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 using the radiopaque drug-carrier and micro-embolic agent Lipiodol, which has been previously establ

4 ential to be a next-generation biofunctional embolic agent that can successfully treat a wide range o

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

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

7 physiology score (SAPS) II, anticoagulation, embolic agent, hematoma volume and location, serum hemog

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

9 7% of patients), risks decreased, and liquid embolic agents and flow diversion were associated with h

10 Embolic agents in clinical practice are limited by recan

11 A wide variety of embolic agents including metallic coils, calibrated micr

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

13 is a minimally invasive procedure that uses embolic agents to intentionally block diseased or injure

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

15 led to the development of novel preclinical embolic agents.

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

17 going cardiac catheterization face risks for embolic and bleeding events, yet information on strategi

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

19 microcatheter to administer 300- to 500-mum embolic beads.

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

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

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

23 Systemic evaluation for embolic causes was unrevealing in 2 patients, and 3 pati

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

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

26 ion syndrome, tumor burden, and drug-eluting embolic chemoembolization as predictors of protracted re

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

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

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

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

31 Ischemic/embolic complications and major bleeding remain importan

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

33 microorganism type, vegetation location, and embolic complications but not early or late mortality, d

34 Embolic complications during stenting of degenerated sap

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

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

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

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

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

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

41 Embolic debris traveling to the brain was captured in 75

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

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

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

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

46 The embolic efficacy of the shear-thinning ECM-based hydroge

47 only independent predictor of the composite embolic end point (hazard ratio, 3.99 [95% CI, 1.54-10.3

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

49 resulting from arterial recanalization or an embolic episode.

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

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

52 y and safety endpoints of stroke or systemic embolic event (SSEE) and major bleeding were assessed st

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

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

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

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

57 .67; 95% CI, 0.52-0.86), and stroke/systemic embolic event rates were similar for warfarin and dabiga

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

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

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

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

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

63 ation for cardiovascular indication, and new embolic event.

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

65 HA(2)DS(2)-VASc score for stroke or systemic embolic events (0.67 [95% CI, 0.65-0.70] versus 0.59 [95

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

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

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

69 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

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

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

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

73 rkers to estimate risk of stroke or systemic embolic events and bleeding, respectively, in patients w

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

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

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

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

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

79 Embolic events from vegetations are commonly accepted as

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

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

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

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

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

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

86 .3; 95% CI: 1.3 to 4.5; p = 0.03) and to new embolic events in PVE (HR: 7.5; 95% CI: 1.24 to 45.2; p

87 ch as pericardial sequelae, myocarditis, and embolic events is also addressed.

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

89 Potentially preventable embolic events outnumbered warfarin-related intracerebra

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

91 Cerebral embolic events related to carotid and cardiac disease ha

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

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

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

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

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

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

98 Embolic events were less common with anticoagulation pro

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

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

101 No delayed ischemic or embolic events were reported.

102 ctive of major cardiac events in PVE and new embolic events within the first year following IE.

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

104 ated with higher rates of stroke or systemic embolic events, and elevated hsTnT and GDF-15 were indep

105 Alterations of brain perfusion from embolic events, bleeding, and rhythm-related hypoperfusi

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

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

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

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

110 -cause mortality, unplanned cardiac surgery, embolic events, or relapse of bacteremia with the primar

111 were the independent predictors of definite embolic events.

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

113 tinal arteriolar macroaneurysm formation and embolic events.

114 es, whereas low-grade HAT was not related to embolic events.

115 ical clots and anticoagulation did not incur embolic events.

116 ed the long-term incidence of a composite of embolic events: stroke, transient ischemic attack, or ex

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

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

119 Embolic infarcts were defined as new foci of reduced dif

120 51 consecutive ischemic stroke patients with embolic large vessel occlusion of the anterior circulati

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

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

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

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

125 performed to identify factors predictive for embolic lesions.

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

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

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

129 Here, a novel blood-derived embolic material (BEM) with regenerative properties, tha

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

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

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

133 ant biodegradation such that only 25% of the embolic material remains at 14 days.

134 Limitations and challenges in embolic materials are also discussed to promote advancem

135 The BEM has significant advantages over embolic materials used today, making it a promising new

136 ess differences in infarction with different embolic materials.

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

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

139 Embolic microspheres that have the ability to release a

140 PAE was performed with 100-500-mum embolic microspheres.

141 ic fundus was performed using 300- to 500-um embolic microspheres.

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

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

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

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

146 ly transcranial Doppler ultrasonography with embolic monitoring.

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

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

149 Embolic occlusion of the pulmonary arterial system is re

150 Embolic occlusions may also alter local hemodynamic pres

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

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

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

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

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

156 dictive for cerebral ischemic lesions during embolic protected CAS.

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

158 events in patients with or without cerebral embolic protection (CEP) during transcatheter aortic val

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

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

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

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

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

164 istics and clinical outcomes associated with embolic protection device use during contemporary saphen

165 d procedural characteristics associated with embolic protection device use were assessed, as well as

166 1.9% (n = 461) and rate of failure to use an embolic protection device was 4.8% (n = 1173).

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

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

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

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

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

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

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

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

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

176 Guidelines recommend use of embolic protection devices during percutaneous coronary

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

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

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

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

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

182 and Drug Administration-approved stents and embolic protection devices were represented.

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

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

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

186 Embolic protection during carotid artery stenting reduce

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

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

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

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

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

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

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

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

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

196 F (Watchman Left Atrial Appendage System for Embolic PROTECTion in Patients With Atrial Fibrillation)

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

198 is significant site variation in the use of embolic protection independent of patient characteristic

199 Use of embolic protection is decreasing with time and occurs in

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

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

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

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

204 Use of embolic protection was associated with reduced risk of u

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

206 dentified 7266 vein graft interventions, and embolic protection was used in 37.9% of cases, with a si

207 Using proximal embolic protection whenever possible during treatment of

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

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

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

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

212 ficant institutional variation in the use of embolic protection, with a 15.50 (95% credible interval,

213 cutive patients undergoing CAS with cerebral embolic protection.

214 oduced outcomes similar to those with distal embolic protection.

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

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

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

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

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

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

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

222 Two thoracic radiologists assessed embolic severity using the Mastora system and evaluated

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

240 20-microm embolic particles injected at each embolic stage.

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

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

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

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

245 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

246 8 or more emboli per hour was predictive of embolic stroke (P = 0.0076).

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

248 In embolic stroke animals, positron emission tomographic-co

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

250 Following embolic stroke in male C57bl/6 mice, thrombolysis using

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

252 Embolic stroke is the most devastating consequence of at

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

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

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

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

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

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

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

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

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

262 The term embolic stroke of undetermined source (ESUS) was introdu

263 e, for the treatment of patients with recent embolic stroke of undetermined source and indirect evide

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

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

266 of Systemic Embolism in Patients With Recent Embolic Stroke of Undetermined Source) and the RE-SPECT

267 Secondary Stroke Prevention in Patients With Embolic Stroke of Undetermined Source).

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

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

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

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

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

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

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

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

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

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

278 Following embolic stroke, pharmacological thrombolysis limited inf

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

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

281 ) to control atrial fibrillation and prevent embolic stroke.

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

283 they require tPA administration following an embolic stroke.

284 tly involved in vascular damage following an 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 Accordingly, we propose that embolic strokes of undetermined source are a therapeutic

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

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

292 ation with ship strikes and with gas and fat embolic syndrome.

293 large tumor burden (P = .004), drug-eluting embolic TACE (P = .03), doxorubicin dose (P = .003), his

294 story of PES, tumor burden, and drug-eluting embolic TACE were identified as the strongest predictors

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

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

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

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

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

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