Section: New Results

Medical applications of numerical models

• [26] : We computed some bidomain solutions for use by M. Pop and M. Sermesant in the STACOM'11 challenge from the MICCAI 2011 conference and derived collaborative article [26] .

• [18] : The aim of this study was to describe a new familial cardiac phenotype and to elucidate the electrophysiological mechanism responsible for the disease. Mutations in several genes encoding ion channels, especially SCN5A, have emerged as the basis for a variety of inherited cardiac arrhythmias. Three unrelated families comprising 21 individuals affected by multifocal ectopic purkinje-related premature contractions (MEPPC) characterized by narrow junctional and rare sinus beats competing with numerous premature ventricular contractions with right and/or left bundle branch block patterns were identified. All the affected subjects carried the same transition in the SCN5A gene. Patch-clamp studies revealed a net gain of function of the sodium channel, leading, in silico, to incomplete repolarization in Purkinje cells responsible for premature ventricular action potentials. In vitro and in silico studies recapitulated the normalization of the ventricular action potentials in the presence of quinidine.

• [22] : In some cases, the standard methods to construct activation maps based on the derivatives of the signals may lead to inaccurate results. In this paper, we evaluated a novel Directional Activation Algorithm (DAA) based on EGM analysis. The DAA calculates the time delays between adjacent EGMs and assigns to each a localized propagation vector. The accuracy of the proposed methodology is compared with known activities obtained from a monodomain, isotrope, Beeler-Reuter model of the atria.

• [20] : Although the ECG is a widely used tool, the ionic basis underlying its changes caused by drugs and diseases are often unclear. In this work we present a computational model of the human ECG capable of representing drug-induced effects from the ionic to the surface potential level. We use the state-of-the-art bidomain model coupled to a membrane kinetics model in the heart and the Laplace equation in the torso. The membrane kinetics are represented by a detailed physiological human action potential model. We modified the potassium (respectively sodium) representation in the model in order to introduce the ion channel/drug interactions representing classIII (respectively class I) drugs. The drug model is represented by an ion channel conduction block depending on the IC50 value and the drug dose. We conduct numerical simulation of the ECGs measured on the surface of the thorax and could assess each of the potassium and sodium block effects (for class I and class III drugs).