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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
Jazyk angličtina Země Švýcarsko
Grantová podpora
NR8334
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Článek
Zdroj
NLK
Karger Journals
od 1981 do 2009
ProQuest Central
od 1996-01-01 do 2015-11-30
Medline Complete (EBSCOhost)
od 2005-01-01 do Před 1 rokem
Nursing & Allied Health Database (ProQuest)
od 1996-01-01 do 2015-11-30
Health & Medicine (ProQuest)
od 1996-01-01 do 2015-11-30
- MeSH
- arterie fyziologie ultrasonografie MeSH
- cévní endotel fyziologie MeSH
- diabetes mellitus patofyziologie MeSH
- dialýza ledvin MeSH
- duplexní dopplerovská ultrasonografie MeSH
- financování organizované MeSH
- fyziologická adaptace MeSH
- hypercholesterolemie patofyziologie MeSH
- hypertriglyceridemie patofyziologie MeSH
- lidé středního věku MeSH
- lidé MeSH
- pevnost ve smyku MeSH
- senioři MeSH
- vazodilatace fyziologie MeSH
- Check Tag
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví 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 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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