Determination of in vivo velocity and endothelial shear stress patterns with phasic flow in human coronary arteries: a methodology to predict progression of coronary atherosclerosis.

BACKGROUND Although the coronary arteries are equally exposed to systemic risk factors, coronary atherosclerosis is focal and eccentric, and each lesion evolves in an independent manner. Variations in shear stress elicit markedly different humoral, metabolic, and structural responses in endothelial cells. Areas of low shear stress promote atherosclerosis, whereas areas of high shear stress prevent atherosclerosis. Characterization of the shear stresses affecting coronary arteries in humans in vivo may permit prediction of progression of coronary disease, prediction of which plaques might become vulnerable to rupture, and prediction of sites of restenosis after percutaneous coronary intervention. METHODS To determine endothelial shear stress, the 3-dimensional anatomy of a segment of the right coronary artery was determined immediately after directional atherectomy by use of a combination of intracoronary ultrasound and biplane coronary angiography. The geometry of the segment was represented in curvilinear coordinates and a computational fluid dynamics technique was used to investigate the detailed phasic velocity profile and shear stress distribution. The results were analyzed with several conventional indicators and one novel indicator of disturbed flow. RESULTS Our methodology identified areas of minor flow reversals, significant swirling, and large variations of local velocity and shear stress--temporally, axially, and cirumferentially--within the artery, even in the absence of significant luminal obstruction. CONCLUSIONS We have described a system that permits, for the first time, the in vivo determination of pulsatile local velocity patterns and endothelial shear stress in the human coronary arteries. The flow phenomena exhibit characteristics consistent with the focal nature of atherogenesis and restenosis.

[1]  C F Dewey,et al.  Shear stress gradients remodel endothelial monolayers in vitro via a cell proliferation-migration-loss cycle. , 1997, Arteriosclerosis, thrombosis, and vascular biology.

[2]  P. Stone,et al.  Effects of curvature and stenosis-like narrowing on wall shear stress in a coronary artery model with phasic flow. , 1997, Computers and biomedical research, an international journal.

[3]  B. Fox,et al.  Distribution of fatty and fibrous plaques in young human coronary arteries. , 1982, Atherosclerosis.

[4]  B E Bouma,et al.  High resolution in vivo intra-arterial imaging with optical coherence tomography , 1999, Heart.

[5]  M. Sonka,et al.  Geometrically correct 3-D reconstruction of coronary wall and plaque: combining biplane angiography and intravascular ultrasound , 1996, Computers in Cardiology 1996.

[6]  D D Duncan,et al.  Effects of arterial compliance and non-Newtonian rheology on correlations between intimal thickness and wall shear. , 1992, Journal of biomechanical engineering.

[7]  W. Roberts,et al.  Hemodynamic shear force in rupture of coronary arterial atherosclerotic plaques. , 1990, The American journal of cardiology.

[8]  S. Alper,et al.  Hemodynamic shear stress and its role in atherosclerosis. , 1999, JAMA.

[9]  O. Tricot,et al.  Relation between endothelial cell apoptosis and blood flow direction in human atherosclerotic plaques. , 2000, Circulation.

[10]  G. Bearman,et al.  Thermal detection of cellular infiltrates in living atherosclerotic plaques: possible implications for plaque rupture and thrombosis , 1996, The Lancet.

[11]  R M Nerem,et al.  Oscillatory shear stress stimulates adhesion molecule expression in cultured human endothelium. , 1998, Circulation research.

[12]  Edward W. Merrill,et al.  The Rheology of Human Blood—Measurement Near and at Zero Shear Rate , 1963 .

[13]  A. Barakat,et al.  Mechanisms of shear stress transmission and transduction in endothelial cells. , 1998, Chest.

[14]  K. J. De Witt,et al.  Pulsatile flow through a bifurcation with applications to arterial disease. , 1976, Journal of biomechanics.

[15]  B. Berk,et al.  Laminar shear stress: mechanisms by which endothelial cells transduce an atheroprotective force. , 1998, Arteriosclerosis, thrombosis, and vascular biology.

[16]  R. Nerem Vascular fluid mechanics, the arterial wall, and atherosclerosis. , 1992, Journal of biomechanical engineering.

[17]  H N Sabbah,et al.  Blood velocity in the right coronary artery: relation to the distribution of atherosclerotic lesions. , 1984, The American journal of cardiology.

[18]  V. Fuster,et al.  Influence of Arterial Damage and Wall Shear Rate on Platelet Deposition: Ex Vivo Study in a Swine Model , 1986, Arteriosclerosis.

[19]  M. Gimbrone,et al.  Identification of vascular endothelial genes differentially responsive to fluid mechanical stimuli: cyclooxygenase-2, manganese superoxide dismutase, and endothelial cell nitric oxide synthase are selectively up-regulated by steady laminar shear stress. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[20]  D. Ku,et al.  Pulsatile Flow and Atherosclerosis in the Human Carotid Bifurcation: Positive Correlation between Plaque Location and Low and Oscillating Shear Stress , 1985, Arteriosclerosis.

[21]  R. Ross,et al.  ApoE-deficient mice develop lesions of all phases of atherosclerosis throughout the arterial tree. , 1994, Arteriosclerosis and thrombosis : a journal of vascular biology.

[22]  W D Wagner,et al.  A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis. A report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. , 1995, Arteriosclerosis, thrombosis, and vascular biology.

[23]  B. Rosner,et al.  Effect on coronary atherosclerosis of decrease in plasma cholesterol concentrations in normocholesterolaemic patients , 1994, The Lancet.

[24]  M. Texon The hemodynamic basis of atherosclerosis. , 1977, Advances in experimental medicine and biology.

[25]  B. Rosner,et al.  Lesion-to-lesion independence of restenosis after treatment by conventional angioplasty, stenting, or directional atherectomy. Validation of lesion-based restenosis analysis. , 1993, Circulation.

[26]  Michael M. Resch,et al.  Pulsatile non-Newtonian blood flow in three-dimensional carotid bifurcation models: a numerical study of flow phenomena under different bifurcation angles. , 1991, Journal of biomedical engineering.

[27]  J Kilian,et al.  Determination of blood flow and endothelial shear stress in human coronary artery in vivo. , 1999, The Journal of invasive cardiology.

[28]  C. von Birgelen,et al.  ANGUS: a new approach to three-dimensional reconstruction of coronary vessels by combined use of angiography and intravascular ultrasound , 1995, Computers in Cardiology 1995.

[29]  R. Virmani,et al.  Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. , 2000, Arteriosclerosis, thrombosis, and vascular biology.

[30]  J. Guyton,et al.  Development of the lipid-rich core in human atherosclerosis. , 1996, Arteriosclerosis, thrombosis, and vascular biology.

[31]  T. Karino,et al.  Flow patterns and spatial distribution of atherosclerotic lesions in human coronary arteries. , 1990, Circulation research.