Toledo, Toledo, OH, USA.Department of Engineering, Norfolk State University, Norfolk, VA, USA.Atherothrombosis, Imaging and Epidemiology Department, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.Department of Cardiology, Hospital Universitario Quirón, Universidad Europea de Madrid, Madrid, Spain.Atherothrombosis, Imaging and Epidemiology Department, Centro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.Cardiology Department, Hospital Universitario La Paz, Madrid, Spain.Cardiology Department, Hospital Universitario La Paz, Madrid, Spain.Center for Arrhythmia Research, Department of Internal Medicine, University of Michigan, Ann Arbor, MI, USA.EECS Department, College of Engineering, University of Toledo, Toledo, OH, USA.Myocardial fibrosis detected via delayed-enhanced magnetic resonance imaging (MRI) has been shown to be a strong indicator for ventricular tachycardia (VT) inducibility. However, little is known regarding how inducibility is affected by the details of the fibrosis extent, morphology, and border zone configuration. The objective of this article is to systematically study the arrhythmogenic effects of fibrosis geometry and extent, specifically on VT inducibility and maintenance. We present a set of methods for constructing patient-specific computational models of human ventricles using in vivo MRI data for patients suffering from hypertension, hypercholesterolemia, and chronic myocardial infarction. Additional synthesized models with morphologically varied extents of fibrosis and gray zone (GZ) distribution were derived to study the alterations in the arrhythmia induction and reentry patterns. Detailed electrophysiological simulations demonstrated that (1) VT morphology was highly dependent on the extent of fibrosis, which acts as a structural substrate, (2) reentry tended to be anchored to the fibrosis edges and showed transmural conduction of activations through narrow channels formed within fibrosis, and (3) increasing the extent of GZ within fibrosis tended to destabilize the structural reentry sites and aggravate the VT as compared to fibrotic regions of the same size and shape but with lower or no GZ. The approach and findings represent a significant step toward patient-specific cardiac modeling as a reliable tool for VT prediction and management of the patient. Sensitivities to approximation nuances in the modeling of structural pathology by image-based reconstruction techniques are also implicated.https://doi.org/10.4137/CMC.S15712
collection DOAJ
language English
format Article
sources DOAJ
author Jordan Ringenberg
Makarand Deo
David Filgueiras-Rama
Gonzalo Pizarro
Borja Ibañez
Rafael Peinado
José L. Merino
Omer Berenfeld
Vijay Devabhaktuni
spellingShingle Jordan Ringenberg
Makarand Deo
David Filgueiras-Rama
Gonzalo Pizarro
Borja Ibañez
Rafael Peinado
José L. Merino
Omer Berenfeld
Vijay Devabhaktuni
Effects of Fibrosis Morphology on Reentrant Ventricular Tachycardia Inducibility and Simulation Fidelity in Patient-Derived Models
Clinical Medicine Insights: Cardiology
author_facet Jordan Ringenberg
Makarand Deo
David Filgueiras-Rama
Gonzalo Pizarro
Borja Ibañez
Rafael Peinado
José L. Merino
Omer Berenfeld
Vijay Devabhaktuni
author_sort Jordan Ringenberg
title Effects of Fibrosis Morphology on Reentrant Ventricular Tachycardia Inducibility and Simulation Fidelity in Patient-Derived Models
title_short Effects of Fibrosis Morphology on Reentrant Ventricular Tachycardia Inducibility and Simulation Fidelity in Patient-Derived Models
title_full Effects of Fibrosis Morphology on Reentrant Ventricular Tachycardia Inducibility and Simulation Fidelity in Patient-Derived Models
title_fullStr Effects of Fibrosis Morphology on Reentrant Ventricular Tachycardia Inducibility and Simulation Fidelity in Patient-Derived Models
title_full_unstemmed Effects of Fibrosis Morphology on Reentrant Ventricular Tachycardia Inducibility and Simulation Fidelity in Patient-Derived Models
title_sort effects of fibrosis morphology on reentrant ventricular tachycardia inducibility and simulation fidelity in patient-derived models
publisher SAGE Publishing
series Clinical Medicine Insights: Cardiology
issn 1179-5468
publishDate 2014-01-01
description Myocardial fibrosis detected via delayed-enhanced magnetic resonance imaging (MRI) has been shown to be a strong indicator for ventricular tachycardia (VT) inducibility. However, little is known regarding how inducibility is affected by the details of the fibrosis extent, morphology, and border zone configuration. The objective of this article is to systematically study the arrhythmogenic effects of fibrosis geometry and extent, specifically on VT inducibility and maintenance. We present a set of methods for constructing patient-specific computational models of human ventricles using in vivo MRI data for patients suffering from hypertension, hypercholesterolemia, and chronic myocardial infarction. Additional synthesized models with morphologically varied extents of fibrosis and gray zone (GZ) distribution were derived to study the alterations in the arrhythmia induction and reentry patterns. Detailed electrophysiological simulations demonstrated that (1) VT morphology was highly dependent on the extent of fibrosis, which acts as a structural substrate, (2) reentry tended to be anchored to the fibrosis edges and showed transmural conduction of activations through narrow channels formed within fibrosis, and (3) increasing the extent of GZ within fibrosis tended to destabilize the structural reentry sites and aggravate the VT as compared to fibrotic regions of the same size and shape but with lower or no GZ. The approach and findings represent a significant step toward patient-specific cardiac modeling as a reliable tool for VT prediction and management of the patient. Sensitivities to approximation nuances in the modeling of structural pathology by image-based reconstruction techniques are also implicated.
url https://doi.org/10.4137/CMC.S15712
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