Stent strut streamlining and thickness reduction promote endothelialization

Stent strut streamlining and thickness reduction promote endothelialization
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DOI:
10.1098/rsif.2021.0023
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发表时间:
2021-08
影响因子:
3.9
通讯作者:
Duy T. Nguyen;Alexander F. Smith;J. M. Jiménez
Duy T. Nguyen;Alexander F. Smith;J. M. Jiménez
中科院分区:
综合性期刊2区
文献类型:
--
作者:
Duy T. Nguyen;Alexander F. Smith;J. M. Jiménez

文献摘要

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支架内血栓形成(ST)具有心肌梗死和死亡的高风险。缺乏内皮覆盖是支架植入术后ST的重要预后指标。虽然支架支撑厚度是ST的关键因素,但对其作用的机制理解有限,血流动力学的作用尚不清楚。使用伤口愈合试验和五种不同的支架支撑模型来测试内皮化情况,支架支撑模型的高度在50到150µm之间,适用于圆弧(CA)和矩形(RT)几何形状,以及没有支撑的对照组。在静态条件下,所有支架支撑表面完全内皮化。除100µm和150µm RT几何形状的支架支撑表面外,反向脉动扰动流导致支架支撑表面完全内皮化,而具有更高平均壁剪应力的完全顺行脉动无扰动流仅导致对照和50µm CA几何形状的支架支架完全内皮化。适度的流线型和支架支架高度的降低以血流动力学依赖的方式改善支架支架周围和支架支架表面的内皮覆盖。本研究强调支架支撑高度(厚度)和几何形状(形状)对局部血流动力学的影响,调节支架植入术后的再内皮化,这是降低支架血栓形成风险的重要因素。
Stent thrombosis (ST) carries a high risk of myocardial infarction and death. Lack of endothelial coverage is an important prognostic indicator of ST after stenting. While stent strut thickness is a critical factor in ST, a mechanistic understanding of its effect is limited and the role of haemodynamics is unclear. Endothelialization was tested using a wound-healing assay and five different stent strut models ranging in height between 50 and 150 µm for circular arc (CA) and rectangular (RT) geometries and a control without struts. Under static conditions, all stent strut surfaces were completely endothelialized. Reversing pulsatile disturbed flow caused full endothelialization, except for the stent strut surfaces of the 100 and 150 µm RT geometries, while fully antegrade pulsatile undisturbed flow with a higher mean wall shear stress caused only the control and the 50 µm CA geometries to be fully endothelialized. Modest streamlining and decrease in height of the stent struts improved endothelial coverage of the peri-strut and stent strut surfaces in a haemodynamics dependent manner. This study highlights the impact of the stent strut height (thickness) and geometry (shape) on the local haemodynamics, modulating reendothelialization after stenting, an important factor in reducing the risk of stent thrombosis.