Altered haemodynamics are implicated in the blood cells damage that leads to thromboembolic complications in presence of prosthetic cardiovascular devices, with platelet activation being the underlying mechanism for cardioemboli formation in blood flow past mechanical heart valves (MHVs). Platelet activation can be initiated and maintained by flow patterns arising from blood flowing through the MHV, and can lead to an enhancement in the aggregation of platelets, increasing the risk for thromboemboli formation. Hellums and colleagues compiled numerous experimental results to depict a locus of incipient shear related platelet activation on a shear stress – exposure time plane, commonly used as a standard for platelet activation threshold [1]. However, platelet activation and aggregation is significantly greater under pulsatile or dynamic condition relative to exposure to constant shear stress [2]. Previous studies do not allow to determine the relationship existing between the measured effect — the activation of a platelet, and the cause — the time-varying mechanical loading, and the time of exposure to it as might be expected in vivo when blood flows through the valve. The optimization of the thrombogenic performance of MHVs could be facilitated by formulating a robust numerical methodology with predictive capabilities of flow-induced platelet activation. To achieve this objective, it is essential (i) to quantify the link between realistic valve induced haemodynamics and platelet activation, and (ii) to integrate theoretical, numerical, and experimental approaches that allow for the estimation of the thrombogenic risk associated with a specific geometry and/or working conditions of the implantable device. In this work, a comprehensive analysis of the Lagrangian systolic dynamics of platelet trajectories and their shear histories in the flow through a bileaflet MHV is presented. This study uses information extracted from the numerical simulations performed to resolve the flow field through a realistic model of MHV by means of an experimentally validated fluid-structure interaction approach [3]. The potency of the device to mechanically induce activation/damage of platelets is evaluated using a Lagrangian-based blood damage cumulative model recently identified using in vitro platelet activity measurements [4,5].

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