Coronary artery atherosclerosis is a leading cause of morbidity and mortality in western societies. Atherosclerosis is a progressive fibroinflammatory disease identified by intimal thickening, the focal accumulation of lipids, fibrous elements, and cellular elements within the walls of large arteries. These lesions preferentially develop at arterial branches, the outer walls of bifurcations, and the inner walls of curved sections; the cause of this focal vasculopathy is not fully understood. It is, however, understood from epidemiological and clinical studies that individual susceptibility to the development and progression of atherosclerotic lesions is influenced by “traditional” systemic risk factors, including smoking, diabetes mellitus, obesity, hypertension, and high cholesterol. However, these risk factors cannot account for half of the variability in occurrence of this disease; this indicates additional risk factors have not been identified. One prevalent explanation of the focal nature of the disease is that the local fluid mechanical stresses at the walls of coronary arteries, as well as mechanical stresses within the vessel wall, may mediate the phenotype of endothelial cells thereby producing atherosusceptible sites. Therefore, it has been speculated [1] that certain aspects of arterial geometry and motion, which vary substantially among individuals, may increase an individual’s susceptibility to developing atherosclerosis — “geometric risk factors”.

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