ライフサイエンスコーパス: restenosis

1 ant issues for vascular bifurcations (15-28% restenosis).

2 ions, chronic total occlusions, and in-stent restenosis).

3 out bare metal stenting (BMS) is hampered by restenosis.

4 tive diseases, including atherosclerosis and restenosis.

5 segment to reduce neointimal hyperplasia and restenosis.

6 ntially improving vessel patency by reducing restenosis.

7 mited by the occurrence of vessel recoil and restenosis.

8 to investigate the role of miRNA in in-stent restenosis.

9 athogenic events of vascular remodeling i.e. restenosis.

10 diagnostic tools in risk stratification for restenosis.

11 us vein grafts, ostial lesions, and in-stent restenosis.

12 ntimal proliferation and subsequent clinical restenosis.

13 l proliferation, a key component of in-stent restenosis.

14 4, and rs164390 affects the risk of in-stent restenosis.

15 rative disorders such as atherosclerosis and restenosis.

16 ous vein grafts, ostial lesions, or in-stent restenosis.

17 fibroproliferative processes and ultimately restenosis.

18 effects on all 3 major processes involved in restenosis.

19 ul tools in risk stratification for in-stent restenosis.

20 r pathologies, including atherosclerosis and restenosis.

21 ention strategies based on predicted risk of restenosis.

22 cle cell (SMC) subset in atherosclerosis and restenosis.

23 nsecutive symptomatic patients with in-stent restenosis.

24 pheral arteries are limited by high rates of restenosis.

25 s for the progression of atherosclerosis and restenosis.

26 (MMP-1) in triggering PAR1-mediated arterial restenosis.

27 be attributed to segments with >70% in-stent restenosis.

28 s to pathologies such as atherosclerosis and restenosis.

29 ffective tools in the prevention or delay of restenosis.

30 as also independently related to the risk of restenosis.

31 s recommended based on the specific cause of restenosis.

32 tal stent (BMS) and drug-eluting stent (DES) restenosis.

33 between baseline characteristics and risk of restenosis.

34 ic target for atherosclerosis and postinjury restenosis.

35 ng stents has decreased the rate of in-stent restenosis.

36 ducing neointimal proliferation and in-stent restenosis.

37 uced neointima formation in a mouse model of restenosis.

38 implantation in patients at high risk for FP restenosis.

39 ncluding atherosclerosis and postangioplasty restenosis.

40 nd smooth muscle cells and can contribute to restenosis.

41 le results for treatment of bare-metal stent restenosis.

42 s to vascular remodelling, atherogenesis and restenosis.

43 hese (57%) were due to new AR and 9 (43%) to restenosis.

44 a potential target for the control of vessel restenosis.

45 rization and related to atherothrombosis and restenosis.

46 hypercholesterolemic swine model of femoral restenosis.

47 th major adverse clinical events or in-stent restenosis.

48 gical conditions such as atherosclerosis and restenosis.

49 el dissection and recoil, and a high rate of restenosis.

50 onstrated effectiveness in treating in-stent restenosis.

51 and provide reasons for stent thrombosis or restenosis.

52 balloon catheters with proven inhibition of restenosis.

53 d adults but in neonates results in frequent restenosis.

54 th reduced occurrence of atherosclerosis and restenosis.

55 echanical and molecular bases for vein graft restenosis.

56 with a marked diminution in the incidence of restenosis.

57 planned two-stent bifurcations, and in-stent restenosis.

58 s (EES) in the treatment of bare metal stent restenosis.

59 in-treated patients ran an increased risk of restenosis (1.54 [1.39-1.71]) and stent thrombosis (1.56

60 ssociated with similar rates of angiographic restenosis (10% vs. 14.6%; p = 0.35), [corrected] target

61 ex assessment demonstrated lack of recurrent restenosis (100% rate of Secondary patency).

62 patients enrolled, 262 (86%) had symptomatic restenosis, 153 (50%) had access thrombosis, and 25 (8%)

63 95% CI, 0.13-0.38; P<0.00001), angiographic restenosis (18.7% versus 45.5%; OR, 0.26; 95% CI, 0.14-0

64 ding was uncovered struts (33.3%) and severe restenosis (19.1%); and for very late ST, the most commo

65 oplasty for BMS restenosis compared with DES restenosis (3.8% vs. 9.6%, p < 0.001).

66 d NA was observed in 40 stents with in-stent restenosis (62%), was more prevalent in DES than bare-me

67 stented segment without significant in-stent restenosis (71%).

68 luting stent and non-paclitaxel-eluting sten restenosis (8.3% vs. 10.8%, p = 0.46).

69 fference in the incidence of repeated binary restenosis (8.7% versus 19.12%; P=0.078) and 12-month ma

70 uring angiogenesis, vessel remodeling during restenosis after angioplasty and atherosclerosis.

71 Arterial calcification predicts accelerated restenosis after angioplasty and stenting.

72 accelerated arterial intima hyperplasia and restenosis after angioplasty, especially in diabetes.

73 scular disorders such as atherosclerosis and restenosis after angioplasty, how control of VSMC phenot

74 cell (ECs) promote or inhibit, respectively, restenosis after angioplasty, vein graft intimal thicken

75 Restenosis after balloon angioplasty and stenting (BAS)

76 optimal treatment strategy for patients with restenosis after CEA remains unknown.

77 In patients with restenosis after CEA, CAS and CEA showed similar low rat

78 high levels predicted cardiovascular events, restenosis after endovascular intervention, cardiovascul

79 tine, treated animals also exhibited reduced restenosis after injury.

80 ion of severe PVS, and examined the risk for restenosis after intervention using either balloon angio

81 n events responsible for bare metal in-stent restenosis after percutaneous coronary intervention.

82 here is evidence that SES reduce the risk of restenosis after percutaneous infrapopliteal artery reva

83 ht represent an attractive target to prevent restenosis after vascular interventions.

84 etarded re-endothelialization, contribute to restenosis after vascular reconstructions.

85 mporal spatial measurement and prediction of restenosis after venous-arterial transition as well as m

86 e events (thrombosis, myocardial infarction, restenosis) after 1 year.

87 more stable early results and lower rates of restenosis, although early stent thrombosis and neointim

88 points were the incidence of binary in-stent restenosis and 12-month major adverse cardiac events.

89 ed in 1,523 patients (72.7%) with DES or BMS restenosis and 572 patients (27.3%) with de novo lesions

90 restenosis is associated with less recurrent restenosis and a better clinical outcome than POBA witho

91 In an experimental rat model of coronary restenosis and a mouse model of systemic bacterial infec

92 cture rate and its association with in-stent restenosis and adverse outcomes in the ACT-1 trial (Caro

93 d treatment strategies for coronary in-stent restenosis and are under clinical investigation for lesi

94 enotype occur in pathological states such as restenosis and atherosclerosis.

95 f vascular proliferative diseases, including restenosis and atherosclerosis.

96 In-stent restenosis and bypass graft failure are characterized by

97 nts with superficial femoral artery in-stent restenosis and chronic limb ischemia were recruited over

98 gh-risk population, yielding similar rate of restenosis and clinically driven target lesion revascula

99 condary end points were: angiographic binary restenosis and late lumen loss and all-cause mortality.

100 ed by a Paclitaxel-Coated Balloon to Inhibit Restenosis and Maintain Vessel Patency-A Pilot Study of

101 resulted in stable lumen dimensions and low restenosis and major adverse cardiac event rates.

102 ents associates with a high risk of in-stent restenosis and need for future revascularization, perhap

103 ng-term complications, including thrombosis, restenosis and neoatherosclerosis.

104 Restenosis and neointima formation were studied with ang

105 High rates of restenosis and neointimal formation have driven increasi

106 Limb surveillance aims to identify restenosis and new disease beyond the intervened segment

107 l occlusions are at especially high risk for restenosis and new revascularizations.

108 Restenosis and occlusion were assessed by duplex ultraso

109 Restenosis and occlusion were infrequent and rates were

110 Nine months after PCI, 5 patients had LMCA restenosis and PCI was successfully repeated.

111 dary endpoints were stent thrombosis (ST) or restenosis and peri-procedural complications.

112 is frequently associated with complications, restenosis and poor quality of life for the affected ind

113 ing balloons (DEB) may reduce infrapopliteal restenosis and reintervention rates versus percutaneous

114 peripheral artery disease is compromised by restenosis and risk of stent fracture or distortion.

115 Secondary end points were binary restenosis and Rutherford class change at 6 months, and

116 omplications such as acute stent thrombosis, restenosis and stent fractures.

117 that serious side effects including in-stent restenosis and stent thrombosis can be avoided and long-

118 edge on the biological mechanisms underlying restenosis and stent thrombosis, revealing novel promisi

119 the drug has been eluted might trigger late restenosis and stent thrombosis.

120 The results of binary restenosis and target lesion revascularization were simi

121 een consistently shown to reduce the risk of restenosis and target vessel revascularization compared

122 Restenosis and thrombosis are potentially fatal complica

123 odynamic parameters known affect the risk of restenosis and thrombosis at coronary bifurcations after

124 nding of the pathophysiologic role of ESS in restenosis and thrombosis might dictate hemodynamically

125 l effect may play an important role in stent restenosis and thrombosis.

126 stresses appear to play an important role in restenosis and thrombosis.

127 rix (ECM) remodeling contributes to in-stent restenosis and thrombosis.

128 re shown to be effective in the treatment of restenosis and vascular inflammation but with adverse si

129 redictors of repeat revascularization due to restenosis and/or progression of disease are largely unk

130 , thrombosis, ipsilateral amputation, binary restenosis, and all-cause mortality at 6 and 24 months.

131 elated disorders, including atherosclerosis, restenosis, and cancers.

132 infarction, target-lesion revascularization, restenosis, and stent thrombosis did not differ signific

133 pposed stent struts at 6 months; (5) 6-month restenosis; and (6) 6-month major adverse cardiovascular

134 a reduced incidence of 1-year MACE, TVF, and restenosis as compared with PES implantation.

135 The primary end point of recurrent in-stent restenosis assessed by ultrasound at 6 months was 15.4%

136 Binary restenosis, assessed by angiography in >90% of patients,

137 y endpoint was 12-month target lesion binary restenosis, assessed using Doppler ultrasound.

138 positively correlated with amputation after restenosis at 12 months postrevascularization of CLI typ

139 Primary endpoint was binary restenosis at 12 months, defined as >/=2.5-fold increase

140 rates for death, double-lung transplant, or restenosis at 36 months were 5% and 30%, respectively.

141 ectively prevented clinically relevant focal restenosis at 6-month follow-up.

142 Binary in-segment restenosis at a 1-year angiographic or ultrasonographic

143 tion is likely to arrest atherosclerosis and restenosis at early stages.

144 Serum miR-15a additionally correlated with restenosis at follow-up.

145 owed similar low rates of stroke, death, and restenosis at short-term follow-up.

146 ble reduction in the development of in-stent restenosis at the cost of an increased risk of late sten

147 The presence of an occlusive restenosis at the time of treatment was not associated w

148 nosis rate, when compared with non-occlusive restenosis, at 1 year.

149 ontributes to vascular pathologies including restenosis, atherosclerosis and vascular calcification.

150 stent thrombosis at 1 year and angiographic restenosis based on analysis of the left main coronary a

151 ective in the treatment of coronary in-stent restenosis, but data are limited regarding their efficac

152 ting stents reduce the incidence of in-stent restenosis, but they result in delayed arterial healing

153 ntima, we established a novel mouse model of restenosis by grafting a decellularized vessel to the ca

154 ther, it exhibited therapeutic potential for restenosis by inhibiting SMC accumulation in a rat reste

155 s inhibition plays crucial roles in vascular restenosis by preventing neointimal hyperplasia at the e

156 rimary endpoint was 1-year in-segment binary restenosis by quantitative angiography.

157 est a novel therapeutic strategy to suppress restenosis by targeting noncanonical MMP-1-PAR1 signalin

158 ation with cryoplasty balloon reduced binary restenosis compared to conventional balloon angioplasty.

159 wer in patients with PCB angioplasty for BMS restenosis compared with DES restenosis (3.8% vs. 9.6%,

160 PCB angioplasty was more effective in BMS restenosis compared with DES restenosis, with no differe

161 -p27-126TS-treated animals exhibited reduced restenosis, complete reendothelialization, reduced hyper

162 d points included angiographic parameters of restenosis, device-oriented composite end point, their i

163 Also, the risk of restenosis during a median follow-up of 13 months was si

164 for VLScT include scaffold discontinuity and restenosis during the resorption process, which appear d

165 s, the related pathological events-including restenosis, endothelial dysfunction, and stent thrombosi

166 Finally, restenosis enhanced the expression of calpain-1/2, but r

167 in vivo rat carotid balloon-injury model of restenosis evidenced that AC8 de novo expression coincid

168 of drugs for vascular diseases, particularly restenosis following angioplasty, stent implantation, or

169 hod of perivascular drug-delivery to prevent restenosis following open surgical procedures.

170 delivery particularly suited for preventing restenosis following open vascular surgery.

171 cells (SMCs) is an important contributor to restenosis following percutaneous coronary interventions

172 till a significant difference in the risk of restenosis for BA versus stenting (hazard ratio, 2.46; 9

173 roke or death and the secondary endpoint was restenosis greater than 50% during follow-up, comparing

174 EB group and also in subgroups with in-stent restenosis >10 mm (0.05 versus 0.26 mm; P=0.0002) and ar

175 Angiographic binary restenosis (>/= 50% lumen diameter stenosis) was reporte

176 Reocclusion rate was 7.5%, whereas binary restenosis (>50%) or reocclusion rate was 20%.

177 In the EES group, repetitive binary restenosis had a significantly greater chance of occurri

178 While failure from restenosis has dropped to below 5%, the risk of stent th

179 ed veins and 25% of stented veins developing restenosis (hazard ratio, 2.77; 95% confidence interval,

180 l [CI]: 0.73 to 0.89; p < 0.001), and ST and restenosis (hazard ratio: 0.74; 95% CI: 0.57 to 0.96; p

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

182 Treatments aimed at inhibiting restenosis in calcified arteries may differ from those t

183 educes the risk of subsequent pulmonary vein restenosis in comparison with BA.

184 minal angioplasty (PTA) for the reduction of restenosis in diabetic patients with critical limb ische

185 eration ZES and EES have reduced the risk of restenosis in large patient cohorts.

186 a lower risk of long-term mortality, ST, and restenosis in patients undergoing PCI for stable angina

187 round Drug-eluting stents reduce the risk of restenosis in patients undergoing percutaneous coronary

188 ts is associated with high rates of in-stent restenosis in patients with diabetes mellitus.

189 l CTP improves diagnosis of CAD and in-stent restenosis in patients with stents compared with CTA alo

190 Overall, 42% of veins developed restenosis including 27% of veins (n=23) treated with st

191 erence tomography, we investigated causes of restenosis, including the contribution of late scaffold

192 Moreover, simvastatin improved restenosis indicators by suppressing the HIF-1alpha/calp

193 oon vs Everolimus-Eluting Stent) and RIBS V (Restenosis Intra-Stent of Bare Metal Stents: Paclitaxel-

194 A pooled analysis of the RIBS IV (Restenosis Intra-Stent of Drug-Eluting Stents: Paclitaxe

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

196 theter approaches are acutely successful but restenosis is common and rapid.

197 local immune response in the development of restenosis is not fully understood.

198 s has acceptable clinical outcomes, in-stent restenosis (ISR) and stent thrombosis remain clinically

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

200 al presentation of bare metal stent in-stent restenosis (ISR) in patients undergoing target lesion re

201 a paucity of data on the burden of in-stent restenosis (ISR) in the United States as well as on its

202 ients with drug-eluting stent (DES) in-stent restenosis (ISR) is more challenging than that of patien

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

204 ous coronary intervention (PCI) for in-stent restenosis (ISR) randomized to short (6 months) versus l

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

206 ients with drug-eluting stent (DES) in-stent restenosis (ISR) remains a major challenge.

207 Management of patients with in-stent restenosis (ISR) remains an important clinical problem.

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

209 tients with bare-metal stents (BMS) in-stent restenosis (ISR).

210 tients with bare-metal stents (BMS) in-stent restenosis (ISR).

211 ion (PCI) can lead to a decrease in in-stent restenosis (ISR).

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

213 al left main coronary artery (UDLM) in-stent restenosis (ISR).

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

215 ent of chronic total occlusions and in-stent restenosis lesions, and had higher 12-month major advers

216 Restenosis limits the efficacy of vascular percutaneous

217 tency, defined as freedom from target-lesion restenosis (luminal narrowing of >/=50%) as detected by

218 Secondary endpoints were in-stent binary restenosis, major adverse cardiac events (MACE: cardiac

219 and binary restenosis rate was 2% (the only restenosis mentioned above).

220 osis by inhibiting SMC accumulation in a rat restenosis model.

221 ), 70 complications were observed, including restenosis (n=53), thrombosis (n=7), bleeding (n=6), and

222 Why did thrombosis or restenosis occur in this stent?

223 0.36 mm, respectively, and in-segment binary restenosis occurred in 2.0% and 7.6% of patients, respec

224 Angiographic restenosis occurred in 21.5% of patients in the ZES grou

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

226 e the efficacy in the prevention of clinical restenosis of everolimus-eluting stent (Xience V) and BM

227 The pathomechanisms underlying restenosis of the bioabsorbable sirolimus-eluting metall

228 was primary patency, defined as freedom from restenosis or clinically driven target lesion revascular

229 ents) for the treatment of coronary in-stent restenosis or de novo lesions.

230 at 12 months (defined as freedom from binary restenosis or from the need for target-lesion revascular

231 62 who had carotid endarterectomy (6.3%) had restenosis or occlusion (hazard ratio [HR] 0.90, 95% CI

232 7, 1.01-4.26) were independent predictors of restenosis or occlusion after the two procedures.

233 alysis, the main endpoint was a composite of restenosis or occlusion at 2 years.

234 ial was to compare the composite endpoint of restenosis or occlusion.

235 patients at high risk for the development of restenosis or thrombosis and might thereby guide individ

236 Cr-EES versus SES), whereas fracture-related restenosis or thrombosis was comparable among the groups

237 composite end point of all-cause mortality, restenosis, or definite stent thrombosis (hazard ratio,

238 d stent oversizing, progressive decreases of restenosis (P=0.002) and target lesion revascularization

239 e and the primary end point (P=0.86) or with restenosis (P=0.53).

240 by vascular injury, such as atherosclerosis, restenosis, peripheral vascular disease, sepsis, and acu

241 ve agents significantly lowered the rates of restenosis, permitting widespread use of percutaneous co

242 ndard balloon angioplasty (POBA) in terms of restenosis prevention for de novo superficial femoral ar

243 e to limit mainly proliferative processes in restenosis-prone diabetic patients, particularly those p

244 +/- 22% vs. 30 +/- 22%; p < 0.01) and binary restenosis rate (11% vs. 19%; p = 0.06), compared with p

245 mm vs. 0.14 +/- 0.5 mm, p = 0.14) and binary restenosis rate (4.7% vs. 9.5%, p = 0.22) were very low

246 The 1-year restenosis rate after balloon angioplasty of long lesion

247 All BVS were widely patent, and binary restenosis rate was 2% (the only restenosis mentioned ab

248 The in-segment restenosis rate was 5.2% in the EES group and 15.6% in t

249 Restenosis rate was significantly reduced from 58.1% to

250 eatment was not associated with an increased restenosis rate, when compared with non-occlusive resten

251 bare stents are limited by a relatively high restenosis rate, which could be potentially improved by

252 r superiority), with no difference in binary restenosis rates (diameter stenosis>/=50%) at 9 months f

253 option for specific arterial sites, although restenosis rates are higher.

254 The cumulative restenosis rates in 1, 2, 3, 4, and 5-years in the exper

255 in 12 of 29 allergy patients revealed binary restenosis rates of 27% in bare metal stents and 0% in d

256 However, restenosis rates remain high.

257 ptomatic coronary artery disease by reducing restenosis rates; however, a significant clinical conseq

258 Intimal hyperplasia produces restenosis (re-narrowing) of the vessel lumen following

259 over the bare stent in terms of reducing the restenosis, recurrence, and secondary interventional the

260 bosis-related MI (n=63; 24.0%), and in-stent restenosis-related MI (n=58; 22.1%).

261 oles of calpastatin and calpains in vascular restenosis remain unclear.

262 However, restenosis remains an unsolved clinical problem after va

263 rculating lymphocytes and increased in-stent restenosis risk (OR, 1.43; 95% CI, 1.00-1.823; P=0.039).

264 he development of diagnostic tools to assess restenosis risk after stent deployment may enable the in

265 d who on the basis of thrombotic bleeding or restenosis risk criteria, qualified as uncertain candida

266 morphisms in CCNB1 associated with increased restenosis risk in a cohort of 284 patients undergoing c

267 ata are available in patients who have a low restenosis risk.

268 een investigated with the intent of limiting restenosis similarly to DES for the coronary arteries.

269 with the risk of late complications such as restenosis, stent fracture or dislocation.

270 In particular, restenosis still represents a challenge, even though it

271 Early endothelialization and restenosis studies were performed using the porcine coro

272 Secondary end points were binary restenosis, target lesion revascularization, and definit

273 Secondary endpoints were angiographic restenosis, target lesion revascularization, and major a

274 s compared with PTA strikingly reduce 1-year restenosis, target lesion revascularization, and target

275 For in-stent restenosis, the benefit of DCBA over POBA remains uncert

276 hypercholesterolemic swine model of femoral restenosis, the implantation of an FP-PES resulted in lo

277 Primary end points were restenosis, thrombosis, and failure of vascular access.

278 These alterations potentially lead to restenosis, thrombosis, or endothelial dysfunction in th

279 were potentially related to BVS: 1 in-stent restenosis (treated 7 months after pPCI with drug-elutin

280 aintain Vessel Patency-A Pilot Study of Anti-Restenosis Treatment) was a multicenter randomized trial

281 Treatment of bare metal stent restenosis using PEB led to significantly less 12-month

282 ers such as atherosclerosis, postangioplasty restenosis, vein graft stenosis, and allograft vasculopa

283 The rate of binary angiographic restenosis was 10.8% and 9.1% in patients allocated to s

284 mm, and 0.21 +/- 0.32 mm (p < 0.01); binary restenosis was 26.2%, 28.6%, and 4.7% (p = 0.01); and MA

285 in the MGuard was 0.99+/-0.80 mm, and binary restenosis was 31.6%.

286 The 3-year overall rate of restenosis was 37%, with 49% of BA-treated veins and 25%

287 At 5 years, in-scaffold and -segment binary restenosis was 7.8% (5 of 64) and 12.5% (8 of 64).

288 The frequency of restenosis was calculated by Kaplan-Meier survival estim

289 At the same time point, binary restenosis was comparable between BVS and DES (7.8% vers

290 Restenosis was defined as >/=75% area stenosis within th

291 Here, restenosis was induced by ligating the left carotid arte

292 Twelve-month target lesion restenosis was observed in 22% of DCB-treated versus 21%

293 Similarly, binary restenosis was significantly lower after treatment with

294 At 12 months, binary restenosis was significantly lower in the cryoplasty gro

295 ng reserve coronary circulation, if in-stent restenosis were to occur in the treated left main.

296 ic approach to specifically inhibit vascular restenosis while preserving EC function.

297 inhibit proliferative VSMCs, thus preventing restenosis, while selectively promoting reendothelializa

298 omized trial showing a reduction of clinical restenosis with a new-generation DES in comparison with

299 ffective in BMS restenosis compared with DES restenosis, with no difference regarding the type of DES

300 imal hyperplasia in a mouse model of carotid restenosis without modifying vital cardiovascular parame