Preventing AVF thrombosis: the rationale and design of the Omega-3 fatty acids (Fish Oils) and Aspirin in Vascular access OUtcomes in REnal Disease (FAVOURED) study

Background: Haemodialysis (HD) is critically dependent on the availability of adequate access to the systemic circulation, ideally via a native arteriovenous fistula (AVF). The Primary failure rate of an AVF ranges between 20-54%, due to thrombosis or failure of maturation. There remains limited evidence for the use of anti-platelet agents and uncertainty as to choice of agent(s) for the prevention of AVF thrombosis. We present the study protocol for a randomised, double-blind, placebo-controlled, clinical trial examining whether the use of the anti-platelet agents, aspirin and omega-3 fatty acids, either alone or in combination, will effectively reduce the risk of early thrombosis in de novo AVF

Analysis of arterial intimal hyperplasia: review and hypothesis

which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Background: Despite a prodigious investment of funds, we cannot treat or prevent arteriosclerosis and restenosis, particularly its major pathology, arterial intimal hyperplasia. A cornerstone question lies behind all approaches to the disease: what causes the pathology? Hypothesis: I argue that the question itself is misplaced because it implies that intimal hyperplasia is a novel pathological phenomenon caused by new mechanisms. A simple inquiry into arterial morphology shows the opposite is true. The normal multi-layer cellular organization of the tunica intima is identical to that of diseased hyperplasia; it is the standard arterial system design in all placentals at least as large as rabbits, including humans. Formed initially as one-layer endothelium lining, this phenotype can either be maintained or differentiate into a normal multi-layer cellular lining, so striking in its resemblance to diseased hyperplasia that we have to name it "benign intimal hyperplasia". However, normal or "benign " intimal hyperplasia, although microscopically identical to pathology, is a controllable phenotype that rarely compromises blood supply. It is remarkable that each human heart has coronary arteries in which a single-layer endothelium differentiates earl

Femoral arteriovenous fistula following cardiac catheterization: An anatomic explanation

The exact etiology of femoral iatrogenic arteriovenous fistula (AVF) following cardiac catheterization is not known. The most common explanation is simultaneous placement of arterial and venous catheters for left and right heart catheterization. Using a strict protocol for groin examination before and after cardiac catheterization, seven patients were found to have a groin thrill and/or bruit as a result of AVF after catheterization in the period from July 1986 to December 1990; one patient had two fistulas, making a total of eight. During the same period, a total of 2609 cardiac catheterizations were performed using the Seldinger technique; the incidence of AVF after the procedure was thus 0.22%. Arteriography was used to confirm the presence of the fistulas and identify their exact location. All eight lesions originated below the bifurcation of the common femoral artery (CFA). Three originated at the superficial femoral artery (SFA) and five at the profunda femoris artery (PFA). In the patient with two fistulas, one originated at the SFA and one at the PFA. The veins involved were the superficial femoral (SFV) in two AVFs and the profunda femoris (PFV) or its lateral circumflex branch in six. The fact that all eight fistulas originated below the bifurcation of the CFA points to a possible anatomic explanation for the formation of iatrogenic AVF. The CFA and common femoral vein (CFV) are located side by side, which makes it difficult to puncture both with one stick Below the bifurcation, the PFV crosses laterally behind the proximal SFA and then lies in a posterior location to the PFA. In addition, the SFV moves laterally behind the SFA to rest posterior to it. A through-and-through puncture of the SFA or PFA can cause direct communication between these arteries and the SFV or PFV, leading to formation of an AVF. Puncturing the CFA or CFV above their bifurcations will lead to a marked decrease in the incidence of AVF following cardiac catheterization. © 1993, SAGE Publications. All rights reserved