Coronary hemodynamics and atherosclerotic wall stiffness: a vicious cycle.
Local hemodynamic environment, including low shear stress and increased tensile stress, determines the localization, growth and progression of coronary atherosclerosis. As atherosclerotic lesions evolve, the diseased coronary arteries undergo local quantitative and qualitative changes in their wall, and progressively become stiff. Arterial stiffening amplifies the atherogenic local hemodynamic environment, initiating a self-perpetuating vicious cycle, which drives the progression of atherosclerosis and the formation of atherosclerotic plaque. In vivo evidence indicates that endothelial dysfunction is associated with arterial stiffness, an association that creates a challenging perspective of utilizing stiffness as an early marker of endothelial dysfunction and future atherosclerosis. Coronary stiffening is also associated with vascular remodeling, which is a major determinant of the natural history of atherosclerotic plaques. Thus, arterial stiffness may constitute a useful marker for the identification of the remodeling pattern, in particular expansive remodeling, which is closely associated with high-risk plaques. The early identification of endothelial dysfunction, or a high-risk plaque may enable the early adoption of preventive measures to improve endothelial function, or justify pre-emptive local interventions in high-risk regions to prevent future acute coronary syndromes. Further experimental and perspective clinical studies are needed for the investigation of these perspectives, whereas the development of new modalities for non-invasive and reliable assessment of coronary stiffness is anticipated to serve these studies.
Chatzizisis
Yiannis S
YS
Cardiovascular Engineering and Atherosclerosis Laboratory, 1st Cardiology Department, AHEPA University Hospital, Aristotle University Medical School, Thessaloniki, Greece. joc@med.auth.gr <joc@med.auth.gr>
Giannoglou
George D
GD
D003324:Coronary Artery Disease / Q000503:physiopathology*; D003326:Coronary Circulation / Q000502:physiology*; D003331:Coronary Vessels / Q000502:physiology / Q000503:physiopathology*; D006801:Humans