Platelet Aggregation Study in Arterial Cavities Using the Lattice-Boltzmann Algorithm

Hemostasis is the mechanism that leads to the cessation of bleeding from a blood vessel affected by accidents. Initially, it uses multiple interlinked steps to build a platelet-made plug that closes up the injured site in a process known as platelet aggregation. Despite being widely studied, this process is not yet fully understood, given the complex and tightly intricated relations between the transport phenomena and the biological processes happening simultaneously around the wounded areas. Therefore, many in silico studies have been used to model different stages of hemostasis and have proven useful to solve those complex relations using traditional numerical methods. However, they all share the downside of requiring high computational resources. Hence the need to develop a method suitable for computational parallelization to decrease the simulation times. The medical community could use such computational models to develop patient-specific therapies once the processing times require less than a few minutes to simulate complex scenarios. For those reasons, this work focuses on developing an algorithm based on the Lattice-Boltzmann method (LBM) to reproduce the platelet aggregation process. LBM is an alternative to the traditional numeric methods capable of reducing computing times. The developed algorithm models a cylindric blood vessel as a 2-dimensional rectangle in which a wound is imposed on the lower wall. Once the vessel’s wall is damaged, a series of reactions take place around the wounded area attracting platelets to build a plug. Different simulations were carried out to assess the effect of different flow and chemical conditions over 1) The shape of the plug and 2) The platelets concentration inside the plug. In general, the obtained results show good agreement with previous works. More importantly, the results suggest that the shear rate strongly affects the concentration profiles of the platelet-activating species. It was found that there may be a positive feedback loop in which the shear rate initially activates some platelets (due to surface proteins unfolding) that in turn release activating chemicals that are dragged and diffused towards specific areas where platelet activation is enhanced even more. This conclusion could be an important breakthrough because most of the state-of-the-art research on the shear rate influence over platelet activation focuses on effects at a molecular scale, but the current approach is based on a systems biology approach. However, the computational algorithm still requires further refinement to reduce the computation times.