Haematocrit and Shear Rate Modulate Local Cell-free Layer Thickness and Platelet Margination in Blood Flow Along a Sinusoidal Wall

TL;DR

This study uses simulations to explore how hematocrit and shear rate influence platelet behavior and local flow dynamics near sinusoidal vessel walls, shedding light on thrombus formation mechanisms.

Contribution

It reveals the dominant role of hematocrit in platelet margination and how sinusoidal geometry affects shear gradients and platelet distribution.

Findings

Platelet margination is mainly governed by hematocrit levels.

Low hematocrit promotes platelet accumulation at crests, aiding aggregate growth.

Shear rate gradients vary along the sinusoidal surface, influencing adhesion pathways.

Abstract

The geometry of blood vessels strongly affects hemostasis and thrombosis through red blood cell (RBC) dynamics and platelet margination. Growing platelet aggregates, in turn, reshape the local vessel wall topography, leading to a strongly coupled system. However, it is not well understood how surface heterogeneities alter local hemodynamics and platelet margination, thereby driving further aggregate growth. This study investigates how hematocrit (Ht) and shear rate affect RBC dynamics, cell-free layer (CFL) thickness, and platelet margination near a sinusoidal wall. The sinusoidal wall, with crests and valleys aligned with the flow direction, serves as a model of the flow-aligned platelet aggregates observed in microfluidic experiments [Pero et al., CRPS, 2024]. We perform three-dimensional immersed-boundary-lattice-Boltzmann simulations of particulate blood flow with deformable RBCs and nearly rigid spherical platelets. Our results show that platelet margination is primarily governed by Ht and is more pronounced in regions where the CFL thickness is similar to the platelet size. At low Ht, platelets preferentially accumulate at crests, promoting high-amplitude aggregate growth. Increasing Ht leads to a more uniform platelet distribution along the surface, consistent with experimental observations. The sinusoidal geometry generates a pronounced crest-valley wall shear rate gradient, suggesting that distinct shear-dependent adhesion pathways may dominate at different surface locations. Our findings provide mechanistic insights into the morphological evolution of platelet aggregates and may ultimately inform targeted therapeutic strategies for thrombosis based on shear-sensitive drug-delivery.