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ollowing the development of drug-eluting stents (DES) the interventional cardiologist seems to have overcome the nemesis of restenosis. The First-InMan study and a randomized comparison of a sirolimuseluting stent (SES) with a standard stent for coronary revascularization reported complete inhibition of restenosis in simple discrete lesions at 6 months. 1,2 However, recent randomized clinical trials using DES for lesions with lowor intermediate restenosis risk reported restenosis rates ranging from 2.3% to 16.7%. [3][4][5][6][7][8][9][10][11][12] Furthermore, the number of DES used and the stent length required for each lesion are both substantially increasing based on the recent recommended policy of full lesion coverage to avoid any potential injury at the stent edges. popularity of DES technologies worldwide, the precise mechanisms responsible for DES restenosis remain unclear. Several case reports have highlighted the occurrence of stent fracture (absence or deformity of a stent strut inside the stent) at follow-up, especially in patients experiencing restenosis with SES, however, the incidence of fracture and its impact on restenosis are poorly understood. [12][13][14][15][16][17][18] The purpose of this study was to investigate the predictors of restenosis following SES implantation and to determine the incidence and impact of stent fracture. We prospectively performed the SES implantation under intravascular ultrasound (IVUS) Guidance in Native coronary Artery Lesions (SIGNAL) study at the Fujita Health University hospital. Methods Study Design and EndpointsThe SIGNAL study was designed as a prospective, single-center, angiographic and IVUS follow-up study to evaluate the acute and late efficacy, as well as safety of deployment, of SES. The primary endpoint was angiographic restenosis. The principal clinical endpoint was a composite Circ J 2007; 71: 1669 -1677 (Received September 19, 2006 revised manuscript received July 5, 2007; accepted July 19, 2007 Although multivariate logistic regression analysis revealed that minimal lumen area (min-LA) post (p=0.027), total stent length (p=0.003) and diabetes (p=0.032) were significant independent predictors of restenosis, univariate analysis showed that stent fracture was more common in the restenosis than in the non-restenosis groups (p=0.001).Conclusions Although min-LA post by IVUS, total stent length by QCA and diabetes are independent predictors for angiographic restenosis, stent fracture occurred in 4 lesions (2.4%) and all of them resulted in restenosis (31% of the restenosis). The impact of stent fracture and its potential role in the development of restenosis deserves further study. (Circ J 2007; 71: 1669 -1677)

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Implantation of 2.5-mm SES in vessels with reference diameters less than 2.5 mm using lower deployment pressures and predilatation and postdilatation may lead to reduced risks of restenosis and MACE without an increased risk of stent thrombosis up to 1 year.

Background: Recently, stent fracture (SF) of sirolimus-eluting stents (SES) has been shown to be associated with an increased risk of restenosis after SES implantation. We sought to assess the incidence, predictors, and clinical outcome of SF after implantation of SES. Methods: A consecutive series of 430 lesions of 382 patients treated with SES followed by coronary angiography at 6 to 9 months were analyzed. SF was defined as complete transverse liner separation or single or multiple stent strut fracture. Results: At follow up, SF occurred in 33 of 430 lesions (7.7%), and 32 of 382 patients (8.4%). In 23 of 33 lesions (69.7%), SF was found in a single point, whereas SF occurred in 2 or more points per lesion in 10 lesions (30.3%). Minimal lumen diameter was significantly smaller in patients with SF (2.11±0.64 mm vs. 2.52±0.60 mm, P <0.001), presumably due to greater late lumen loss (0.36±0.57 mm vs. 0.08±0.50 mm, P =0.005). Consequently, in-stent restenosis in lesions with SF was observed more frequently than non-SF lesions (15.2% vs. 4.0%, P =0.004). At 450 days, however, the cumulative rate of major adverse cardiac events (death, myocardial infarction, or target lesion revascularization) was similar in patients with and without SF (9.1% vs. 7.1%, P =0.722). Multivariable predictors of SF were shown in Figure . Conclusions: The occurrence of SF 6 to 9 months after implantation of SES in consecutive “real-world” patients was relatively common, which did not lead to an increased risk of adverse cardiac events at 450 days. Total stent length, the reduction in the lesion angle by stenting, and lesions located on the right coronary artery were identified as predictors of SF after implantation of SES.