In-vivo assessment of the natural history of coronary atherosclerosis: Vascular remodeling and endothelial shear stress determine the complexity of atherosclerotic disease progression

Michail I. Papafaklis, Konstantinos C. Koskinas, Yiannis S. Chatzizisis, Peter H. Stone, Charles L. Feldman

Research output: Contribution to journalReview article

22 Citations (Scopus)

Abstract

PURPOSE OF REVIEW: Atherosclerotic disease progression is determined by localized plaque growth, which is induced by systemic and local hemodynamic factors, and the nature of the wall remodeling response. The purpose of this review is to summarize the processes underlying the heterogeneity of coronary atherosclerosis progression in relation to the local hemodynamic and arterial remodeling environment. RECENT FINDINGS: Multiple competing biological processes in the extracellular matrix define the extent of vascular remodeling and disease progression. The remodeling phenomenon is not consistent but is characterized by great phenotypical heterogeneity which reflects the complex effect of systemic, genetic and hemodynamic factors on the arterial wall response to plaque formation and progression. The exaggeration of expansive remodeling (i.e., excessive expansive remodeling) likely contributes to the transformation of an initially favorable action into an excessive course of vessel expansion, continued disease progression and plaque instability. Extremely low endothelial shear stress and excessive expansive remodeling establish a vicious cycle which leads to the formation of severe plaques with high-risk characteristics. SUMMARY: The dynamic interplay between the local hemodynamic environment and the wall remodeling behavior determines the complexity of the natural history of atherosclerosis and explains the development of localized plaque vulnerability.

Original languageEnglish (US)
Pages (from-to)627-638
Number of pages12
JournalCurrent Opinion in Cardiology
Volume25
Issue number6
DOIs
StatePublished - Nov 1 2010

Fingerprint

Disease Progression
Coronary Artery Disease
Hemodynamics
Biological Phenomena
Vascular Diseases
Extracellular Matrix
Atherosclerosis
Vascular Remodeling
Growth

Keywords

  • atherosclerosis
  • extracellular matrix
  • imaging modalities
  • remodeling
  • shear stress

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

In-vivo assessment of the natural history of coronary atherosclerosis : Vascular remodeling and endothelial shear stress determine the complexity of atherosclerotic disease progression. / Papafaklis, Michail I.; Koskinas, Konstantinos C.; Chatzizisis, Yiannis S.; Stone, Peter H.; Feldman, Charles L.

In: Current Opinion in Cardiology, Vol. 25, No. 6, 01.11.2010, p. 627-638.

Research output: Contribution to journalReview article

@article{a6dc1cd86b0e4b989b3d551ed9928e71,
title = "In-vivo assessment of the natural history of coronary atherosclerosis: Vascular remodeling and endothelial shear stress determine the complexity of atherosclerotic disease progression",
abstract = "PURPOSE OF REVIEW: Atherosclerotic disease progression is determined by localized plaque growth, which is induced by systemic and local hemodynamic factors, and the nature of the wall remodeling response. The purpose of this review is to summarize the processes underlying the heterogeneity of coronary atherosclerosis progression in relation to the local hemodynamic and arterial remodeling environment. RECENT FINDINGS: Multiple competing biological processes in the extracellular matrix define the extent of vascular remodeling and disease progression. The remodeling phenomenon is not consistent but is characterized by great phenotypical heterogeneity which reflects the complex effect of systemic, genetic and hemodynamic factors on the arterial wall response to plaque formation and progression. The exaggeration of expansive remodeling (i.e., excessive expansive remodeling) likely contributes to the transformation of an initially favorable action into an excessive course of vessel expansion, continued disease progression and plaque instability. Extremely low endothelial shear stress and excessive expansive remodeling establish a vicious cycle which leads to the formation of severe plaques with high-risk characteristics. SUMMARY: The dynamic interplay between the local hemodynamic environment and the wall remodeling behavior determines the complexity of the natural history of atherosclerosis and explains the development of localized plaque vulnerability.",
keywords = "atherosclerosis, extracellular matrix, imaging modalities, remodeling, shear stress",
author = "Papafaklis, {Michail I.} and Koskinas, {Konstantinos C.} and Chatzizisis, {Yiannis S.} and Stone, {Peter H.} and Feldman, {Charles L.}",
year = "2010",
month = "11",
day = "1",
doi = "10.1097/HCO.0b013e32833f0236",
language = "English (US)",
volume = "25",
pages = "627--638",
journal = "Current Opinion in Cardiology",
issn = "0268-4705",
publisher = "Lippincott Williams and Wilkins",
number = "6",

}

TY - JOUR

T1 - In-vivo assessment of the natural history of coronary atherosclerosis

T2 - Vascular remodeling and endothelial shear stress determine the complexity of atherosclerotic disease progression

AU - Papafaklis, Michail I.

AU - Koskinas, Konstantinos C.

AU - Chatzizisis, Yiannis S.

AU - Stone, Peter H.

AU - Feldman, Charles L.

PY - 2010/11/1

Y1 - 2010/11/1

N2 - PURPOSE OF REVIEW: Atherosclerotic disease progression is determined by localized plaque growth, which is induced by systemic and local hemodynamic factors, and the nature of the wall remodeling response. The purpose of this review is to summarize the processes underlying the heterogeneity of coronary atherosclerosis progression in relation to the local hemodynamic and arterial remodeling environment. RECENT FINDINGS: Multiple competing biological processes in the extracellular matrix define the extent of vascular remodeling and disease progression. The remodeling phenomenon is not consistent but is characterized by great phenotypical heterogeneity which reflects the complex effect of systemic, genetic and hemodynamic factors on the arterial wall response to plaque formation and progression. The exaggeration of expansive remodeling (i.e., excessive expansive remodeling) likely contributes to the transformation of an initially favorable action into an excessive course of vessel expansion, continued disease progression and plaque instability. Extremely low endothelial shear stress and excessive expansive remodeling establish a vicious cycle which leads to the formation of severe plaques with high-risk characteristics. SUMMARY: The dynamic interplay between the local hemodynamic environment and the wall remodeling behavior determines the complexity of the natural history of atherosclerosis and explains the development of localized plaque vulnerability.

AB - PURPOSE OF REVIEW: Atherosclerotic disease progression is determined by localized plaque growth, which is induced by systemic and local hemodynamic factors, and the nature of the wall remodeling response. The purpose of this review is to summarize the processes underlying the heterogeneity of coronary atherosclerosis progression in relation to the local hemodynamic and arterial remodeling environment. RECENT FINDINGS: Multiple competing biological processes in the extracellular matrix define the extent of vascular remodeling and disease progression. The remodeling phenomenon is not consistent but is characterized by great phenotypical heterogeneity which reflects the complex effect of systemic, genetic and hemodynamic factors on the arterial wall response to plaque formation and progression. The exaggeration of expansive remodeling (i.e., excessive expansive remodeling) likely contributes to the transformation of an initially favorable action into an excessive course of vessel expansion, continued disease progression and plaque instability. Extremely low endothelial shear stress and excessive expansive remodeling establish a vicious cycle which leads to the formation of severe plaques with high-risk characteristics. SUMMARY: The dynamic interplay between the local hemodynamic environment and the wall remodeling behavior determines the complexity of the natural history of atherosclerosis and explains the development of localized plaque vulnerability.

KW - atherosclerosis

KW - extracellular matrix

KW - imaging modalities

KW - remodeling

KW - shear stress

UR - http://www.scopus.com/inward/record.url?scp=78049265832&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=78049265832&partnerID=8YFLogxK

U2 - 10.1097/HCO.0b013e32833f0236

DO - 10.1097/HCO.0b013e32833f0236

M3 - Review article

C2 - 20838338

AN - SCOPUS:78049265832

VL - 25

SP - 627

EP - 638

JO - Current Opinion in Cardiology

JF - Current Opinion in Cardiology

SN - 0268-4705

IS - 6

ER -