Hemodynamic Analysis Of Blood Flow In Embryonic Hearts Developing Persistent Truncus Arteriosus
In the congenital heart defect persistent truncus arteriosus (PTA), the developing outflow tract fails to septate into the pulmonary artery and the aorta. Hearts with PTA develop compact myocardium with the passive elastic modulus increased by factors of two (left ventricle) and four (right ventricle) compared to control. This research aims to create a computational model of blood flow through both normal and the mutant (PTA) ED12.5 mouse hearts to determine whether differences in pressure or wall shear stress could be associated with the observed modulus changes.
Each model geometry created in Solidworks consists of two ventricles and the inflow and outflow tracts. The geometric models were imported into COMSOL® 5.4 for finite element analysis. Both ventricles were comprised of a free inner channel and a surrounding porous, trabeculated myocardium. Blood flow was modeled using laminar flow equations for the inner channel and the Brinkman equations for the trabeculated domain. The control and mutant models were compared using the calculated pressure and shear stresses in each ventricle.
While average shear stresses at the open/porous and compact/porous interfaces in both the control and mutant models ranged from 0.08 – 0.25 Pa, average pressures were significantly higher, from 6 – 10 kPa. Additionally, the fluid pressures in both the left and right ventricles were found to be 40% lower in the mutant heart than in the control. Overall, the cushions restrict the cross sectional area of the outflow tract. To overcome this greater resistance, the control heart exhibits higher pressures in the ventricles.