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WIREs Syst Biol Med
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Advances in modeling ventricular arrhythmias: from mechanisms to the clinic

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Modern cardiovascular research has increasingly recognized that heart models and simulation can help interpret an array of experimental data and dissect important mechanisms and interrelationships, with developments rooted in the iterative interaction between modeling and experimentation. This article reviews the progress made in simulating cardiac electrical behavior at the level of the organ and, specifically, in the development of models of ventricular arrhythmias and fibrillation, as well as their termination (defibrillation). The ability to construct multiscale models of ventricular arrhythmias, representing integrative behavior from the molecule to the entire organ, has enabled mechanistic inquiry into the dynamics of ventricular arrhythmias in the diseased myocardium, in understanding drug‐induced proarrhythmia, and in the development of new modalities for defibrillation, to name a few. In this article, we also review the initial use of ventricular models of arrhythmia in personalized diagnosis, treatment planning, and prevention of sudden cardiac death. Implementing individualized cardiac simulations at the patient bedside is poised to become one of the most thrilling examples of computational science and engineering approaches in translational medicine. WIREs Syst Biol Med 2014, 6:209–224. doi: 10.1002/wsbm.1256 This article is categorized under: Models of Systems Properties and Processes > Organ, Tissue, and Physiological Models Translational, Genomic, and Systems Medicine > Translational Medicine

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(a and b) Wavefront dynamics during reentry are qualitatively similar in ventricular models with (a) and without (b) high‐resolution representation of anatomical microstructures. (Reprinted with permission from Ref . Copyright 2012 John Wiley & Sons)
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Low‐voltage defibrillation with a train of pulses. Low‐energy shocks (250 mV/cm) delivered at the instants when the maximal amount of myocardial volume was excitable terminated ventricular fibrillation (VF). (Reprinted with permission from Ref . Copyright 2013 Elsevier)
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(a and b) Comparison between simulation‐guided and standard electrophysiological approaches for identifying ablation targets in two patients with infarct‐related ventricular tachycardias (VTs). Left column: propagation pathways (green) and lines of conduction block (blue) are overlaid over VT activation maps simulated in image‐based patient heart models. Middle column: preablation infarct geometry (infarct scar: orange, border zone: yellow, and noninfarcted: gray) along with ablation lesions delivered by the standard approach (red circles) and conduction block lines as calculated from ventricular simulations. Right column: optimal ablation zones (green shading) predicted by simulations, with narrowest isthmuses indicated (cyan); in both cases, only a fraction of the ablation sites from the standard approach were within the predicted optimal ablation zone (yellow circles). (Reprinted with permission from Ref . Copyright 2013 Elsevier)
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(a and b) Clinical magnetic resonance imaging (MRI) scan of an infarcted patient heart and the corresponding segmentation. (c) 3D geometric model of the patient heart with the epicardium and the infarct border zone rendered semitransparent. (d) Estimated fiber orientations. (e) Simulated activation map of ventricular tachycardia (VT) revealing reentry on the left ventricular endocardium. VT frequency is 3.05 Hz. (Reprinted with permission from Ref . Copyright 2012 The American Association for the Advancement of Science)
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(a) High‐resolution magnetic resonance imaging (MRI)‐based model of the infarcted rabbit ventricle with fibroblasts incorporated in the zone of infarct. (b) Coupling of fibroblasts to myocytes results in arrhythmia. Red arrow indicates the location of the premature activation. (Reprinted with permission from Ref . Copyright 2011 Elsevier)
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(a) Model of the rabbit ventricles and Purkinje system (PS) with two possible overdrive pacing sites for supraventricular tachycardia diagnosis. (b and c) Pseudo‐ECG recordings (leads I, II, and III) during overdrive pacing from sites 1 and 2, respectively; sites closer to the PS are a poor choice in terms of diagnostic quality because they fail to produce distinct QRS complexes in simulations with (left) versus without (right) the accessory pathway. (Reprinted with permission from Ref . Copyright 2013 Elsevier)
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Translational, Genomic, and Systems Medicine > Translational Medicine
Models of Systems Properties and Processes > Organ, Tissue, and Physiological Models

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