Intimal hyperplasia and hemodynamic factors in arterial bypass and arteriovenous grafts: a review

Abstract

Stenosis at the graft-vein junction caused by intimal hyperplasia (IH) is the major cause of failure of vascular access grafts used for hemodialysis. There is a strong relationship between hemodynamic factors and formation of IH. The hemodynamic pattern and the location of IH are different in arterial bypass grafts (ABGs) compared with arteriovenous grafts (AVGs). In an ABG, end-to-side anastomosis of the expanded polytetrafluoroethylene graft and artery produces hemodynamic changes around the junction. IH develops at the arterial floor and the toe and heel of the distal anastomosis. Low shear stress and oscillating shear forces at the arterial floor and the heel plus a high wall sheer stress (WSS) gradient at the toe probably promote IH development. Compliance mismatch between the graft and artery causes turbulence that may contribute to IH formation. The blood flow rate in AVGs is 5-10 times greater than that in ABGs. High flow causes turbulence that injures endothelial cells and eventually results in IH. The peak WSS in AVGs is about 6 N/m(2), much higher than that in ABGs. Excessively high WSS may effect IH formation in AVGs. Several venous cuff or patch anastomotic designs have been used in attempts to regulate hemodynamic factors in grafts. In ABGs, these designs appear to help decrease IH formation. In AVGs, however, they generally have not improved patency rates. In a high-flow system such as an AVG, more drastic changes in anastomotic design may be required.

Novel Paradigms for Dialysis Vascular Access

“…In activated ECs, increased expression of growth factors at the gene and protein levels (such as HDAC3 and PDGF-2) promote SMC migration from the media to the intima as well as proliferation (10). Proliferation of SMCs in the intima is associated with deposition of extracellular matrix, a process analogous to scar formation (9,11). The overall result is the rapid formation of a neointimal layer over the site of injury.…”

“…Thus, low WSS activates a cascade of molecular events that lead to leukocyte adhesion and migration into the intimal layer of the vasculature. Hemodynamically induced neointimal hyperplasia has been related not only to low WSS but also to stagnation points of the circulation (11). That low WSS is the major determinant of intimal thickness was demonstrated in vivo in dogs by Morinaga and colleagues in 1985 (34), who clearly showed that the change in WSS, but not the rate of blood flow, is the essential hemodynamic factor related to neointimal hyperplasia in autogenous vein grafts.…”

Expression of Versican Isoform V3 in the Absence of Ascorbate Improves Elastogenesis in Engineered Vascular Constructs

“…Numerous studies have shown that synthetic TEBVs and autologous vein grafts exhibit compliance and caliber mismatch with their recipient arteries, which elicits intimal hyperplasia leading to graft apatency. [43][44][45] Therefore, achieving a close match of caliber and compliance between the graft and the recipient artery is of critical importance. Using the methods described here, TEBVs can be fabricated with diameters that match recipient vessels and with compliances within natural ranges.…”

SANS Characterization of an Anisotropic Poly(vinyl alcohol) Hydrogel with Vascular Applications

“…It is believed that this plays a major role in postoperative complications and ultimate graft failure. [4][5][6] Thus, there is a need to create a biomaterial with properties tuned for specific cardiovascular device applications.…”