ライフサイエンスコーパス: stenosis

1 ultilevel, or rest group with no significant stenosis).

2 nificant coronary artery disease (CAD; >=50% stenosis).

3 media thickness, carotid plaque, and carotid stenosis.

4 risk patients with symptomatic severe aortic stenosis.

5 ic valve area in patients with severe aortic stenosis.

6 ase is common in patients with severe aortic stenosis.

7 or patients with cirrhosis and severe aortic stenosis.

8 th increased cardiovascular risks, including stenosis.

9 Scans were visually interpreted for coronary stenosis.

10 s with chronic heart failure (HF) and aortic stenosis.

11 ity of CT-FFR in patients with severe aortic stenosis.

12 sociated with increased risk of aortic valve stenosis.

13 particularly in regard to functional mitral stenosis.

14 onic, n=4103) for treatment of native aortic stenosis.

15 or occlusion, arterial disease, and central stenosis.

16 to SAH due to an aneurysm, improving CTT and stenosis.

17 een validated in patients with severe aortic stenosis.

18 s II or higher, and had severe native aortic stenosis.

19 einterventions for concomitant valvar aortic stenosis.

20 t valves in the treatment of bicuspid aortic stenosis.

21 treatment of symptomatic severe aortic valve stenosis.

22 99% symptomatic or asymptomatic intracranial stenosis.

23 intestinal atresia, and recurrent intestinal stenosis.

24 uld predict outcomes in patients with aortic stenosis.

25 and feasible in patients with severe aortic stenosis.

26 values, and carotid stenosis as 50% or more stenosis.

27 within 6 months for detecting central venous stenosis.

28 media thickness, carotid plaque, and carotid stenosis.

29 s in comparison with those with tricuspid AV stenosis.

30 emia, hypertensive heart disease, and aortic stenosis.

31 rence of stroke independent of the degree of stenosis.

32 ectomy for severe symptomatic carotid artery stenosis.

33 t of the severity of the underlying coronary stenosis.

34 risks for intracranial than for extracranial stenosis.

35 bleeding, filter migration, CCA thrombus, or stenosis.

36 ence of CAD was 27.8% defined by a >=70% QCA stenosis.

37 associated with a risk of functional mitral stenosis.

38 chemic symptoms in participants with carotid stenosis.

39 rtery calcium score, or coronary artery area stenosis.

40 the treatment of patients with central vein stenosis.

41 t variables and the degree of improvement in stenosis.

42 factor for cardiovascular disease and aortic stenosis.

43 for IC is not determined by the location of stenosis.

44 , and best medical treatment of intracranial stenosis.

45 ase severity even in patients with HG aortic stenosis.

46 , color flow gain (0%-100%), and flow past a stenosis.

47 atients with 50-99% symptomatic intracranial stenosis, 14 (14.9%) had recurrent strokes (12 ischaemic

48 000 vs 150 mum) and contraction angle of the stenosis (15 degrees vs 80 degrees ).

49 n only in participants with greater than 70% stenosis (16 of 28 patients; P < .001) and were associat

50 ho underwent TCAR and CEA for carotid artery stenosis (2016- 2019) were included.

51 ications were pulmonary insufficiency (28%), stenosis (23%), and mixed (49%).

52 on between history of symptoms and degree of stenosis (27 patients with >=70% stenosis and 17 patient

53 h at least 1 intermediate stenosis (diameter stenosis, 30%-70%) was treated or deferred according to

54 noted as bronchiectasis (77%) and bronchial stenosis (4%) but none with broncholithiasis.

55 ilter (A 0%, B 31%, C 69%), and renal artery stenosis (A 0%, B 67%, C 33%).

56 d cardiac abnormalities, such as mild aortic stenosis; a similar proportion consider these candidates

57 Bicuspid aortic stenosis accounts for almost 50% of patients undergoing

58 ss, as present in patients with aortic valve stenosis, activates multiple monocyte functions, and we

59 associated stroke risk of 50-99% and 70-99% stenosis (adjusted for age and vascular risk factors) du

60 chaemic stroke compared with no intracranial stenosis (adjusted hazard ratio 1.43, 95% CI 1.04-1.96),

61 ronary ostium might create artificial ostial stenosis, affecting the hyperemic flow.

62 l efficacy were improvement in the degree of stenosis after endovascular treatment and improvement or

63 ings in low-risk patients with severe aortic stenosis after surgical aortic valve replacement (SAVR)

64 0.63 (95% CI 0.27-1.46) and for intracranial stenosis alone it was 1.06 (0.46-2.42; p(interaction)=0.

65 For extracranial stenosis alone the HR was 0.63 (95% CI 0.27-1.46) and fo

66 hesis that gradual formation of mild carotid stenosis along the life course leads to progressive dama

67 Myocardial tissue from patients with aortic stenosis also showed evidence of UPR(mt) activation, whi

68 o assess the physiological significance of a stenosis, analogous to diagnostic threshold for FFR.

69 d degree of stenosis (27 patients with >=70% stenosis and 17 patients with <70%; P = .54), IPH (12 pa

70 carotid artery dilatation, terminal segment stenosis and absent basal collaterals.

71 illance, and whether or not they have severe stenosis and are candidates for surgery, can depend on w

72 ired in 30 subjects (15 patients with aortic stenosis and associated secondary hypertrophic cardiomyo

73 typically cause haemodynamically significant stenosis and can mimic arterial dissection, non-calcifie

74 reatest value for combined quantification of stenosis and characterization of atherosclerosis in rela

75 her or not a person is said to have moderate stenosis and enters surveillance, and whether or not the

76 stical analysis showed that echolucent, high-stenosis and high-risk plaques exhibited higher phase sh

77 e replacement in patients with severe aortic stenosis and intermediate surgical risk.

78 also included percentages of artery luminal stenosis and interstitial fibrosis/tubular atrophy (IF/T

79 ts across 12 centers with symptomatic aortic stenosis and large aortic annuli underwent transcatheter

80 randomized 1000 patients with severe aortic stenosis and low surgical risk to undergo either transfe

81 In patients with severe aortic stenosis and low surgical risk, TAVR with the SAPIEN 3 v

82 tients (544 women [37%]), with severe aortic stenosis and preserved left ventricular ejection fractio

83 ted with causal risk ratios for aortic valve stenosis and replacement, respectively, of 1.52 (95% CI:

84 associated with higher risk of aortic valve stenosis and replacement.

85 ausally associated with risk of aortic valve stenosis and replacement.

86 ate metabolism can lead to prenatal aqueduct stenosis and resultant hydrocephalus.

87 e-specific prevalence of 50-99% intracranial stenosis and the associated stroke risk of 50-99% and 70

88 owering Lp(a) will reduce progression aortic stenosis and the need for aortic valve replacement.

89 and the coronary microcirculation in aortic stenosis and their impact on myocardial remodeling, aort

90 ogs were performed with and without coronary stenosis and validated with simultaneously acquired nitr

91 (stent expansion with <20% in-stent residual stenosis) and safety outcomes (procedural complications,

92 ial fibrosis/tubular atrophy, artery luminal stenosis, and arteriolar hyalinosis to measure nephroscl

93 prostate cancer, androgenic alopecia, spinal stenosis, and hypertension; and context-dependent effect

94 ng of a CTO may overestimate the severity of stenosis, and that after revascularization of a CTO, the

95 atients with symptomatic severe aortic valve stenosis; and antiplatelet agents vorapaxar and prasugre

96 vascular features such as aplastic arteries, stenosis, aneurysms, and vessel caliper for endovascular

97 They were grouped according to level of stenosis (aortoiliac, femoropopliteal, multilevel, or re

98 ranscatheter heart valves in bicuspid aortic stenosis are lacking.

99 Causal risk factors for aortic valve stenosis are poorly understood, limiting the possibility

100 rongly with the severity of luminal coronary stenosis (area stenosis, r=0.83; P<0.001).

101 large enough lesions without the risk of PV stenosis, artery, nerve, or esophageal damage.

102 d intima-media thickness values, and carotid stenosis as 50% or more stenosis.

103 Older patients with severe aortic stenosis (AS) are increasingly identified as having card

104 In patients with severe aortic stenosis (AS) at intermediate surgical risk, treatment w

105 In patients with severe aortic stenosis (AS) at low surgical risk, treatment with trans

106 uces a study on the classification of aortic stenosis (AS) based on cardio-mechanical signals collect

107 Aortic stenosis (AS) contributes to cardiovascular mortality an

108 The management of patients with aortic stenosis (AS) crucially depends on accurate diagnosis.

109 atients with low-gradient (LG) severe aortic stenosis (AS) despite preserved left ventricular ejectio

110 esting poor survival in patients with aortic stenosis (AS) who do not undergo treatment are largely c

111 ound Paradoxical low-flow (LF) severe aortic stenosis (AS) with preserved left ventricular ejection f

112 Valve morphology, aortic stenosis (AS), and aortic insufficiency (AI) have been p

113 ed outcome predictor in patients with aortic stenosis (AS), but the prognostic impact of right ventri

114 benefit in high-gradient (HG) severe aortic stenosis (AS), the results in low-gradient (LG, mean gra

115 risk stratification in patients with aortic stenosis (AS).

116 ement (SAVR) for patients with severe aortic stenosis (AS).

117 d changes in the definition of severe aortic stenosis (AS).

118 s a defining characteristic of severe aortic stenosis (AS).

119 f cardiac magnetic resonance (CMR) in aortic stenosis (AS).

120 use of TAVI in severe bicuspid aortic valve stenosis, asymptomatic severe aortic stenosis, moderate

121 isk patients with severe, symptomatic aortic stenosis at 57 centers.

122 at warranted the diagnosis of severe carotid stenosis at centers in the 5th percentile, but not in th

123 I in patients with symptomatic severe aortic stenosis at low operative risk have set the stage for a

124 Our cohort consisted of patients with aortic stenosis at low surgical risk with a mean age of 73.4+/-

125 The agreement between CT FFR (<= 0.80) and stenosis at triple-rule-out CT angiography (>= 50%), as

126 Aortic valve stenosis (AVS), which is the most common valvular heart

127 c valve regurgitation (AVR) and aortic valve stenosis (AVS).

128 re we used a bilateral common carotid artery stenosis (BCAS) mouse model of VaD to investigate its ef

129 SAVR), or conservative management for aortic stenosis between 2015 and 2017, using overlap propensity

130 tigated the effects of varying the degree of stenosis, blood flow rate, and viscosity on two diagnost

131 ssess physiological significance of coronary stenosis, but requires an invasive procedure.

132 y of flurpiridaz PET (for detection of >=50% stenosis by ICA) was 71.9% (95% confidence interval [CI]

133 onary artery disease (CAD), defined as >=50% stenosis by quantitative invasive coronary angiography (

134 sions were categorized as obstructive (>=70% stenosis by visual angiographic assessment) or nonobstru

135 reason and received the diagnosis of carotid stenosis, carotid dissection, and extra or intracranial

136 ggest that approximately one-third of aortic stenosis cases are associated with highly elevated lipop

137 patients had a UOC (most frequently ureteral stenosis) close to biopsy.

138 easure of AVA in patients with severe aortic stenosis compared to AVA(Fick) measured using a modified

139 PFA significantly reduced risk of PV stenosis compared with IRF postprocedure in a canine mod

140 in particular for concomitant valvar aortic stenosis compared with patients with WBS.

141 Although symptomatic intracranial stenosis conveyed an increased risk of ischaemic stroke

142 Heart Valve in Low-Risk Patients With Aortic Stenosis) CT substudy randomized 435 patients with low-s

143 rotid endarterectomy for symptomatic carotid stenosis decreased over an 8-year period, independent of

144 9 and 0.90 for echogenicity, symptomaticity, stenosis degree and plaque risk, respectively.

145 ostic metrics - pressure gradient across the stenosis (DeltaP) and wall shear stress (WSS) - by perfo

146 Outcomes of TAVR in bicuspid aortic stenosis depend on valve morphology.

147 or patients with bicuspid aortic valve (BAV) stenosis despite the exclusion of bicuspid anatomy in al

148 ect the defect while 30% have no appreciable stenosis, despite sharing the same basic genetic lesion.

149 osis >=50%, in which at least 1 intermediate stenosis (diameter stenosis, 30%-70%) was treated or def

150 Individuals with carotid stenosis enter surveillance or are considered for surger

151 yperaemic coronary pressure measurements for stenosis evaluation, the current evidence base for the a

152 We found that mild carotid stenosis, even in a unilateral occlusion, creates behavi

153 sis of intra-abdominal complications such as stenosis, fistulas, and abscesses.

154 terials and MethodsParticipants with carotid stenosis from two ongoing prospective studies who underw

155 ntermediate-risk patients with severe aortic stenosis given transcatheter aortic valve replacement (T

156 (CTA) may be used to exclude coronary artery stenosis >=50% in patients with NSTEACS.

157 A coronary stenosis >=50% was found by coronary CTA in 68.9% and by

158 st 2-vessel disease defined as with diameter stenosis >=50%, in which at least 1 intermediate stenosi

159 scularization in the 2,479 patients with QCA stenosis >=60% (2.5%/year vs. 4.2%/year; hazard ratio [H

160 ary outcome was reduced in patients with QCA stenosis >=60% (2.9%/year vs. 6.9%/year; HR: 0.43; 95% C

161 s, the treatment effect in patients with QCA stenosis >=60% versus <60% on the first coprimary outcom

162 of coronary CTA to rule out coronary artery stenosis (>=50% stenosis) in the entire population, expr

163 rosclerotic disease burden or if presence of stenosis has independent predictive value.

164 stroke impact of asymptomatic carotid artery stenosis has proved difficult over the last decade.

165 disease on hemodialysis (ESRD-HD) and aortic stenosis have poor prognosis.

166 cs in patients with and without Renal Artery stenosis (HERA), NL40795.018.12 at the Dutch national tr

167 The indication for redo-TAVR was THV stenosis in 12 (16.2%) and 51 (37.0%) (p = 0.002) and re

168 orted all-cause adverse events were ureteric stenosis in 31 (44%) of 71 patients, urinary tract infec

169 s, and prognosis of symptomatic intracranial stenosis in a population-based cohort of patients with t

170 invasive coronary angiography revealed <50% stenosis in all major arteries, multivessel OCT was perf

171 tive invasive angiography, with at least 50% stenosis in at least 1 coronary artery considered signif

172 atic severe aortic stenosis, moderate aortic stenosis in combination with heart failure with reduced

173 utcomes of TAVR in patients with bicuspid AV stenosis in comparison with those with tricuspid AV sten

174 threshold for detecting CAD was a >=67% QCA stenosis in GadaCAD1 and >=63% QCA stenosis in GadaCAD2.

175 >=67% QCA stenosis in GadaCAD1 and >=63% QCA stenosis in GadaCAD2.

176 ecropsy showed expansive PFA lesions without stenosis in the proximal PV sites, compared with more co

177 subclavian vein dialysis catheter because of stenosis in the superior vena cava.

178 o underwent surgery for asymptomatic carotid stenosis in the Vascular Quality Initiative registry (n=

179 to rule out coronary artery stenosis (>=50% stenosis) in the entire population, expressed as the neg

180 media thickness, carotid plaque, and carotid stenosis increased consistently with age and was higher

181 revalence of symptomatic 50-99% intracranial stenosis increased from 29 (4.9%) of 596 at younger than

182 revalence of 50-99% symptomatic intracranial stenosis increases steeply with age in predominantly Cau

183 etermine whether FAV for midgestation aortic stenosis increases survival from fetal diagnosis to age

184 of regions of recirculatory flow distal to a stenosis, increasing mean blood residence time relative

185 Pulmonary vein (PV) stenosis is a highly morbid condition that can result af

186 Coronary artery stenosis is a narrowing of coronary lumen space caused b

187 Whether aortic valve stenosis is accelerated by inflammation and whether it i

188 Aortic valve stenosis is an increasingly prevalent degenerative and i

189 Symptomatic vertebral artery stenosis is associated with a high risk of recurrent str

190 edical treatment of symptomatic intracranial stenosis is consistent with the two previous randomised

191 tage change of 58.97% from 2000; and carotid stenosis is estimated to be 1.5% (1.1-2.1), equivalent t

192 This occurs mostly when the stenosis is located in proximal and middle coronary segm

193 Aortic stenosis is the most common valvular heart disease in th

194 lung disease in the setting of severe aortic stenosis, likely representing a better alternative to co

195 hether DeltaFFR(eng)-FFR(dis) related to the stenosis location, that is, proximal and middle versus d

196 .79), but not in the 1,372 patients with QCA stenosis <60% (3.0%/year vs. 2.9%/year; HR: 1.04; 95% CI

197 ) to a greater extent than patients with QCA stenosis <60% (3.3%/year vs. 5.2%/year; HR: 0.65; 95% CI

198 and symptomatic patients with >=50% carotid stenosis, <=80 years of age, and at standard or high ris

199 ic and symptomatic participants with carotid stenosis.Materials and MethodsParticipants with carotid

200 Aortic stenosis may contribute to cardiorenal syndrome that imp

201 02 participants to 5 groups: moderate aortic stenosis (ModAS) (n=13), SevAS, left ventricular (LV) ej

202 increased dilatation rate were severe aortic stenosis, moderate and severe aortic regurgitation, and

203 c valve stenosis, asymptomatic severe aortic stenosis, moderate aortic stenosis in combination with h

204 In ESRD-HD patients with aortic stenosis, mortality was lower in the short-term with TAV

205 Prevalence of calcific mitral stenosis (MS) increases with age; however, its natural h

206 Significant residual mitral stenosis (MS) was defined as mean gradient >=10 mm Hg an

207 ations of obesity with incident aortic valve stenosis (n = 1,215) and replacement (n = 467) for a med

208 f the coronary artery anatomy to demonstrate stenosis (noninvasively with cardiac CT).

209 ents with an angiographically nonobstructive stenosis not intended for PCI but with IVUS plaque burde

210 ute ischemic stroke with ipsilateral carotid stenosis of >=50% underwent FDG-positron-emission tomogr

211 for coronary revascularization and MACE than stenosis of 50% and greater at triple-rule-out CT angiog

212 In humans, carotid stenosis of 70% and above might be the cause of clinical

213 ts with ischemic stroke with atherosclerotic stenosis of cerebral vasculature.

214 The median angiographic diameter stenosis of the randomized lesions was 41.6%; by near-in

215 megaly in Gldc-deficient mice is preceded by stenosis of the Sylvian aqueduct and malformation or abs

216 rm complications of GCA include aneurysm and stenosis of vessels, even in patients with apparently cl

217 Patients with isolated mitral stenosis often benefit from percutaneous balloon mitral

218 Coronary artery disease and aortic stenosis often coexist.

219 n stress cardiac MRI or significant coronary stenosis on coronary CTA were referred for conventional

220 udy aimed to assess the impact of aortoiliac stenosis on graft and patient survival.

221 ly intermediate disease (40% to 69% diameter stenosis on visual inspection).

222 dial infarction without significant coronary stenosis or atherosclerosis in patients with MPNs sugges

223 mic cholangiopathy (IC), vascular thrombosis/stenosis or graft, and patient survival was seen between

224 12 781), all with either symptomatic carotid stenosis or major acute stroke.

225 moderate agreement in their ability to grade stenosis or occlusion (kappa = 0.59).

226 sensitivity and specificity for detection of stenosis or occlusion was 99% and 98%, respectively.

227 dent readers evaluated vessels for diameter, stenosis or occlusion, arterial disease, and central ste

228 luated by three radiologists for presence of stenosis or occlusion.

229 icity for detection of thoracic central vein stenosis or occlusion.(C) RSNA, 2020See also the comment

230 tion without moderate or severe mitral valve stenosis or prosthetic mechanical heart valves, treatmen

231 % CI, 0.77-1.39]; P=0.810), and aortic valve stenosis (OR, 1.03 [95% CI, 0.56-1.90]; P=0.926).

232 mplications on lifetime management of aortic stenosis, particularly in younger patients.

233 Plaque burden, not stenosis per se, is the main predictor of risk for CVD e

234 In dogs with coronary stenosis, perfusion anomalies were detected on the basis

235 nd MRI scans were analyzed for the degree of stenosis, plaque surface structure, presence of intrapla

236 The degree of stenosis, plaque ulceration, and intraplaque hemorrhage

237 ected tetralogy of Fallot (TOF) or pulmonary stenosis (PS) referred for pulmonary valve replacement (

238 severity of luminal coronary stenosis (area stenosis, r=0.83; P<0.001).

239 olic velocity threshold for moderate (>=50%) stenosis ranged from 110 to 245 cm/s (median, 125; 5th a

240 d 150), and the threshold for severe (>=70%) stenosis ranged from 175 to 340 cm/s (median, 230; 5th a

241 cores, presence of coronary stents, coronary stenosis, REACH and SMART scores, the Duke coronary arte

242 e for the treatment of bicuspid aortic valve stenosis) registry included 353 consecutive patients who

243 %) (p = 0.002) and regurgitation or combined stenosis-regurgitation in 62 (83.8%) and 86 (62.3%) (p =

244 cts with a medical diagnosis of aortic valve stenosis (remaining n=308 683 individuals), phenome-wide

245 idney function stage in patients with aortic stenosis remains poorly understood.

246 pulsed field ablation (PFA) would reduce PV stenosis risk and collateral injury compared with irriga

247 For detection of a 50% QCA stenosis, sensitivity was 64.6% and specificity was 86.6

248 ge artery stroke (LAS) and NASCET 50% to 69% stenosis served as an additional comparison group.

249 some but not all patients with severe aortic stenosis (SevAS) develop otherwise unexplained reduced s

250 to determine the effect of nonculprit-lesion stenosis severity measured by quantitative coronary angi

251 utcomes to a greater extent in patients with stenosis severity of >=60% compared with <60%, as determ

252 zed in the COMPLETE trial, nonculprit lesion stenosis severity was measured using QCA in the angiogra

253 ary artery calcium score, or coronary artery stenosis severity.

254 dictors for myocardial infarction, including stenosis severity.

255 no cardiac damage associated with the valve stenosis (Stage 0), left ventricular damage (Stage 1), l

256 IT) did not show superiority of intracranial stenosis stenting over intensive medical management alon

257 Supravalvular aortic stenosis (SVAS) is a narrowing of the aorta caused by el

258 in ELN cause nonsyndromic supravalvar aortic stenosis (SVAS).

259 In patients with symptomatic severe aortic stenosis, TAVI has now been explored across the entire s

260 intracranial stenosis than for extracranial stenosis (ten (16%) of 64 patients vs one (1%) of 121 pa

261 atients with 70-99% symptomatic intracranial stenosis tended to be less than those reported in the no

262 stroke or death was higher for intracranial stenosis than for extracranial stenosis (ten (16%) of 64

263 ess echocardiography abnormality caused by a stenosis, the greater the reduction in symptoms from PCI

264 For detection of a >=70% QCA stenosis, the sensitivity of CMR was 78.9%, specificity

265 y prevent progression of midgestation aortic stenosis to hypoplastic left heart syndrome.

266 t used to assess the potential of a coronary stenosis to induce myocardial ischemia and guide decisio

267 would assign a diagnosis of moderate carotid stenosis to twice as many individuals as the 95th percen

268 lled patients with symptomatic severe aortic stenosis to undergo TAVR using a commercially available

269 d 435 patients with low-surgical-risk aortic stenosis to undergo transcatheter aortic valve replaceme

270 (Bicuspid Aortic Valve Stenosis Transcatheter Aortic Valve Replacement Registry

271 n the diagnostics of transplant renal artery stenosis (TRAS).

272 tive registry of patients with severe aortic stenosis treated with the commercially available SAPIEN

273 on mortality in patients with severe aortic stenosis undergoing surgical aortic valve replacement (A

274 In patients with severe aortic stenosis undergoing TAVR, even with baseline impaired eG

275 on (DD) and outcomes in patients with aortic stenosis undergoing transcatheter aortic valve replaceme

276 randomized trial of 447 patients with aortic stenosis undergoing transfemoral transcatheter aortic va

277 Among patients with aortic stenosis undergoing transfemoral transcatheter aortic va

278 ng in the treatment of unprotected left main stenosis: updated 5-year outcomes from the randomised, n

279 sively detecting atherosclerotic plaques and stenosis using NETs may lay a groundwork for future clin

280 In aortic stenosis, valvulo-arterial impedance (Zva) estimates the

281 The diagnostic threshold for carotid stenosis varies considerably.

282 d sex-adjusted hazard ratio for aortic valve stenosis was 1.3 (95% confidence interval [CI]: 1.0 to 1

283 The mean improvement in the degree of stenosis was 18%+/-11.65% in the ICA, 30.67%+/-18.45% in

284 osis of hemodynamically significant coronary stenosis was 98% and 96% respectively, compared with FFR

285 Symptomatic intracranial stenosis was perceived to convey a high risk of recurren

286 Patients with bicuspid aortic valve (AV) stenosis were excluded from the pivotal evaluations of t

287 Patients without aortoiliac stenosis were functioning as controls.

288 A total of 8107 ESRD-HD patients with aortic stenosis were included, 4130 (50%) underwent TAVR, 2565

289 risk patients with severe symptomatic aortic stenosis were recruited from 52 medical centres experien

290 Patients had severe aortic stenosis, were treated with TAVR or SAVR, and were analy

291 ating its use in most patients with coronary stenosis who are eligible for coronary intervention, the

292 nsecutive patients with cirrhosis and aortic stenosis who underwent TAVR (n = 55) or SAVR (n = 50) be

293 Among patients with aortic stenosis who were at intermediate surgical risk, there w

294 In patients with severe aortic stenosis who were at low surgical risk, TAVR with a self

295 nd-stage lung disease and significant aortic stenosis who were successfully bridged to lung transplan

296 5% CI 0.96 to 2.10) and ipsilateral arterial stenosis with 50%-99% narrowing (HR 1.54, 95% CI 0.98 to

297 tional Flow Reserve in Intermediate Coronary Stenosis With Guiding Catheter Disengagement) registry,

298 ed 240 patients with single de novo coronary stenosis with reference vessel diameter 2.5 to 3.5 mm di

299 Among urgent CS patients (left main stenosis with unstable angina, acute endocarditis, valvu

300 o accurately assess the severity of coronary stenosis without resorting to invasive techniques.