The role of the endothelium in the reduction of restenosis following balloon angioplasty
Muller, C. J.
Rossouw, D. J.
Doubell, A. F.
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Objective. Coronary angioplasty is complicated in one-third of cases by restenosis due to intimal hyperplasia. This is the result of the migration and proliferation of vascular smooth-muscle cells (SMCs) and correlates with the extent of endothelial stripping. To study the effect of rapid re-endothelialisation on preventing intimal hyperplasia, a model of vessel injury is needed which allows for the retention and adhesion of cultured vascular endothelial cells (VECs) in the injured segment. Methods. The abdominal aortas of BD9 rats were injured with an embolectomy catheter and the response to injury assessed on days 1, 3, 7, 14 and 28. Cultured vascular endothelial cells (VECs) were then placed into injured vessels. Introduction of 51Cr-labelled cells was used first-to confirm adhesion, and then unlabelled cells were used to study the effect on intimal hyperplasia. Results. Medial necrosis and complete stripping of the endothelium was seen on days 1 and 3. By day 7 all rats had VECs lining part of the lumen. Intimal hyperplasia was present by day 14. Complete restitution of the endothelium was present at day 28 and medial SMC numbers were also back to normal at this time. Cells producing the intimal hyperplasia were identified as SMCs by staining for smooth-muscle actin and electron microscopy. Re-endothelialisation was confirmed by autoradiography following introduction of 51Cr-labelled VECs. In animals receiving VECs after injury (N = 15), intimal hyperplasia involved a smaller percentage of the lumen circumference compared with controls (N = 15), where only medium was introduced (52.00 ± 6.83% v. 63.47 ± 6.39%; P = 0.03). Conclusion. The response to balloon-induced injury in the rat aorta has been well characterised. This model enabled us to repopulate a damaged vessel with cultured VECs, resulting in a decrease in intimal hyperplasia.