Abstract
There has been increasing evidence that severe stenosis may cause artery compression and plaque cap rupture leading to heart attack and stroke. The physiological conditions under which that may occur and mechanisms involved are not well understood. It has been known that severe stenosis causes critical flow and wall mechanical conditions such as flow limitation, flow separation, low and oscillating shear stress distal to the stenosis, high shear stress and low or even negative flow pressure at the throat of stenosis, artery compression or even collapse. Those conditions are related to limitation of blood supply, intimal thickening and thrombosis formation, endothelism damage, platelet activation and aggregation, plaque cap rupture (for review, see [1,2]). Due to the complexity of the problem and lack of experimental data for mechanical properties of arteries under both expansion and compression, previous models were limited primarily to flow behaviors and with various limitations (axisymmetry, rigid wall, small strain, small pressure gradient). In this paper, experimental data for artery mechanical properties under physiological conditions were measured and a 3-d computational model is introduced to investigate flow behaviors and wall stress and strain distributions with fluid-structure interactions to better understand the mechanism involved in artery compression and plaque cap rupture.
Effects of Caveolin-1-ERK1/2 pathway on endothelial cells and smooth muscle cells under shear stress
