Image‐based models of cardiac structure in health and disease

Vadakkumpadan, Fijoy; Arevalo, Hermenegild; Prassl, Anton J.; Chen, Junjie; Kickinger, Ferdinand; Kohl, Peter; Plank, Gernot; Trayanova, Natalia A.

doi:10.1002/wsbm.76

Cited by 114 publications

(125 citation statements)

References 67 publications

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“…As well as examining normal cardiac structure, DT-MRI can also be used to identify and segment pathological cardiac tissue-FA, for example, has been used to segment infarcted tissue [76]. Figure 8 illustrates this for an infarct produced by coronary artery ligation in a rabbit.…”

Section: Going Beyond the Healthy Heart: Infarctionmentioning

confidence: 99%

Construction and validation of anisotropic and orthotropic ventricular geometries for quantitative predictive cardiac electrophysiology

et al. 2010

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Reaction -diffusion computational models of cardiac electrophysiology require both dynamic excitation models that reconstruct the action potentials of myocytes as well as datasets of cardiac geometry and architecture that provide the electrical diffusion tensor D, which determines how excitation spreads through the tissue. We illustrate an experimental pipeline we have developed in our laboratories for constructing and validating such datasets. The tensor D changes with location in the myocardium, and is determined by tissue architecture. Diffusion tensor magnetic resonance imaging (DT-MRI) provides three eigenvectors e i and eigenvalues l i at each voxel throughout the tissue that can be used to reconstruct this architecture. The primary eigenvector e 1 is a histologically validated measure of myocyte orientation (responsible for anisotropic propagation). The secondary and tertiary eigenvectors (e 2 and e 3 ) specify the directions of any orthotropic structure if l 2 is significantly greater than l 3 -this orthotropy has been identified with sheets or cleavage planes. For simulations, the components of D are scaled in the fibre and cross-fibre directions for anisotropic simulations (or fibre, sheet and sheet normal directions for orthotropic tissues) so that simulated conduction velocities match values from optical imaging or plunge electrode experiments. The simulated pattern of propagation of action potentials in the models is partially validated by optical recordings of spatio-temporal activity on the surfaces of hearts. We also describe several techniques that enhance components of the pipeline, or that allow the pipeline to be applied to different areas of research: Q ball imaging provides evidence for multi-modal orientation distributions within a fraction of voxels, infarcts can be identified by changes in the anisotropic structure-irregularity in myocyte orientation and a decrease in fractional anisotropy, clinical imaging provides human ventricular geometry and can identify ischaemic and infarcted regions, and simulations in human geometries examine the roles of anisotropic and orthotropic architecture in the initiation of arrhythmias.

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Section: Going Beyond the Healthy Heart: Infarctionmentioning

confidence: 99%

Construction and validation of anisotropic and orthotropic ventricular geometries for quantitative predictive cardiac electrophysiology

et al. 2010

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“…The rhythm is generated by pacemaking activity in specialized cardiomyocytes that drive propagating waves of excitation in the myocardium and conducting system, and that trigger the alternating contractions of the atria and ventricles. The computational biology of the electrodynamics of the heart [1] is largely based on models and datasets that have been constructed from in vitro and in vivo experiments on isolated cells, tissue and organs extracted from laboratory animals. These computational models require datasets of cardiac geometry, its spatially heterogeneous architecture and electrophysiology, from which the spatio-temporal patterns of excitation and the resulting deformations can be computed [2,3].…”

Section: Introductionmentioning

confidence: 99%

Antenatal architecture and activity of the human heart

et al. 2013

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One contribution of 25 to a Theme Issue 'The virtual physiological human: integrative approaches to computational biomedicine'. We construct the components for a family of computational models of the electrophysiology of the human foetal heart from 60 days gestational age (DGA) to full term. This requires both cell excitation models that reconstruct the myocyte action potentials, and datasets of cardiac geometry and architecture. Fast lowangle shot and diffusion tensor magnetic resonance imaging (DT-MRI) of foetal hearts provides cardiac geometry with voxel resolution of approximately 100 mm. DT-MRI measures the relative diffusion of protons and provides a measure of the average intravoxel myocyte orientation, and the orientation of any higher order orthotropic organization of the tissue. Such orthotropic organization in the adult mammalian heart has been identified with myocardial sheets and cleavage planes between them. During gestation, the architecture of the human ventricular wall changes from being irregular and isotropic at 100 DGA to an anisotropic and orthotropic architecture by 140 DGA, when it has the smooth, approximately 1208 transmural change in myocyte orientation that is characteristic of the adult mammalian ventricle. The DT obtained from DT-MRI provides the conductivity tensor that determines the spread of potential within computational models of cardiac tissue electrophysiology. The foetal electrocardiogram (fECG) can be recorded from approximately 60 DGA, and RR, PR and QT intervals between the P, R, Q and T waves of the fECG can be extracted by averaging from approximately 90 DGA. The RR intervals provide a measure of the pacemaker rate, the QT intervals an index of ventricular action potential duration, and its rate-dependence, and so these intervals constrain and inform models of cell electrophysiology. The parameters of models of adult human sinostrial node and ventricular cells that are based on adult cell electrophysiology and tissue molecular mapping have been modified to construct preliminary models of foetal cell electrophysiology, which reproduce these intervals from fECG recordings. The PR and QR intervals provide an index of conduction times, and hence propagation velocities (approx. 1-10 cm s 21, increasing during gestation) and so inform models of tissue electrophysiology. Although the developing foetal heart is small and the cells are weakly coupled, it can support potentially lethal re-entrant arrhythmia.

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“…13,27,[29][30][31] Accurate reconstruction of ventricular geometry has been validated with ex-vivo and in-vivo imaging datasets. 12,32 The approach to construct a model of the iv64 infarcted ventricles by thresholding the infarct into only scar and (homogeneous) grey zone, as done in the present study, without accounting for additional small-scale heterogeneities in the grey zone, has been recently validated with experimental data. Specifically, Deng et al 13 used sock epicardial data for infarct-related VT, obtained from in-vivo swine heart, and demonstrated that ventricular models reconstructed from MRI data of the corresponding hearts were able to predict fairly accurately the morphology of each VT reentrant circuit and its organizing centre (e.g.…”

Section: 31mentioning

confidence: 99%