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Factors associated with impaired arterial adaptation to chronically high wall shear rate in the feeding artery of PTFE grafts
V Tuka, M Slavikova, Z Kasalova, J Malik
Language English Country Switzerland
Grant support
NR8334
MZ0
CEP Register
Digital library NLK
Full text - Article
Source
NLK
Karger Journals
from 1981 to 2009
ProQuest Central
from 1996-01-01 to 2015-11-30
Medline Complete (EBSCOhost)
from 2005-01-01 to 1 year ago
Nursing & Allied Health Database (ProQuest)
from 1996-01-01 to 2015-11-30
Health & Medicine (ProQuest)
from 1996-01-01 to 2015-11-30
- MeSH
- Arteries physiology ultrasonography MeSH
- Endothelium, Vascular physiology MeSH
- Diabetes Mellitus physiopathology MeSH
- Renal Dialysis MeSH
- Ultrasonography, Doppler, Duplex MeSH
- Financing, Organized MeSH
- Adaptation, Physiological MeSH
- Hypercholesterolemia physiopathology MeSH
- Hypertriglyceridemia physiopathology MeSH
- Middle Aged MeSH
- Humans MeSH
- Shear Strength MeSH
- Aged MeSH
- Vasodilation physiology MeSH
- Check Tag
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
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(-1) and to 1,159 +/- 109 s(-1), 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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- $a Third Department of Internal Medicine, General University Hospital and First School of Medicine, Charles University, Prague, Czech Republic. Vladimir.Tuka@vfn.cz
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- $a 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(-1) and to 1,159 +/- 109 s(-1), 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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