Background Endothelial integrity is essential for maintaining Vascular
homeostasis, and endothelial denudation results in neointimal thicken
ing. Balloon-expandable endovascular stents provide a luminal scaffold
ing within atherosclerotic arteries with minimal direct contact betwee
n balloon and endothelium. We wondered whether stents cause diminished
endothelial ablation, and if so, whether the degree of endothelial da
mage might deter mine later proliferative sequelae. Methods and Result
s Stainless steel stents were expanded in normal or previously denuded
iliac arteries of New Zealand White rabbits. Stented arteries were ha
rvested 15 minutes, 1 hour, 3 days, or 14 days later. En face staining
of the luminal surfaces of stented arteries demonstrated that endothe
lial cell loss began immediately after stent expansion and was restric
ted to interstices between stent struts. Remnant endothelium adjacent
to struts provided the foundation for complete endothelial regeneratio
n of the stented segment within 3 days. Both early monocyte adhesion a
nd later intimal macrophage accumulation were reduced >80% in nonballo
oned but stented arteries, in concert with a twofold reduction in inti
mal thickening after 14 days, compared with ar teries completely denud
ed with a balloon before stent expansion. Conclusions It is accepted t
hat deep injury caused by balloon-expanded endovascular stents is a cr
itical contributor to experimental stent-induced neointimal hyperplasi
a. Our data indicate that the degree of endothelial injury may also be
an important component of vascular repair after stenting and an impor
tant consideration in stent and balloon design and use. The use of ste
nts for primary endovascular intervention may allow partial retention
of endothelium within treated arteries, thereby modulating vascular re
pair with less need for adjunctive pharmacological therapy.