High wall shear stress and high-risk plaque: an emerging concept.

High wall shear stress and high-risk plaque: an emerging concept.
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DOI:
10.1007/s10554-016-1055-1
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发表时间:
2017-07
期刊:
The international journal of cardiovascular imaging
影响因子:
--
通讯作者:
Samady H
Samady H
中科院分区:
其他
文献类型:
--
作者:
Eshtehardi P;Brown AJ;Bhargava A;Costopoulos C;Hung OY;Corban MT;Hosseini H;Gogas BD;Giddens DP;Samady H

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近年来,在急性事件发生之前,已经有了大量的努力来识别体内的高风险斑块。虽然已经开发了许多成像方式来识别高危斑块的形态特征,但前瞻性的自然历史观察研究表明,易损性并不仅仅取决于斑块的形态,而且可能涉及其他的促进机制。高壁剪切应力(WSS)最近被认为是一个可能的致病因素,促进了高风险斑块的发展。高WSS已被证明会诱导内皮细胞行为的特异性改变,加剧炎症并刺激动脉粥样硬化脂质核心的进展。与实验和尸检研究一致,一些人体研究表明高WSS与已知的高危斑块形态学特征之间存在关联。然而,尽管越来越多的证据,仍然没有纵向数据将高WSS与临床事件联系起来。由于动脉粥样硬化斑块、动脉和WSS之间的相互作用是高度动态的,因此包括WSS测量在内的动脉粥样硬化的大型自然历史研究现在是有必要的。这篇综述将总结现有的临床证据,高WSS可能是高危斑块形成的病因机制。
In recent years, there has been a significant effort to identify high-risk plaques in vivo prior to acute events. While number of imaging modalities have been developed to identify morphologic characteristics of high-risk plaques, prospective natural-history observational studies suggest that vulnerability is not solely dependent on plaque morphology and likely involves additional contributing mechanisms. High wall shear stress (WSS) has recently been proposed as one possible causative factor, promoting the development of high-risk plaques. High WSS has been shown to induce specific changes in endothelial cell behavior, exacerbating inflammation and stimulating progression of the atherosclerotic lipid core. In line with experimental and autopsy studies, several human studies have shown associations between high WSS and known morphological features of high-risk plaques. However, despite increasing evidence, there is still no longitudinal data linking high WSS to clinical events. As the interplay between atherosclerotic plaque, artery, and WSS is highly dynamic, large natural history studies of atherosclerosis that include WSS measurements are now warranted. This review will summarize the available clinical evidence on high WSS as a possible etiological mechanism underlying high-risk plaque development.