ライフサイエンスコーパス: nonobstructive

1 It is usually polypoid, intraluminal, and nonobstructive.

2 ed as obstructive (coronary stenosis 50%) or nonobstructive.

3 30% and/or fractional flow reserve >0.80 was nonobstructive.

4 However, the prognostic significance of nonobstructive (1%-49% stenosis) LM CAD, including sex-s

5 1.7-, 1.8-, 2.3-, and 2.6-fold for 3-vessel nonobstructive, 1-vessel obstructive, 2-vessel obstructi

6 with angiographic data, women more often had nonobstructive (15% vs 8%) and less often had 2-vessel (

7 Among 883 women, 62%, 17%, 11%, and 10% had nonobstructive and 1-vessel, 2-vessel, and 3-vessel CAD,

8 .51 for group 3; P = 0.01) were lower in the nonobstructive and higher in the latent HCM group.

9 or positron emission tomography after normal/nonobstructive and mildly abnormal study findings.

10 ation referral rate in the setting of normal/nonobstructive and mildly abnormal test results.

11 Among individuals without known CAD, nonobstructive and obstructive CAD by CCTA are associate

12 ct cardiovascular events among patients with nonobstructive and obstructive coronary artery disease (

13 fication on computed tomography scan or both nonobstructive and obstructive lesions on angiography.

14 enosis by visual angiographic assessment) or nonobstructive, and as thin-cap fibroatheroma (TCFA) or

15 ate ASCVD risk, CAD, including noncalcified, nonobstructive, and vulnerable plaque, was highly preval

16 d Meta-Analyses guidelines, the terms "MI," "nonobstructive," "angiography," and "prognosis" were sea

17 tomographic angiography allows detection of nonobstructive atherosclerosis that would not be identif

18 nctional studies because of the detection of nonobstructive atherosclerosis.

19 rm to the ejaculate in up to 56% of men with nonobstructive azoospermia (NOA) following varicocele re

20 Nonobstructive azoospermia (NOA) remains a challenging c

21 cular markers in the testes of patients with nonobstructive azoospermia (NOA) revealed enhanced expre

22 This mutation was present in a man with nonobstructive azoospermia (that is, no sperm was detect

23 management of patients with varicoceles and nonobstructive azoospermia and to review predictors of s

24 The genetic basis of nonobstructive azoospermia is unknown in the majority of

25 elated men of Middle Eastern descent who had nonobstructive azoospermia were found to carry mutations

26 he importance of DNA repair defects in human nonobstructive azoospermia.

27 res appear to be more beneficial in cases of nonobstructive azoospermia.

28 erapy make up a small subgroup of males with nonobstructive azoospermia.

29 from 924 men who had received a diagnosis of nonobstructive azoospermia.

30 sis-generating analysis, among patients with nonobstructive but extensive CAD, statin use after CCTA

31 events (n=74/137) occurred in patients with nonobstructive CAD (1%-69% stenosis).

32 i-ischemic therapy was higher for women with nonobstructive CAD (15% versus 12% for 1-vessel to 3-ves

33 ty was significantly higher in patients with nonobstructive CAD (5.2% versus 1.6%; hazard ratio [95%

34 variable analysis, the presence of extensive nonobstructive CAD (hazard ratio, 3.1; 95% confidence in

35 ant associations with mortality for 3-vessel nonobstructive CAD (HR, 1.6; 95% CI, 1.1-2.5), 1-vessel

36 ouped according to obstructive CAD (n = 60), nonobstructive CAD (n = 80), or no CAD (n = 114).

37 erapy significantly increased for those with nonobstructive CAD (odds ratio, 3.6; 95% confidence inte

38 Stratifying by no CAD, nonobstructive CAD (worst stenosis <50%), or obstructive

39 The presence of obstructive vs nonobstructive CAD among those with a CAC score of 0 was

40 g 37,674 patients, 8384 patients (22.3%) had nonobstructive CAD and 20,899 patients (55.4%) had obstr

41 ropensity matching yielded 117 patients with nonobstructive CAD and 331 patients with obstructive CAD

42 fied by obstructive (>/=50% stenosis) versus nonobstructive CAD and a high (>5) versus a low (</=5) C

43 current evidence on risk stratification for nonobstructive CAD and discuss its implications and medi

44 Patients with nonobstructive CAD and high CT-LeSc had hard event-free

45 gnificant association between 1- or 2-vessel nonobstructive CAD and mortality, but there were signifi

46 hese findings suggest clinical importance of nonobstructive CAD and warrant further investigation of

47 tients with chest pain who are found to have nonobstructive CAD are limited, and, in clinical practic

48 central emerging paradigm is the concept of nonobstructive CAD as a cause of IHD and related adverse

49 structive CAD compared with in patients with nonobstructive CAD as defined by coronary CTA (hazard ra

50 with no apparent CAD, patients with 1-vessel nonobstructive CAD had a hazard ratio (HR) for 1-year MI

51 with the highest risk among those exhibiting nonobstructive CAD in 3 epicardial vessels (HR: 4.75, 95

52 was performed in 93 patients (91%), showing nonobstructive CAD in eight patients (9%) and normal cor

53 tive was therefore to evaluate the impact of nonobstructive CAD in patients with non-ST-segment-eleva

54 Emerging data document that more extensive, nonobstructive CAD involvement, hypertension, and diabet

55 uctive CAD net reclassification index, 0.44; nonobstructive CAD net reclassification index, 0.49; P<0

56 Medical management of nonobstructive CAD plays an essential role in plaque sta

57 g MBF impairment due to obstructive CAD from nonobstructive CAD remains challenging.

58 ngina despite nonobstructive CAD, underlying nonobstructive CAD warrants attention.

59 Nonobstructive CAD was found in 479 patients, the CAD(-)

60 reased rate of events, whereas nonextensive, nonobstructive CAD was not.

61 Higher mortality for nonobstructive CAD was observed even among patients with

62 se and introduced new risk categories within nonobstructive CAD with a risk continuum between primary

63 Event-free survival in nonobstructive CAD with high CT-LeSc (78.6%) was similar

64 g any degree of abnormality, including mild (nonobstructive CAD), moderate, and severe findings, conf

65 20%) and increased progressively by 1-vessel nonobstructive CAD, 0.24% (n = 10, 95% CI, 0.10%-0.40%);

66 .24% (n = 10, 95% CI, 0.10%-0.40%); 2-vessel nonobstructive CAD, 0.56% (n = 13, 95% CI, 0.30%-1.00%);

67 .56% (n = 13, 95% CI, 0.30%-1.00%); 3-vessel nonobstructive CAD, 0.59% (n = 6, 95% CI, 0.30%-1.30%);

68 For women with nonobstructive CAD, average lifetime cost estimates were

69 ts undergoing elective coronary angiography, nonobstructive CAD, compared with no apparent CAD, was a

70 fidence interval [CI], 0.79-2.33; P = 0.298; nonobstructive CAD, HR, 1.53; 95% CI, 0.84-2.77; P = 0.1

71 for chest pain occurred in 20% of women with nonobstructive CAD, increasing to 38% to 55% for women w

72 , by identifying patients at risk because of nonobstructive CAD, provides better prognostic informati

73 Among patients with nonobstructive CAD, those with extensive plaque experien

74 t pain are found to have true angina despite nonobstructive CAD, underlying nonobstructive CAD warran

75 , n=163), women showed a higher frequency of nonobstructive CAD, whereas men showed a higher frequenc

76 ients with elevated troponin, 197 (8.8%) had nonobstructive CAD.

77 in patients identified as having extensive, nonobstructive CAD.

78 associated with higher risk than presence of nonobstructive CAD.

79 om-driven care is costly even for women with nonobstructive CAD.

80 prevalent, but the majority of patients had nonobstructive CAD.

81 in increased identification of patients with nonobstructive CAD.

82 atification, and management of patients with nonobstructive CAD.

83 ny symptomatic individuals are found to have nonobstructive CAD.

84 y degree (no apparent CAD: no stenosis >20%; nonobstructive CAD: >/=1 stenosis >/=20% but no stenosis

85 eroma to the low-risk, quiescent, eccentric, nonobstructive calcified plaque.

86 A nonobstructive constant renal pelvic pressure model was

87 elevation myocardial infarction (STEMI) with nonobstructive coronaries (MINOCA) are largely unknown.

88 Angina with nonobstructive coronary arteries (ANOCA) is increasingly

89 o the diagnosis and treatment of angina with nonobstructive coronary arteries (ANOCA).

90 spasm (CAS) is a common cause of angina with nonobstructive coronary arteries (ANOCA).

91 scular function in patients with angina with nonobstructive coronary arteries (ANOCA).

92 nction testing in patients with ischemia and nonobstructive coronary arteries (INOCA) commonly includ

93 MI with nonobstructive coronary arteries (MINOCA [<50% stenosis]

94 ors in women with myocardial infarction with nonobstructive coronary arteries (MINOCA) and those with

95 Myocardial infarction with nonobstructive coronary arteries (MINOCA) constitutes 3-

96 Myocardial infarction with nonobstructive coronary arteries (MINOCA) is a puzzling

97 working diagnosis Myocardial Infarction with Nonobstructive Coronary Arteries (MINOCA) is being incre

98 Suspected myocardial infarction (MI) with nonobstructive coronary arteries (MINOCA) occurs in 5% t

99 Myocardial infarction with nonobstructive coronary arteries (MINOCA) occurs in 5% t

100 Myocardial infarction with nonobstructive coronary arteries (MINOCA) occurs in 6% t

101 nary arteries and myocardial infarction with nonobstructive coronary arteries (MINOCA) were enrolled.

102 therosclerotic vs myocardial infarction with nonobstructive coronary arteries [MINOCA]) in women who

103 ere were 161 (56.1%) myocardial ischemia and nonobstructive coronary arteries and 126 (43.9%) MINOCA

104 es for ischemia in patients with angina with nonobstructive coronary arteries and a MB in the left an

105 Patients with angina with nonobstructive coronary arteries and a MB were compared

106 In patients with angina and nonobstructive coronary arteries and an MB confirmed by

107 atients with chronic myocardial ischemia and nonobstructive coronary arteries and myocardial infarcti

108 es and a MB were compared with 2 angina with nonobstructive coronary arteries groups with no MB: 1 wi

109 Angina with nonobstructive coronary arteries is a common condition f

110 Myocardial infarction with nonobstructive coronary arteries is a relatively common

111 Patients with angina with nonobstructive coronary arteries underwent blinded invas

112 Patients with angina with nonobstructive coronary arteries underwent the acquisiti

113 identification of patients with angina with nonobstructive coronary arteries who would benefit from

114 ectively studied 64 patients with angina and nonobstructive coronary arteries, all of whom had an MB

115 otypically similar patients with angina with nonobstructive coronary arteries, only those with an imp

116 ection, ischemia, myocardial infarction with nonobstructive coronary arteries, or stress-induced card

117 luding myocardial infarction associated with nonobstructive coronary arteries, spontaneous coronary a

118 ge (MB) is an important cause of angina with nonobstructive coronary arteries.

119 cardial infarction with both obstructive and nonobstructive coronary arteries.

120 ry abnormalities in patients with angina and nonobstructive coronary arteries.

121 unction (CMD) in patients with ischemia with nonobstructive coronary arteries.

122 h myocardial ischemia and/or infarction with nonobstructive coronary arteries.

123 nd a higher frequency of 1-vessel disease or nonobstructive coronary artery disease (39.6% versus 29.

124 ronary disorders in patients with angina and nonobstructive coronary artery disease (ANOCA).

125 osis of patients with troponin elevation and nonobstructive coronary artery disease (CAD) is unknown.

126 t cardiac adverse events among patients with nonobstructive coronary artery disease (CAD).

127 are available in patients with ischemia and nonobstructive coronary artery disease (INOCA).

128 CED) causes angina/ischemia in patients with nonobstructive coronary artery disease (NOCAD).

129 uses of myocardial ischemia in patients with nonobstructive coronary artery disease (NOCAD).

130 Patients with nonobstructive coronary artery disease (NOCAD; wall irre

131 56 consecutive patients with de novo HF with nonobstructive coronary artery disease divided into HF w

132 Patients with angina and nonobstructive coronary artery disease had simultaneous

133 ovascular angina, patients with ischemia and nonobstructive coronary artery disease receiving intraco

134 Patients with angina and nonobstructive coronary artery disease underwent simulta

135 y adults and 17 arteries in 14 patients with nonobstructive coronary artery disease were studied.

136 ; NCT03508609) in patients with ischemia and nonobstructive coronary artery disease with persistent a

137 ismatch (2b: 2.4% women; 1.1% men); class 3, nonobstructive coronary artery disease with supply-deman

138 d normal coronary arteries, 297 patients had nonobstructive coronary artery disease, 264 patients had

139 s with multiple cardiovascular risk factors, nonobstructive coronary artery disease, and coronary end

140 In patients with angina and nonobstructive coronary artery disease, diminished coron

141 Beyond ischemia with nonobstructive coronary artery disease, testing for CMD

142 Among patients with angina and nonobstructive coronary artery disease, those with coron

143 ascular events in patients with subclinical, nonobstructive coronary artery disease.

144 dial infarction among cocaine users, 48% had nonobstructive coronary artery disease.

145 ts with coronary endothelial dysfunction and nonobstructive coronary artery disease.

146 dysfunction to acetylcholine in humans with nonobstructive coronary artery disease.

147 sting for CMD in patients with ischemia with nonobstructive coronary artery disease.

148 armacological vasodilator in the presence of nonobstructive coronary artery disease.

149 e in evaluating patients with chest pain and nonobstructive coronary artery disease.

150 identify an ischemic cause in patients with nonobstructive coronary artery disease.

151 es in patients with evidence of ischemia and nonobstructive coronary artery disease; however, no spec

152 Lipid content in untreated nonobstructive coronary artery lesions is associated wit

153 The prognostic significance of nonobstructive coronary artery plaques by CCTA is poorly

154 Among patients with ischemia with nonobstructive coronary artery, CSF was not associated w

155 identifying mild perfusion defects of early nonobstructive coronary atherosclerosis as the basis for

156 ction for managing symptomatic patients with nonobstructive coronary atherosclerosis because current

157 entive measures in millions of patients with nonobstructive coronary heart disease.

158 Nonobstructive coronary plaques manifesting high-risk mo

159 assess the efficacy of sealing intermediate nonobstructive coronary saphenous vein graft (SVG) lesio

160 atients known to have or suspected of having nonobstructive Crohn disease were recruited.

161 ule endoscopy and CT enterography may depict nonobstructive Crohn disease when techniques such as ile

162 inguish significant epicardial stenosis from nonobstructive, diffuse atherosclerosis or microvascular

163 ge, 0-273] vs 19 AU [0-225], P = .046), more nonobstructive disease (48% vs 37%, P = .02), and higher

164 Patients with normal or nonobstructive disease (CAD angiographic score of 0), mi

165 HCM patients with nonobstructive disease appear to experience a relatively

166 st that regardless of whether obstructive or nonobstructive disease is present, the extent of plaque

167 ee of coronary artery disease (CAD), 31% had nonobstructive disease, and 19% had inconclusive or posi

168 e need for timely detection and treatment of nonobstructive disease, in addition to traditional risk

169 icular contractility in both obstructive and nonobstructive forms of HCM, suggesting common disease m

170 ation, and distinguishing obstructive versus nonobstructive forms.

171 Eleven patients were classified as nonobstructive (group 1), 12 as obstructive (group 2), a

172 ebo-controlled design, 178 participants with nonobstructive HCM (age, 23.3+/-10.1 years; 61% men) wer

173 and gender (p = 0.2) nor from patients with nonobstructive HCM (p = 0.8).

174 onal frames in patients with obstructive and nonobstructive HCM and in normal patients.

175 f advanced heart failure among patients with nonobstructive HCM and preserved systolic function.

176 ES of nonobstructive HCM has an expanded and more diverse clin

177 Forty-six nonobstructive HCM patients (2.2%) either received or we

178 Twenty nonobstructive HCM patients (age, 48.3+/-12.3 years; 14

179 A small minority of nonobstructive HCM patients progress to heart transplant

180 Nonobstructive HCM patients were less likely to experien

181 following physiological exercise (<30 mm Hg; nonobstructive HCM) and retrospectively assembled clinic

182 lic frames of 95% of obstructive HCM, 22% of nonobstructive HCM, and 11% of normal patients (p < 0.00

183 compared 82 patients (22 obstructive HCM, 23 nonobstructive HCM, and 37 normal) by measuring 164 LV p

184 as noted in 82% of the obstructed HCM, 9% of nonobstructive HCM, and none (0%) of the control patient

185 her patients with obstruction, compared with nonobstructive HCM, demonstrate significant differences

186 ar to have a worse prognosis than those with nonobstructive HCM.

187 ructive HR, 4.6 (95% CI, 2.0-10.5); 3-vessel nonobstructive HR, 4.5 (95% CI, 1.6-12.5); 1-vessel obst

188 1-year MI of 2.0 (95% CI, 0.8-5.1); 2-vessel nonobstructive HR, 4.6 (95% CI, 2.0-10.5); 3-vessel nono

189 interval [CI]: 1.94 to 3.49; p < 0.0001) and nonobstructive (HR: 1.60; 95% CI: 1.18 to 2.16; p = 0.00

190 ctive CAD, with increasing risk observed for nonobstructive (HR: 1.62; 95% CI: 1.20 to 2.19; p = 0.00

191 ment appeared normal, newborn mice developed nonobstructive hydrocephalus, suggesting excessive cereb

192 Loss of Rab35 leads to nonobstructive hydronephrosis because of loss of ureter

193 our understanding of the molecular basis of nonobstructive hydronephrosis in humans.

194 8-Tetrachlorodibenzo-p-dioxin (TCDD) induces nonobstructive hydronephrosis in mouse neonates through

195 Loss of Rab35 leads to nonobstructive hydronephrosis, making the Rab35 mutant m

196 Nonobstructive hypertrophic cardiomyopathy (HCM) has bee

197 ion (peak Vo(2) <75% of predicted) caused by nonobstructive hypertrophic cardiomyopathy (mean age, 55

198 Symptomatic nonobstructive hypertrophic cardiomyopathy (nHCM) lacks

199 Patients with nonobstructive hypertrophic cardiomyopathy (nHCM) often

200 In nonobstructive hypertrophic cardiomyopathy (nHCM), there

201 ow obstruction, treatment of obstructive and nonobstructive hypertrophic cardiomyopathy with negative

202 large Czech family with 3 males affected by nonobstructive hypertrophic cardiomyopathy with severe l

203 c cardiac variant of Fabry disease mimicking nonobstructive hypertrophic cardiomyopathy.

204 ) isolated basal hypertrophy; and (4) milder nonobstructive hypertrophy enriched for familial sarcome

205 Nonobstructive hypertrophy localized to the cardiac apex

206 ntly performed procedures in women; however, nonobstructive (ie, < 50% stenosis) coronary artery dise

207 gg fusion and is often defective in men with nonobstructive infertility.

208 0.80, as well as decreasing the frequency of nonobstructive invasive coronary angiography.

209 , but we now recognize the need to attend to nonobstructive lesions as well.

210 of myocardial infarction have clarified that nonobstructive lesions progressively enlarged relatively

211 For nonobstructive lesions, TCFA lesions had similar lesion

212 y harbored vulnerable plaque morphology than nonobstructive lesions.

213 ents were categorized as having normal LM or nonobstructive LM (18% of cohort).

214 rly 80% higher risk for events than men with nonobstructive LM CAD (adjusted hazard ratio, 1.78; P=0.

215 In subgroup analysis, women with nonobstructive LM CAD had a nearly 80% higher risk for e

216 Nonobstructive LM CAD was frequently detected on coronar

217 ultivariable Cox regression, the presence of nonobstructive LM plaque increased the risk for the comp

218 the sex-specific prognostic significance of nonobstructive LM plaque may augment risk stratification

219 scularization was higher among patients with nonobstructive LM than normal LM in both women and men:

220 We studied 80 subjects with nonobstructive (<30% stenosis) coronary artery disease.

221 mination findings were classified as normal, nonobstructive (<50% stenosis), or obstructive (>/=50%).

222 ts were divided into the following 3 groups: nonobstructive (LVOTG < 30 mm Hg at rest and after provo

223 Nodules with nonobstructive morphologies, dependent portions of airwa

224 CAD was common for nonobstructive (n = 1452, 27%) and obstructive (n = 629,

225 truction without operation (n = 228); and 3) nonobstructive (n = 820).

226 alve thrombosis episodes (obstructive, n=15; nonobstructive, n=13).

227 ndergoing cardiac catheterization with >or=1 nonobstructive native coronary artery atheroma were rand

228 ssment, revealed both BRSs to be patent with nonobstructive neointimal hyperplasia.

229 VC < 0.70, n = 993) and age- and sex-matched nonobstructive (NO) referents were recruited from popula

230 level, the prevalence of 2-feature high-risk nonobstructive nonculprit plaques was slightly higher in

231 Drug treatment was highest for those with nonobstructive or 1-vessel CAD (P < 0.0001).

232 r CVD events regardless of whether they have nonobstructive or obstructive CAD.

233 However, 7 nonobstructive patients (2.8%) did require heart transpl

234 a median follow-up of 6.5 years, 225 of 249 nonobstructive patients (90%) remained in classes I/II,

235 HCM-related mortality among nonobstructive patients was low (n = 8; 0.5%/year), with

236 the broad HCM clinical spectrum consists of nonobstructive patients with advanced heart failure, in

237 occasionally, heart transplant for end-stage nonobstructive patients.

238 ec [FEV(1)]: vital capacity [VC] <0.7) and a nonobstructive pattern (FEV(1):VC >/=0.7) in pulmonary f

239 atients with moderate-to-severe symptoms and nonobstructive pattern recognized as overactive bladder

240 s: Patients without plaque and patients with nonobstructive plaque and at most mild to moderate steno

241 ents with obstructive CAD, greater extent of nonobstructive plaque was associated with higher event r

242 ed for CAD risk factors, the presence of any nonobstructive plaque was associated with higher mortali

243 o coronary plaque or stenosis, 288 (49%) had nonobstructive plaque, 22 (4%) had moderate stenosis, an

244 s other patterns (eg, location or extent) of nonobstructive plaque.

245 nary stenosis category, even in vessels with nonobstructive plaques (n = 169), 38% of which had abnor

246 The presence and extent of nonobstructive plaques augment prediction of incident mo

247 isk in relation to extent and composition of nonobstructive plaques by 64-detector row coronary compu

248 atients with stable angina also contain many nonobstructive plaques, which are prone to fissures or r

249 the three groups: 1) no family witness; 2) a nonobstructive "quiet" family witness; and 3) a family w

250 Nonobstructive, single, and multivessel disease was pres

251 s: small-bowel obstruction in 17 (6%) cases, nonobstructive small-bowel narrowing in six (2%), extral

252 Patients with an angiographically nonobstructive stenosis not intended for PCI but with IV

253 th a CAC score of 0, 84% had no CAD, 13% had nonobstructive stenosis, and 3.5% had >/=50% stenosis (1

254 ft who had developed at least 1 intermediate nonobstructive SVG lesion (30%-60% diameter stenosis by

255 Sealing intermediate nonobstructive SVG lesions with DES was safe but was not

256 of the potential risk of asthma attacks, but nonobstructive symptoms occur frequently and may also ca

257 n rates ranged from 4% to 38% for women with nonobstructive to 3-vessel CAD (P < 0.0001).

258 with visualized cortical atrophy (P = .01), nonobstructive urinary incontinence (18.5% vs 3.9%; P =

259 However, the mechanism by which such nonobstructive valve lesions impart excess cardiovascula

260 ing to race; for example, classifications of nonobstructive ventilatory impairment may change dramati

261 alizations was 1.8-fold higher in women with nonobstructive versus 1-vessel CAD after 1 year of follo

262 anagement of both overactivity syndromes and nonobstructive voiding dysfunction.