In silico analysis of the haemodynamic disturbances caused by the subaortic membrane pathology

Subaortic stenosis, a heart disease characterised by a narrowing of the left ventricular outflow tract, is frequently caused by the presence of a subaortic membrane (SAM) located at the aortic valve inlet. This anatomical obstruction leads to significant haemodynamic alterations and leaflets fluttering, whose mechanisms are not yet fully understood. This research investigates, through computer simulations, the SAM's haemodynamic impact and the mechanism behind leaflets fluttering. A mono-physics fluid-structure interaction approach, based on the meshless smoothed particle hydrodynamics method, was employed. This approach represents both blood and structures with particles without defining interfaces, efficiently capturing large deformations and dynamic phenomena. Two common types of SAMs were investigated - a discrete thin SAM layer (flexible) and a thick fibromuscular ridge SAM (stiff) - and compared with a healthy aortic valve. Projected dynamic valve area (PDVA) was used as a reference parameter to quantify leaflet oscillation. While the PDVA in the healthy aortic valve stabilised at 283 mm² without oscillation, both pathological cases exhibited self-sustained periodic fluctuations. In the presence of discrete thin SAM layer, the mean PDVA decreased by 3% compared to the healthy control. This reduction was more pronounced for thick fibromuscular ridge configurations, where the mean PDVA was 9% lower than the healthy case. Notably, stiffer SAM configurations more than doubled the oscillation amplitude (from 3.12 mm² to 6.77 mm²) and increased the oscillation frequency by 8% relative to flexible membranes. Vortices dynamics was analysed, determining the phases of their formation, growth and migration. Through the analysis of velocity, vorticity, and shear stress maps, this study provides critical insights into the origin of fluttering and its influence over these key haemodynamic parameters. Findings demonstrate that the oscillatory leaflet motion is the result of vortices formation and shedding. The stiffness of the SAM significantly modulates the fluttering behaviour. While structural damage and haematological complications were not directly simulated, the identified oscillations represent haemodynamic conditions associated in literature with such pathologies. The observed alterations in wall shear stress magnitude and direction provide a physical basis for the mechanical environment that could contribute to endothelial cell dysfunction in the presence of SAM.