ライフサイエンスコーパス: in-stent

1 as associated with a greater late lumen loss in stent and more frequent angiographic restenosis regar

2 vascular injury and is a prominent component in stented and nonstented restenotic lesions.

3 The 30-day MACCE rates were 3.7% and 1.5% in stented and unstented patients, respectively (p < 0.0

4 are addressed, including novel developments in stents and stent coatings, conventional drugs, nuclei

5 ivalent, we defined the relationship between in-stent and analysis segment late loss, the shape of th

6 sions showed similar vessel response in both in-stent and reference segments regardless of the DES ty

7 The final in-stent angiographic minimum lumen diameter was 2.99+/-

8 Secondary outcomes included final in-stent angiographic minimum lumen diameter, procedure

9 as included use of new metal alloys, changes in stent architecture, and use of bioresorbable polymers

10 In stented arteries, there was an increase in intima-med

11 g rapid and stable cell homing and expansion in stented arteries.

12 was assumed, late loss accurately estimated in-stent binary angiographic restenosis for the control

13 (0.6 +/- 0.5 mm vs. 0.7 +/- 0.5 mm; p = NS), in-stent binary restenosis (7.1% vs. 6.9%; p = NS), in-s

14 Secondary endpoints were in-stent binary restenosis, major adverse cardiac events

15 d MNPs to achieve site-specific transduction in stented blood vessels.

16 ta-analysis that accounted for the variation in stent choice.

17 nd progression of neointimal hyperplasia and in-stent clotting.

18 After successful demonstration, in-stent coronary thrombosis was induced by x-ray-guided

19 The composition of the in-stent ECM has not been well characterized in humans.

20 sess stent tissue coverage and malapposition in stent evaluation trials.

21 ificant advances have also occurred recently in stent graft research and development.

22 use, and highlights the recent developments in stent graft treatment of abdominal aortic aneurysms.

23 In stent-implanted vessels, real-time imaging illuminate

24 The primary endpoint of in-stent (in-balloon) late loss was significantly less w

25 endpoint was noninferiority of angiographic in-stent (in-balloon) late loss with a delta of 0.25 mm.

26 o model of SM cell (SMC) differentiation and in stent-induced pig coronary vessel injury.

27 of preinterventional arterial remodeling on in-stent intimal hyperplasia (IH) after implantation of

28 In-stent late loss at 9 months was 0.29+/-0.60 versus 0.

29 The primary end point was in-stent late loss at 9 months.

30 The primary end point was in-stent late loss at 9-month angiographic follow-up (no

31 The observed difference in in-stent late loss between both groups was -0.16 mm (95%

32 In the sirolimus-eluting stent arm, in-stent late loss correlated better with target-lesion

33 he primary angiographic endpoint was 6-month in-stent late loss measured by quantitative coronary ang

34 We hypothesized that mean in-stent late loss might be a more stable estimator of r

35 The mean in-stent late loss observed in the SIRIUS trial was 0.17

36 with an acute gain of 1.41 mm (0.46 mm) and in-stent late loss of 1.08 mm (0.49 mm).

37 The 6-month in-stent late loss was 0.15 +/- 0.34 mm for PROMUS Eleme

38 of reference vessel diameter on TLR than on in-stent late loss.

39 Primary endpoint was 6-month angiographic in-stent late lumen loss (LLL) within a noninferiority s

40 The mean in-stent late lumen loss at 6 months and 9 months were 0

41 found noninferior for the primary end point in-stent late lumen loss at 9 months.

42 nt (X-EES) in terms of the primary end point in-stent late lumen loss at 9 months.

43 luting stent, P=0.75); 13-month angiographic in-stent late lumen loss was 0.22+/-0.41 mm and 0.23+/-0

44 he primary endpoint was 6-month angiographic in-stent late-luminal loss.

45 In the post-transplant patients, in-stent LL was closely coupled to control segment LL (R

46 n de novo lesions showed significantly lower in-stent LLL at 6 months than the Taxus Liberte stent di

47 In-stent LLL was significantly lower in Cre8 group (0.14

48 In-stent LLL was similar between patients treated with B

49 Visualization of the in-stent lumen at CT angiography with a 16-detector row

50 Mean in-stent lumen loss was 0.90 +/- 0.59 mm for PF-PES and

51 Estimated values for in-stent luminal diameter were lower with CT than with c

52 computed tomographic (CT) measurement of the in-stent luminal diameter.

53 rotrusion (hazard ratio [HR], 2.35; P<0.01), in-stent minimum lumen area (MLA) <4.5 mm(2) (HR, 2.72;

54 nfarction was associated with a larger final in-stent minimum lumen diameter.

55 se in PA gradient or post-procedure ratio of in-stent minimum to pre-stent distal diameter >80%.

56 polymer-based, paclitaxel-eluting stents on in-stent neointima formation and late incomplete stent a

57 es injection concurrent with injury, reduces in-stent neointimal formation and arterial stenosis in h

58 ulated bisphosphonates inhibits experimental in-stent neointimal formation.

59 limus treatment groups significantly reduced in-stent neointimal growth (46% reduction and 42% reduct

60 de of the same family as sirolimus) inhibits in-stent neointimal growth in rabbit iliac arteries.

61 Oral everolimus suppresses in-stent neointimal growth in the rabbit iliac artery.

62 ility of drug-eluting stents has reduced the in-stent neointimal proliferation that causes restenosis

63 In-stent noise, signal-to-noise ratio(SNR), stent-lumen

64 , SAFIRE was superior to FBP with regards to in-stent noise, SNR, SAIR, and image quality score.

65 ediate and impressive, 14 patients developed in-stent or in-segment restenosis, requiring repeated in

66 thods will be required to decrease recurrent in-stent or in-segment restenosis.

67 Urinary tract infections were more common in stented patients (RR 1.49), unless the patients were

68 ns of Non-Adherence to Anti-Platelet Regimen in Stented Patients [PARIS]; NCT00998127).

69 s of Non-Adherence to Anti-Platelet Regimens in Stented Patients Registry), 4222 patients who underwe

70 s of non-adherence to anti-platelet regimens in stented patients) registry is a prospective observati

71 ns of Non-Adherence to Anti-Platelet Regimen in Stented Patients) registry, separate risk scores were

72 Non-Adherence to Dual Anti-Platelet Regimen in Stented Patients) was a prospective multicenter obser

73 s of Non-Adherence to Anti-Platelet Regimens in Stented Patients) were categorized according to their

74 In stented patients, an antibiotic with anti-enterococca

75 The 13-month angiographic in-stent percent diameter stenosis amounted to 12.0 +/-

76 primary prespecified IVUS end point was the in-stent percent net volume obstruction at follow-up.

77 The primary prespecified end point was the in-stent percent net volume obstruction at follow-up.

78 t binary restenosis (7.1% vs. 6.9%; p = NS), in-stent percent volume obstruction by IVUS (29% vs. 24%

79 In stented pig coronary vessels, LPP was expressed in th

80 y using a Rotarex system followed by a stent-in-stent placement procedure.

81 d to fully study this issue; and 5) advances in stent platforms for drug elution as well as adjunctiv

82 EC p-S6RP expression in stented porcine arteries confirmed our in vitro findi

83 no data on the feasibility and safety of RDN in stented RA.

84 -magnetic delivery conditions, were observed in stented rat carotid arteries.

85 strategy success (stent expansion with <20% in-stent residual stenosis) and safety outcomes (procedu

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

135 In-stent restenosis and bypass graft failure are charact

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 In-stent restenosis is a major limitation of intracorona

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

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

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

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

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

170 1025 consecutive native coronary artery, non-in-stent restenosis lesions undergoing PCI, 72 hematomas

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

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

173 % in drug-eluting stents, with mean diameter in-stent restenosis of 36% and 8%, respectively.

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

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

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

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

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

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

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

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

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

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

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

185 332 patients with in-stent restenosis underwent successful coronary interv

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

212 have demonstrated effectiveness in treating in-stent restenosis.

213 %) could be attributed to segments with >70% in-stent restenosis.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 smoker, multivessel disease, treatment of an in-stent restenotic lesion), laboratory findings (low ba

252 Treatment of bare-metal in-stent restenotic lesions with paclitaxel-eluting sten

253 treatment group included 68 patients with 74 in-stent restenotic lesions.

254 We analyzed 29 coronary arterial in-stent restenotic tissue samples (14 left anterior des

255 nitroglycerin in mean lumen diameter of the in-stent/scaffold segment at 12 months with superiority

256 Therefore, this study aimed to compare the in-stent/scaffold vasomotion between MgBRS and permanent

257 Changes in stent section shape after balloon deflation are impor

258 ut gap), and V (with transection causing gap in stent segment).

259 p-ERK/p-Akt ratio in stented segments uniquely correlated with neointimal

260 stance and diabetes on Akt and ERK signaling in stented segments.

261 d ratio, 0.32; P=0.015) and from significant in-stent stenosis (hazard ratio, 0.14; P=0.002).

262 s included stent migration (one patient) and in-stent stenosis (three patients).

263 No significant focal in-stent stenosis analyzed with angiography (percentage

264 sociation studies of human neointima-induced in-stent stenosis confirmed the association of the ROS1

265 on was documented in 9 cases and significant in-stent stenosis in 17 cases.

266 y is effective in reducing the recurrence of in-stent stenosis in native coronary arteries.

267 lantation to intravascular brachytherapy for in-stent stenosis of bare metal stents.

268 The role of intravascular brachytherapy for in-stent stenosis of drug eluting stents is very much in

269 Even with in-stent stenosis, the role of intravascular brachythera

270 from a stent platform significantly reduced in-stent stenosis, while promoting re-endothelialization

271 is already decreasing the clinical impact of in-stent stenosis.

272 01), resulting in a 50% reduction of percent in-stent stenosis.

273 owed restriction of growth within an area of in-stent stenosis.

274 failure of previous treatment such as "stent in stent" technique.

275 Current innovations in stent technologies, including biodegradable stents, n

276 f MACE progressively declined with evolution in stent technology (BMS: 24.1% versus DES1: 17.9% versu

277 role of cholangioscopy, and recent advances in stent technology are reviewed.

278 remains a clinical problem despite advances in stent technology in both bare-metal and drug-eluting

279 In-stent thin-cap neoatheroma is more prevalent, is dist

280 In-stent thrombi: in-stent thrombosis was observed in al

281 f rivaroxaban is associated with a reduction in stent thrombosis among patients with acute coronary s

282 on DES entails a tradeoff between reductions in stent thrombosis and MI and increases in major hemorr

283 xaban 2.5 mg was associated with a reduction in stent thrombosis and mortality.

284 There were no significant differences in stent thrombosis or bleeding complications.

285 The reduction in stent thrombosis with ticagrelor was numerically grea

286 VUS guidance was associated with a reduction in stent thrombosis, myocardial infarction, and major ad

287 s, which is relevant to reports of very late in-stent thrombosis at altitude.

288 l applications include detection of coronary in-stent thrombosis or thrombus burden in patients with

289 Both of these patients developed acute in-stent thrombosis postoperatively (days 5 and 2) despi

290 feasibility of MRI of coronary thrombus and in-stent thrombosis using a novel fibrin-binding molecul

291 In-stent thrombi: in-stent thrombosis was observed in all stents after EP-

292 , inflammatory response, and mechanism(s) of in-stent thrombosis were assessed.

293 ion is essential for the prevention of early in-stent thrombosis, but clopidogrel use among older DES

294 ar medicine include clopidogrel and risk for in-stent thrombosis, steady-state warfarin dose, myotoxi

295 ), in a swine model of coronary thrombus and in-stent thrombosis.

296 Endoleaks and in-stent thrombus of thoracic aorta were detectable to 1

297 ties in each vessel, as well as the ratio of in-stent to PV flow, were compared before and after TIPS

298 Ureteral complication rate was 1.9% in stent versus 5.8% in no-stent group (P=0.007).

299 The adjacent wall stresses were very minimal in stents with 180/100 and 70/70 mum struts after embedd

300 flammatory cell content was 2.4-fold greater in stents with restenosis versus no restenosis, and infl