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Author Notes:

Corresponding Author: Ajit P. Yoganathan, The Wallace H. Coulter Department of Biomedical Engineering, Georgia Institute of Technology and Emory University, Room 2119 U. A. Whitaker Building, 313 Ferst Drive, Atlanta, GA 30332-0535, USA. ajit.yoganathan@bme.gatech.edu

Authors wish to thank the Cardiovascular Fluid Mechanics Lab, Dr. Hanjoong Jo’s lab, Dr. Robert M. Nerem’s Lab members, and all other researchers for their contributions to thework presented in this paper.

Finally, the authors acknowledge the kindness of Mr. Holifield for donating porcine heart valves, and thank the machine shop crew at School of Chemical and Biomolecular Engineering,

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Research Funding:

Authors also would like to thank all the relevant funding sources for the Cardiovascular Fluid Mechanics lab at Georgia Tech: American Heart Association under the Post-doctoral Research Awards (0625620B, 10POST3050054) and Predoctoral Research Award (09PRE2060605), National Science Foundation through the Engineering Research Center program at the Georgia Tech under the award EEC 9731643, National Heart, Lung and Blood Institute grant number HL-07262, the Wallace H. Coulter Distinguished Faculty Chair funds, Petit Undergraduate Research Scholars Program, a gift from Tom and Shirley Gurley, and all other sources.

Keywords:

  • Science & Technology
  • Technology
  • Engineering, Biomedical
  • Engineering
  • ENGINEERING, BIOMEDICAL
  • Aortic valve
  • Mechanobiology
  • Shear stress
  • Pressure
  • Stretch
  • Bicuspid
  • Calcification
  • VALVULAR ENDOTHELIAL-CELLS
  • FLUID SHEAR-STRESS
  • ENGINEERED HEART-VALVES
  • SMOOTH-MUSCLE-CELLS
  • INTERSTITIAL-CELLS
  • CYCLIC STRETCH
  • ORGAN-CULTURE
  • BIOLOGICAL-PROPERTIES
  • EX-VIVO
  • TRANSFORMING GROWTH-FACTOR-BETA-1

Aortic Valve: Mechanical Environment and Mechanobiology

Tools:

Journal Title:

Annals of Biomedical Engineering

Volume:

Volume 41, Number 7

Publisher:

, Pages 1331-1346

Type of Work:

Article | Post-print: After Peer Review

Abstract:

The aortic valve (AV) experiences a complex mechanical environment, which includes tension, flexure, pressure, and shear stress forces due to blood flow during each cardiac cycle. This mechanical environment regulates AV tissue structure by constantly renewing and remodeling the phenotype. In vitro, ex vivo and in vivo studies have shown that pathological states such as hypertension and congenital defect like bicuspid AV (BAV) can potentially alter the AV's mechanical environment, triggering a cascade of remodeling, inflammation, and calcification activities in AV tissue. Alteration in mechanical environment is first sensed by the endothelium, which in turn induces changes in the extracellular matrix, and triggers cell differentiation and activation. However, the molecular mechanism of this process is not understood very well. Understanding these mechanisms is critical for advancing the development of effective medical based therapies. Recently, there have been some interesting studies on characterizing the hemodynamics associated with AV, especially in pathologies like BAV, using different experimental and numerical methods. Here, we review the current knowledge of the local AV mechanical environment and its effect on valve biology, focusing on in vitro and ex vivo approaches. © 2013 Biomedical Engineering Society.

Copyright information:

Copyright © 2013, Biomedical Engineering Society

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