Computational Modeling of Inertial Effects on Electromechanics of the Heart

Abstract

Abstract Computational modeling of cardiac function has gradually progressed during the past four decades and now beginning to translate toward clinical use as a noninvasive mean of optimizing cardiac treatment options. Recent experimental findings and numerical investigations have suggested an important role of mechanical and intrinsic properties of cardiac tissues in overall electromechanical dynamics of the heart. The inertial effects, which were usually neglected in earlier computational studies, have now been found to alter cardiac dynamics through stretch activated channels (SAC) and can lead to cardiac disorders under specific set of physiological conditions. Considering possible role of inertia in cardiac dynamics, we have modeled electromechanical activity of the heart with inertia terms for computing pressure volume relation and action potentials over a complete cardiac cycle. To this end, we use the continuum balance laws to capture physiological function of the human left ventricle (LV) on an idealized geometry and solve the resulting equations using a python-based finite element platform. For the same set of pressure boundary conditions, the finite element models for quasi-static (less inertia) and dynamic (with inertia terms) formulation yielded a difference of 4.2% end diastolic volume (EDV), 3.1% ejection fraction, and variations in fiber strain pattern. The mechano-electric transduction channels sensitive to small mechanical perturbations in combination with changes in electrical conductivity due to deformation caused quantitative variations over cardiac electrical activity up to 2.75–5% reduction in action potential duration (APD) at 50% repolarization (APD50) and 3.5–5.75% reduction at 90% repolarization (APD90). Catering the effect of inertia can help the research community to improve future computational models in investigating the electromechanics of the heart.