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J Am Coll Cardiol, 2007; 49:2379-2393, doi:10.1016/j.jacc.2007.02.059 (Published online 7 June 2007).
© 2007 by the American College of Cardiology Foundation
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STATE-OF-THE-ART PAPER

Role of Endothelial Shear Stress in the Natural History of Coronary Atherosclerosis and Vascular Remodeling

Molecular, Cellular, and Vascular Behavior

Yiannis S. Chatzizisis, MD, MSc*,{dagger}, Ahmet Umit Coskun, PhD{ddagger}, Michael Jonas, MD{dagger}, Elazer R. Edelman, MD, PhD, FACC*,{dagger},3, Charles L. Feldman, ScD*,2 and Peter H. Stone, MD, FACC*,1,*

* Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts
{ddagger} Mechanical and Industrial Engineering, Northeastern University, Boston, Massachusetts
{dagger} Harvard-MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge, Massachusetts.

Manuscript received January 2, 2007; revised manuscript received February 22, 2007, accepted February 26, 2007.

* Reprint requests and correspondence: Dr. Peter H. Stone, Cardiovascular Division, Brigham and Women’s Hospital, Harvard Medical School, 75 Francis Street, Boston, Massachusetts. (Email: pstone{at}partners.org).

Although the entire coronary tree is exposed to the atherogenic effect of the systemic risk factors, atherosclerotic lesions form at specific arterial regions, where low and oscillatory endothelial shear stress (ESS) occur. Low ESS modulates endothelial gene expression through complex mechanoreception and mechanotransduction processes, inducing an atherogenic endothelial phenotype and formation of an early atherosclerotic plaque. Each early plaque exhibits an individual natural history of progression, regression, or stabilization, which is dependent not only on the formation and progression of atherosclerosis but also on the vascular remodeling response. Although the pathophysiologic mechanisms involved in the remodeling of the atherosclerotic wall are incompletely understood, the dynamic interplay between local hemodynamic milieu, low ESS in particular, and the biology of the wall is likely to be important. In this review, we explore the molecular, cellular, and vascular processes supporting the role of low ESS in the natural history of coronary atherosclerosis and vascular remodeling and indicate likely mechanisms concerning the different natural history trajectories of individual coronary lesions. Atherosclerotic plaques associated with excessive expansive remodeling evolve to high-risk plaques, because low ESS conditions persist, thereby promoting continued local lipid accumulation, inflammation, oxidative stress, matrix breakdown, and eventually further plaque progression and excessive expansive remodeling. An enhanced understanding of the pathobiologic processes responsible for atherosclerosis and vascular remodeling might allow for early identification of a high-risk coronary plaque and thereby provide a rationale for innovative diagnostic and/or therapeutic strategies for the management of coronary patients and prevention of acute coronary syndromes.

Abbreviations and Acronyms
  EC = endothelial cell
  ECM = extracellular matrix
  eNOS = endothelial nitric oxide synthase
  ESS = endothelial shear stress
  IEL = internal elastic lamina
  IL = interleukin
  LDL = low-density lipoprotein cholesterol
  MAPK = mitogen-activated protein kinase
  MMP = matrix metalloproteinase
  NF-{kappa}B = nuclear factor-kappa B
  NO = nitric oxide
  ROS = reactive oxygen species
  SREBP = sterol regulatory elements binding protein
  TCFA = thin cap fibroatheroma
  TF = transcription factor
  VSMC = vascular smooth muscle cell




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L. Ai, M. Rouhanizadeh, J. C. Wu, W. Takabe, H. Yu, M. Alavi, R. Li, Y. Chu, J. Miller, D. D. Heistad, et al.
Shear stress influences spatial variations in vascular Mn-SOD expression: implication for LDL nitration
Am J Physiol Cell Physiol, June 1, 2008; 294(6): C1576 - C1585.
[Abstract] [Full Text] [PDF]

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 Arterioscler. Thromb. Vasc. Bio.Home page
E. R. Mohler III, L. Sarov-Blat, Y. Shi, D. Hamamdzic, A. Zalewski, C. MacPhee, R. Llano, D. Pelchovitz, S. K. Mainigi, H. Osman, et al.
Site-Specific Atherogenic Gene Expression Correlates With Subsequent Variable Lesion Development in Coronary and Peripheral Vasculature
Arterioscler Thromb Vasc Biol, May 1, 2008; 28(5): 850 - 855.
[Abstract] [Full Text] [PDF]

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 VascularHome page
H. E. Achneck, B. Sileshi, and J. H. Lawson
Review of the Biology of Bleeding and Clotting in the Surgical Patient
Vascular, April 2, 2008; 16(suppl_1): S6 - S11.
[Abstract] [Full Text] [PDF]

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 CirculationHome page
Y. S. Chatzizisis, M. Jonas, A. U. Coskun, R. Beigel, B. V. Stone, C. Maynard, R. G. Gerrity, W. Daley, C. Rogers, E. R. Edelman, et al.
Prediction of the Localization of High-Risk Coronary Atherosclerotic Plaques on the Basis of Low Endothelial Shear Stress: An Intravascular Ultrasound and Histopathology Natural History Study
Circulation, February 26, 2008; 117(8): 993 - 1002.
[Abstract] [Full Text] [PDF]

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 J Am Coll Cardiol IntvHome page
B. De Bruyne and E. Barbato
Drug-eluting stent implantation technique matters, more than ever.
J. Am. Coll. Cardiol. Intv., February 1, 2008; 1(1): 32 - 33.
[Full Text] [PDF]

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 J Am Coll CardiolHome page
H. Kaneda
Complex Roles of Endothelial Shear Stress in Vascular Remodeling Response
J. Am. Coll. Cardiol., November 27, 2007; 50(22): 2171 - 2171.
[Full Text] [PDF]

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 J Am Coll CardiolHome page
Y. Chatzizisis, A. U. Coskun, M. Jonas, E. R. Edelman, C. L. Feldman, and P. H. Stone
Reply
J. Am. Coll. Cardiol., November 27, 2007; 50(22): 2171 - 2172.
[Full Text] [PDF]

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 Circ. Res.Home page
J. P. De Bono and K. M. Channon
Endothelial Cell Tetrahydrobiopterin: Going With the Flow
Circ. Res., October 12, 2007; 101(8): 752 - 754.
[Full Text] [PDF]


 
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