Patient-specific computational models have tremendous potential in revolutionizing disease management and advancing heart failure treatments. Significant advances have been made in the last twenty years on the theoretical and computational developments of cardiac computational models. However, there is currently a lack of a complete computational model that is capable of taking into account all the principal physics occurring in a beating heart, specifically, electrical conduction in the heart, dynamics of blood flow, mechanics of the cardiac wall motion, and the long-term changes in heart function and geometry. The lack of such a modeling framework is a critical barrier to the development of in-depth knowledge about the heart function and diseases. This is especially so as the interactions of these physics are important aspects that need to be taken into account when designing heart disease treatments and understanding heart function. The proposed project aims to develop a strongly-coupled cardiac electromechanics-fluid-growth computational modeling framework that takes into account the key principal physics occurring in the beating heart. Both graduate and undergraduate students will be involved with the research project.
The proposed bottom-up multiscale model will be versatile to allow for arbitrary 3D heart geometries as well as multiscale physics, including: (i) cellular excitation-contraction coupling processes, (ii) contribution of constituents found in the cardiac tissue to its anisotropic mechanical behavior, (iii) macroscale fluid-structure interactions between the heart wall and blood, and (iv) long term growth and remodeling processes. Specific goals that will be accomplished in this project are as follows. First, a strongly coupled cardiac electromechanics-fluid modeling framework will be developed based on a hybrid Fictitious-Domain Arbitrary-Lagrange-Eulerian formulation to describe the short-term bidirectional fluid-elastic-structure interactions between blood flow and ventricular wall deformation driven by the cellular excitation-contraction coupling processes. Second, a cardiac growth model will be integrated into the modeling framework based on the principle of timescale separation to describe long-term changes in the heart geometry and function driven by pathophysiological insults. Last, with clinical data obtained from collaborators, the PIs will apply the modeling framework to develop new understanding concerning normal and abnormal heart functions, such as the short- and long-term effects arising from flow obstruction due to abnormalities in the geometry and deformation of the ventricular wall in hypertrophic cardiomyopathy.
