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Reduction in Mechanical Wall Strain Precedes Intimal Hyperplasia Formation in a Murine Model of Arterial Occlusive Disease

[+] Author Affiliations
John T. Favreau, Glenn R. Gaudette

Worcester Polytechnic Institute, Worcester, MA

Chengwei Liu

Brigham and Women’s Hospital, Boston, MAThe First Affiliated Hospital of Jiamusi University, Jiamusi, Heilongjiang, China

Peng Yu, Christine Mauro, Ming Tao, C. Keith Ozaki

Brigham and Women’s Hospital, Boston, MA

Paper No. SBC2013-14475, pp. V01AT04A016; 2 pages
doi:10.1115/SBC2013-14475
From:
  • 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

abstract

Coronary artery disease and peripheral artery disease remain a significant source of mortality and vascular morbidity in the United States; both affecting over 14 million Americans.[1] Although a number of both open and endovascular procedures are available for treating occlusive lesions, post-procedure intimal hyperplasia (IH) and pathological wall adaptation in treated arteries cause further need for treatment. As on average 50% of patients receiving these treatments must receive further vascular intervention to prevent the continued expansion of IH into the vessel lumen, there is a need to improve our understanding of the underlying causes of IH formation.[2]

Copyright © 2013 by ASME
Topics: Diseases

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