Shear-induced activation and transport of platelets in artificial heart valve flows

Despite extensive hemodynamic studies on prosthetic heart valves, it remains unclear whether local high concentrations of activated platelets near these valves result from local shear-induced activation or from transport-driven accumulation. Here, we computationally disentangle the role of activation vs transport toward platelet activation levels in two designs of mechanical heart valves (MHVs), namely, a trileaflet MHV (TMHV) and a bileaflet MHV (BMHV), and compare them with a bioprosthetic heart valve (BHV) as a control. We observe that transport acts as a mitigating mechanism to the local shear-induced activation, washing out activated platelets and driving the system toward a cyclic state. At the end of diastole in a cyclic state, the volumetric integral of shear-induced activation is over 138% and 45% higher in BMHV and TMHV, respectively, compared to BHV. This increase is accompanied by a greater washout, which is over 151% and 53% higher in BMHV and TMHV, respectively, relative to BHV. Histogram of residence time shows that over 50% of platelets remain nearby between one and two cycles in the domain, with BHV demonstrating the highest portions of platelets (about 15%) residing over two cycles. 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 lower residence time (i.e., a better washout). Conversely, the subclinical thrombosis in BHVs is probably due to prolonged platelet residence time than MHVs.