Multidimensional optimization of stent design for endothelial shear stress regulation: Geometric structuring, surface functionalization strategies to mitigate thrombosis and restenosis

Figures

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  Fig. 1. Cardiovascular disease (CVD). Suboptimal stent design following implantation may lead to reduced distribution of ESS, elevating the likelihood of restenosis and thrombosis. Enhancing stent design by refining geometry, utilizing computational fluid dynamics (CFD) simulations, incorporating microstructural inner wall modifications, and developing novel stent configurations to promote endothelialization can alleviate ESS non-uniformity.

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  Fig. 2. Flow PRISMA diagram of the screening and selection procedure.

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  Fig. 3. In the arterial vasculature, the change of endothelial shear stress (ESS) gradient has important clinical and engineering significance gradient change in endothelial shear stress formation. There is a shear gradient forming at the point indicated by the curved arrow In regions without plaques, there is no significant gradient change in endothelial shear, and in regions with plaques, the gradient change in endothelial shear is more pronounced, which may form disturbing currents that can affect the rupture of plaques.

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  Fig. 4. Illustrates a schematic of laminar and disturbed blood flow in arterial branches. In the main arterial trunk, which is typically straight with a larger diameter, blood flow is stable and orderly, resulting in laminar flow and uniform ESS. At bifurcations, changes in flow direction and velocity occur, leading to flow separation, disturbed blood flow, and uneven ESS.

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  Fig. 5. Diagram of endothelial shear stress response signal transduction. After stent implantation, ESSG formated, blood flow is redistributed as it impinges on the stent struts. Homogeneous and heterogeneous ESS stimulate integrins, ion channels, G protein-coupled receptors (GPCRs), and cytoskeletal mechanosensors on ECs, respectively, in response to complex downstream molecular mechanisms[44].

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  Fig. 6. Following stent implantation, a high ESS region is observed upstream, while a low ESS region is found downstream. The low ESS region can lead to endothelial cell dysfunction and the release of inflammatory factors[49]. This diagram depicts a classic NF-κB inflammatory signaling pathway: A stimulus (P) triggers IκB phosphorylation and degradation, releasing NF-κB, which translocates to the nucleus and promotes IL6 expression. This cascade ultimately leads to increased endothelial permeability, a key mechanism in vascular inflammation and atherosclerosis.

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  Fig. 7. Simulation diagram of stent implantation. Effect of stent adherence on ESS. (a)The stent is well adhered to the wall and the ESS is more evenly distributed, (b)With poor stent adherence, blood flow creates a zone of slow stagnation, resulting in a significant change from high to low local ESS[68], It can help us have a deeper understanding of the impact of poor stent adhesion.

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  Fig. 8. Stent loading MNP promotes ECs enrichment under the action of external magnetic field and promotes endothelialization process[86].