Abstract
Background/Aims: The feeding artery of dialysis vascular access is subjected to unusually high wall shear stress (WSS), a hemodynamic factor leading to vasodilatation, for at least several months after access creation. Physiologically, high WSS leads to compensatory endothelium-dependent vasodilatation. We supposed that the dilatation of the feeding artery continues to lower WSS during longer time period after access creation and that this process is limited by risk factors of endothelial dysfunction. Methods: We examined the feeding artery of vascular accesses within 3 months, 1 and 2 years after access creation. By ultrasonography, we obtained internal diameter and blood velocity in the feeding arteries. We calculated wall shear rate (WSR). Results: We examined 75 patients. Internal diameter rose from 3.9 ± 0.1 mm (3 months) to 4.3 ± 0.2 mm within the first year and to 4.6 ± 0.2 mm within the second. Similarly, mean WSR decreased from 1,839 ± 117 to 1,629 ± 123 s<sup>–1</sup> and to 1,159 ± 109 s<sup>–1</sup>, respectively. The vasodilatation was limited by diabetes mellitus, hypercholesterolemia and hypertriglyceridemia. Conclusions: The feeding artery continues to dilate 2 years after access creation, with a simultaneous decrease in WSR. This process is dampened in patients with diabetes mellitus and dyslipidemia.
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