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内皮剪切应力在支架再狭窄和血栓形成中的作用:病理生理机制及其对临床转化的意义。

Role of endothelial shear stress in stent restenosis and thrombosis: pathophysiologic mechanisms and implications for clinical translation.

机构信息

1st Cardiology Department, AHEPA University Hospital, Aristole University Medical School, Thessaloniki, Greece.

出版信息

J Am Coll Cardiol. 2012 Apr 10;59(15):1337-49. doi: 10.1016/j.jacc.2011.10.903.

DOI:10.1016/j.jacc.2011.10.903
PMID:22480478
Abstract

Restenosis and thrombosis are potentially fatal complications of coronary stenting with a recognized multifactorial etiology. The effect of documented risk factors, however, cannot explain the preponderance of certain lesion types, stent designs, and implantation configurations for the development of these complications. Local hemodynamic factors, low endothelial shear stress (ESS) in particular, are long known to critically affect the natural history of atherosclerosis. Increasing evidence now suggests that ESS may also contribute to the development of restenosis and thrombosis upon stenting of atherosclerotic plaques, in conjunction with well-appreciated risk factors. In this review, we present in vivo and mechanistic evidence associating ESS with the localization and progression of neointimal hyperplasia and in-stent clotting. Clinical studies have associated stent design features with the risk of restenosis. Importantly, computational simulations extend these observations by directly linking specific stent geometry and positioning characteristics with the post-stenting hemodynamic milieu and with the stent's thrombogenicity and pro-restenotic potential, thereby indicating ways to clinical translation. An enhanced understanding of the pathophysiologic role of ESS in restenosis and thrombosis might dictate hemodynamically favorable stent designs and deployment configurations to reduce the potential for late lumen loss and thrombotic obstruction. Recent methodologies for in vivo ESS profiling at a clinical level might allow for early identification of patients at high risk for the development of restenosis or thrombosis and might thereby guide individualized, risk-tailored treatment strategies to prevent devastating complications of endovascular interventions.

摘要

再狭窄和血栓形成是冠状动脉支架置入术的潜在致命并发症,其发病机制具有多因素特征。然而,已确定的危险因素的影响并不能解释某些病变类型、支架设计和植入方式在这些并发症中的优势。局部血液动力学因素,尤其是低内皮剪切应力(ESS),长期以来一直被认为对动脉粥样硬化的自然病程有重要影响。越来越多的证据表明,ESS 也可能与动脉粥样硬化斑块支架置入后再狭窄和血栓形成的发展有关,这与公认的危险因素有关。在这篇综述中,我们提出了与 ESS 与新生内膜增生和支架内血栓形成的定位和进展相关的体内和机制证据。临床研究将支架设计特征与再狭窄风险联系起来。重要的是,计算模拟通过直接将特定的支架几何形状和定位特征与支架置入后的血液动力学环境以及支架的血栓形成和促再狭窄潜力联系起来,从而为临床转化提供了途径。对 ESS 在再狭窄和血栓形成中的病理生理作用的深入了解可能会决定有利于血液动力学的支架设计和部署配置,以降低晚期管腔丢失和血栓阻塞的潜在风险。最近在临床水平上进行 ESS 分析的方法可能可以早期识别出有再狭窄或血栓形成风险的患者,并据此指导个体化的、风险定制的治疗策略,以预防血管内介入治疗的灾难性并发症。

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