Journal ArticleDOI
Hemodynamic shear stress and its role in atherosclerosis.
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TLDR
The functional regulation of the endothelium by local hemodynamic shear stress provides a model for understanding the focal propensity of atherosclerosis in the setting of systemic factors and may help guide future therapeutic strategies.Abstract:
Atherosclerosis, the leading cause of death in the developed world and
nearly the leading cause in the developing world, is associated with systemic
risk factors including hypertension, smoking, hyperlipidemia, and diabetes
mellitus, among others. Nonetheless, atherosclerosis remains a geometrically
focal disease, preferentially affecting the outer edges of vessel bifurcations.
In these predisposed areas, hemodynamic shear stress, the frictional force
acting on the endothelial cell surface as a result of blood flow, is weaker
than in protected regions. Studies have identified hemodynamic shear stress
as an important determinant of endothelial function and phenotype. Arterial-level
shear stress (>15 dyne/cm2) induces endothelial quiescence and
an atheroprotective gene expression profile, while low shear stress (<4
dyne/cm2), which is prevalent at atherosclerosis-prone sites, stimulates
an atherogenic phenotype. The functional regulation of the endothelium by
local hemodynamic shear stress provides a model for understanding the focal
propensity of atherosclerosis in the setting of systemic factors and may help
guide future therapeutic strategies.read more
Citations
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ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction--executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction).
Elliott M. Antman,Daniel T. Anbe,Paul W. Armstrong,Eric R. Bates,Lee A. Green,Mary M. Hand,Judith S. Hochman,Harlan M. Krumholz,Frederick G. Kushner,Gervasio A. Lamas,Charles J. Mullany,Joseph P. Ornato,David L. Pearle,Michael A. Sloan,Sidney C. Smith,Joseph S. Alpert,Jeffrey L. Anderson,David P. Faxon,Valentin Fuster,Raymond J. Gibbons,Gabriel Gregoratos,Jonathan L. Halperin,Loren F. Hiratzka,Sharon A. Hunt,Alice K. Jacobs +24 more
TL;DR: Elliott M. Antman,MD, FACC, FAHA, Chair; Daniel T. Anbe, MD, F ACC,FAHA; Paul Wayne Armstrong, MD; Eric R. Bates; Lee A. Green; Mary Hand; Judith S. Kushner; and Sidney C. Sloan.
Journal ArticleDOI
ACC/AHA Guidelines for the Management of Patients With ST-Elevation Myocardial Infarction
Elliott M. Antman,Daniel T. Anbe,Paul W. Armstrong,Eric R. Bates,Lee A. Green,Mary M. Hand,Judith S. Hochman,Harlan M. Krumholz,Frederick G. Kushner,Gervasio A. Lamas,Charles J. Mullany,Joseph P. Ornato,David L. Pearle,Michael A. Sloan,Sidney C. Smith,Joseph S. Alpert,Jeffrey L. Anderson,David P. Faxon,Valentin Fuster,Raymond J. Gibbons,Gabriel Gregoratos,Jonathan L. Halperin,Loren F. Hiratzka,Sharon A. Hunt,Alice K. Jacobs +24 more
TL;DR: This document was approved by the American College of Cardiology Foundation Board of Trustees on May 7, 2004 and by theAmerican Heart Association Science Advisory and Coordinating Committee on May 5, 2004.
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Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis
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Effects of Disturbed Flow on Vascular Endothelium: Pathophysiological Basis and Clinical Perspectives
Jeng Jiann Chiu,Shu Chien +1 more
TL;DR: Current knowledge on the role of disturbed flow in EC physiology and pathophysiology, as well as its clinical implications are summarized to contribute to the understanding of the etiology of lesion development in vascular niches with disturbed flow and help to generate new approaches for therapeutic interventions.
Journal ArticleDOI
Role of endothelial shear stress in the natural history of coronary atherosclerosis and vascular remodeling: molecular, cellular, and vascular behavior.
Yiannis S. Chatzizisis,Ahmet U. Coskun,Michael Jonas,Elazer R. Edelman,Elazer R. Edelman,Charles L. Feldman,Peter Stone +6 more
TL;DR: The molecular, cellular, and vascular processes supporting the role of low ESS in the natural history of coronary atherosclerosis and vascular remodeling are explored and likely mechanisms concerning the different natural history trajectories of individual coronary lesions are indicated.
References
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Journal ArticleDOI
Localizing Role of Hemodynamics in Atherosclerosis in Several Human Vertebrobasilar Junction Geometries
TL;DR: Modulation of the various parameters in the models changed the size of the regions with low wall shear stress and/or recirculation areas dramatically and a comparable effect was found in the occurrence of plaques in the human vertebrobasilar junction; eg, for an atherosclerotic plaque at the apex, a predicted probability larger than 0.5 was computed.
Journal ArticleDOI
Hemodynamic forces modulate the effects of cytokines on fibrinolytic activity of endothelial cells
Yohko Kawai,Yutaka Matsumoto,Kiyoaki Watanabe,Hiroshi Yamamoto,Kumi Satoh,Mitsuru Murata,Makoto Handa,Yasuo Ikeda +7 more
TL;DR: A role for hemodynamic forces in regulating fibrinolytic activity with or without cytokine stimulation is indicated, using a modified cone-plate viscometer in which well-controlled and -defined shear forces were generated.
Journal ArticleDOI
Fluid Shear Stress Increases the Production of Granulocyte-Macrophage Colony-Stimulating Factor by Endothelial Cells via mRNA Stabilization
TL;DR: It is suggested that fluid shear stress increases the production of GM-CSF in HUVECs via mRNA stabilization, which depended on protein synthesis, because it was blocked by cycloheximide.
Journal ArticleDOI
Flow-induced prostacyclin production is mediated by a pertussis toxin-sensitive G protein.
TL;DR: It is found that flow stimulates prostacyclin production via a pertussis toxin‐sensitive G protein and modulates the stimulus‐response coupling of other agonists.
Journal ArticleDOI
Relation between coronary artery geometry and the distribution of early sudanophilic lesions
TL;DR: Results would appear to be consistent with the notion that atherosclerosis is favored where a larger extent of the vessel experiences fluid dynamic wall shears near zero for an appreciable part of the pulsatile cycle.