Summary. Background: Plaque erosion is a cause of atherothrombosis that preferentially occurs on smooth muscle cell (SMC)-and proteoglycan-rich rather than lipid-rich plaques. However, its underlying mechanisms remain unknown. Objective: To determine whether disturbed blood flow induces erosive injury and thrombus formation on SMC-rich neointima. Methods: Three weeks after balloon injury, SMC-rich neointima with increased tissue factor (TF) activity developed in rabbit femoral arteries that were narrowed with a vascular occluder to disturb blood flow after stenosis. Neointimal injury and thrombus formation were assessed at 15, 30, and 180 min after the vascular narrowing. Results: Endothelial detachment, platelet adhesion and neointimal cell apoptosis became evident at the post-stenotic regions of all femoral arteries (n = 5) within 15 min of narrowing. Mural thrombi composed of platelet and fibrin developed after 30 min, and then occlusive thrombi were generated in three out of five vessels after 180 min. The identical vascular narrowing of normal femoral arteries also induced endothelial detachment with small platelet thrombi at poststenotic regions, but fibrin and occlusive thrombi did not develop. Computational simulation analysis indicated that oscillatory shear stress contributes to the development of erosive damage to the neointima. Conclusions: These results suggest that disturbed post-stenotic blood flow can induce erosive injury in SMC-rich plaques and promote thrombus formation that results in vascular events.
Aim:To clarify the contribution of hemodynamic factors to the onset of plaque erosion in smooth muscle cell (SMC)-rich atherosclerotic plaque.
Methods:We developed a rabbit model of SMC-rich atherosclerotic plaque with various degree of stenosis induced by incomplete ligation and generated three-dimensional models of five rabbit femoral arteries based on 130-162 serial histological cross-sections at 100-μm intervals per artery. We performed a computational blood flow simulation using the Reynolds-averaged Navier-Stokes model and calculated the wall shear stress (WSS), turbulence kinetic energy (TKE), blood pressure (BP) and blood pressure gradients (BPG) in eight sections (the inlet, the stenotic portion and areas 1, 2 and 5 mm from the stenotic portion) in each rabbit. We also investigated whether the magnitude of WSS or TKE was related to the presence or absence of erosive injury by evaluating six points (the locally highest, median and lowest of WSS or TKE) in each section.
A high plasma PTX3 level in elderly hypertensive patients, particularly in those with a high 24-hour BP level, could be a significant predictor of cognitive impairment. A high PTX3 level may be a marker of frailty in elderly hypertensive patients.
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