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Abstract

Atherosclerosis is the leading cause of death in the United States and most Western countries. Despite intense research efforts, much is still unknown about the etiology of the disease. While many clinical and biochemical factors have been linked to atherosclerosis, none of these factors can account for the extreme localization of this disease within the vascular system.1 The carotid bifurcation, the coronary arteries, the distal abdominal aorta and the major arteries of the leg are susceptible, while most other medium-sized and large arteries, including the pulmonary and mesenteric arteries and the vessels of the arm, remain disease-free.2 Even within these specific vessels, atherosclerosis is not uniformly distributed, but diseased and healthy regions of the vessel are often separated by less than 1 cm. Hemodynamic forces likely account for this localization as they can vary greatly over very small distances. Attempts to correlate lesion development with hemodynamic forces have demonstrated that intimal thickening co-localizes with region with oscillatory and low mean wall shear stress (Figs. 2.1 and 2.2).

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Gooch, K.J., Tennant, C.J. (1997). Endothelial Cells. In: Gooch, K.J., Tennant, C.J. (eds) Mechanical Forces: Their Effects on Cells and Tissues. Biotechnology Intelligence Unit. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-03420-0_2

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