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Surgically-created blood conduits used for chronic hemodialysis, including native arteriovenous fistulas (AVFs) and synthetic AV grafts (AVGs), are the lifeline for kidney failure patients. Unfortunately, each has its own limitations: AVFs often fail to mature to become useful for dialysis and AVGs often fail due to stenosis as a result of neointimal hyperplasia, which preferentially forms at the graft-venous anastomosis. No clinical therapies are currently available to significantly promote AVF maturation or prevent neointimal hyperplasia in AVGs. Central to devising strategies to solve these problems is a complete mechanistic understanding of the pathophysiological processes. The pathology of arteriovenous access problems is likely multi-factorial. This review focuses on the roles of fluid-wall shear stress (WSS) and endothelial cells (ECs). In arteriovenous access, shunting of arterial blood flow directly into the vein drastically alters the hemodynamics in the vein. These hemodynamic changes are likely major contributors to non-maturation of an AVF vein and/or formation of neointimal hyperplasia at the venous anastomosis of an AVG. ECs separate blood from other vascular wall cells and also influence the phenotype of these other cells. In arteriovenous access, the responses of ECs to aberrant WSS may subsequently lead to AVF non-maturation and/or AVG stenosis. This review provides an overview of the methods for characterizing blood flow and calculating WSS in arteriovenous access and discusses EC responses to arteriovenous hemodynamics. This review also discusses the role of WSS in the pathology of arteriovenous access, as well as confounding factors that modulate the impact of WSS.

Purpose To develop an arrhythmia‐insensitive rapid (AIR) cardiac T1 mapping pulse sequence for quantification of diffuse fibrosis. Methods An arrhythmia‐insensitive cardiac T1 mapping pulse sequence was developed based on saturation recovery T1 weighting, which is inherently insensitive to heart rate and rhythm, and two single‐shot balanced steady‐state free precession image acquisitions with centric k‐space ordering, where T1 calculation is inherently insensitive to T2 effects. Its performance against conventional cardiac T1 mapping based on inversion recovery (i.e., MOLLI) is compared. Phantom experiments (T1 ranging from 535 to 2123 ms) were performed with heart rate and rhythm simulated at 60 and 120 beats per minute (bpm) and arrhythmia using an external triggering device. Ten human subjects and 17 large animals were scanned precontrast and 5, 10, and 15 min after contrast agent administration. Results Compared with the reference T1 mapping, AIR yielded lower normalized root‐mean‐square error than MOLLI (8% vs. 3%, respectively, at 60 bpm, 28% vs. 3%, respectively, at 120 bpm, and 22% vs. 3%, respectively, at arrhythmia). In vivo studies showed that T1 measurements made by MOLLI and AIR were strongly correlated (r = 0.99) but in poor agreement (mean difference = 161.8 ms, upper and lower 95% limits of agreements = 347.5 ms and −24.0 ms). Conclusion Our AIR pulse sequence may be clinically useful for assessment of diffuse myocardial fibrosis in patients. Magn Reson Med 70:1274–1282, 2013. © 2012 Wiley Periodicals, Inc.

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