Abstract
A mechanical heart valve, an essential prosthetic for managing valvular heart disease, consists of a metal frame housing two or three leaflets (depending on the design) that control blood flow within the heart. However, leaflet dysfunction can impede their movement, leading to valve defects. This study extensively investigates the hemodynamics of such a bileaflet mechanical heart valve with dysfunctions of various extents with the help of direct numerical simulations (DNS) under both steady inflow and pulsatile flow conditions. The results are presented and discussed in terms of spatial variations of velocity magnitude, Reynolds stresses, and surface and time-averaged clinically important parameters such as wall shear stress (WSS), pressure drop, and blood damage. Under steady inflow conditions, the flow field becomes unsteady and turbulent even at a modest Reynolds number of 750 when the valve has 50% defective conditions, in contrast to a steady and laminar flow for a fully functional heart valve with 0% defect condition. The values of WSS also increase by around 50%, and net pressure drops by more than 200% with these defective conditions, which further increase as the defective condition increases. On the other hand, the same trend is also seen under pulsatile flow conditions, with maximum values of wall shear stress and blood damage seen during the peak systolic stage of the cardiac cycle, increasing by more than 200% as the defect condition increases from 0% to 50% for the latter parameter. Furthermore, the present study also investigates the effect of blood rheological behaviors such as shear-thinning and yield stress on hemodynamics past this dysfunctional heart valve. It is seen that blood rheological behavior has a substantial influence on hemodynamics at low Reynolds numbers, diminishing as the Reynolds number increases. Under pulsatile flow conditions, blood exhibiting non-Newtonian characteristics such as shear-thinning shows higher values of wall shear stress and blood damage values compared to Newtonian ones. Therefore, the present study highlights the importance of accounting for blood rheology in clinical assessments. However, this study simulates the cases where both valve leaflets are fixed in position, thereby excluding fluid–structure interaction (FSI) from the present simulations. Such conditions are representative of common occurrences in dysfunctional heart valves. All in all, the in-depth analysis and information obtained from this study are expected to facilitate early detection of valve leaflet dysfunction, thereby contributing to improved clinical management of patients with valvular heart disease.
Published Version
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