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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Journal Article
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.
Journal ArticleDOI
Endothelial Cell Dysfunction and the Pathobiology of Atherosclerosis
TL;DR: This review traces the evolution of the concept of endothelial cell dysfunction, focusing on recent insights into the cellular and molecular mechanisms that underlie its pivotal roles in atherosclerotic lesion initiation and progression; explores its relationship to classic, as well as more recently defined, clinical risk factors for atherosclerosis.
Journal ArticleDOI
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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Association between multiple cardiovascular risk factors and atherosclerosis in children and young adults. The Bogalusa Heart Study
Gerald S. Berenson,Sathanur R. Srinivasan,Weihang Bao,William P. Newman,Richard E. Tracy,Wendy A. Wattigney +5 more
TL;DR: Findings indicate that as the number of cardiovascular risk factors increases, so does the severity of asymptomatic coronary and aortic atherosclerosis in young people.
Journal ArticleDOI
Flow-mediated endothelial mechanotransduction
TL;DR: The transmission of hemodynamic forces throughout the endothelium and the mechanotransduction mechanisms that lead to biophysical, biochemical, and gene regulatory responses of endothelial cells to hemodynamic shear stresses are reviewed.
Journal ArticleDOI
Nitric oxide-generating vasodilators and 8-bromo-cyclic guanosine monophosphate inhibit mitogenesis and proliferation of cultured rat vascular smooth muscle cells.
Uttam Garg,Aviv Hassid +1 more
TL;DR: Results suggest that endogenous nitric oxide may function as a modulator of vascular smooth muscle cell mitogenesis and proliferation, by a cGMP-mediated mechanism.
Journal ArticleDOI
The Emerging Concept of Vascular Remodeling
Gary H. Gibbons,Victor J. Dzau +1 more
TL;DR: Vascular remodeling is an active process of structural alteration that involves changes in at least four cellular processes -- cell growth, cell death, cell migration, and production or degradation of extracellular matrix -- and is dependent on a dynamic interaction between locally.
Journal ArticleDOI
Carotid bifurcation atherosclerosis. Quantitative correlation of plaque localization with flow velocity profiles and wall shear stress.
Christopher K. Zarins,Don P. Giddens,B. K. Bharadvaj,V S Sottiurai,R.F. Mabon,Seymour Glagov +5 more
TL;DR: It is concluded that in the human carotid bifurcation, regions of moderate to high shear stress, where flow remains unidirectional and axially aligned, are relatively spared of intimal thickening.