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Author Notes:

Address for Correspondence: Habib Samady, MD, FACC, Professor of Medicine, Division of Cardiology, Emory University School of Medicine, 1364 Clifton Road F622, Atlanta, GA 30322, Telephone: 404-778-1237, Fax: 404-712-7102, hsamady@emory.edu.

Disclosures: 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


Research Funding:

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.


  • Science & Technology
  • Life Sciences & Biomedicine
  • Cardiac & Cardiovascular Systems
  • Radiology, Nuclear Medicine & Medical Imaging
  • Cardiovascular System & Cardiology
  • Acute coronary syndrome
  • Coronary artery disease
  • Computational fluid dynamics
  • High-risk plaque
  • Wall shear stress

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


Journal Title:

International Journal of Cardiovascular Imaging


Volume 33, Number 7


, Pages 1089-1099

Type of Work:

Article | Post-print: After Peer Review


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.

Copyright information:

© 2017, Springer Science+Business Media Dordrecht.

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