Stents are small, usually metallic tubes that are intended to prop open arteries blocked with atherosclerotic plaques. While stents have been used successfully in recent years, they still suffer from failure due to development of new tissue in stented segment (restenosis). Variations in the failure rates associated with different stent designs have led researchers to investigate the role of near-wall flow patterns. While there is no direct evidence yet, the patterns of flow stagnation as the blood flows past the stent struts may affect the restenosis process. Computational fluid dynamics (CFD) approaches are well suited for obtaining detailed information on stent flow patterns. Many CFD simulations make use of a two-dimensional model. The strong dependence of flow stagnation on stent strut spacing has been clearly demonstrated. These results have been employed to interpret the results of in vitro experiments designed to elucidate the mechanisms of restenosis.
Vascular stenosis is defined as a narrowing or constriction to the body or opening of a vessel conduit. Stenosis and thrombus formations are the result of vascular injury and inflammation due to vascular cell dysfunction, resulting in any of the following pathological or healing injury responses: an initial coagulation/thrombus (blood clot) on the vascular inner wall to promote healing or further injury and inflammation; vascular smooth muscle cell proliferation and migration into the blood vessel lumen promoting stenosis following an initial disruption to the endothelium; atherosclerosis in which both early thrombus and smooth muscle cell proliferation and migration participate; and atherothrombosis that interacts with a mature atherosclerotic plaque to form a blood clot on the surface of the plaque resulting in further stenosis or possible emboli. Changes in vascular function are governed by the dynamic mechanical environment consisting of shear stress, wall stresses, and pressure imposed on the cells within the vascular wall as a result of blood flow. Endothelial cells in the intima and the smooth muscle cells within the vessel media are stimulated with these mechanical stresses that alter their behavior. Atherosclerosis and other causes of stenosis develop at localized regions within the vasculature that correlate to localized mechanical conditions. Disease typically occurs at arterial sites where endothelial cells would be exposed to low and oscillatory shear stress. Localized variations in the inner to outer wall stresses also appear to be related to disease‐formation. This chapter reviews studies integrating biology with vascular mechanical events that explain the current theories on stenosis and thrombosis.
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