Modelling electromechanical interaction of myocardium and coronary circulation for investigation of heart diseases

Interaction between cardiac mechanics and coronary blood flow is fundamental for cardiac physiology as these systems are mutually dependent. There is a growing and active research effort toward developing comprehensive mathematical models of cardiac electromechanics and myocardial perfusion to better understand and investigate cardiac and coronary diseases. However, integrating these multiphysics models into a unified framework is inherently complex and remains computational challenging. Many existing studies rely on simplifications such as modelling only the left side of the heart, assuming rigid arteries and neglecting myocardial poromechanics. This thesis presents a computational framework that couples anatomically realistic 3D biventricular electromechanical model with 3D epicardial coronary blood flow dynamics and myocardial perfusion to investigate cardiac-coronary interactions in both healthy and diseased heart conditions. Diseased cases include a non-moving coronary artery model, a failing heart with reduced myocardial contractility and a left bundle branch block (LBBB) in a failing heart. The framework integrates core electromechanical elements - cardiac fibre architecture, electrophysiology, active and passive mechanics, and open-loop Windkessel circulation, with coronary circulation model, combining 3D Navier-Stokes equations for the epicardial coronary flow and a single-compartment Darcy poromechanical model for the myocardial perfusion. A coupling operator was utilized to mathematically synchronize the biventricular motion and the coronary arterial displacement without physically attaching the two domains. Results revealed that diseased heart cases showed delayed ventricular activation, lower ventricular pressure and volume, and impaired ventricular mechanics compared with the healthy case. Cardiac-induced coronary arterial motion strongly influenced coronary flow patterns, generating regions with varying velocity and wall shear stress (WSS). Arterial motion also disrupted the formation of secondary Dean vortices observed in non-moving arteries, highlighting its critical role in shaping coronary hemodynamic. In failing heart conditions, local coronary hemodynamic including pressure, velocity and flowrate were reduced relative to the healthy heart. In the coupled cardiac electromechanics-coronary flow framework incorporating the Darcy perfusion model, myocardial perfusion was shown to vary across different myocardial regions, with arterial inflow occurred predominantly during diastole and venous outflow was higher during systole. Negative arterial inflow during early systole indicated retrograde flow caused by increased pore pressure from the ventricular contraction and poromechanical effect. Overall, this study establishes a simplified yet comprehensive coupled framework of cardiac electromechanics and coronary flow dynamics, providing a strong foundation for future computational simulations of various cardiac and coronary diseases.