The purpose of this manuscript is to develop a reaction-diffusion heart model for closed-loop evaluation of heart-pacemaker interaction, and to provide a hardware setup for the implementation of the closed-loop system. The heart model, implemented on a workstation, is based on the cardiac monodomain formulation and a phenomenological model of cardiac cells, which we fitted to the electrophysiological properties of the different cardiac tissues. We modelled the pacemaker as a timed automaton, deployed on an Arduino 2 board. The Arduino and the workstation communicate through a PCI acquisition board. Additionally, we developed a graphical user interface for easy handling of the framework. The myocyte model resembles the electrophysiological properties of atrial and ventricular tissue. The heart model reproduces healthy activation sequence and proved to be computationally efficient (i.e., 1 s simulation requires about 5 s). Furthermore, we successfully simulated the interaction between heart and pacemaker models in three well-known pathological contexts. Our results showed that the PDE formulation is appropriate for the simulation in closed-loop. While computationally more expensive, a PDE model is more flexible and allows to represent more complex scenarios than timed or hybrid automata. Furthermore, users can interact more easily with the framework thanks to the graphical representation of the spatiotemporal evolution of the membrane potentials. By representing the heart as a reaction-diffusion model, the proposed closed-loop system provides a novel and promising framework for the assessment of cardiac pacemakers.INDEX TERMS Cardiovascular Implantable Electronic Devices (CIEDs), endless loop tachycardia, heart modelling, in silico closed-loop models, reaction-diffusion models This article has been accepted for publication in IEEE Access.

In this work, we developed a closed loop model of the interaction between the heart and a cardiac pacemaker. The main novelty of our framework is the employment of a reaction-diffusion heart model, which could enhance the assessment of cardiac pacing. Additionally, we provided a specific hardware setup for the deployment of our framework. Our results show that the heart model reproduces the healthy activation sequence and is feasible for closed loop simulations. Furthermore, we successfully simulated the interaction between heart and pacemaker models during the insurgence of endless loop tachycardia. Finally, we believe that our closed loop system could be an effective supporting tool to evaluate the safety and efficacy of the therapeutic effect of cardiac pacemakers.

This manuscript presents a novel finite difference method to solve cardiac bidomain equations in anatomical models of the heart. The proposed method employs a smoothed boundary approach that represents the boundaries between the heart and the surrounding medium as a spatially diffuse interface of finite thickness. The bidomain boundary conditions are implicitly implemented in the smoothed boundary bidomain equations presented in the manuscript without the need of a structured mesh that explicitly tracks the heart-torso boundaries. We reported some significant examples assessing the method’s accuracy using nontrivial test geometries and demonstrating the applicability of the method to complex anatomically detailed human cardiac geometries. In particular, we showed that our approach could be employed to simulate cardiac defibrillation in a human left ventricle comprising fiber architecture. The main advantage of the proposed method is the possibility of implementing bidomain boundary conditions directly on voxel structures, which makes it attractive for three dimensional, patient specific simulations based on medical images. Moreover, given the ease of implementation, we believe that the proposed method could provide an interesting and feasible alternative to finite element methods, and could find application in future cardiac research guiding electrotherapy with computational models.