ライフサイエンスコーパス: embolic

1 Conclusion: The use of minimally embolic (90)Y glass microspheres to treat patients with

2 ned to three groups depending on the type of embolic agent injected: 70-150-mum radiopaque microspher

3 The visibility of the embolic agent was assessed with all modalities before an

4 The embolic agent was selectively delivered in the LAD in si

5 antly higher risk was associated with liquid embolic agents (8.1%; 99% CI: 4.7%, 13.7%) versus simple

6 7% of patients), risks decreased, and liquid embolic agents and flow diversion were associated with h

7 s of intervention technique, indications and embolic agents since Duggan introduced embolization to m

8 of an anticancer-in-oil emulsion followed by embolic agents, is widely used in the treatment of hepat

9 et therapy was associated with a low rate of embolic and bleeding events after a mean follow-up of 20

10 rochloride elution from drug-loaded hydrogel embolic beads within a microfluidic device consisting of

11 RV/LV diameter ratio and embolic burden are not associated with short-term death

12 Neither RV/LV diameter ratio nor embolic burden was associated with increased risk of dea

13 ventricle (RV) and left ventricle (LV), and embolic burden-are associated with short-term death, def

14 ial growth factor (VEGF) in a model of focal embolic cerebral ischemia in the rat.

15 Atrial fibrillation and related cardio-embolic cerebrovascular accidents are two well-defined m

16 month incidences of death or readmission for embolic (cerebrovascular accident, transient ischemic at

17 A transmural MI was created by implanting an embolic coil in the left anterior descending artery in Y

18 vascular stent insertion, or introduction of embolic coils.

19 imited data about the risk of thrombotic and embolic complication (TEC) in adults with atrial arrhyth

20 lesion in 35 patients (74.5%): 18 showed an embolic complication, 8 showed pathologic uptake on the

21 vs. 19 [5.9%], respectively; p = 0.602), or embolic complications (1 [0.3%] vs. 1 [0.3%], respective

22 ilter may be associated with a lower rate of embolic complications associated with carotid stent plac

23 Embolic complications during stenting of degenerated sap

24 osure is now standard practice and may limit embolic complications for at least 10 years.

25 Bleeding and embolic complications occurred in 47 (7.3%) and 2 (0.3%)

26 complications related to scoliosis surgery, embolic complications of joint arthroplasty, and complic

27 For this analysis, embolic complications were evaluated during the 30 days

28 essary to prevent devastating thrombotic and embolic complications, but bleeding is a major source of

29 es, associated with elevated risk for thromo-embolic complications.

30 TCEP was safe, captured embolic debris in 99% of patients, and did not change ne

31 Embolic debris traveling to the brain was captured in 75

32 Particles of embolic debris within the filters were quantified by pho

33 sical parameters governing drug-elution from embolic devices under physiologically relevant fluidic c

34 Anticancer treatment using embolic drug-eluting beads (DEBs) has shown multifarious

35 n dose with fewer particles, likely reducing embolic effects.

36 ng offers the potential to target functional embolic end points during TAE.

37 resulting from arterial recanalization or an embolic episode.

38 ot ischemic events including stroke/systemic embolic event (HRadj: 1.16; 95% CI: 0.89 to 1.51; p = 0.

39 score (OR, 1.07; 95% CI, 1.01 to 1.12), and embolic event (OR, 2.79; 95% CI, 1.15 to 6.80).

40 confidence interval [CI]: 0.66 to 0.96) and embolic event (RR: 0.52, 95% CI: 0.35 to 0.76) but a hig

41 risons were made of rates of stroke/systemic embolic event (SSEE), major bleeding, additional efficac

42 Therefore, its presence may signal vascular embolic event and damage not only in the brain but also

43 ng LAA morphology are less likely to have an embolic event even after controlling for comorbidities a

44 For dabigatran 150 mg, stroke/systemic embolic event rates were lower compared with warfarin in

45 .67; 95% CI, 0.52-0.86), and stroke/systemic embolic event rates were similar for warfarin and dabiga

46 The primary end point of stroke/systemic embolic event was lower in those patients with paroxysma

47 ation via pathology evaluation or documented embolic event within 6 months after CMR.

48 rug strongly depended on the location of the embolic event within the embolised channel (e.g. fractio

49 endpoint was a composite of stroke, systemic embolic event, myocardial infarction, and cardiovascular

50 patic disease, incident diabetes, thrombotic/embolic event, nontraumatic fracture, non-AIDS-defining

51 roke, transient ischemic attack, or systemic embolic event.

52 n compared with warfarin (stroke or systemic embolic event: higher dose pinteraction=0.85, lower dose

53 bus (51% versus 16%, P<0.001) and more fatal embolic events (26% versus 8%, P<0.03).

54 of stroke/transient ischemic attack/systemic embolic events (6 versus 10, iECG versus RC; hazard rati

55 f vegetation (MLV)>/=10 mm is a predictor of embolic events (EEs) in patients with infective endocard

56 k of death (RR: 1.01, 95% CI: 0.80 to 1.27), embolic events (RR: 0.95, 95% CI: 0.61 to 1.47), and ble

57 lation-related stroke, extracranial systemic embolic events (SEEs) remain poorly defined.

58 p; four [4%] vs eight [8%] postoperatively), embolic events (six [4%] vs eight [6%] preoperatively; t

59 nfidence intervals (CIs) for stroke/systemic embolic events (SSEE), major bleeding, intracranial hemo

60 to warfarin in preventing stroke or systemic embolic events and significantly reduced bleeding and ca

61 in for the prevention of stroke and systemic embolic events and significantly reduced intracranial bl

62 rrent incidence rates, numbers of AF-related embolic events at age >/=80 years will treble again by 2

63 nts significantly reduced stroke or systemic embolic events by 19% compared with warfarin (RR 0.81, 9

64 dentified 394 ischemic stroke and peripheral embolic events during 15,494 person-years of follow-up o

65 s a triad of heart failure, arrhythmias, and embolic events from mural thrombi.

66 Recently, cerebral embolic events have become a focus of clinical importanc

67 w-up, and 219 adjudicated stroke or systemic embolic events in anticoagulated patients with atrial fi

68 oted no heterogeneity for stroke or systemic embolic events in important subgroups, but there was a g

69 cal trials for stroke prevention or systemic embolic events in patients with atrial fibrillation.

70 th a lower risk of stroke and other systemic embolic events in patients with atrial fibrillation.

71 rin for preventing strokes or other systemic embolic events in patients with atrial fibrillation?

72 ion monitoring, prevents stroke and systemic embolic events in patients with nonvalvular AF as effect

73 gnificant reduction in the risk of recurrent embolic events or death as compared with medical therapy

74 Potentially preventable embolic events outnumbered warfarin-related intracerebra

75 as well calibrated with 0.76 stroke/systemic embolic events per 100 person-years in the predefined lo

76 Cerebral embolic events related to carotid and cardiac disease ha

77 composite of death, end-stage renal disease, embolic events resulting in end-organ damage, renovascul

78 Complex have been found to precede vascular embolic events secondary to cardiac myxoma, thus early d

79 explain the increased frequency and size of embolic events seen with pFVIII.

80 lar overall reductions in stroke or systemic embolic events to warfarin (1.03, 0.84-1.27; p=0.74), an

81 significantly higher cumulative incidence of embolic events was observed in patients with high predic

82 Hazard ratios for stroke/systemic embolic events were 1.95 for medium- versus low-risk gro

83 No embolic events were detected in group 3 patients.

84 Embolic events were less common with anticoagulation pro

85 s 3 and 30, an excess of stroke and systemic embolic events were observed in participants assigned to

86 Death and embolic events were relatively rare in the first 3 month

87 No major hemorrhagic or embolic events were reported.

88 No delayed ischemic or embolic events were reported.

89 -month adverse events were low (death, 3.0%; embolic events, 1.0%; bleeding events, 1.0%).

90 associated with a reduced risk of death and embolic events, but at the cost of an increased bleeding

91 The main outcomes were stroke and systemic embolic events, ischaemic stroke, haemorrhagic stroke, a

92 etermine the probability of stroke, systemic embolic events, or death by assigning tiered points for

93 nhanced risk assessment for stroke, systemic embolic events, or death compared with traditional clini

94 ical clots and anticoagulation did not incur embolic events.

95 were the independent predictors of definite embolic events.

96 dominantly by CMR imaging), including 2 with embolic events.

97 tinal arteriolar macroaneurysm formation and embolic events.

98 Two patients had subsequent embolic events: one death despite treatment and one recu

99 idly evolving and the recent introduction of embolic filtration devices (EFD) proved to reduce peripr

100 ion, and fatal or nonfatal stroke (ischemic, embolic, hemorrhagic, or unknown origin) were all lower

101 suggest that neurological events are mainly embolic in nature; however, there is significant discrep

102 ano accurately and expressively following an embolic infarct of the right angular and supramarginal g

103 one patient was discovered to have multiple embolic infarcts of the spleen, kidneys, and brain that

104 Embolic infarcts were defined as new foci of reduced dif

105 Knowledge of risk factors for cerebral embolic lesions during CAS may impact treatment decision

106 e predictive for procedural-related cerebral embolic lesions during embolic protected CAS.

107 n magnetic resonance imaging showed positive-embolic lesions in control pigs.

108 In 25% of these patients embolic lesions were also found in the contralateral hem

109 performed to identify factors predictive for embolic lesions.

110 ve of this study was to compare the cerebral embolic load of filter-protected versus proximal balloon

111 GuardWire aspirates was also similar: median embolic load per filter was 16 mm3 (range 2 to 84 mm3).

112 Median embolic load per GuardWire was also 16 mm3 (range 7 to 4

113 Total embolic load per lesion for both filters and GuardWire a

114 filter protection significantly reduced the embolic load to the brain.

115 croembolized in six pigs with small-diameter embolic material (40-120 microm, 250000 count).

116 ture understanding and diligent selection of embolic material are helpful in preventing this adverse

117 nts for embolotherapy may cause migration of embolic material from the external to the internal carot

118 rug eluting beads (DEBs), in which a uniform embolic material is loaded with a drug and delivered in

119 ess differences in infarction with different embolic materials.

120 was smaller in GK rats with both suture and embolic MCAO, but expanded with longer reperfusion perio

121 lusion with the suture model, but not in the embolic MCAO.

122 Embolic mechanism, distal territory location, and basila

123 Embolic microspheres that have the ability to release a

124 Male Wistar rats (n=28) were subjected to embolic middle cerebral artery (MCA) occlusion.

125 Ischemia induced either by embolic middle cerebral artery occlusion (MCAO) in vivo

126 We then used the murine suture and embolic middle cerebral artery occlusion models of strok

127 Rats subjected to embolic middle cerebral artery occlusion were treated wi

128 Rats were subjected to embolic middle cerebral artery occlusion.

129 allogeneic clot, we previously developed an embolic model of MCA occlusion in the rat, which recapit

130 intracranial bleeding in both mechanical and embolic models of stroke in rats, and reduced brain edem

131 rysms are safely treated with daily aspirin, embolic monitoring, and radiographic surveillance.

132 ly transcranial Doppler ultrasonography with embolic monitoring.

133 (n = 2), and late strokes thought to be non-embolic (n = 2).

134 ruction of normal native valves and to cause embolic occlusion of large arteries and its resistance t

135 alutary effect in ischemic stroke induced by embolic occlusion of the middle cerebral artery (MCAO).

136 Embolic occlusion of the pulmonary arterial system is re

137 Embolic occlusions may also alter local hemodynamic pres

138 During follow-up, no embolic or septic events occurred.

139 oportion of patients and is assumed to be of embolic origin.

140 with approximately 0.5 million 40-120-microm embolic particles injected at each embolic stage.

141 ypercoagulability, which might enhance their embolic potential and affect treatment and prevention, i

142 ural-related cerebral embolic lesions during embolic protected CAS.

143 dictive for cerebral ischemic lesions during embolic protected CAS.

144 gh previous reports of carotid stenting with embolic protection (CAS) have focused on clinical outcom

145 teraction was observed between abciximab and embolic protection (P<0.05), favoring combination treatm

146 ) may be reduced with transcatheter cerebral embolic protection (TCEP).

147 al, we compared carotid-artery stenting with embolic protection and carotid endarterectomy in patient

148 however, have not been quantified, rendering embolic protection approaches empiric.

149 lacement with the use of a dual filter-based embolic protection device (Montage Dual Filter System, C

150 ould be further improved, we investigated an embolic protection device placed proximal to the target

151 1.9% (n = 461) and rate of failure to use an embolic protection device was 4.8% (n = 1173).

152 usion-weighted MRI, or the use of a cerebral embolic protection device was found to be independently

153 replacement procedures where a filter-based embolic protection device was used.

154 ters were randomly assigned to an open-label embolic protection device, Angioguard, or double-blind u

155 ines give a class I recommendation to use of embolic protection devices (EPD) for saphenous vein graf

156 carotid artery intervention with filter-type embolic protection devices (EPDs) and to determine its p

157 limited on contemporary use and outcomes of embolic protection devices (EPDs) in saphenous vein graf

158 ates are reduced significantly by the use of embolic protection devices (EPDs), neither the level of

159 Use of 1 of 2 cerebral embolic protection devices (n = 118 for suction-based ex

160 of the updated ongoing clinical research on embolic protection devices and present its major caveats

161 Among patients undergoing SAVR, cerebral embolic protection devices compared with a standard aort

162 desired goal, the current research design of embolic protection devices focuses on surrogate markers

163 TriActiv System was not inferior to approved embolic protection devices for the treatment of diseased

164 uality of life, the clinical significance of embolic protection devices has yet to be determined, and

165 the efficacy and adverse effects of cerebral embolic protection devices in reducing ischemic central

166 rug-eluting stents, antiplatelet agents, and embolic protection devices may improve clinical outcomes

167 stent procedures, whether adjunctive use of embolic protection devices or glycoprotein IIb/IIIa inhi

168 Combined with filter embolic protection devices, both a randomized control tr

169 has been associated with the development of embolic protection devices.

170 reentry devices; thrombectomy catheters; and embolic protection devices.

171 opment and to the clinical research of novel embolic protection devices.

172 Embolic protection during carotid artery stenting reduce

173 Patients undergoing CAS with cerebral embolic protection for internal carotid artery stenosis

174 tection flush and extraction device, with an embolic protection group during treatment of saphenous v

175 erated SVGs who underwent PCI without distal embolic protection in a single center.

176 e use of conventional guidewires, and permit embolic protection in anatomy unfavorable for distal dev

177 e on the role of mechanical thrombectomy and embolic protection in native coronary arteries during pr

178 e incremental cost and cost-effectiveness of embolic protection in patients undergoing percutaneous r

179 he Watchman Left Atrial Appendage System for Embolic Protection in Patients With AF (PROTECT AF) rand

180 F (Watchman Left Atrial Appendage System for Embolic Protection in Patients With Atrial Fibrillation)

181 y (Watchman Left Atrial Appendage System for Embolic Protection in Patients With Atrial Fibrillation)

182 F (WATCHMAN Left Atrial Appendage System for Embolic Protection in Patients With Atrial Fibrillation)

183 F (Watchman Left Atrial Appendage System for Embolic Protection in Patients with Atrial Fibrillation)

184 F (Watchman Left Atrial Appendage System for Embolic Protection in Patients with Atrial Fibrillation)

185 Left Atrial Appendage Closure Technology for Embolic Protection in Patients With Atrial Fibrillation)

186 rectomy, carotid artery stenting with distal embolic protection is a reasonable alternative for revas

187 that CAS with the WALLSTENT plus FilterWire embolic protection is non-inferior (equivalent or better

188 Treatment of SVGs with embolic protection reduces adverse cardiac events.

189 Self-Expanding Nitinol Stent and the SPIDER Embolic Protection System (ev3 Inc., Plymouth, Minnesota

190 point was significantly lower for the Wirion Embolic Protection System group, compared with historica

191 carotid artery stenting with a unique distal embolic protection system in high-risk patients with sev

192 aluated the safety and performance of Wirion Embolic Protection System in patients undergoing carotid

193 The Wirion Embolic Protection System is used to deploy an independe

194 placebo (0+/-27% versus -10+/-20%; P<0.05), embolic protection was not (-1+/-28% versus -10+/-20%; P

195 Using proximal embolic protection whenever possible during treatment of

196 ith coronary ischemia and lesions in SVGs to embolic protection with the TriActiv System or control g

197 with a device to capture and remove emboli ("embolic protection") is an effective alternative to caro

198 n better antithrombotic pharmacology, distal embolic protection, and devices for crossing chronic tot

199 With stenting alone, stenting and embolic protection, and stenting with abciximab alone, g

200 Renal artery stenting alone, stenting with embolic protection, and stenting with abciximab were ass

201 Embolic protection, improving stent designs, and ever-in

202 cutive patients undergoing CAS with cerebral embolic protection.

203 oduced outcomes similar to those with distal embolic protection.

204 th >/=50 patients, that had exclusive use of embolic-protection devices, and that compared CAS agains

205 Commercially available polymeric embolics range from gelatin foam to synthetic polymers s

206 ography (ACUTE) trial found no difference in embolic rates between the two approaches.

207 validate a simple calculator to quantify the embolic risk (ER) at admission of patients with infectiv

208 ns in the low-flow left atrium, but cerebral embolic risk in ventricular ablation has not been evalua

209 CHADS(2), except for patients with very low embolic risk; the CHA(2)DS(2)-VASc was able to identify

210 (V/Q) scans were performed for evaluation of embolic risks, and clinical and imaging examinations wer

211 ction in heart failure and the prevention of embolic sequelae.

212 psilateral stroke was 3.62% in patients with embolic signals and 0.70% in those without.

213 eline and 2 years was 7.13% in patients with embolic signals and 3.04% in those without, and for ipsi

214 nvestigate whether detection of asymptomatic embolic signals by use of transcranial doppler (TCD) cou

215 ck from baseline to 2 years in patients with embolic signals compared with those without was 2.54 (95

216 Assessment of the presence of embolic signals on TCD might be useful in the selection

217 nsient ischaemic attack for patients who had embolic signals on the recording preceding the next 6-mo

218 Embolic signals were present in 77 of 467 patients at ba

219 To detect the presence of embolic signals, patients had two 1 h TCD recordings fro

220 he displacement of the bead from the primary embolic site.

221 Echocardiography revealed an embolic source in 61% of CRAO and 53% of BRAO compared t

222 cause (SDIs >/= 15mm or SDIs with potential embolic source) (n = 32) was predicted using the derived

223 carotid artery stenosis and plaques, cardiac embolic source, TIA/stroke and myocardial ischemia diffe

224 microparticulate debris that approximate the embolic sources from catheter ablation can create hyperi

225 Secondary prevention for high-risk embolic sources generally involves anticoagulation, but

226 om any of several well established potential embolic sources, including minor-risk or covert cardiac

227 formed at baseline and after each subsequent embolic stage (10 minutes between stages).

228 Reductions to AUC and MUS after each embolic stage were statistically significant (P<.006 for

229 20-microm embolic particles injected at each embolic stage.

230 7); arrhythmic sudden death (SD) (n=17); and embolic stroke (n=2).

231 ation in the chronic stage of a rat model of embolic stroke (n=6), and (ii) whether this process can

232 elated mortality events (0.64%/y), including embolic stroke (n=6), progressive heart failure or trans

233 tid crush injury (mural thrombosis model) or embolic stroke (occlusive thrombosis model) followed by

234 enosis (OR, 7.52; CI, 6.22-9.09; P < 0.001), embolic stroke (OR, 4.43; CI, 3.05-6.42; P < 0.001), hyp

235 8 or more emboli per hour was predictive of embolic stroke (P = 0.0076).

236 cific WMH lesion pattern among patients with embolic stroke aetiology.

237 diac arrhythmia, is the most common cause of embolic stroke and death associated with heart failure.

238 Male Wistar rats were subjected to embolic stroke and received treatment via a femoral vein

239 Male Wistar rats were subjected to embolic stroke and treated with the combination of rtPA

240 In embolic stroke animals, positron emission tomographic-co

241 hort of consecutive patients presenting with embolic stroke at an academic hospital and tertiary refe

242 Administration of sildenafil to rats with embolic stroke enhances angiogenesis and selectively inc

243 lasminogen activator, or both, 4 hours after embolic stroke improves the functional outcome and reduc

244 In a clinically relevant model of embolic stroke in rodents, we now show that administrati

245 emorrhage after transient brain ischemia and embolic stroke in rodents.

246 onal cortical blood flow (RCBF) following an embolic stroke is beneficial to neurological outcome.

247 Embolic stroke is the most devastating consequence of at

248 ients with non-valvular atrial fibrillation, embolic stroke is thought to be associated with left atr

249 cerebral ischemia using a rabbit small clot embolic stroke model (RSCEM) using clinical rating score

250 used a modification of the rabbit small clot embolic stroke model (RSCEM), a multiple infarct ischemi

251 ical ATP content using the rabbit small clot embolic stroke model (RSCEM), the model originally used

252 infarct ischemia using the rabbit small clot embolic stroke model (RSCEM).

253 The rabbit large clot embolic stroke model has been used for over 23 years to

254 hemic damage in both size and severity in an embolic stroke model of rat with and without a therapeut

255 Lastly, we show that in the rabbit embolic stroke model, hemorrhages are adjacent to areas

256 a fully blinded and randomized manner in an embolic stroke model, we determined if CEPO would be use

257 s has not been demonstrated using an in vivo embolic stroke model.

258 In experimental embolic stroke models, MMP inhibitors decreased cerebral

259 isease, leading to the recent formulation of embolic stroke of undetermined source as a distinct targ

260 , recent clinical trials have indicated that embolic stroke of undetermined source may often stem fro

261 ial cardiomyopathy may explain many cases of embolic stroke of undetermined source, and oral anticoag

262 ested for stroke prevention in patients with embolic stroke of undetermined source, including specifi

263 he prevention of thrombosis in patients with embolic stroke of unknown source, heart failure, coronar

264 ion burden as assessed on the Fazekas scale, embolic stroke pattern, infarct distribution and pertine

265 gnificant impact on clot trajectory and thus embolic stroke propensity through the left common caroti

266 o HT data measured histologically at 48 h in embolic stroke rats, the enhanced areas by Gd-DTPA at 24

267 se middle cerebral occlusion (MCAO) model of embolic stroke to study neuronal degeneration following

268 with Gd-DTPA to detect HT in a rat model of embolic stroke treated with rtPA and a glycoprotein IIb/

269 Embolic stroke was induced in 8 male Wistar rats and mag

270 Acute ischemic or embolic stroke was seen in 7 patients (16%) with an over

271 of sildenafil, male Wistar rats subjected to embolic stroke were treated with sildenafil (n=11) or sa

272 ch curvature is an important risk factor for embolic stroke which should be tested in future clinical

273 cerebral perfusion is impaired directly (eg, embolic stroke) or indirectly (eg, raised intracranial p

274 with in-hospital death, nonfatal recurrence, embolic stroke, or delayed normalization of ejection fra

275 y cause of death in HCM virtually limited to embolic stroke, supporting a low threshold for initiatin

276 In conclusion, following an embolic stroke, TNFalpha administration increased the in

277 ) to control atrial fibrillation and prevent embolic stroke.

278 the LAA is believed to decrease the risk of embolic stroke.

279 they require tPA administration following an embolic stroke.

280 tly involved in vascular damage following an embolic stroke.

281 ion during stroke recovery in a rat model of embolic stroke.

282 ceptor antagonist, 7E3 F(ab')2, at 4 h after embolic stroke.

283 d delayed rht-PA treatment in a rat model of embolic stroke.

284 ound to be independent predictors of thrombo-embolic stroke.

285 lity of life and is associated with risk for embolic stroke.

286 iated with a substantially increased risk of embolic stroke/TIA.

287 s document provides the current views on (1) embolic/stroke risk, (2) ischemic/thrombotic cardiac ris

288 (NILT) improves behavioral outcome following embolic strokes in embolized rabbits and clinical rating

289 t improving behavioral performance following embolic strokes in rabbits.

290 Accordingly, we propose that embolic strokes of undetermined source are a therapeutic

291 l anticoagulants for secondary prevention of embolic strokes of undetermined source are warranted.

292 imvastatin-induced neuroprotection following embolic strokes, we used pharmacological intervention wi

293 l use appeared to be most pronounced for the embolic subtype.

294 ith improved safety profiles, and radiopaque embolics that are trackable in vivo.

295 PFO is a potential route for embolic transit from the systemic venous circulation to

296 Occlusive agents, referred to as embolics, vary in material characteristics including che

297 ncidence of AF-related stroke and peripheral embolic vascular events is uncertain.

298 he probability of positive DWI was higher in embolic versus nonembolic MVL (28 vs 8%, p = 0.04), in M

299 188 (9%) peripheral vascular (43 aortic, 53 embolic visceral or limb ischaemia, 92 critical limb isc

300 glycol) derivatives, in situ gelling liquid embolics with improved safety profiles, and radiopaque e