Cardiac Electromechanics: The effect of contraction model on the mathematical problem and accuracy of the numerical scheme

Models of cardiac electromechanics usually contain a contraction model determining the active tension induced at the cellular level, and the equations of nonlinear elasticity to determine tissue deformation in response to this active tension. All contraction models are dependent on cardiac electro-physiology, but can also be dependent on\ud the stretch and stretch-rate in the fibre direction. This fundamentally affects the mathematical problem being solved, through classification of the governing PDEs, which affects numerical schemes that can be used to solve the governing equations. We categorise contraction models into three types, and for each consider questions such as classification and the most appropriate choice from two numerical methods (the explicit and implicit schemes). In terms of mathematical classification, we consider the question of strong ellipticity of the total strain energy (important for precluding ‘unnatural’ material behaviour) for stretch-rate-independent contraction models; whereas for stretch-rate-dependent contraction models we introduce a corresponding third-order problem and explain how certain choices of boundary condition could lead to constraints on allowable initial condition. In terms of suitable numerical methods, we show that an explicit approach (where the contraction model is integrated in the timestep prior to the bulk deformation being computed) is: (i) appropriate for stretch-independent contraction models; (ii) only conditionally-stable, with the stability criterion independent of timestep, for contractions models which just depend on stretch (but not stretch-rate), and (iii) inappropriate for stretch-rate-dependent models

Modeling and simulation of the electric activity of the heart using graphic processing units

Mathematical modelling and simulation of the electric activity of the heart (cardiac electrophysiology) offers and ideal framework to combine clinical and experimental data in order to help understanding the underlying mechanisms behind the observed respond under physiological and pathological conditions. In this regard, solving the electric activity of the heart possess a big challenge, not only because of the structural complexities inherent to the heart tissue, but also because of the complex electric behaviour of the cardiac cells. The multi- scale nature of the electrophysiology problem makes difficult its numerical solution, requiring temporal and spatial resolutions of 0.1 ms and 0.2 mm respectively for accurate simulations, leading to models with millions degrees of freedom that need to be solved for thousand time steps. Solution of this problem requires the use of algorithms with higher level of parallelism in multi-core platforms. In this regard the newer programmable graphic processing units (GPU) has become a valid alternative due to their tremendous computational horsepower. This thesis develops around the implementation of an electrophysiology simulation software entirely developed in Compute Unified Device Architecture (CUDA) for GPU computing. The software implements fully explicit and semi-implicit solvers for the monodomain model, using operator splitting and the finite element method for space discretization. Performance is compared with classical multi-core MPI based solvers operating on dedicated high-performance computer clusters. Results obtained with the GPU based solver show enormous potential for this technology with accelerations over 50× for three-dimensional problems when using an implicit scheme for the parabolic equation, whereas accelerations reach values up to 100× for the explicit implementation. The implemented solver has been applied to study pro-arrhythmic mechanisms during acute ischemia. In particular, we investigate on how hyperkalemia affects the vulnerability window to reentry and the reentry patterns in the heterogeneous substrate caused by acute regional ischemia using an anatomically and biophysically detailed human biventricular model. A three dimensional geometrically and anatomically accurate regionally ischemic human heart model was created. The ischemic region was located in the inferolateral and posterior side of the left ventricle mimicking the occlusion of the circumflex artery, and the presence of a washed-out zone not affected by ischemia at the endocardium has been incorporated. Realistic heterogeneity and fi er anisotropy has also been considered in the model. A highly electrophysiological detailed action potential model for human has been adapted to make it suitable for modeling ischemic conditions (hyperkalemia, hipoxia, and acidic conditions) by introducing a formulation of the ATP-sensitive K+ current. The model predicts the generation of sustained re-entrant activity in the form single and double circus around a blocked area within the ischemic zone for K+ concentrations bellow 9mM, with the reentrant activity associated with ventricular tachycardia in all cases. Results suggest the washed-out zone as a potential pro-arrhythmic substrate factor helping on establishing sustained ventricular tachycardia.Colli-Franzone P, Pavarino L. A parallel solver for reaction-diffusion systems in computational electrocardiology, Math. Models Methods Appl. Sci. 14 (06):883-911, 2004.Colli-Franzone P, Deu hard P, Erdmann B, Lang J, Pavarino L F. Adaptivity in space and time for reaction-diffusion systems in electrocardiology, SIAM J. Sci. Comput. 28 (3):942-962, 2006.Ferrero J M(Jr), Saiz J, Ferrero J M, Thakor N V. Simulation of action potentials from metabolically impaired cardiac myocytes: Role of atp-sensitive K+ current. Circ Res, 79(2):208-221, 1996.Ferrero J M (Jr), Trenor B. Rodriguez B, Saiz J. Electrical acticvity and reentry during acute regional myocardial ischemia: Insights from simulations.Int J Bif Chaos, 13:3703-3715, 2003.Heidenreich E, Ferrero J M, Doblare M, Rodriguez J F. Adaptive macro finite elements for the numerical solution of monodomain equations in cardiac electrophysiology, Ann. Biomed. Eng. 38 (7):2331-2345, 2010.Janse M J, Kleber A G. Electrophysiological changes and ventricular arrhythmias in the early phase of regional myocardial ischemia. Circ. Res. 49:1069-1081, 1981.ten Tusscher K HWJ, Panlov A V. Alternans and spiral breakup in a human ventricular tissue model. Am. J.Physiol. Heart Circ. Physiol. 291(3):1088-1100, 2006.<br /

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