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


RESULTS
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.


CONCLUSIONS
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.
Papafaklis
Michail I
MI
Cardiovascular Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA.
Koskinas
Konstantinos C
KC
Chatzizisis
Yiannis S
YS
Stone
Peter H
PH
Feldman
Charles L
CL
D000222:Adaptation, Physiological; D001783:Blood Flow Velocity; D003324:Coronary Artery Disease / Q000473:pathology*; D003331:Coronary Vessels / Q000473:pathology*; D018450:Disease Progression; D004730:Endothelium, Vascular / Q000473:pathology*; D006439:Hemodynamics; D006801:Humans; D007249:Inflammation / Q000473:pathology; D012307:Risk Factors; D033081:Shear Strength; D013312:Stress, Physiological; D013997:Time Factors; D020257:Ventricular Remodeling