P10.03: Evaluation of Arterial Stiffness in Atherosclerotic Rabbits in Vivo Via Echotracking

Objectives We have shown that large artery stiffening, a major risk factor in cardiovascular diseases, can be evaluated in hypertensive rats by echotracking, analysing arterial compliance and also the arterial pulsatile diameter distension. We aimed to analyze similarly arterial stiffness in a model...

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Veröffentlicht in:Artery research 2011, Vol.5 (4), p.189-189
Hauptverfasser: Vayssettes-Courchay, C., Ragonnet, C., Simonet, S., Verbeuren, T. J., Vilaine, J. P.
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Sprache:eng
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Zusammenfassung:Objectives We have shown that large artery stiffening, a major risk factor in cardiovascular diseases, can be evaluated in hypertensive rats by echotracking, analysing arterial compliance and also the arterial pulsatile diameter distension. We aimed to analyze similarly arterial stiffness in a model of atherosclerosis. Methods Male 9 week-old rabbits were fed 0.3 % cholesterol diet (ATH) or standard diet (CON) during 28 weeks. Then, under anaesthesia, blood pressure was recorded by catheterization and diameter via an ArtLab device, in a motion mode to detect pulsatile displacement of aortic walls (distension). Results Compliance, distension and distension/pressure loop were greatly decreased in ATH aorta versus CON, without mean diameter or blood pressure alteration. Basal femoral artery parameters were lower than aortic parameters. In ATH femoral artery, compliance, distension and the distension/pressure loop were reduced when recorded at a plaque level but increased at the upstream adjacent site; mean diameter was increased at both sites versus CON. Aortic endothelial function, assessed by ACh relaxation ex vivo was abolished in aorta and reduced in femoral artery; the lesions area in aorta (55 %) was 4x that observed in femoral artery. Conclusions This study analysed for the first time the in vivo dynamic arterial compliance in atherosclerotic rabbit. The data indicate a reduced arterial compliance and pulsatile distension and also show that the upstream adjacent site of a plaque is submitted to a higher stress and increased distension, in agreement with human data, which may participate to the plaque progression.
ISSN:1872-9312
1876-4401
1876-4401
DOI:10.1016/j.artres.2011.10.147