Abstract 11003: Delayed Inflammatory Response as a Feature of In-Stent Restenosis after Drug-Eluting Stent Implantation
Backgrounds: Restenosis after stenting is an overreaction of the wound healing response after vascular injury, which is characterized by a sequence of inflammation, granulation, extracellular matrix remodeling, and smooth muscle cell proliferation and migration. Recent advances in drug-eluting stent (DES) technology could greatly succeed in inhibiting this sequence of events. To examine the difference of mechanisms of in-stent restenosis (ISR) after DES implantation from that after bare metal stent (BMS) implantation, we compared pathological features among ISR lesions after DES (sirolimus-eluting stent: SES) placement, and those after BMS placement.
Methods: Tissues obtained by directional atherectomy (SES: 7 specimens, BMS: 17 specimens and de-novo: 15 specimens) were immunostained for T lymphocytes (CD45), macrophages (CD68), smooth muscle cells (α-smooth muscle actin), endothelial cells (von Willebrand factor: vWV) and activated platelets (P-selectin). Accumulation of T lymphocytes and macrophages, and smooth-muscle cell migration were quantitatively assessed by calculating “area rate” as extraction area/image processing area, using a specific image analysis software for immunostained area/entire tissue area. Endothelial cell coverage and accumulation of activated platelets and were assessed qualitatively.
Results: The area rate for lymphocytes accumulation was higher in SES lesions, compared to BMS lesions and de-novo lesions (9.1±11.2%, 3.2±4.2% and 6.1±8.8%, respectively, p<0.05) . The area rate for macrophages accumulation was also higher in the SES lesions, compared to the BMS and de-novo lesions (9.3±12.6%, 1.9±2.5% and 8.9±12.8%, respectively, P<0.01). Smooth muscle cell migration and accumulation of endothelial cells and activated platelets were similarly seen in the SES, BMS and de-novo lesions.
Conclusions: Restenotic tissues after SES stenting showed persistent signs of delayed or incomplete wound healing and inflammation, compared to BMS. Thus, the mechanism of restenosis after DES stenting may be different from that observed after BMS stenting.
- © 2010 by American Heart Association, Inc.