Analysis of Haemodynamics in Arteriovenous Fistulas

Haemodialysis is the most common treatment for end stage renal disease (ESRD) whereby an external machine (a dialyser) cleanses the blood, thus performing the function of the failing kidneys. For haemodialysis to be viable, a functional vascular access (VA) capable of managing 300-400ml extraction of blood per minute is required. Arteriovenous fistulas (AVFs) are preferred over other VA because of their association with prolonged survival, fewer infections, lower hospitalisation, and reduced costs in comparison with other types. An AVF consists of a surgically created anastomosis joining a peripheral artery and vein. This joining can be accomplished in different configurations and in this study we concentrate on one configuration – an end-to-side anastomosis. This is where the vein is surgically cut and the end leading back to the heart is surgically stitched onto the side of the artery. The introduction of arterial blood flow, at a significantly higher blood pressure, into a vein should induce vein expansion and cause its walls to remodel. This expansion and remodelling, known as maturation, allows regular cannulation, accommodates the 300-400ml per minute required and is critical for successful long-term haemodialysis; however, some AVFs fail to ever mature. The maturation process is dependent on the local haemodynamics within the AVF with the endothelial cells lining the venous walls capable of sensing the flow conditions and releasing chemical messengers in response that influence how other cells within the venous wall behave. For instance, endothelial cells can release growth factors in response to low wall shear stress (WSS) which cause vascular smooth muscle cells (VSMCs) to proliferate and migrate into the inner lining of the venous wall. This proliferation, called intimal hyperplasia can result in a stenosis in a newly-formed or possibly in a matured AVF which would then require further endovascular intervention to remain patent for haemodialysis. With this in mind the question then is why some AVFs fail to ever mature with rates between 20-50% never considered a viable VA. One hypothesis as to why this happens is that the haemodynamics within the AVF are not typical of what is usually experienced in the vasculature and depending on the AVF geometry can in some instances result in stenosis. There is significant variability between AVFs in different patients because of their individual vasculature, and different surgical techniques and locations. Modelling the haemodynamics within patient-specific AVFs is warranted to elucidate if there are particular geometrical features or perhaps the existence of certain flow conditions that cause failure. This could produce recommendations for future surgical techniques in AVF creation that could be employed to mitigate these effects.