Assessment of Wall Shear Stress Changes in Arteries and Veins of Arteriovenous Polytetrafluoroethylene Grafts Using Magnetic Resonance Imaging

Abstract

The purpose of the study was to determine simultaneously the temporal changes in luminal vessel area, blood flow, and wall shear stress (WSS) in both the anastomosed artery (AA) and vein (AV) of arteriovenous polytetrafluoroethylene (PTFE) grafts. PTFE grafts were placed from the iliac artery to the ipsilateral iliac vein in 12 castrated juvenile male pigs. Contrast-enhanced magnetic resonance angiography with cine phase-contrast magnetic resonance imaging was performed. Luminal vessel area, blood flow, and WSS in the aorta, AA, AV, and inferior vena cava were determined at 3 days (D3), 7 days (D7), and 14 days (D14) after graft placement. Elastin von Gieson staining of the AV was performed. The average WSS of the AA was highest at D3 and then decreased by D7 and D14. In contrast, the average WSS and intima-to-media ratio of the AV increased from D3 to D7 and peaked by D14. Similarly, the average area of the AA was highest by D7 and began to approximate the control artery by D14. The average area of the AV had decreased to its lowest by D7. High blood flows through the AA causes a decrease in average WSS and increase in the average luminal vessel area, whereas at the AV, the average WSS and intima-to-media ratio both increase while the average luminal vessel area decreases.

Increased shear stress with upregulation of VEGF-A and its receptors and MMP-2, MMP-9, and TIMP-1 in venous stenosis of hemodialysis grafts

“…To assess hemodynamic changes and vascular remodeling of the vein-to-graft anastomosis and control vessels, MRI was performed as previously described (35,40). Animals were anesthetized for the procedure as previously described.…”

“…Our laboratory has been especially interested in the effect of WSS (the dragging force of the blood on the endothelium) because we and others have shown that it is increased at the vein-to-graft anastomosis of hemodialysis grafts (11,40) and because it regulates the expression of many proteins including MMP-2, MMP-9, VEGF-A, and VEGF receptor (VEGFR)-2 (1,53,58). Recently, there have been several reports describing the use of phase-contrast magnetic resonance angiography with MRI (PC MRA/MRI) to determine blood flow and luminal vessel area to estimate WSS (3,33,40,44). Thus, our overall hypothesis is that the formation of intimal hyperplasia resulting in venous stenosis is in part related to changes in WSS that results in the activation of matrix regulatory proteins causing subsequent venous stenosis formation.…”

Novel Paradigms for Dialysis Vascular Access

“…Large-animal models are advantageous because they have vessel anatomy similar to that of humans and provide the opportunity to study in detail hemodynamics and histology, but also allow for testing of experimental drug therapies and devices. The main large-animal models to date in dialysis access have been porcine models (47,64,65). One main disadvantage of both small and large animal models is the inability to simulate the long-term effects and consequences of CKD and endothelial dysfunction.…”

Hemodialysis Vascular Access Dysfunction

“…Hemodynamic sheer stresses play a significant role in development of neointimal hyperplasia 87,112,206,207 . Therefore, altering the sheer stress pattern to prevent turbulent, lowflow, and low-sheer stresses could reduce the development of neointimal hyperplasia.…”

“…In order to advance the field further, we need to further our current understanding of both the clinical and experimental pathways that result in venous neointimal hyperplasia and mechanisms that lead to biofilm and fibrin sheath production in C V C s b y u s i n g t h e a d v a n c e d technologies and tools in cellular and molecular biology, bioengineering, genomics, proteomics, and vascular imaging (ultrasound, computed tomography, and magnetic resonance imaging) 65,124,214 . Finally, small and large animal models of AVF and AVG, which a number of investigators in this field have already developed 61,93,207,[215][216][217] , will play an essential role in "translating" our knowledge of pathophysiologic mechanisms in vascular access dysfunction to novel therapies for patients.…”