Relative contribution of wall shear stress and injury in experimental intimal thickening at PTFE end-to-side arterial anastomoses
Relative contribution of wall shear stress and injury in experimental intimal thickening at PTFE end-to-side arterial anastomoses
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DOI：
10.1115/1.1428554
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发表时间：
2002-02-01
影响因子：
1.7
通讯作者：
Bassiouny, HS
中科院分区：
文献类型：
--
作者：
Loth, F;Jones, SA;Bassiouny, HS
背景：内膜增厚（IHT）是人工心脏旁路移植失败的常见原因。HIT的诱发和进展被认为涉及与导管的流量、场、损伤和假体性质的变化有关的许多机制。本研究旨在研究全切应力和损伤对实验端侧义肢吻合端特定区域IHT诱导的相对贡献。方法与结果：对7例犬髂股四氟乙烯（PTFE）植入术12周后远端端侧吻合口HIT分布进行了测定。利用活体吻合几何构造了一个放大的透明模型，并通过激光多普勒风速法测定了24个轴向位置的壁面剪切应力，测量了与活体相似的脉动流动条件下的近壁面速度。利用计算机辅助形态测量法测定端侧聚四氟乙烯移植物的HIT分布。累及原生动脉的IHT范围为0.0 +/- 0.1 mm至0.05 +/- 0.03 mm。在接枝罩（PTFE）上发现了较大的IHT，范围为0.09 +/- 0.06至0.24 +/- 0.06 mm。使用非线性多变量logistic分析将IHT建模为壁面剪切应力、与缝合线的距离和血管导管类型（即PTFE与宿主动脉）的倒数函数。血管导管类型和离缝合线的距离是导致IHT的独立因素，而壁面剪应力与HIT之间的负相关关系仅存在于吻合区旁的聚四氟乙烯移植物上。结论：该数据与一个内膜增厚模型一致，在该模型中，从缝合线迁移的内膜增厚膜通过降低聚四氟乙烯移植物/宿主动脉界面的壁剪切应力水平而增强。在邻近的动脉壁上没有这种损伤性HIT的血流动力学调节。
Background: Intimal hyperplastic thickening (IHT) is a frequent cause of prosthetic bypass graft failure. Induction and progression of HIT is thought to involve a number Of mechanisms related to variation in the flow, field, injury and the prosthetic nature of the conduit. This study was designed to examine the relative contribution of it-all shear stress and injury to the induction of IHT at defined regions of experimental end-to-side Prosthetic anastomoses. Methods and Results: The distribution of HIT was determined at the distal end-to-side anastomosis of seven canine Iliofemoral PTFE grafts after 12 weeks of I. implantation. An upscaled transparent model was constructed using the in vivo anastomotic geometry, and wall shear stress was determined at 24 axial locations from laser Doppler anemometry, measurements of the near wall velocity under conditions of pulsatile flow similar to that present in vivo. The distribution of HIT at the end-to-side PTFE graft was determined using computer assisted morphometry. IHT involving the native artery ranged from 0.0 +/- 0.1 mm to 0.05 +/- 0.03 mm. A greater amount of IHT was found on the graft hood (PTFE) and ranged from 0.09 +/- 0.06 to 0.24 +/- 0.06 mm. Nonlinear multivariable logistic analysis was used to model IHT as a function of the reciprocal of wall shear stress, distance from the suture line, and vascular conduit type (i.e. PTFE versus host artery). Vascular conduit type and distance from the suture line independently, contributed to IHT An inverse correlation between wall shear stress and HIT was found only, for those regions located on the juxta-anastomotic PTFE graft. Conclusions: The data are consistent with a model of intimal thickening in which the intimal hyperplastic pannus migrating from the suture line was enhanced by reduced levels of wall shear stress at the PTFE graft/host artery, interface. Such hemodynamic modulation of injury induced HIT was absent at the neighboring artery wall.