ライフサイエンスコーパス: in-stent restenosis

1 (bifurcations, chronic total occlusions, and in-stent restenosis).

2 have demonstrated effectiveness in treating in-stent restenosis.

3 y supersede VBT as the therapy of choice for in-stent restenosis.

4 in the stented main branch that can lead to in-stent restenosis.

5 use of a stent to deliver a drug may reduce in-stent restenosis.

6 iction of progression of atherosclerosis and in-stent restenosis.

7 r brachytherapy for the treatment of diffuse in-stent restenosis.

8 ESS may have a limited role in in-stent restenosis.

9 the rate of recurrent restenosis in diffuse in-stent restenosis.

10 a 90Sr/90Y beta-source for the treatment of in-stent restenosis.

11 in patients undergoing treatment for diffuse in-stent restenosis.

12 nary radiation therapy reduces recurrence of in-stent restenosis.

13 seful adjunct for the clinical prevention of in-stent restenosis.

14 e for preventing recurrence in patients with in-stent restenosis.

15 giographic outcomes of patients with diffuse in-stent restenosis.

16 hought to be important for coronary arterial in-stent restenosis.

17 bo after interventional treatment of diffuse in-stent restenosis.

18 ogical data on the morphological features of in-stent restenosis.

19 percutaneous coronary intervention (PCI) for in-stent restenosis.

20 proliferation contribute to later stages of in-stent restenosis.

21 temic delivery nanoparticle PXL for reducing in-stent restenosis.

22 racoronary gamma-radiation reduces recurrent in-stent restenosis.

23 lusions, planned two-stent bifurcations, and in-stent restenosis.

24 adiation for the prevention of recurrence of in-stent restenosis.

25 delaying, although probably not preventing, in-stent restenosis.

26 enting recurrent restenosis in patients with in-stent restenosis.

27 fective form of nonionizing energy to reduce in-stent restenosis.

28 become a useful approach to the treatment of in-stent restenosis.

29 onary radiation therapy for the treatment of in-stent restenosis.

30 on is a promising modality for inhibition of in-stent restenosis.

31 in the first 6 months after the treatment of in-stent restenosis.

32 emitters has been shown to reduce recurrent in-stent restenosis.

33 therapies aimed at reducing the incidence of in-stent restenosis.

34 e the effect of gamma-radiation on recurrent in-stent restenosis.

35 l and angiographic outcomes of patients with in-stent restenosis.

36 stent oversizing may lower the frequency of in-stent restenosis.

37 mmatory approaches may be of value to reduce in-stent restenosis.

38 timal hyperplasia, reducing the incidence of in-stent restenosis.

39 minimizing the total stent length may reduce in-stent restenosis.

40 e most consistent predictors of angiographic in-stent restenosis.

41 on shortly after catheter-based treatment of in-stent restenosis.

42 strate effectiveness of strategies to reduce in-stent restenosis.

43 ed in a study of intracoronary radiation for in-stent restenosis.

44 smaller final MLD were strong predictors of in-stent restenosis.

45 SMC) hyperplasia is the most likely cause of in-stent restenosis.

46 in 25 stents without restenosis and 24 with in-stent restenosis.

47 esions were in small vessels, and 17.8% were in-stent restenosis.

48 ed lesion; 4) chronic total occlusion; or 5) in-stent restenosis.

49 suboptimal stent deployment, and preexisting in-stent restenosis.

50 orting their use as a first-line therapy for in-stent restenosis.

51 ment strategy for the management of coronary in-stent restenosis.

52 ere used to investigate the role of miRNA in in-stent restenosis.

53 re a preferred treatment option for coronary in-stent restenosis.

54 treatment option for patients with coronary in-stent restenosis.

55 -coated balloon (SCB) compared with a PCB in in-stent restenosis.

56 of repeat angiogram, revascularization, and in-stent restenosis.

57 f saphenous vein grafts, ostial lesions, and in-stent restenosis.

58 lates cell proliferation, a key component of in-stent restenosis.

59 , rs350104, and rs164390 affects the risk of in-stent restenosis.

60 y, saphenous vein grafts, ostial lesions, or in-stent restenosis.

61 e as useful tools in risk stratification for in-stent restenosis.

62 tents) consecutive symptomatic patients with in-stent restenosis.

63 %) could be attributed to segments with >70% in-stent restenosis.

64 rug-eluting stents has decreased the rate of in-stent restenosis.

65 ive in reducing neointimal proliferation and in-stent restenosis.

66 ntrolled targeting of MNPs with efficacy for in-stent restenosis.

67 obstruction post stenting, a disorder termed in-stent restenosis.

68 clinically on drug-eluting stents to inhibit in-stent restenosis.

69 efficacy in limiting recurrence of existing in-stent restenosis.

70 ciated with major adverse clinical events or in-stent restenosis.

71 tomotic device stenosis, possibly similar to in-stent restenosis.

72 tive alternative to VBT for the treatment of in-stent restenosis.

73 e plaque prolapse (2 cases); and (5) diffuse in-stent restenosis (1 case).

74 elerated re-endothelialization and decreased in-stent restenosis 28 days after implantation.

75 After successful catheter-based treatment of in-stent restenosis, 476 patients were randomly assigned

76 y-verified NA was observed in 40 stents with in-stent restenosis (62%), was more prevalent in DES tha

77 s of the stented segment without significant in-stent restenosis (71%).

78 patients undergoing coronary angioplasty for in-stent restenosis, a paclitaxel-coated balloon was sup

79 To evaluate strategies to reduce in-stent restenosis, accurate measurement of in-stent ne

80 adiation for the prevention of recurrence of in-stent restenosis achieved similar rates of restenosis

81 f the main events responsible for bare metal in-stent restenosis after percutaneous coronary interven

82 lular composition of human coronary arterial in-stent restenosis after various periods of time follow

83 arization: AHR, 1.85; 95% CI, 1.37-2.50; and in-stent restenosis: AHR, 3.89; 95% CI, 2.16-7.01).

84 mechanical effect may play an important role in stent restenosis and thrombosis.

85 sty (ELCA)+adjunct PTCA for the treatment of in-stent restenosis and (via lesion matching) compared t

86 dary end points were the incidence of binary in-stent restenosis and 12-month major adverse cardiac e

87 stent fracture rate and its association with in-stent restenosis and adverse outcomes in the ACT-1 tr

88 e accepted treatment strategies for coronary in-stent restenosis and are under clinical investigation

89 ailure and in those undergoing treatment for in-stent restenosis and bifurcations.

90 In-stent restenosis and bypass graft failure are charact

91 een patients with superficial femoral artery in-stent restenosis and chronic limb ischemia were recru

92 nical outcome; however, due to potential for in-stent restenosis and high costs of stents, there is i

93 ed release of NO donor significantly reduces in-stent restenosis and is associated with increase in v

94 nts has been established as a major cause of in-stent restenosis and late stent thrombosis.

95 metal stents associates with a high risk of in-stent restenosis and need for future revascularizatio

96 y appear to be associated with high rates of in-stent restenosis and repeat target lesion revasculari

97 tents so that serious side effects including in-stent restenosis and stent thrombosis can be avoided

98 ndpoint was the occurrence of stent failure (in-stent restenosis and stent thrombosis).

99 n which are harbingers for increased risk of in-stent restenosis and stent thrombosis.

100 The incidence of repeat in-stent restenosis and target vessel revascularization

101 Drug-eluting stents reduce the occurrence of in-stent restenosis and the need for subsequent target v

102 lular matrix (ECM) remodeling contributes to in-stent restenosis and thrombosis.

103 nts with recurrent symptoms had angiographic in-stent restenosis and were successfully revascularized

104 e records of 473 patients who presented with in-stent restenosis and who were enrolled in various rad

105 es (repeat angiogram, revascularization, and in-stent restenosis), and clinical outcomes (heart failu

106 s coronary dissection, no reflow phenomenon, in-stent restenosis, and stent thrombosis requires accur

107 artery PCI (aOR, 2.28 [2.00, 2.59]), PCI for in-stent restenosis (aOR, 1.55 [1.40, 1.72]), and surgic

108 Native atherosclerosis and in-stent restenosis are focal and evolve independently.

109 d reference segments during the treatment of in-stent restenosis are unknown.

110 Mechanisms of recurrence after treatment of in-stent restenosis are unknown.

111 e success of irradiation (brachytherapy) for in-stent restenosis argues that DNA-damage p53 responses

112 apy, renal failure, bifurcation lesions, and in-stent restenosis as significant correlates of ST (P<0

113 The primary end point of recurrent in-stent restenosis assessed by ultrasound at 6 months w

114 However, current approved stents suffer from in-stent restenosis associated with neointimal hyperplas

115 erior descending artery, length > or =20 mm, in-stent restenosis at baseline, and use of rotablator.

116 considerable reduction in the development of in-stent restenosis at the cost of an increased risk of

117 Five of the 11 patients had previous in-stent restenosis before CABG.

118 to be effective in the treatment of coronary in-stent restenosis, but data are limited regarding thei

119 Drug-eluting stents reduce the incidence of in-stent restenosis, but they result in delayed arterial

120 on therapy can effectively prevent recurrent in-stent restenosis by inhibiting neointimal formation w

121 ter stent implantation significantly reduces in-stent restenosis by inhibiting neointimal hyperplasia

122 Gene therapy to treat in-stent restenosis by using gene vector delivery from t

123 trasound (IVUS) analysis was performed in 30 in-stent restenosis cases treated with a 40-mm (90)Sr/Y

124 the treatment of coronary drug-eluting stent in-stent restenosis compared with PCB.

125 ntimal hyperplasia and significantly reduced in-stent restenosis compared with the control group by a

126 ctional atherectomy from 10 patients in whom in-stent restenosis complicated percutaneous revasculari

127 te as compared with balloon angioplasty, but in-stent restenosis continues to be an important clinica

128 Unfortunately, in-stent restenosis continues to plague this procedure,

129 Beyond the treatment of in-stent restenosis, DCBs provide an additional tool for

130 for the ability to predict the occurrence of in-stent restenosis defined as a diameter stenosis > or

131 iabetics are at increased risk of developing in-stent restenosis for unclear reasons.

132 udy was performed to determine predictors of in-stent restenosis from a high volume, single-center pr

133 in the PEB group and also in subgroups with in-stent restenosis >10 mm (0.05 versus 0.26 mm; P=0.000

134 Of 252 eligible patients in whom in-stent restenosis had developed, 131 were randomly ass

135 In-stent restenosis has a high recurrence rate after per

136 However, its impact on in-stent restenosis has not been systematically investig

137 Patients with in-stent restenosis have an increased risk of recurrence

138 f systemic pharmacotherapy aimed at reducing in-stent restenosis have been consistently disappointing

139 sed stent use and the difficulty in managing in-stent restenosis have provided the impetus to develop

140 ibitors, including atherothrombotic disease, in-stent restenosis, heart failure, and sepsis.

141 nts has demonstrated efficacy for preventing in-stent restenosis; however, both the inflammatory effe

142 he Gamma-1 trial, coronary brachytherapy for in-stent restenosis improved clinical outcomes but incre

143 ts and is associated with a 30% reduction of in-stent restenosis in comparison with BMS.

144 adiation for the prevention of recurrence of in-stent restenosis in native coronaries and saphenous v

145 A total of 120 patients with diffuse in-stent restenosis in native coronary arteries (lesion

146 tal of 120 consecutive patients with diffuse in-stent restenosis in native coronary arteries and vein

147 ectively, with late (> 1 year) TSR driven by in-stent restenosis in only 3 patients (1.7%).

148 gamma-radiation therapy for the treatment of in-stent restenosis in patients with bypass grafts.

149 ding stents is associated with high rates of in-stent restenosis in patients with diabetes mellitus.

150 myocardial CTP improves diagnosis of CAD and in-stent restenosis in patients with stents compared wit

151 A total of 120 patients with in-stent restenosis in saphenous-vein grafts, the majori

152 al novel therapeutic approach for inhibiting in-stent restenosis in such patients.

153 lated with AAV2-apoA1(4WF) failed to prevent in-stent restenosis in the atherosclerotic vasculature o

154 nalysis, ACS was an independent predictor of in-stent restenosis in the cohort treated with bare-meta

155 a intracoronary radiation therapy (ICRT) for in-stent restenosis (IRS).

156 In-stent restenosis is a complication after coronary ste

157 In-stent restenosis is a major limitation of intracorona

158 In-stent restenosis is associated with a high incidence

159 Intracoronary radiation for patients with in-stent restenosis is associated with a high rate of LT

160 DCBA for superficial femoral artery in-stent restenosis is associated with less recurrent re

161 Furthermore, if the capacity of DES to treat in-stent restenosis is confirmed in randomized trials, t

162 the past few years, it has become clear that in-stent restenosis is largely due to the migration and

163 diabetes mellitus (DM), especially IDDM, on in-stent restenosis is not known.

164 As a result, in-stent restenosis is now an important clinical problem

165 Serial IVUS studies have shown that in-stent restenosis is secondary to intimal hyperplasia.

166 Presently, in-stent restenosis is the condition with the most robus

167 intimal formation and its role in preventing in-stent restenosis (ISR) after percutaneous coronary in

168 ic, and histological features of concomitant in-stent restenosis (ISR) and cardiac allograft vasculop

169 l segments has acceptable clinical outcomes, in-stent restenosis (ISR) and stent thrombosis remain cl

170 aneous treatment of drug-eluting stent (DES) in-stent restenosis (ISR) and the correlates for recurre

171 However, the incidence of in-stent restenosis (ISR) and the resultant need for rep

172 intervention (PCI) in patients with coronary in-stent restenosis (ISR) as well as de novo coronary ar

173 roved treatment option for the management of in-stent restenosis (ISR) based on superior outcomes com

174 Recent successes in the treatment of in-stent restenosis (ISR) by drug-eluting stents belie t

175 In-stent restenosis (ISR) cases presented as chronic cor

176 In-stent restenosis (ISR) complicates revascularization

177 As a result, in-stent restenosis (ISR) has become a widespread proble

178 for bare metal stent and drug-eluting stent in-stent restenosis (ISR) have not been established.

179 Re-stenting of in-stent restenosis (ISR) improves acute angiographic re

180 Clinical presentation of bare metal stent in-stent restenosis (ISR) in patients undergoing target

181 There is a paucity of data on the burden of in-stent restenosis (ISR) in the United States as well a

182 In-stent restenosis (ISR) is a novel pathobiologic proce

183 Current therapy for in-stent restenosis (ISR) is based on drug-eluting stent

184 nt of patients with drug-eluting stent (DES) in-stent restenosis (ISR) is more challenging than that

185 Treatment of in-stent restenosis (ISR) is still challenging.

186 In-stent restenosis (ISR) is the major drawback of super

187 ry gamma-irradiation in preventing recurrent in-stent restenosis (ISR) is well established.

188 It is unclear whether PCI of in-stent restenosis (ISR) lesions in degenerated SVGs is

189 ual distribution of gamma radiation in human in-stent restenosis (ISR) lesions, and 2) to analyze the

190 The angiographic presentation of in-stent restenosis (ISR) may convey prognostic informat

191 ectomy for de novo atherosclerosis (n=55) or in-stent restenosis (ISR) of a bare metal stent (n=34).

192 outcomes of patients who developed coronary in-stent restenosis (ISR) or stent thrombosis (STH) insi

193 percutaneous coronary intervention (PCI) for in-stent restenosis (ISR) randomized to short (6 months)

194 In-stent restenosis (ISR) remains a difficult problem in

195 nt of patients with drug-eluting stent (DES) in-stent restenosis (ISR) remains a major challenge.

196 Management of patients with in-stent restenosis (ISR) remains an important clinical

197 ng stent (DES) technology, the prevalence of in-stent restenosis (ISR) remains relatively unchanged,

198 ggests that drug-coated balloons may benefit in-stent restenosis (ISR) treatment.

199 examined long-term outcomes of patients with in-stent restenosis (ISR) who underwent different percut

200 s in 66 patients with native coronary artery in-stent restenosis (ISR) who were treated with (192)Ir

201 Patients with coronary in-stent restenosis (ISR) within multiple layers of sten

202 phic angiography (CTA) and their relation to in-stent restenosis (ISR), stent fracture (SF), and over

203 x lesions also introduced a new problem: DES in-stent restenosis (ISR), which occurs in 3% to 20% of

204 erapy (IRT) is the only proven treatment for in-stent restenosis (ISR).

205 ts of vascular brachytherapy (VBT) on ostial in-stent restenosis (ISR).

206 radiation therapy (IRT) for the treatment of in-stent restenosis (ISR).

207 tion therapy (IRT) in diabetic patients with in-stent restenosis (ISR).

208 racoronary gamma-radiation reduces recurrent in-stent restenosis (ISR).

209 tion of intracoronary irradiation to prevent in-stent restenosis (ISR).

210 ntages over other modalities in treatment of in-stent restenosis (ISR).

211 in graft (SVG) versus native coronary artery in-stent restenosis (ISR).

212 gioplasty, PTCA) in the treatment of diffuse in-stent restenosis (ISR).

213 ry gamma-radiation therapy reduces recurrent in-stent restenosis (ISR).

214 ary angioplasty [PTCA]) for the treatment of in-stent restenosis (ISR).

215 anatomy, potentially addressing the issue of in-stent restenosis (ISR).

216 ES) in patients with bare-metal stents (BMS) in-stent restenosis (ISR).

217 EES in patients with bare-metal stents (BMS) in-stent restenosis (ISR).

218 intervention (PCI) can lead to a decrease in in-stent restenosis (ISR).

219 reatment of superficial femoral artery (SFA) in-stent restenosis (ISR).

220 cted distal left main coronary artery (UDLM) in-stent restenosis (ISR).

221 luting stent (SES) implantation treatment of in-stent restenosis (ISR).

222 ary radiation therapy (IRT) in patients with in-stent restenosis (ISR).

223 Catheter for the Treatment of Subjects With In-Stent Restenosis [ISR] [AGENT IDE]; NCT04647253).

224 Although MSA is a consistent predictor of in-stent restenosis, its predictive value in BMS is stil

225 t were 6 to 10 mm proximal and distal to the in-stent restenosis lesion.

226 ) extended >10 mm proximal and distal to the in-stent restenosis lesion.

227 d clinical trial, enrolled 600 patients with in-stent restenosis (lesion length <26 mm and reference

228 confidence interval, 0.98-12.20; P=0.05) and in-stent restenosis lesions (odds ratio, 5.30; 95% confi

229 ion protocol of (90)Sr/Y radiation to native in-stent restenosis lesions may provide substantial inhi

230 1025 consecutive native coronary artery, non-in-stent restenosis lesions undergoing PCI, 72 hematomas

231 th treatment of chronic total occlusions and in-stent restenosis lesions, and had higher 12-month maj

232 More careful consideration of the type of in-stent restenosis may aid in identifying when alternat

233 Balloon angioplasty of in-stent restenosis may, therefore, fail due to ECM chan

234 d stent struts were also assessed in the pig in-stent restenosis model.

235 roliferative activity, in a porcine coronary in-stent restenosis model.

236 When severe forms of in-stent restenosis occur, they tend to present earlier

237 At a mean follow-up of 13+/-5 months, repeat in-stent restenosis occurred in 28% of patients with TVR

238 % in drug-eluting stents, with mean diameter in-stent restenosis of 36% and 8%, respectively.

239 nity-based institutions in 396 patients with in-stent restenosis of a previously implanted bare-metal

240 travascular gamma radiation in patients with in-stent restenosis of saphenous-vein bypass grafts.

241 luting stents) for the treatment of coronary in-stent restenosis or de novo lesions.

242 tion lesion involving side-branches >2.5 mm, in-stent restenosis, or long-lesions (estimated stent le

243 The process of in-stent restenosis parallels wound healing responses.

244 Treatment of in-stent restenosis presents a critical limitation of in

245 The binary in-stent restenosis rate was 2% for the sirolimus stent

246 ent thrombosis-related MI (n=63; 24.0%), and in-stent restenosis-related MI (n=58; 22.1%).

247 Intimal hyperplasia and subsequent in-stent restenosis remain a major limitation after sten

248 In-stent restenosis remains a challenging problem, and i

249 estenosis compared with balloon angioplasty, in-stent restenosis remains a major clinical problem.

250 ever, arterial reobstruction after stenting, in-stent restenosis, remains an important problem.

251 These findings support the notion that in-stent restenosis results from SMC hyperplasia and sug

252 In-stent restenosis results primarily from neointimal hy

253 ion in circulating lymphocytes and increased in-stent restenosis risk (OR, 1.43; 95% CI, 1.00-1.823;

254 on used as adjunct therapy for patients with in-stent restenosis significantly reduces both angiograp

255 Using a porcine coronary artery model of in-stent restenosis, single Palmaz-Schatz stents were im

256 rom normal vessels (n-VSMCs) and angioplasty/in-stent restenosis sites (r-VSMCs).

257 However, challenges such as in-stent restenosis, stent fracture, and in-stent thromb

258 ansion is associated with increased risks of in-stent restenosis, stent thrombosis, and myocardial in

259 For in-stent restenosis, the benefit of DCBA over POBA remai

260 After conventional treatment of in-stent restenosis, the incidence of recurrent clinical

261 a reduction in re-stenting for patients with in-stent restenosis treated with gamma-radiation is well

262 ee events were potentially related to BVS: 1 in-stent restenosis (treated 7 months after pPCI with dr

263 ail" (192)Ir intracoronary brachytherapy for in-stent restenosis, treatment with (192)Ir delays the t

264 The Washington Radiation for In-Stent Restenosis Trial (WRIST) PLUS, which involved 6

265 R patients from the Washington Radiation for In-Stent restenosis Trial (WRIST) that met the following

266 In the Washington Radiation for In-Stent restenosis Trial (WRIST), patients with in-sten

267 rachytherapy in the Washington Radiation for In-Stent Restenosis Trial (WRIST).

268 ere enrolled in the Washington Radiation for In-Stent Restenosis Trial (WRIST; ISR length, 10 to 47 m

269 The Washington Radiation for In-Stent Restenosis Trial for long lesions (Long WRIST)

270 The Washington Radiation for In-Stent Restenosis Trial is a double-blinded randomized

271 ery ISR from WRIST (Washington Radiation for In-Stent Restenosis Trial) and 31 patients with SVG ISR

272 study, BETA WRIST (Washington Radiation for In-Stent restenosis Trial) was designed to examine the e

273 lled in (1) Long WRIST (Washington Radiation In-Stent Restenosis Trial), a double-blind, placebo-cont

274 essel ISR in WRIST (Washington Radiation for In-Stent Restenosis Trial), in which patients with ISR w

275 In the Washington Radiation for In-Stent Restenosis Trial, patients with ISR treated wit

276 332 patients with in-stent restenosis underwent successful coronary interv

277 One hundred thirty patients with in-stent restenosis underwent successful coronary interv

278 ted to dramatically reduce the recurrence of in-stent restenosis, up to 24% of these patients will st

279 egy against vaso-occlusive disorders such as in-stent restenosis, vein-graft stenosis, and transplant

280 In-stent restenosis was 0 in the proximal LAD sirolimus-

281 In-stent restenosis was angiographically documented in 2

282 In-stent restenosis was defined as a stent area stenosis

283 secutive series of 456 coronary lesions with in-stent restenosis was evaluated for the type of resten

284 In-stent restenosis was excluded.

285 Underlying in-stent restenosis was present in only 4 (31%) of 13 ca

286 hundred one patients with drug-eluting stent in-stent restenosis were enrolled in 2 identical randomi

287 tent restenosis Trial (WRIST), patients with in-stent restenosis were first treated with conventional

288 cember 1997 and July 1998, 252 patients with in-stent restenosis were randomized to receive brachythe

289 Late lumen loss and in-stent restenosis were the result of neointimal tissue

290 by offering reserve coronary circulation, if in-stent restenosis were to occur in the treated left ma

291 asty and stenting is a common treatment, but in-stent restenosis, where the artery re-narrows, is a f

292 enter, randomized trial of 384 patients with in-stent restenosis who were enrolled between February 2

293 l occlusion (LTO, >30 days) in-patients with in-stent restenosis who were treated with intracoronary

294 ic choice for patients with complex, diffuse in-stent restenosis who would otherwise have a very poor

295 ly performed, the prevalence of renal artery in-stent restenosis will increase.

296 fect resulted in a significant inhibition of in-stent restenosis with a relatively low dose of MNP-en

297 (PEPCAD DES-Treatment of DES-In-Stent Restenosis With SeQuent(R) Please Paclitaxel El

298 urrent restenotic lesion, after treatment of in-stent restenosis with vascular brachytherapy in the W

299 ng may potentially reduce costs and rates of in-stent restenosis without compromising the quality of

300 crog/mm2, reduced angiographic indicators of in-stent restenosis without short- or medium-term side e