3D & 4D CORONARY HEMODYNAMICS AND LOCAL ATHEROSCLEROSIS

局部冠状动脉血流动力学可预测导致心肌梗死的动脉粥样硬化斑块的发生和发展。最近对正常外周动脉节段和存在不同程度动脉粥样硬化的血流动力学的研究表明，内膜增厚是对低壁切应力的正常反应，在某些情况下这种增厚可以发展为动脉粥样硬化斑块。在正常的、动脉粥样硬化的或最近受冠状动脉干预影响的冠状动脉中，没有类似的研究。我们的主要假设是，根据冠状动脉三维管腔形态、动脉血流速度及其随时间的变化计算出的局部剪应力变量与局部动脉粥样硬化斑块的严重程度有关。我们建议：1)完成一个综合的血管几何表示系统的开发，该系统结合了冠状动脉造影和血管内超声图像序列，以便正确地描述冠状动脉的几何形状和斑块的形态。2)发展了一种计算流体动力学分析来描述冠状动脉的三维和四维时空表示中的局部流动动力学，考虑了人体的非定常流动、管壁扩张性和血管运动。3)确定局部流体动力学指标(包括最小和最大壁面切应力和振荡切应力指数)与这些区域动脉粥样硬化斑块的严重程度和血管形态之间的关系。计算局部血流动力学和血流动力学指标，并与斑块严重程度的定量指标和血管重塑指标进行比较，以统计学方式确定它们之间的关系。血管不同节段的斑块沉积与局部血流动力学状况之间的关系可能对我们理解动脉粥样硬化的发展具有重要意义。它可能会增加我们对较小血管或有偏心斑块的血管中不同程度的代偿性血管扩大(重塑)的了解，以及一些邻近血管节段没有这种反应的知识，它可能有助于理解冠状动脉介入治疗后对损伤(再狭窄)反应的个体差异。

Atherosclerotic plaque initiation and progression that lead to myocardial infarction may be predicted by local coronary hemodynamics. Recent studies on blood flow dynamics in normal peripheral arterial segments and in the presence of varying degrees of atherosclerosis have suggested that intimal thickening is a normal response to low wall shear stress, and this thickening can develop into atherosclerotic plaque under certain circumstances. No similar studies exist in coronary vessels which are normal, atherosclerotic, or recently affected by coronary interventions. Our main hypothesis is that local shear stress variables calculated from three-dimensional coronary lumen morphology, arterial flow velocity, and their changes over time are associated with regional atherosclerotic plaque severity. We propose to: 1) Finish development of a comprehensive system for geometrically correct vessel representation which combines coronary angiographic and intravascular ultrasound image sequences in order to correctly describe coronary vessel geometry and plaque morphology. 2) Develop a computational fluid dynamic analysis to delineate the local flow dynamics in 3-D and 4-D spatio-temporal representations of coronary arteries, considering unsteady flow, wall distensibility, and vessel motion in humans. 3) Determine the relationship between local indices of fluid dynamics (including minimum and maximum wall shear stress and oscillatory shear stress index) and the severity of underlying atherosclerotic plaque and vessel morphology in these regions. Local hemodynamic and flow dynamic indices will be calculated and compared with quantitative indices of plaque severity and measures of vessel remodeling to statistically determine their relationship. The association between plaque deposition within different segments of vessel and the local hemodynamic conditions may be important in our understanding of atherosclerosis development. It may add to our knowledge of differential degrees of compensatory vessel enlargement (remodeling) in smaller vessels or vessels with eccentric plaque, the absence of this response in some neighboring vessel segments, and it may aid in understanding individual variability in the response to injury (restenosis) after coronary interventions.