Abstract 2168: Sirolimus-eluting Stent Implantation at Proximal Site Inhibits In-stent Restenosis in Bare Metal Stent Placed at Distal Site of de novo Lesion in Same Coronary Artery

Drug-eluting stent (DES) suppresses peri-stent distal edge stenosis via a local diffusion of the drug. Diffusion of sirolimus into coronary blood flowing may cause an accumulation of this drug in coronary bed beyond the distal edge of sirolimus-eluting stent (SES). Thus, this study examined whether SES implantation may exert anti-proliferative action on bare metal stent (BMS) placed distally in the same coronary artery. Methods and Results: We prospectively examined 114 consecutive patients with stable coronary artery disease who met the following inclusion criteria: elective, successful percutaneous coronary intervention for a long de novo lesion or two adjacent de novo lesions treated with more than two stents in the same coronary artery, implantation of BMS (2.25 mm in size, 12 ~ 18 mm in length) in the distal site because no DES was available due to small vessel size, quantitative coronary angiography (QCA) and intravascular ultrasound (IVUS) at stent placement and at 6 months or during the 6 months follow up after the stenting. At the proximal site adjacent to the distal BMS, SES was implanted without gap in 57 patients (SES-BMS), and BMS in the remaining 57 patients (BMS-BMS). Patients with in-stent restenosis (ISR, defined as > 50% diameter stenosis), developed at the proximal stent during the 6 months follow up, were excluded from the further analysis (all of them were 14 patients with BMS-BMS). Clinical, lesion, and procedural variables at stenting were comparable between SES-BMS (n = 57) and BMS-BMS (n = 43) groups. The QCA of the distal BMS showed less late luminal loss (0.49 ± 0.06 vs. 0.91 ± 0.08 mm, p < 0.01) and a lower ISR rate (13% vs. 36%, p < 0.01) in the SES-BMS group than the BMS-BMS group. The SES-BMS group also had less neointimal hyperplasia volume (25.1 ± 2.2 vs. 37.1 ± 2.5 mm 3 , p < 0.01) than the BMS-BMS group in the IVUS which examined a 10-mm length of the distal BMS from the distal edge of the proximal stent. Target lesion revascularization (TLR) of the distal BMS was less frequent in the SES-BMS group compared with the BMS-BMS group (9% vs. 19%, p < 0.01). Conclusions: SES implantation inhibits ISR and TLR in BMS at distal site of de novo lesion in same coronary artery. These findings may have an implication for stent strategy in long lesions.