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Cardiovascular Research 2002 56(1):164-172; doi:10.1016/S0008-6363(02)00503-5
© 2002 by European Society of Cardiology
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Copyright © 2002, European Society of Cardiology

Increased intimal hyperplasia in experimental vein graft stenting compared to arterial stenting: comparisons in a new rabbit model of stent injury

Nicholas J Alpa, Nick E.J Westa, Nadine Arnoldb, Julian Gunnb, Adrian P Banninga and Keith M Channona,*

aDepartment of Cardiovascular Medicine, University of Oxford, John Radcliffe Hospital, Oxford OX3 9DU, UK
bCardiovascular Research Group, University of Sheffield, Clinical Sciences Centre, Northern General Hospital, Herries Road, Sheffield S5 7AU, UK

keith.channon{at}cardiov.ox.ac.uk

* Corresponding author. Tel.: +44-1865-851-085; fax: +44-1865-222-077

Background: In-stent restenosis due to intimal hyperplasia is an important clinical problem. Animal models of stent injury are limited by inconsistent arterial responses to stenting, and less intimal hyperplasia than diseased human vessels. To address these issues, we aimed to compare the degree of intimal hyperplasia in stented rabbit jugular–carotid interposition grafts (vein grafts) versus stented carotid arteries. Methods: Jugular–carotid vein grafts were constructed in rabbits, then stented or left unstented. Carotid arteries were treated with similar stents or left instrumented only. After 3 or 28 days, vessels were perfusion fixed, embedded in resin, and sections were cut with a diamond saw. Intimal and medial thicknesses were measured in stained sections. Results: After 3 days, inflammatory changes were observed in the intima of all stented vessels. After 28 days, intimal thickness in stented vein grafts was 2-fold greater than in control vein grafts and approximately 4-fold greater than in stented carotid arteries. In addition, the intimal hyperplasia response was markedly more consistent in stented vein grafts compared with stented carotid arteries. Conclusions: Stent deployment in experimental vein grafts results in increased and more reproducible smooth muscle cell intimal hyperplasia than carotid arterial stenting. This is a promising small-animal model for investigating the intimal response to stenting.

KEYWORDS Coronary disease; Histo(path)ology; Restenosis; Stents; Veins


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