Sensitivity of Ablation Targets Prediction to Electrophysiological Parameter Variability in Image-Based Computational Models of Ventricular Tachycardia in Post-infarction Patients

Sensitivity of reentrant driver localization to electrophysiological parameter variability in image-based computational models of persistent atrial fibrillation sustained by a fibrotic substrate

Chaos An Interdisciplinary Journal of Nonlinear Science ◽

10.1063/1.5003340 ◽

2017 ◽

Vol 27 (9) ◽

pp. 093932 ◽

Cited By ~ 28

Author(s):

Dongdong Deng ◽

Michael J. Murphy ◽

Joe B. Hakim ◽

William H. Franceschi ◽

Sohail Zahid ◽

...

Keyword(s):

Atrial Fibrillation ◽

Computational Models ◽

Persistent Atrial Fibrillation ◽

Electrophysiological Parameter

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

Clinical Medicine Insights Cardiology ◽

10.4137/cmc.s15712 ◽

2014 ◽

Vol 8s1 ◽

pp. CMC.S15712 ◽

Cited By ~ 8

Author(s):

Jordan Ringenberg ◽

Makarand Deo ◽

David Filgueiras-Rama ◽

Gonzalo Pizarro ◽

Borja Ibañez ◽

...

Keyword(s):

Ventricular Tachycardia ◽

Computational Models ◽

Border Zone ◽

Patient Specific ◽

Narrow Channels ◽

Simulation Fidelity ◽

Strong Indicator ◽

Significant Step ◽

Magnetic Resonance Imaging Mri

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.

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