Search

The cardiac electrophysiology (EP) problem is governed by a nonlinear anisotropic reaction-diffusion system with a very rapidly varying reaction term associated with the transmembrane cell current. The nonlinearity associated with the cell models requires a stabilization process before any simulation is performed. More importantly, when used in a 3-dimensional (3D) anatomy, it is not sufficient to perform this stabilization on the basis of isolated cells only, since the coupling of the different cells through the tissue greatly modulates the dynamics of the system. Therefore, stabilization of the system must be performed on the entire 3D model. This work develops a novel procedure for the initialization of reaction-diffusion systems for numerical simulations of cardiac EP from steady-state conditions. We exploit surface point correspondence to establish volumetric point correspondence. Upon introduction of a new 3D anatomy with surface point correspondence, a prediction of the cell model steady states is derived from the set of earlier biophysical simulations. We show that the prediction error is typically less than 10% for all model variables, with most variables showing even greater accuracy. When initializing simulations with the predicted model states, it is demonstrated that simulation times can be cut by at least two-thirds and potentially more, which saves hours or days of high-performance computing. Overall, these results increase the clinical applicability of detailed computational EP studies on personalized anatomies. [ABSTRACT FROM AUTHOR]

Abstract: The reconstruction of the ventricular cardiac conduction system (CCS) from patient‐specific data is a challenging problem. High‐resolution imaging techniques have allowed only the segmentation of proximal sections of the CCS from images acquired ex vivo. In this paper, we present an algorithm to estimate the location of a set of Purkinje‐myocardial junctions (PMJs) from electro‐anatomical maps, as those acquired during radio‐frequency ablation procedures. The method requires a mesh representing the myocardium with local activation time measurements on a subset of nodes. We calculate the backwards propagation of the electrical signal from the measurement points to all the points in the mesh to define a set of candidate PMJs that is iteratively refined. The algorithm has been tested on several Purkinje network configurations, with simulated activation maps, subject to different error amplitudes. The results show that the method is able to build a set of PMJs that explain the observed activation map for different synthetic CCS configurations. In the tests, the average error in the predicted activation time is below the amplitude of the error applied to the data. [ABSTRACT FROM AUTHOR]