3D & 4D CORONARY HEMODYNAMICS AND LOCAL ATHEROSCLEROSIS

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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.