Shear-Induced Activation and Transport of Platelets in Artificial Heart Valve Flows

TL;DR

This study investigates how shear stresses in artificial heart valves activate and transport platelets, revealing differences in thrombosis risk between mechanical and bioprosthetic valves based on shear-induced activation and washout dynamics.

Contribution

It provides a comparative analysis of platelet activation and transport in different valve designs, highlighting mechanisms underlying thrombosis risk.

Findings

MHVs show higher platelet activation than BHV.

Activation levels are significantly higher in BMHV and TMHV compared to BHV.

Differences in washout and residence time influence thrombosis risk.

Abstract

Albeit the hemodynamics of artificial heart valves has been investigated for several decades, the local shear-induced activation potential and subsequent transport phenomena of activated platelets in different valve designs, which mediate thrombosis, remains poorly understood. Here, platelet activation due to local shear stresses and the associated transport phenomena are investigated in two designs of mechanical heart valves (MHVs), namely a trileaflet MHV (TMHV) and a bileaflet MHV (BMHV) and compared against a surgical bioprosthetic heart valve (BHV) as a control. It is observed that the local activation and transport of platelets in any aortic region reach a cyclic state, with MHVs showing higher levels of both activation and transport than BHV. When integrated over the volume of the aortic sinuses and central lumen, the local activation is, respectively, 5.90 and 2.26 times higher in BMHV whereas 2.97 and 1.39 times higher in TMHV than in BHV. The washout of activated platelets from the sinuses and central lumen is, respectively, 10.40 and 2.39 times higher in BMHV while 4.90 and 1.40 times higher in TMHV compared to BHV. The low washout of sinuses in BHV is also demonstrated by higher residence time in sinuses compared to MHVs. These findings indicate that the risk of clinical thrombosis in MHVs is likely due to higher levels of local shear-induced activation than BHV despite the lower residence time (i.e. a better washout). Conversely, the subclinical thrombosis in BHVs is probably due to prolonged platelet residence time relative to MHVs.