Endogenous Cell Seeding

Abstract

Background Endothelial integrity is essential for maintaining vascular homeostasis, and endothelial denudation results in neointimal thickening. Balloon-expandable endovascular stents provide a luminal scaffolding within atherosclerotic arteries with minimal direct contact between balloon and endothelium. We wondered whether stents cause diminished endothelial ablation, and if so, whether the degree of endothelial damage might determine later proliferative sequelae. Methods and Results Stainless steel stents were expanded in normal or previously denuded iliac arteries of New Zealand White rabbits. Stented arteries were harvested 15 minutes, 1 hour, 3 days, or 14 days later. En face staining of the luminal surfaces of stented arteries demonstrated that endothelial cell loss began immediately after stent expansion and was restricted to interstices between stent struts. Remnant endothelium adjacent to struts provided the foundation for complete endothelial regeneration of the stented segment within 3 days. Both early monocyte adhesion and later intimal macrophage accumulation were reduced >80% in nonballooned but stented arteries, in concert with a twofold reduction in intimal thickening after 14 days, compared with arteries completely denuded with a balloon before stent expansion. Conclusions It is accepted that deep injury caused by balloon-expanded endovascular stents is a critical contributor to experimental stent-induced neointimal hyperplasia. Our data indicate that the degree of endothelial injury may also be an important component of vascular repair after stenting and an important consideration in stent and balloon design and use. The use of stents for primary endovascular intervention may allow partial retention of endothelium within treated arteries, thereby modulating vascular repair with less need for adjunctive pharmacological therapy.