106 research outputs found
Incorporating Inductances in Tissue-Scale Models of Cardiac Electrophysiology
In standard models of cardiac electrophysiology, including the bidomain and
monodomain models, local perturbations can propagate at infinite speed. We
address this unrealistic property by developing a hyperbolic bidomain model
that is based on a generalization of Ohm's law with a Cattaneo-type model for
the fluxes. Further, we obtain a hyperbolic monodomain model in the case that
the intracellular and extracellular conductivity tensors have the same
anisotropy ratio. In one spatial dimension, the hyperbolic monodomain model is
equivalent to a cable model that includes axial inductances, and the relaxation
times of the Cattaneo fluxes are strictly related to these inductances. A
purely linear analysis shows that the inductances are negligible, but models of
cardiac electrophysiology are highly nonlinear, and linear predictions may not
capture the fully nonlinear dynamics. In fact, contrary to the linear analysis,
we show that for simple nonlinear ionic models, an increase in conduction
velocity is obtained for small and moderate values of the relaxation time. A
similar behavior is also demonstrated with biophysically detailed ionic models.
Using the Fenton-Karma model along with a low-order finite element spatial
discretization, we numerically analyze differences between the standard
monodomain model and the hyperbolic monodomain model. In a simple benchmark
test, we show that the propagation of the action potential is strongly
influenced by the alignment of the fibers with respect to the mesh in both the
parabolic and hyperbolic models when using relatively coarse spatial
discretizations. Accurate predictions of the conduction velocity require
computational mesh spacings on the order of a single cardiac cell. We also
compare the two formulations in the case of spiral break up and atrial
fibrillation in an anatomically detailed model of the left atrium, and [...].Comment: 20 pages, 12 figure
Comparison of Propagation Models and Forward Calculation Methods on Cellular, Tissue and Organ Scale Atrial Electrophysiology
The bidomain model and the finite element method are an established standard to mathematically describe cardiac electrophysiology, but are both suboptimal choices for fast and large-scale simulations due to high computational costs. We investigate to what extent simplified approaches for propagation models (monodomain, reaction-Eikonal and Eikonal) and forward calculation (boundary element and infinite volume conductor) deliver markedly accelerated, yet physiologically accurate simulation results in atrial electrophysiology. Methods: We compared action potential durations, local activation times (LATs), and electrocardiograms (ECGs) for sinus rhythm simulations on healthy and fibrotically infiltrated atrial models. Results: All simplified model solutions yielded LATs and P waves in accurate accordance with the bidomain results. Only for the Eikonal model with pre-computed action potential templates shifted in time to derive transmembrane voltages, repolarization behavior notably deviated from the bidomain results. ECGs calculated with the boundary element method were characterized by correlation coefficients >0.9 compared to the finite element method. The infinite volume conductor method led to lower correlation coefficients caused predominantly by systematic overestimations of P wave amplitudes in the precordial leads. Conclusion: Our results demonstrate that the Eikonal model yields accurate LATs and combined with the boundary element method precise ECGs compared to markedly more expensive full bidomain simulations. However, for an accurate representation of atrial repolarization dynamics, diffusion terms must be accounted for in simplified models. Significance: Simulations of atrial LATs and ECGs can be notably accelerated to clinically feasible time frames at high accuracy by resorting to the Eikonal and boundary element methods
A multiresolution space-time adaptive scheme for the bidomain model in electrocardiology
This work deals with the numerical solution of the monodomain and bidomain
models of electrical activity of myocardial tissue. The bidomain model is a
system consisting of a possibly degenerate parabolic PDE coupled with an
elliptic PDE for the transmembrane and extracellular potentials, respectively.
This system of two scalar PDEs is supplemented by a time-dependent ODE modeling
the evolution of the so-called gating variable. In the simpler sub-case of the
monodomain model, the elliptic PDE reduces to an algebraic equation. Two simple
models for the membrane and ionic currents are considered, the
Mitchell-Schaeffer model and the simpler FitzHugh-Nagumo model. Since typical
solutions of the bidomain and monodomain models exhibit wavefronts with steep
gradients, we propose a finite volume scheme enriched by a fully adaptive
multiresolution method, whose basic purpose is to concentrate computational
effort on zones of strong variation of the solution. Time adaptivity is
achieved by two alternative devices, namely locally varying time stepping and a
Runge-Kutta-Fehlberg-type adaptive time integration. A series of numerical
examples demonstrates thatthese methods are efficient and sufficiently accurate
to simulate the electrical activity in myocardial tissue with affordable
effort. In addition, an optimalthreshold for discarding non-significant
information in the multiresolution representation of the solution is derived,
and the numerical efficiency and accuracy of the method is measured in terms of
CPU time speed-up, memory compression, and errors in different norms.Comment: 25 pages, 41 figure
The LifeV library: engineering mathematics beyond the proof of concept
LifeV is a library for the finite element (FE) solution of partial
differential equations in one, two, and three dimensions. It is written in C++
and designed to run on diverse parallel architectures, including cloud and high
performance computing facilities. In spite of its academic research nature,
meaning a library for the development and testing of new methods, one
distinguishing feature of LifeV is its use on real world problems and it is
intended to provide a tool for many engineering applications. It has been
actually used in computational hemodynamics, including cardiac mechanics and
fluid-structure interaction problems, in porous media, ice sheets dynamics for
both forward and inverse problems. In this paper we give a short overview of
the features of LifeV and its coding paradigms on simple problems. The main
focus is on the parallel environment which is mainly driven by domain
decomposition methods and based on external libraries such as MPI, the Trilinos
project, HDF5 and ParMetis.
Dedicated to the memory of Fausto Saleri.Comment: Review of the LifeV Finite Element librar
Numerical Simulations of Fractionated Electrograms and Pathological Cardiac Action Potential
The aim of this work is twofold. First we focus on the complex phenomenon of electrogram fractionation, due to the presence of discontinuities in the conduction properties of the cardiac tissue in a bidomain model. Numerical simulations of paced activation may help to understand the role of the membrane ionic currents and of the changes in cellular coupling in the formation of conduction blocks and fractionation of the electrogram waveform. In particular, we show that fractionation is independent ofINAalterations and that it can be described by the bidomain model of cardiac tissue. Moreover, some deflections in fractionated electrograms may give nonlocal information about the shape of damaged areas, also revealing the presence of inhomogeneities in the intracellular conductivity of the medium at a distance.The second point of interest is the analysis of the effects of space–time discretization on numerical results, especially during slow conduction in damaged cardiac tissue. Indeed, large discretization steps can induce numerical artifacts such as slowing down of conduction velocity, alteration in extracellular and transmembrane potential waveforms or conduction blocks, which are not predicted by the continuous bidomain model. Several possible numerical and physiological explanations of these effects are given. Essentially, the discrete system obtained at the end of the approximation process may be interpreted as a discrete model of the cardiac tissue made up of isopotential cells where the effective intracellular conductivity tensor depends on the space discretization steps; the increase of these steps results in an increase of the effective intracellular resistance and can induce conduction blocks if a certain critical value is exceeded
Simulation of action potential propagation based on the ghost structure method
In this paper, a ghost structure (GS) method is proposed to simulate the monodomain model in irregular computational domains using finite difference without regenerating body-fitted grids. In order to verify the validity of the GS method, it is first used to solve the Fitzhugh-Nagumo monodomain model in rectangular and circular regions at different states (the stationary and moving states). Then, the GS method is used to simulate the propagation of the action potential (AP) in transverse and longitudinal sections of a healthy human heart, and with left bundle branch block (LBBB). Finally, we analyze the AP and calcium concentration under healthy and LBBB conditions. Our numerical results show that the GS method can accurately simulate AP propagation with different computational domains either stationary or moving, and we also find that LBBB will cause the left ventricle to contract later than the right ventricle, which in turn affects synchronized contraction of the two ventricles
Convergence of discrete duality finite volume schemes for the cardiac bidomain model
We prove convergence of discrete duality finite volume (DDFV) schemes on
distorted meshes for a class of simplified macroscopic bidomain models of the
electrical activity in the heart. Both time-implicit and linearised
time-implicit schemes are treated. A short description is given of the 3D DDFV
meshes and of some of the associated discrete calculus tools. Several numerical
tests are presented
Physiological accuracy in simulating refractory cardiac tissue: the volume-averaged bidomain model vs. the cell-based EMI model
The refractory period of cardiac tissue can be quantitatively described using
strength-interval (SI) curves. The information captured in SI curves is
pertinent to the design of anti-arrhythmic devices including pacemakers and
implantable cardioverter defibrillators. As computational cardiac modelling
becomes more prevalent, it is feasible to consider the generation of
computationally derived SI curves as a supplement or precursor to curves that
are experimentally derived. It is beneficial, therefore, to examine the
profiles of the SI curves produced by different cardiac tissue models to
determine whether some models capture the refractory period more accurately
than others. In this study, we compare the unipolar SI curves of two tissue
models: the current state-of-the-art bidomain model and the recently developed
extracellular-membrane-intracellular (EMI) model. The EMI model's resolution of
individual cell structure makes it a more detailed model than the bidomain
model, which forgoes the structure of individual cardiac cells in favour of
treating them homogeneously as a continuum. We find that the resulting SI
curves elucidate differences between the models, including that the behaviour
of the EMI model is noticeably closer to the refractory behaviour of
experimental data compared to that of the bidomain model. These results hold
implications for future computational pacemaker simulations and shed light on
the predicted refractory properties of cardiac tissue from each model.Comment: 30 pages, 12 figures, 3 table
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