Background-Native atherosclerosis and in-stent restenosis are focal and evolve independently. The endothelium controls local arterial responses by transduction of shear stress. Characterization of endothelial shear stress (ESS) may allow for prediction of progression of atherosclerosis and in-stent restenosis. Methods and Results-By using intracoronary ultrasound, biplane coronary angiography, and measurement of coronary blood flow, we represented the artery in accurate 3D space and determined detailed characteristics of ESS and arterial wall/plaque morphology. Patients who underwent stent implantation and who had another artery with luminal obstruction Ͻ50% underwent intravascular profiling initially and after 6-month follow-up. Twelve arteries in 8 patients were studied: 6 native and 6 stented arteries. In native arteries, regions of abnormally low baseline ESS exhibited a significant increase in plaque thickness and enlargement of the outer vessel wall, such that lumen radius remained unchanged (outward remodeling). Regions of physiological ESS showed little change. Regions with increased ESS exhibited outward remodeling with normalization of ESS. In stented arteries, there was an increase in intima-medial thickness, a decrease in lumen radius, and an increase in ESS at all levels of baseline ESS. Key Words: endothelium Ⅲ atherosclerosis Ⅲ coronary disease Ⅲ shear stress C oronary atherosclerosis is focal and eccentric, 1,2 and each coronary obstruction progresses or regresses in an independent manner, including areas after percutaneous revascularization. 3 Local hemodynamic factors are crucial to determine the evolution of coronary obstructions. 1,4 The vascular endothelium is in a pivotal position to respond to the dynamic forces acting on the vessel wall owing to the complex 3D geometry of the artery. 5 Fluid shear stresses elicit a large number of responses in endothelial cells. 4,5 The response of genes sensitive to local hemodynamic forces likely leads to creation of a raised plaque; subsequent hemodynamic forces created by the plaque may lead to a cycle of cellular recruitment and proliferation, lipid accumulation, and inflammation. 4,6 The pathobiology of restenosis after percutaneous coronary interventions may be due to 2 independent processes: geometric remodeling and neointimal hyperplasia. In segments undergoing angioplasty alone, late lumen loss is largely due to geometric remodeling, whereas in stented arteries, late lumen loss correlates primarily with intimal hyperplasia. 7 The effect of endothelial shear stress (ESS) within the stent or at the stent edges has not been fully explored as a mechanism contributing to in-stent restenosis. 8 Current methodologies cannot provide adequate information about the microenvironment of the coronary arteries. We developed a unique system by using coronary intravascular ultrasound (IVUS), biplane coronary angiography, and measurements of coronary blood flow to represent the artery in accurate 3D space and to produce detailed characteristics of ESS and arter...
The purpose of this study was to assess the reproducibility of an in vivo methodology to reconstruct the lumen, plaque, and external elastic membrane (EEM) of coronary arteries and estimate endothelial shear stress (ESS). Ten coronary arteries without significant stenoses (five native and five stented arteries) were investigated. The 3D lumen and EEM boundaries of each coronary artery were determined by fusing end-diastolic intravascular ultrasound images with biplane coronary angiograms. Coronary flow was measured. Computational fluid dynamics was used to calculate local ESS. Complete data acquisition was then repeated. Analysis was performed on each data set in a blinded manner. The intertest correlation coefficients for all arteries for the two measurements of lumen radius, EEM radius, plaque thickness, and ESS were r = 0.96, 0.96, 0.94, 0.91, respectively (all P values < 0.0001). The 3D anatomy and ESS of human coronary arteries can be reproducibly estimated in vivo. This methodology provides a tool to examine the effect of ESS on atherogenesis, remodeling, and restenosis; the contribution of arterial remodeling and plaque growth to changes in the lumen; and the impact of new therapies.
A mathematical model is presented of the turbulent recirculating two-phase flow in gas-stirred systems. Conservation equations are solved for each phase variables and these are connected through interaction parameters. Allowance is made both for the direct influence of bubble transport on the turbulence field and the additional generation of turbulence energy at the liquid/gas interphase.In addition, the plume shape is a direct result of the computation ratherthan being prescribed a priori Computed flowfields are presented for both air-water and nitrogen-steel systems. The air-water results compare well with established measurements of gas fraction and mean velocities.The steel system results seem to suggest that gas plumes in metals may be narrower than in water
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