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Development of Framework to Examine the Focal Association Between Wall Shear Stress and Coronary Artery Disease Progression in the Clinical Setting

[+] Author Affiliations
Lucas H. Timmins, John N. Oshinski

Georgia Institute of Technology and Emory University School of Medicine, Atlanta, GAEmory University School of Medicine, Atlanta, GA

David S. Molony, Don P. Giddens

Georgia Institute of Technology and Emory University School of Medicine, Atlanta, GA

Parham Eshtehardi

Albert Einstein College of Medicine, Bronx, NY

Michael C. McDaniel, Habib Samady

Emory University School of Medicine, Atlanta, GA

Paper No. SBC2013-14476, pp. V01AT14A004; 2 pages
  • ASME 2013 Summer Bioengineering Conference
  • Volume 1A: Abdominal Aortic Aneurysms; Active and Reactive Soft Matter; Atherosclerosis; BioFluid Mechanics; Education; Biotransport Phenomena; Bone, Joint and Spine Mechanics; Brain Injury; Cardiac Mechanics; Cardiovascular Devices, Fluids and Imaging; Cartilage and Disc Mechanics; Cell and Tissue Engineering; Cerebral Aneurysms; Computational Biofluid Dynamics; Device Design, Human Dynamics, and Rehabilitation; Drug Delivery and Disease Treatment; Engineered Cellular Environments
  • Sunriver, Oregon, USA, June 26–29, 2013
  • Conference Sponsors: Bioengineering Division
  • ISBN: 978-0-7918-5560-7
  • Copyright © 2013 by ASME


Natural history data on clinical coronary artery disease (CAD) indicates that there is a critical need to prospectively identify rapidly progressing and vulnerable coronary lesions that may cause potentially fatal acute coronary events [1]. Recent prospective clinical investigations have evaluated the value of wall shear stress (WSS) as a prognostic marker for identifying rapidly progressing coronary lesions [2,3]. Data indicate that low WSS is associated with significant plaque progression, while regions of high WSS are associated with plaque regression and phenotypic transformation towards a more vulnerable lesion. While these studies provided unprecedented data on the role of hemodynamic-induced mechanical forces in lesion dynamics, they were limited by a lack of focal understanding of the association between WSS and plaque progression. Specifically, despite the understanding that WSS and plaque progression are heterogeneous around the artery’s circumference, in each image slice WSS values were spatially averaged around the circumference and correlated with average values for changes in virtual histology-intravascular ultrasound (VH-IVUS) defined plaque constituent areas.

Copyright © 2013 by ASME



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