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


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.

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Fig. 1
Fig. 2

[Reprinted from EuroIntervention 7/1, Gijsen et al. High shear stress induces a strain increase in human coronary plaques over a 6-month period, 121–127 [45], Copyright (2011), with permission from Europa Digital & Publishing]

Fig. 3

(modified from Stone et al. [36] with permission)

Fig. 4



Acute coronary syndrome


Coronary artery disease


Coronary computed tomography angiography


Computational fluid dynamics




Intraplaque hemorrhage


Optical coherence tomography


Plaque structural stress


Thin-cap fibroatheroma


Thick-cap fibroatheroma


Virtual histology intravascular ultrasound


Wall shear stress


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Correspondence to Habib Samady.

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Conflict of interest

P Eshtehardi and OY Hung received salary support from the Ruth L Kirschstein National Research Service Awards training Grant (5T32HL007745). H Samady receives research funding from the Georgia Research Alliance, the Wallace H. Coulter Foundation, Volcano Corporation, St. Jude Medical, Gilead Sciences Inc., Medtronic Inc. and Abbott Vascular. DP Giddens receives research funding from the Georgia Research Alliance and the Wallace H. Coulter Foundation. AJ Brown is funded by the British Heart Foundation and the Academy of Medical Sciences. C Costopoulos is supported by the British Heart Foundation. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

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Eshtehardi, P., Brown, A.J., Bhargava, A. et al. High wall shear stress and high-risk plaque: an emerging concept. Int J Cardiovasc Imaging 33, 1089–1099 (2017). https://doi.org/10.1007/s10554-016-1055-1

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  • Acute coronary syndrome
  • Coronary artery disease
  • Computational fluid dynamics
  • High-risk plaque
  • Wall shear stress