OBJECTIVES: The aim of this study was to compare pathological features among in-stent restenosis lesions after drug-eluting stent (DES) placement, those after bare metal stent (BMS) placement, and de-novo atherosclerotic lesions. BACKGROUND: Restenosis after stenting is an over-reaction 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 DES technology could considerably succeed in inhibiting this sequence of events. Thus, we hypothesized that the mechanism of in-stent restenosis after DES stenting might be different from that after BMS stenting as well as atherosclerosis. METHODS: Tissues obtained by directional atherectomy (DES: seven 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), and activated platelets (P-selectin). RESULTS: The accumulation of T lymphocytes tended to increase and that of macrophages increased significantly in the DES lesions compared with BMS lesions. No significant differences were observed for the other parameters evaluated. CONCLUSION: Pathological features of restenotic tissues after DES implantation showed a stronger inflammatory response compared with those after BMS implantation. Thus, the mechanism of restenosis after DES implantation may be different from that observed after BMS implantation.
OBJECTIVES: The aim of this study was to compare pathological features among in-stent restenosis lesions after drug-eluting stent (DES) placement, those after bare metal stent (BMS) placement, and de-novo atherosclerotic lesions. BACKGROUND:Restenosis after stenting is an over-reaction 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 DES technology could considerably succeed in inhibiting this sequence of events. Thus, we hypothesized that the mechanism of in-stent restenosis after DES stenting might be different from that after BMS stenting as well as atherosclerosis. METHODS: Tissues obtained by directional atherectomy (DES: seven 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), and activated platelets (P-selectin). RESULTS: The accumulation of T lymphocytes tended to increase and that of macrophages increased significantly in the DES lesions compared with BMS lesions. No significant differences were observed for the other parameters evaluated. CONCLUSION: Pathological features of restenotic tissues after DES implantation showed a stronger inflammatory response compared with those after BMS implantation. Thus, the mechanism of restenosis after DES implantation may be different from that observed after BMS implantation.
Authors: Victor Nauffal; Thomas A Schwann; Maroun B Yammine; Abdul-Karim M El-Hage-Sleiman; Mohamad H El Zein; Ameer Kabour; Milo C Engoren; Robert H Habib Journal: J Thorac Cardiovasc Surg Date: 2015-02-10 Impact factor: 5.209
Authors: Andreas Rudolph; Michael Teske; Sabine Illner; Volker Kiefel; Katrin Sternberg; Niels Grabow; Andreas Wree; Marina Hovakimyan Journal: PLoS One Date: 2015-12-07 Impact factor: 3.240