ライフサイエンスコーパス: stenotic

1 in acute myocardial infarction are severely stenotic.

2 c strain identifies which coronary artery is stenotic.

3 us UEI normalized strain also differentiated stenotic (-0.87) versus adjacent normal small bowel (-1.

4 1) to treatment strategy based on FFR in all stenotic ( 50%) coronary arteries or to a traditional st

5 Fifteen vessels were severely stenotic and 13 were completely occluded.

6 Luminal diameters of stenotic and adjacent vessel segments before and after a

7 functional repertoire of T cells differs in stenotic and aneurysmal lesions, and provide a novel fra

8 sham surgery (n = 5) was performed, and the stenotic and contralateral kidneys were studied longitud

9 s similarly detected the differences between stenotic and contralateral kidneys.

10 In-vivo evaluation included CCTA stenotic and non-stenotic plaques from 41 asymptomatic s

11 ulture, and to study the differences between stenotic and nonstenosed stents.

12 Stenotic and nonstenotic contralateral kidneys were comp

13 CD were studied with UEI and their resected stenotic and normal bowel segments were evaluated by ex

14 The myocardial enhancement ratio between stenotic and normally perfused territories was determine

15 to describe the natural history of combined stenotic and regurgitant aortic valve disease.

16 tinely used clinically to assess severity of stenotic and regurgitant valves.

17 s resection specimens were obtained from non-stenotic and stenotic tissue areas of 15 CD patients.

18 ment (AVR) when the aortic valve is severely stenotic and the patient is symptomatic; however, a subs

19 th fusion of the right-left coronary cusp (6 stenotic) and 3 with fusion of the right and noncoronary

20 disease, high-risk plaques (not necessarily stenotic), and overall burden of the disease.

21 rotid plaques were studied in proximal, most stenotic, and distal regions along the longitudinal bloo

22 ause infarction are not necessarily severely stenotic, and stenotic lesions are not necessarily unsta

23 modynamic changes may occur in patients with stenotic, aneurysmal, dissection of the carotid artery a

24 Last, we stained for monocytes in explanted stenotic aortic human valves.

25 Small differences in function between stenotic aortic mechanical prostheses, undetectable by c

26 oded CMR as a routine method for quantifying stenotic aortic valve area, to compare this method with

27 y tested the hypothesis that the impact of a stenotic aortic valve depends not only on the cross-sect

28 as used to reconstruct a typical spectrum of stenotic aortic valve geometrics from doming to flat.

29 elated Cc (= continuity/planimeter areas) to stenotic aortic valve shape in 35 patients with high-qua

30 (REpositionable Percutaneous Replacement of Stenotic Aortic Valve Through Implantation of Lotus Valv

31 carotid endarterectomy specimens (n=16) and stenotic aortic valves (n=18).

32 Operatively excised stenotic aortic valves (with or without associated aorti

33 s of oxidative stress differ greatly between stenotic aortic valves and atherosclerotic arteries.

34 oxidative stress is increased in calcified, stenotic aortic valves and to examine mechanisms that mi

35 ular peak systolic pressure gradients across stenotic aortic valves correlate better with the weights

36 Excised human stenotic aortic valves display mCRP deposition.

37 Whereas AVIC from stenotic aortic valves exhibit an augmented response to

38 We examined operatively excised, stenotic aortic valves from 932 patients aged 26 to 91 y

39 stress is increased in calcified regions of stenotic aortic valves from humans.

40 We weighed operatively excised stenotic aortic valves in 324 adults who had undergone p

41 As the weights of the operatively excised stenotic aortic valves increased (from <1 g to >6 g), th

42 ting cells, monocytes, while passing through stenotic aortic valves result in proinflammatory effects

43 hearts not suitable for transplantation and stenotic aortic valves that were removed during surgical

44 correlate the weights of operatively excised stenotic aortic valves to preoperative transvalvular pea

45 us publication has correlated the weights of stenotic aortic valves to the transvalvular gradients or

46 Higher expression of Lp-PLA2 in stenotic aortic valves was confirmed by quantitative pol

47 found that n-3 PUFA incorporation into human stenotic aortic valves was higher in noncalcified region

48 s a reliable, user-friendly tool to evaluate stenotic aortic valves.

49 e interstitial cells and is downregulated in stenotic aortic valves.

50 nalyze the intrabeat dynamic behavior of the stenotic-aortic valve and compare these measurements wit

51 on catheter selected was advanced across the stenotic area and the IVUS wire advanced in the guide lu

52 The stenotic area measured by PET was 16% smaller than that

53 f hyperemic myocardial blood flow (MBF) in a stenotic area to hyperemic MBF in a normal perfused area

54 on after stenting was equally effective; the stenotic area was reduced (21% versus 65%, P<0.001).

55 At 29 Gy, the histological stenotic area was reduced by 67% (22% versus 66% in cont

56 Flow velocity at anastomoses and suspected stenotic areas was measured.

57 ation that transition from dilated to normal/stenotic arterial calibre coincides with where the inter

58 of carotid wall composition both in the non-stenotic arterial wall and in severely stenotic plaques.

59 ardial blood flow in territories supplied by stenotic arteries (1.01+/-0.35 to 0.76+/-0.27 mL.min(-1)

60 uded arteries (77%, 36 of 47) and patent but stenotic arteries (84%, 104 of 124).

61 Implantation of expandable stents into stenotic arteries after percutaneous coronary interventi

62 oth muscle cells and macrophage abundance in stenotic arteries and abrogates carotid neointima format

63 o FFR-guided PCI had FFR measurements of all stenotic arteries and PCI was done only if FFR was 0.80

64 thoracic aortic dissections to thrombosis in stenotic arteries following plaque rupture, where local

65 of medial SMC hyperplasia and disarray, and stenotic arteries in the vasa vasorum due to medial SMC

66 nal function and maximal perfusion distal to stenotic arteries when administered before the developme

67 At high shear stresses such as are found in stenotic arteries, both steps are mediated by von Willeb

68 r stress, which resembles flow conditions in stenotic arteries, induces significantly more platelet a

69 closely in vivo conditions such as those in stenotic arteries.

70 rams; dephasing was considered severe if the stenotic artery appeared occluded on phase-contrast angi

71 of subsequent stroke in the territory of the stenotic artery is greatest with stenosis > or =70%, aft

72 tio of maximal coronary blood flow through a stenotic artery to the blood flow in the hypothetical ca

73 Risk of stroke in the territory of the stenotic artery was highest with severe stenosis > or =7

74 hest risk for stroke in the territory of the stenotic artery who would be the target group for a subs

75 e in coronary blood flow (CBF) distal to the stenotic artery, resulting in functional improvement of

76 , designed to mimic the flow conditions in a stenotic artery, showed enhanced platelet aggregation in

77 uent ischemic stroke in the territory of the stenotic artery.

78 f these strokes were in the territory of the stenotic artery.

79 d a significantly higher tissue stiffness in stenotic as compared to non-stenotic tissue sections (p

80 Shunts were occluded or severely stenotic at venography and necropsy in the remaining six

81 ly faintly detected in nondiseased tissue or stenotic atheroma.

82 ) cell responses in human AAAs compared with stenotic atheromas.

83 anastomotic collateral networks that augment stenotic bed flow reserve, but at the expense of the adj

84 Explanted, stenotic bicuspid aortic valves (BAVs) from pediatric pa

85 Furthermore, pediatric stenotic bicuspid aortic valves that have lost normal ex

86 platelet-mediated thrombosis in damaged and stenotic canine coronary arteries, due, in large part, t

87 anced vessel patency in remote, damaged, and stenotic carotid arteries, largely due to adenosine rece

88 een in association with TIPS stenoses in all stenotic cases and was not found in 24 of 26 (92%) cases

89 or greater at angiography in 25 of 32 (78%) stenotic cases and was not present in 71 of 72 (99%) cas

90 Intact DSA regularly elicited markedly stenotic CAV in recipients over 28 days.

91 ex vivo pro-fibrotic protein secretion from stenotic CD biopsies.

92 Seven consecutive patients with stenotic CD were studied with UEI and their resected ste

93 In stenotic chambers containing endothelial cells, flow pro

94 ementary in vitro studies using microfluidic stenotic chambers, designed to mimic the flow conditions

95 e elevated expression of fibrosis markers in stenotic compared to non-stenotic tissue (all p < 0.001)

96 assessed by DHM were significantly higher in stenotic compared to non-stenotic tissue areas (p < 0.00

97 me and blood flow were markedly lower in the stenotic compared with the contralateral kidney and cort

98 roximal to the terminal vessel in normal and stenotic coronary arteries (P<0.001).

99 Fifty-five patients with 67 stenotic coronary arteries underwent coronary angiograph

100 ove subsequent vessel patency in damaged and stenotic coronary arteries via release of adenosine from

101 Bypass of stenotic coronary arteries with autologous saphenous vei

102 w conditions comparable to those existing in stenotic coronary arteries.

103 osine, improve vessel patency in damaged and stenotic coronary arteries.

104 d flow, from a region supplied by a severely stenotic coronary artery to those supplied by less disea

105 ffective procedure to reduce the severity of stenotic coronary atherosclerotic disease, its long-term

106 can be characterized as having impaired post-stenotic coronary flow reserve < 2.0 and pressure-derive

107 ased and surgical treatment of significantly stenotic coronary lesions, the comprehensive and serial

108 nsatory enlargement commonly (54%) occurs at stenotic coronary lesions.

109 assessing the coronary circulation and post-stenotic coronary vasodilatory reserve in patients with

110 The measurement of post-stenotic coronary vasodilatory reserve, now possible in

111 derwent a second TAVR: 57 (33%) for a mainly stenotic degenerated TAV, 97 (56%) for a mainly regurgit

112 Clot size, stenotic degree, and other associated PE findings were e

113 ere risk factors for penetrating (B3) and/or stenotic disease (B2).

114 atins have little effect in well established stenotic disease with calcification, but their effects e

115 ectomy With Significant Extracranial Carotid Stenotic Disease).

116 involves enhanced, flow-mediated dilation of stenotic epicardial conduit vessels and may account at l

117 e 2 and solute carrier family 16 member 1 in stenotic fibroblasts.

118 n but only superficial erosion of a markedly stenotic, fibrotic plaque.

119 for accurately describing thrombus growth in stenotic flows.

120 The shortest stenotic fragment was 10 mm long and the longest occlude

121 t aggregate formation might be caused by the stenotic geometry.

122 nts with CMI underwent stent placement in 79 stenotic (>70%) mesenteric arteries.

123 nderwent revision of their nonthrombosed but stenotic HA were reviewed for patient/graft survival, me

124 matory and progrowth changes observed in the stenotic HC+RAS kidney, which might potentially facilita

125 tithrombotic efficacy at denuded or fissured stenotic high-risk lesions without systemic bleeding.

126 3CR1 and CD68 was significantly increased in stenotic human AVFs.

127 (MSCs) improves perfusion and oxygenation in stenotic human kidneys, but associated atherosclerosis a

128 Histograms showing the numbers of stenotic ICAs in subgroups and for vessels with stenoses

129 utflow obstruction in 29 percent (1610), and stenotic in 2 percent (92).

130 and inflammatory factors linked to improved stenotic kidney (STK) function after percutaneous transl

131 vascular disease (RVD) amplifies damage in a stenotic kidney by inducing pro-inflammatory mechanisms

132 Stenotic kidney cortical/medullary perfusion and RBF wer

133 usion, low-energy shockwave therapy improves stenotic kidney function, likely in part by mechanotrans

134 reduces renal blood flow (RBF) and amplifies stenotic kidney hypoxia.

135 Recovery of the stenotic kidney in RVD after ELP-VEGF therapy may be dri

136 Pigs then received a single stenotic kidney infusion of ELP-VEGF (100 mug/kg), a mat

137 high renal binding of ELP-VEGF 4 hours after stenotic kidney infusion.

138 nuated renovascular hypertension, normalized stenotic kidney microvascular density and oxygenation, s

139 n rate (GFR) were similarly decreased in the stenotic kidney of both RVD groups.

140 Stenotic kidney RBF rose (202+/-29-262+/-115 mL/min; P=0

141 remodeling, and improved IMV function in the stenotic kidney, independent of lipid lowering.

142 In the stenotic kidney, intratubular contrast content has decre

143 In the stenotic kidney, the hemodynamic impairment of the corte

144 Results In the stenotic kidney, the median magnetization transfer ratio

145 effects on the function and structure of the stenotic kidney.

146 icrovascular density, and oxygenation in the stenotic kidney.

147 sed BP, improved serum creatinine levels and stenotic-kidney cortical perfusion and oxygenation, and

148 fer, fractional kidney hypoxia was higher in stenotic kidneys compared with kidneys with EH (17.4% vs

149 To determine the application of imaging the stenotic lacrimal punctum with infrared photographs and

150 In the stenotic LAD zone, MBF did not change significantly.

151 served in the asynergic zone perfused by the stenotic LAD.

152 Human AVIC were isolated from normal and stenotic leaflets.

153 section of the two devices are different in stenotic length (1,000 vs 150 mum) and contraction angle

154 resorbable scaffold implantation in a simple stenotic lesion resulted in stable lumen dimensions and

155 om a stroke), probably culprit (not the most stenotic lesion upstream from a stroke), or nonculprit (

156 assified as either culprit (the only or most stenotic lesion upstream from a stroke), probably culpri

157 e requiring angioplasty of a progressive FMD stenotic lesion.

158 n of the total myocardium in jeopardy from a stenotic lesion.

159 significantly higher in nonstenotic than in stenotic lesions (1.3 +/- 0.2 vs. 1.0 +/- 0.2, p < 0.001

160 icantly different between nonstenotic versus stenotic lesions (20 +/- 8 mm(2), n = 23 vs. 22 +/- 8 mm

161 (OR, 1.32; 95% CI, 1.15-1.53; P < .001), and stenotic lesions (OR, 1.15; 95% CI, 1.01-1.31; P = .03).

162 gration, a key feature in the development of stenotic lesions after balloon injury.

163 n are not necessarily severely stenotic, and stenotic lesions are not necessarily unstable.

164 to standard angioplasty for the treatment of stenotic lesions in dysfunctional hemodialysis arteriove

165 We have shown that cells derived from stenotic lesions in infrainguinal vein grafts were signi

166 tion (PCI) should be considered for severely stenotic lesions in proximal coronaries that subtend a l

167 ss risk in patients with type 2 diabetes for stenotic lesions showed hazard ratios for aortic stenosi

168 Human vein graft-threatening stenotic lesions were identified by duplex scanning with

169 The location and severity of stenotic lesions were recorded.

170 n of the first balloon-expandable valves for stenotic lesions with implantation in the pulmonic posit

171 In five stenotic lesions, "negative remodeling" (Remodeling Inde

172 Notably, stenotic lesions, but not AAAs, contained mature forms o

173 ow often early arterial wall changes lead to stenotic lesions, use of these modalities in combination

174 type 1 and 2 diabetes have greater risk for stenotic lesions, whereas risk for valvular regurgitatio

175 IL-2 and IL-15, which are amply expressed in stenotic lesions.

176 une responses appear to predominate in human stenotic lesions.

177 lecules were correlated with the severity of stenotic lesions.

178 as sudden (abrupt appearance of a normal or stenotic low-resistance signal), stepwise (flow improvem

179 ater, and the intima/medial ratio as well as stenotic luminal area was more pronounced in apoE(-/-) m

180 The developed stenotic microfluidic chamber offers a realistic platfor

181 MSCs engrafted in stenotic mouse kidneys.

182 Of the 31 occluded (n = 8) and stenotic (n = 23) shunts, ultrasonography accurately pre

183 By imaging, defect magnitude (stenotic/normal) was greater for (201)Tl than MIBI (0.57

184 Stenotic/obstructed IFV and IVC may be reconstructed usi

185 fety and efficacy of stent reconstruction of stenotic/occluded iliofemoral veins (IFV) and inferior v

186 One or both ICAs were stenotic on all patient MR arteriograms.

187 and/or management of coronary calcification, stenotic or obstructive disease, high-risk plaques (not

188 Patients with congenital heart defects and stenotic or occluded IFV/IVC may encounter femoral venou

189 rresponding conventional venography, 73 were stenotic or occluded.

190 n staging, i.e., early atheroma versus later stenotic or occlusive atherothrombosis.

191 ervention is dependent on the anatomy of the stenotic or occlusive lesion; percutaneous interventions

192 se due to de novo superficial femoral artery stenotic or occlusive lesions were randomized to treatme

193 saturation, should not be misinterpreted as stenotic or occlusive vascular disease.

194 mineralization remains the leading cause of stenotic or regurgitant failure in native human and porc

195 Surgical treatment of stenotic or regurgitant valvular lesions can alter the n

196 ree-dimensional axisymmetric models of round stenotic orifices were created.

197 showed enhanced platelet aggregation in the stenotic outlet region at 60-80% channel occlusion over

198 d increased endothelial vWF secretion in the stenotic outlet region, contributing to exacerbated plat

199 ncreased platelet aggregate formation in the stenotic outlet region.

200 but not ECs, mitigated the hypermuscular and stenotic phenotype in the aorta of Eln-/- mice.

201 Because severely stenotic plaques are more likely to stimulate collateral

202 Even non-stenotic plaques can precipitate a sudden cerebrovascula

203 vo evaluation included CCTA stenotic and non-stenotic plaques from 41 asymptomatic subjects with 122

204 Vascular disease can manifest as stenotic plaques or ectatic aneurysms, although the mech

205 that 15 of the 17 cases analysed occurred on stenotic plaques with median 31% diameter stenosis (inte

206 ary events result from the rupture of mildly stenotic plaques, based on studies in which angiographic

207 oliferation identified in recurrent coronary stenotic plaques.

208 e non-stenotic arterial wall and in severely stenotic plaques.

209 oronary events arise from ruptures of mildly stenotic plaques.

210 f iFR was similar to resting Pd/Pa and trans-stenotic pressure gradient and significantly inferior to

211 , or according to the magnitude of the trans-stenotic pressure gradient.

212 lar function, number of diseased vessels, or stenotic proximal left anterior descending artery.

213 lar function, number of diseased vessels, or stenotic proximal left anterior descending artery.

214 Balloon dilation of the stenotic pulmonary veins was performed in these patients

215 alloons readily increase the diameter of the stenotic pylorus on average from 6 to 16 mm.

216 n rate (GFR) were decreased similarly in the stenotic RAS and HC+RAS kidneys, but tubular fluid reabs

217 Stenotic RBF was reduced compared with RBF of contralate

218 aximal adenosine stress, MR clearly depicted stenotic regions and showed regional signal differences

219 dominantly occurred in the proximal and most stenotic regions but not in the distal region.

220 ic examination showed that proximal and most stenotic regions exhibited features of plaque vulnerabil

221 que rupture, complex pulsatile flows through stenotic regions producing high wall shear stresses, and

222 Patients with MAC frequently have stenotic, regurgitant, or mixed valvular disease, and th

223 We assessed BP, urinary protein, stenotic renal blood flow, GFR, microvascular structure,

224 pe (WT) mouse (control) undergoes a dramatic stenotic response, which is nearly completely abolished

225 In human stenotic samples from AVFs, we demonstrated increased ge

226 Stents provide effective treatment for stenotic saphenous venous aorto-coronary bypass grafts,

227 to WB (p < 0.01), the device with a shorter stenotic section and steeper contraction angle showed a

228 The stenotic section of the two devices are different in ste

229 -1)) through two microfluidic systems with a stenotic section under constant pressure.

230 xperiments, the flow chamber occluded in the stenotic section.

231 Short-term lipid-lowering therapy increases stenotic segment maximal myocardial blood flow by approx

232 significantly higher than those in the post-stenotic segment of the diseased artery (1.8 +/- 0.6, p

233 Treatment methods included resection of the stenotic segment with primary reanastomosis (n = 17), ao

234 stimulate collateral circulation to the post-stenotic segment, plaque rupture and thrombosis at such

235 maging confirmed balloon location within the stenotic segment.

236 Out of 45 stenotic segments, 29 were single stenotic segments (16 intracranial and 13 extracranial)

237 al and 13 extracranial) and 16 were multiple stenotic segments (8 intracranial and 8 extracranial).

238 In the total number of stenotic segments (single and multiple), there were 24 (

239 largement or vessel constriction occurred in stenotic segments compared with the reference segments a

240 r significant stenosis and a total number of stenotic segments was 45.

241 Seven (18%) of 38 significantly stenotic segments were classified as having < 50% stenos

242 Out of 45 stenotic segments, 29 were single stenotic segments (16

243 only 9 (29%) of the 31 correctly classified stenotic segments, were severely calcified (area > 20 mm

244 Noninvasive assessment of functionally stenotic small-diameter aortic mechanical prostheses is

245 There was no difference between stenotic stents and nonstenosed stents with respect to c

246 However, smooth muscle cells (SMC) from stenotic stents demonstrated both greater cell prolifera

247 oliferative activity in tissues excised from stenotic stents has not been previously reported.

248 ant (accounting for 99% of the total drop in stenotic subjects).

249 enoses, new evidence suggests that opening a stenotic subsidiary branch may create unfavorable hemody

250 patient underwent balloon angioplasty of the stenotic SVC segment with resolution of her bleeding and

251 ive in diagnosing occluded and significantly stenotic tibial artery disease in these patients compare

252 tive in diagnosing occluded or significantly stenotic tibial artery disease.

253 fibrosis markers in stenotic compared to non-stenotic tissue (all p < 0.001).

254 ificantly higher in stenotic compared to non-stenotic tissue areas (p < 0.001).

255 pecimens were obtained from non-stenotic and stenotic tissue areas of 15 CD patients.

256 sue stiffness in stenotic as compared to non-stenotic tissue sections (p < 0.001).

257 , human intestinal fibroblasts isolated from stenotic tissue were characterized by differential level

258 During dobutamine stress, the stenotic-to-normal (99m)Tc-N-NOET activity ratio was 0.6

259 During adenosine stress, the stenotic-to-normal activity ratio for (99m)Tc-N-NOET was

260 The stenotic-to-normal flow ratio was 0.33+/-0.04 at the tim

261 The stenotic-to-normal flow ratio was 0.47+/-0.04 at the tim

262 In dogs with reduced flow reserve, the stenotic-to-normal sestamibi activity ratio (0.86+/-0.03

263 In protocol 1, 2-hour NOET and 201Tl stenotic-to-normal tissue activity ratios were similar (

264 Explanted stenotic tricuspid aortic valves were weighed, and fibro

265 ough experiments on a series of idealized 2D stenotic tube flows.

266 nd corresponding blood damage index (BDI) in stenotic turbulent blood flow.

267 examination of the resected gall bladder and stenotic ureteric segment showed CMV inclusions, confirm

268 strong relevance to clinical measurements of stenotic valve areas by use of the Doppler continuity eq

269 example, the hypothesis that the impact of a stenotic valve depends not only on its limiting orifice

270 In patients with AVD, stenotic valves exposed to high wall shear stress had hi

271 AVICs isolated from stenotic valves had greater expression of TLR2 and TLR4

272 Stenotic valves opened and closed more slowly than norma

273 Superoxide levels in stenotic valves were significantly reduced by inhibition

274 In stenotic valves, superoxide levels were increased 2-fold

275 ty was not increased in calcified regions of stenotic valves.

276 so markedly elevated in calcified regions of stenotic valves.

277 ensional (2D) measurements decreased in less stenotic valves.

278 w was shorter than valve opening in severely stenotic valves.

279 fferences between the dynamics of normal and stenotic valves.

280 augmentation of the TLR4 response in AVIC of stenotic valves.

281 ponse to lipopolysaccharide (LPS) in AVIC of stenotic valves.

282 ease is the primary cause of regurgitant and stenotic valvular lesion in the U.S.

283 in the medial layer (68% of PCNA + cells) of stenotic vein grafts.

284 distal protection device during stenting of stenotic venous grafts was associated with a highly sign

285 on thickening of endothelial cell layer and stenotic versus nonstenotic medial wall thickening.

286 al versus subintimal crossing, location, and stenotic versus occlusive disease.

287 therapeutic combination for the treatment of stenotic vessel disease.

288 roke and stroke in the same territory of the stenotic vessel was compared in patients grouped by mean

289 ic stroke and stroke in the territory of the stenotic vessel.

290 Stenotic vessels were dilated by using 5-6-mm-diameter b

291 gh guide wires were easily passed across the stenotic vessels, occluded vessels required puncture thr

292 ate, however--even in patients with severely stenotic vessels--is relatively low, which suggests that

293 ease systolic thickening was observed in the stenotic zone (2.7+/-0.4 versus 4.6+/-0.3 mm in the norm

294 Stenotic zone flow and thickening did not increase durin

295 After stress, stenotic-zone blood flow and oxygen consumption were red

296 In group 2, stenotic-zone contraction with stress declined versus ba

297 Baseline stenotic-zone endocardial blood flow was reduced versus

298 Stenotic-zone endocardial flow was unchanged versus base

299 Stenotic-zone thickening increased at low but not at hig

300 Finally, a significant reduction in stenotic-zone thickening was seen during postdobutamine