Spiral anchoring in anisotropic media with multiple inhomogeneities: a dynamical system approach

Various PDE models have been suggested in order to explain and predict the dynamics of spiral waves in excitable media. In two landmark papers, Barkley noticed that some of the behaviour could be explained by the inherent Euclidean symmetry of these models. LeBlanc and Wulff then introduced forced Euclidean symmetry-breaking (FESB) to the analysis, in the form of individual translational symmetry-breaking (TSB) perturbations and rotational symmetry-breaking (RSB) perturbations; in either case, it is shown that spiral anchoring is a direct consequence of the FESB. In this article, we provide a characterization of spiral anchoring when two perturbations, a TSB term and a RSB term, are combined, where the TSB term is centered at the origin and the RSB term preserves rotations by multiples of $\frac{2\pi}{\jmath^*}$, where $\jmath^*\geq 1$ is an integer. When $\jmath^*>1$ (such as in a modified bidomain model), it is shown that spirals anchor at the origin, but when $\jmath^* =1$ (such as in a planar reaction-diffusion-advection system), spirals generically anchor away from the origin.Comment: Revised versio

A comparative study of nonequilibrium dynamics in complex and real Ginzburg-Landau equations

Complex and real Ginzburg-Landau equations have been numerically studied by implementing Euler discretization technique. In addition to characterizing the differences and similarities of patterns involving these two continuum dynamical equations, in a wide range of appropriate parameter space, we have also made quantitative comparisons of growth dynamics in the two cases. In most part of the above-mentioned parameter space the complex Ginzburg-Landau equation exhibits frozen spiral dynamics. Results on the unlocking of this freezing are also presented

The Virtual Ventricular Wall: A Tool for Exploring Cardiac Propagation and Arrhythmogenesis

Methods for the experimental and clinical investigation of cardiac arrhythmias are limited to inferring propagation within the myocardium, from surface measurements, or from electrodes at a few sites within the cardiac wall. Biophysically and anatomically detailed computational models of cardiac tissues offer a powerful way for studying the electrical propagation processes and arrhythmias within the virtual heart. We use virtual tissues to study and visualise the effects of patho- and physiological conditions, and pharmacological interventions on transmural propagation in the virtual ventricular walls. Class III drug actions are quantitatively explained by changes induced in the transmural dispersion of action potential duration. We illustrate the automated construction of a virtual anisotropic ventricle from Diffusion Tensor MRI for individual hearts, and use it to explore mechanisms leading to ventricular fibrillation. The virtual ventricular wall provides an effective tool for exploring, evaluating and visualising processes during the initiation and maintenance of ventricular arrhythmias