Cardiac dynamics: a simplified model for action potential propagation

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Cardiac dynamics: a simplified model for action potential propagation Angelina Peñaranda1* , Inma R Cantalapiedra1 , Jean Bragard2 and Blas Echebarria1 *Correspondence: [email protected] 1 Departament de Física Aplicada, Universitat Politècnica de Catalunya. BarcelonaTech, Av. Dr. Marañon 44-50, 08028 Barcelona, Spain Full list of author information is available at the end of the article

Abstract This paper analyzes a new semiphysiological ionic model, used recently to study reexitations and reentry in cardiac tissue [I.R. Cantalapiedra et al, PRE 82 011907 (2010)]. The aim of the model is to reproduce action potencial morphologies and restitution curves obtained, either from experimental data, or from more complex electrophysiological models. The model divides all ion currents into four groups according to their function, thus resulting into fast-slow and inward-outward currents. We show that this simplified model is flexible enough as to accurately capture the electrical properties of cardiac myocytes, having the advantage of being less computational demanding than detailed electrophysiological models. Under some conditions, it has been shown to be amenable to mathematical analysis. The model reproduces the action potential (AP) change with stimulation rate observed both experimentally and in realistic models of healthy human and guinea pig myocytes (TNNP and LRd models, respectively). When simulated in a cable it also gives the right dependence of the conduction velocity (CV) with stimulation rate. Besides reproducing correctly these restitution properties, it also gives a good fit for the morphology of the AP, including the notch typical of phase 1. Finally, we perform simulations in a realistic geometric model of the rabbit’s ventricles, finding a good qualitative agreement in AP propagation and the ECG. Thus, this simplified model represents an alternative to more complex models when studying instabilities in wave propagation.

Introduction Cardiac action potentials (APs) are electrical signals that trigger the synchronous contraction of the heart. As such, the regular propagation of the action potential is necessary for ensuring a correct heart functioning. APs are produced as a result of ion currents that cross the cell membrane, producing a net depolarization or repolarization of the membrane as different currents are invoked in response to the transmembrane voltage changes. The currents are produced by the movement of individual ions through ion channels, which are specialized pore-forming proteins that span the cell membrane, forming a pathway for ions to cross it. Each type of channel is highly selective for a specific type of ion. The most common intracellular ion concentrations considered in cardiac models are calcium, sodium, and potassium. Channelopaties due to mutations that modify the ion channel function can perturb the form of the action potential, sometimes leading to cardiac dysfunctions or altered AP propagation. Following the pioneering mathematical descriptio