A Theoretical Model for Cardiac Mechanics: Effects of Interventricular Interactions

Abstract

The left and right ventricles (LV, RV) of the heart are mechanically linked by the interventricular septum. Changes in volume, pressure and contractility of one ventricle can affect the other by shift and deformation of the septum. This coupling of the systolic and diastolic functions between the ventricles is known as interventricular interactions. Studying the role of ventricular dependence is relevant in several cardiomyopathies in- cluding atrial septal defects, mitral stenosis, cor pulmonale, RV failure after implantation of LV assist device, and pulmonary hypertension. In this work, we present a spatially- resolved, biventricular model of the heart that can be used to investigate the effects of septal displacement and LV-RV interactions in the context of pulmonary hypertension and to quantify its effects on local and global hemodynamics. The model builds from a low- order, computationally efficient model of a prolate spheroidal, axisymmetric LV connected in series to a closed circulation and is adapted to allow for non-axisymmetric deforma- tions, including the introduction of the RV cavity as an appendage to the LV. By using this representation of the complex geometry of both the LV and RV, model parameters can be matched to fit individualized patient geometries from echocardiogram data. Simulations of cardiac cycles in response to acute increases to pulmonary resistance suggest that the heart can only function with increased pulmonary resistance if there is RV hypertro- phy. To represent the effects of RV hypertrophy, the force of RV contractility is increased in proportion to increases in pulmonary resistance. According to the model, increasing pulmonary resistance and RV contractility leads to a large increase in pulmonary artery pressure, but systemic arterial pressure and stroke volume show significant decreases. The inclusion of interventricular interaction had little effect on stroke volume response, but significantly dampened the reduction in LV pressure with decreased preload. The model suggests that increased RV contractility with septal displacement helps maintain LV pres- sure in pulmonary hypertension. This biventricular model is suited for quantifying the role of interventricular interactions in pulmonary hypertension and can be applied to various cardiomyopathies.