ライフサイエンスコーパス: nonobstructive

1 It is usually polypoid, intraluminal, and nonobstructive.

2 30% and/or fractional flow reserve >0.80 was nonobstructive.

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

4 1.7-, 1.8-, 2.3-, and 2.6-fold for 3-vessel nonobstructive, 1-vessel obstructive, 2-vessel obstructi

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

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

7 .51 for group 3; P = 0.01) were lower in the nonobstructive and higher in the latent HCM group.

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

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

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

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

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

13 Nonobstructive azoospermia (NOA) remains a challenging c

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

45 20%) and increased progressively by 1-vessel nonobstructive CAD, 0.24% (n = 10, 95% CI, 0.10%-0.40%);

46 .24% (n = 10, 95% CI, 0.10%-0.40%); 2-vessel nonobstructive CAD, 0.56% (n = 13, 95% CI, 0.30%-1.00%);

47 .56% (n = 13, 95% CI, 0.30%-1.00%); 3-vessel nonobstructive CAD, 0.59% (n = 6, 95% CI, 0.30%-1.30%);

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

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

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

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

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

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

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

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

56 in patients identified as having extensive, nonobstructive CAD.

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

58 A nonobstructive constant renal pelvic pressure model was

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

77 Nonobstructive coronary plaques manifesting high-risk mo

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

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

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

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

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

83 HCM patients with nonobstructive disease appear to experience a relatively

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

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

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

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

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

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

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

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

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

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

94 Nonobstructive HCM patients were less likely to experien

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

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

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

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

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

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

101 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

102 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

103 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

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

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

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

107 8-Tetrachlorodibenzo-p-dioxin (TCDD) induces nonobstructive hydronephrosis in mouse neonates through

108 Nonobstructive hypertrophic cardiomyopathy (HCM) has bee

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

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

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

112 Nonobstructive hypertrophy localized to the cardiac apex

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

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

115 0.80, as well as decreasing the frequency of nonobstructive invasive coronary angiography.

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

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

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

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

120 Nonobstructive LM CAD was frequently detected on coronar

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

158 anagement of both overactivity syndromes and nonobstructive voiding dysfunction.