Brain-Heart Electromechanical Modeling

Abstract

The brain controls the heart through the sympathetic and parasympathetic branches of the autonomic nervous system. It consists of multisynaptic pathways from myocardial cells back to peripheral ganglionic neurons and further to central preganglionic and premotor neurons. Still, there are no reliable cardiovascular markers of the sympathetic tone and of the sympathetic-parasympathetic balance. It is necessary to understand the interaction between the brain and the heart in order to make early detection and treatment of pathological changes in the brain-heart interaction. In this study we present a detailed electro-chemo-mechanical model of heart and torso, so as to simulate the three principal modes of actions of drugs for cardiomyopathy: (i) modulating calcium transients, (ii) changing kinetics of contractile proteins, (iii) changing the macroscopic structure or its boundary conditions. Heart model geometry included seven different regions. Monodomain model of modified FitzHugh-Nagumo model of the cardiac cell was used. Six electrodes were positioned on the chest to model the precordial leads and the results were compared with real clinical measurements. Inverse ECG method was used to optimize potential on the heart. A whole heart was embedded in the electrical activity throughout the torso environment, with spontaneous initiation of activation in the sinoatrial node, incorporating a specialized conduction system with heterogeneous action potential morphologies throughout the heart. We included body surface potential maps in a healthy subject during progression of ventricular activation in nine sequences. The electrical model was coupled with a mechanical model with orthotropic material properties obtained from the experiments of Holzapfel. In future research we will be more focused on in silico clinical trials with the aim to compare some clinical pathology findings on the body surface with standard 12 ECG electrode measurements.