نبذة مختصرة : A multiphysics framework for modelling coupled fluid-electromechanics phenomena in human cardiac ventricles was developed. An idealised ventricular structure was utilised with embedded myocardial anisotropy due to microstructural myocyte fibre, sheet, and normal-to-sheet orientations. Phenomenological representations of action potential activation and excitation-contraction were adapted to trigger myocardial contraction. A reaction-diffusion formulation was discretised within a material frame to emulate gap-junction controlled propagation. An idealised Purkinje network was developed incorporating varying fibre radius with one-way electrical coupling to the surrounding myocardium. Passive myocardial mechanics was represented using a transverse isotropic hyperelastic material, whilst blood dynamics was modelled using incompressible Navier-Stokes equations, with a moving mesh to handle blood domain deformation. A closed-loop Windkessel circuit to govern the circulatory response was also coupled to the model. The model reproduced known myocardial electrical activation and contractile dynamics such as torsion, apico-basal shortening, and myocardial thickening. Known haemodynamic responses, including ventricular pressure-volume loops, along with vortex formation during the filling phase, were also simulated. Interventricular coupling was evident under simulation of pulmonary hypertension, in which right ventricular failure induced left ventricular failure, and the interventricular septum was displaced towards the right ventricle. Model behaviour under abnormal electrical activity was simulated in two modes: ischaemia and left bundle branch block (LBBB). These abnormalities weaken the heart’s mechanical performance, and contribute to worsening of the haemodynamic variables. Direct pacing applied to the late activated region in LBBB showed that the model can predict reversal of LBBB pathologies. Heart-implant interaction was simulated by incorporating a left ventricular assist device (LVAD) into the model. Ventricular ...
No Comments.