ライフサイエンスコーパス: valve stenosis

1 lly associated with increased risk of aortic valve stenosis.

2 is an effective form of treatment for mitral valve stenosis.

3 redictive value for diagnosing severe aortic valve stenosis.

4 tion, and aortic valve replacement in aortic valve stenosis.

5 cardiovascular disease, and calcific aortic valve stenosis.

6 sclerotic cardiovascular disease, and aortic valve stenosis.

7 cardiomyopathies, prior cardiac surgery, and valve stenosis.

8 ESP has a 100% sensitivity for severe aortic valve stenosis.

9 calcification and the development of aortic valve stenosis.

10 s derived from patients with calcific aortic valve stenosis.

11 ial infarction, ischaemic stroke, and aortic valve stenosis.

12 icted risk undergoing TAVR for native aortic valve stenosis.

13 d the treatment of symptomatic severe aortic valve stenosis.

14 valve replacement in the treatment of aortic valve stenosis.

15 y in patients with symptomatic severe aortic valve stenosis.

16 enefit for cardiovascular disease and aortic valve stenosis.

17 r stress (WSS), and classification of aortic valve stenosis.

18 ography in patients with low-gradient aortic valve stenosis.

19 acy) trials in patients with moderate aortic valve stenosis.

20 0 years or older with isolated severe aortic valve stenosis.

21 sed risk of myocardial infarction and aortic valve stenosis.

22 tment option for patients with severe aortic valve stenosis.

23 scending aortic dilation and calcific aortic valve stenosis.

24 ortant mitral valve regurgitation and mitral valve stenosis.

25 ng cardiovascular disease or calcific aortic valve stenosis.

26 gh-risk surgical patients with severe aortic valve stenosis.

27 r cardiovascular disease and calcific aortic valve stenosis.

28 functional characteristics of severe aortic valve stenosis.

29 nal properties of severe degenerative aortic valve stenosis.

30 iovascular disease (CVD) and calcific aortic valve stenosis.

31 e and coarctation of the aorta and pulmonary valve stenosis.

32 ostheses and those with predominant surgical valve stenosis.

33 atment of severe symptomatic calcific aortic valve stenosis.

34 approach to treat neonatal congenital aortic valve stenosis.

35 d regression of SMR following AVR for aortic valve stenosis.

36 ickening to severe calcification with aortic valve stenosis.

37 gnaling, and halts the progression of aortic valve stenosis.

38 therapeutic targets for prevention of aortic valve stenosis.

39 Reasons for second MVR were prosthetic valve stenosis 24 (83%), thrombosis 4 (14%), and endocar

40 normalities, ocular hypertelorism, pulmonary valve stenosis, abnormal genitalia, retardation of growt

41 -surgical risk patients with bicuspid aortic valve stenosis achieved favorable 30-day results, with l

42 r stress, as present in patients with aortic valve stenosis, activates multiple monocyte functions, a

43 phic findings in patients with severe aortic valve stenosis after transcatheter aortic valve replacem

44 rally been the first-line therapy for aortic valve stenosis, although some contemporary studies have

45 Thirty-five patients with aortic-valve stenosis and 10 healthy controls underwent a 27-mi

46 ctive study, participants with severe aortic valve stenosis and clinically indicated CT for transcath

47 iming to prevent PPM in patients with aortic valve stenosis and concomitant SMR.

48 fectively reduce the risk of calcific aortic valve stenosis and CVD.

49 considered first-line therapy for pulmonary valve stenosis and generally results in successful relie

50 rominent cardiac defects in NS are pulmonary valve stenosis and hypertrophic cardiomyopathy.

51 que drivers of atherosclerosis versus aortic valve stenosis and implicates EVs in advanced cardiovasc

52 Aortic valve stenosis and insufficiency develop over time and c

53 s does not always correlate with severity of valve stenosis and left ventricular (LV) function.

54 Eligible patients had severe bicuspid aortic valve stenosis and met American Heart Association/Americ

55 Patients >/= 70 years old with severe aortic valve stenosis and no significant coronary artery diseas

56 k factors for development of calcific aortic valve stenosis and predict severity of the disease.

57 t highlight Lp(a) in CVD and calcific aortic valve stenosis and propose pathways to clinical registra

58 ms, thromboses and calcification; to truncal valve stenosis and regurgitation; to semilunar and atrio

59 ssociated with causal risk ratios for aortic valve stenosis and replacement, respectively, of 1.52 (9

60 usally associated with higher risk of aortic valve stenosis and replacement.

61 x is causally associated with risk of aortic valve stenosis and replacement.

62 is causally associated with calcific aortic valve stenosis and the need for aortic valve replacement

63 nderstand the molecular mechanisms of aortic valve stenosis and to help guide sex-based precision the

64 rdiomyopathy (HOCM), 10 patients with aortic valve stenosis, and 14 healthy individuals using [(11)C]

65 diagnostic tool in the assessment of aortic valve stenosis, and how the results compare with current

66 nical risk factors for development of aortic valve stenosis, and hypercholesterolemia is a putative t

67 t in patients with symptomatic severe aortic valve stenosis; and antiplatelet agents vorapaxar and pr

68 Causal risk factors for aortic valve stenosis are poorly understood, limiting the possi

69 for patients with severe symptomatic aortic valve stenosis (AS) across the whole spectrum of risk.

70 haemodynamic cardiac consequences of aortic valve stenosis (AS) and aortic valve regurgitation (AR).

71 Whether aortic valve stenosis (AS) can adversely affect systemic endoth

72 Aortic valve stenosis (AS) can cause angina despite unobstructe

73 siological shear rates as observed in aortic valve stenosis (AS) can influence protein conformation a

74 lmonary hypertension (PHT) and severe aortic valve stenosis (AS) from 1987 to 1999.

75 Aortic valve stenosis (AS) induces compensatory alterations in

76 Calcific aortic valve stenosis (AS) is a life-threatening disease with n

77 Aortic valve stenosis (AS) is the most common manifestation of

78 presence of syncope in patients with aortic valve stenosis (AS) predicts a grave prognosis.

79 ection time (ET) ratio is a marker of aortic valve stenosis (AS) severity and predicts outcome in mod

80 lue of stress FR for the detection of aortic valve stenosis (AS) severity and the prediction of morta

81 In aortic valve stenosis (AS), the occurrence of heart failure sym

82 ent can modify the natural history of aortic valve stenosis (AS).

83 ity impacted outcome in patients with aortic valve stenosis (AS).

84 The use of TAVI in severe bicuspid aortic valve stenosis, asymptomatic severe aortic stenosis, mod

85 In patients with severe aortic valve stenosis at intermediate surgical risk, transcathe

86 Aortic valve stenosis (AVS) is a progressive disease, wherein m

87 Aortic valve stenosis (AVS) is a sexually dimorphic disease whe

88 Accurate quantification of aortic valve stenosis (AVS) is needed for relevant management d

89 Aortic valve stenosis (AVS) patients experience pathogenic valv

90 Congenital aortic valve stenosis (AVS), coarctation of the aorta (COA) and

91 n was associated with the presence of aortic valve stenosis (AVS), no prospective study has suggested

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

93 aortic valve regurgitation (AVR) and aortic valve stenosis (AVS).

94 vely associate with increased risk of aortic valve stenosis (AVS).

95 erity and hemodynamic consequences of aortic valve stenosis (AVS).

96 sed by FFR in 54 patients with severe aortic valve stenosis before and after transcatheter aortic val

97 ycerides is likely to prevent CAD and aortic valve stenosis but may increase thromboembolic risk.

98 r cardiovascular disease and calcific aortic valve stenosis, but no approved specific therapy exists

99 ic valve replacement (AVR) for severe aortic valve stenosis, but whether or not frail patients derive

100 In patients with low-gradient aortic valve stenosis, catheter-induced premature ventricular c

101 Congenital aortic valve stenosis (CAVS) affects up to 10% of the world pop

102 Calcific aortic valve stenosis (CAVS) is a frequent and life-threatening

103 Calcific aortic valve stenosis (CAVS) is a major health problem facing a

104 iovascular disease (CVD) and calcific aortic valve stenosis (CAVS) is substantial.

105 Calcific aortic valve stenosis (CAVS) is the most frequent valve disorde

106 ), ischemic stroke (IS), and calcific aortic valve stenosis (CAVS).

107 o medical therapy to prevent calcific aortic valve stenosis (CAVS).

108 Patients with severe aortic valve stenosis deemed to be at intermediate or increased

109 Patients with severe aortic valve stenosis deemed to be at intermediate risk of 30-d

110 As aortic valve stenosis develops, valve tissue becomes stiffer.

111 trophy was also seen in patients with aortic valve stenosis: ERK(Thr188) phosphorylation was increase

112 ological treatments for fibrocalcific aortic valve stenosis (FCAVS) have been elusive for >50 years.

113 t TAVR for treatment of severe native aortic valve stenosis from June 2010 to May 2021 across all US

114 with respect to echocardiographic indexes of valve stenosis, functional status, and quality of life.

115 is (AS) according to the new proposed aortic valve stenosis grading classification.

116 d risk factors described for critical aortic valve stenosis have been shown to be inapplicable to pat

117 R) in low-risk patients with bicuspid aortic valve stenosis have not been studied in a large scale, m

118 CAD risk, peripheral artery disease, aortic valve stenosis, heart failure, and lifespan.

119 efect, pulmonary artery anomalies, pulmonary valve stenosis, hydrocephalus) with trends in malformati

120 a better prognosis when experiencing aortic valve stenosis, hypertrophic cardiomyopathy, or heart fa

121 alve sclerosis was present in 26% and aortic valve stenosis in 2% of the entire study cohort; in subj

122 f cardiovascular disease and calcific aortic valve stenosis in patients with elevated Lp(a) concentra

123 Aortic valve stenosis is a sexually dimorphic disease, with wom

124 Whether aortic valve stenosis is accelerated by inflammation and whethe

125 Aortic valve stenosis is an increasingly prevalent degenerative

126 Although aortic-valve stenosis is clearly associated with adverse cardio

127 of myofibroblasts from patients with aortic valve stenosis is more condensed than that of myofibrobl

128 ng is the dominant mechanism by which mitral valve stenosis is relieved by this technique, and thus c

129 tension in patients with asymptomatic aortic valve stenosis is scarce.

130 Aortic valve stenosis is the most common type of congenital lef

131 Aortic valve stenosis may influence fractional flow reserve (FF

132 In contrast to patients with aortic valve stenosis, MEE was not improved in patients with HO

133 Atrial fibrillation, calcific aortic valve stenosis, mitral regurgitation, and left atrial vo

134 abetes, atrial fibrillation, calcific aortic valve stenosis, mitral regurgitation, and left atrial vo

135 In moderate and severe aortic valve stenosis, mPAP/CO slope and percent-predicted peak

136 associations of obesity with incident aortic valve stenosis (n = 1,215) and replacement (n = 467) for

137 TAVR were moderate-severe prosthetic aortic valve stenosis (n=10, 21.7%), moderate-severe central pr

138 Patients with severe aortic valve stenosis (n=161) undergoing aortic valve replaceme

139 efects, atrial septal defects, and pulmonary valve stenosis) occurred in 2.0 per 1000 births, of whic

140 valve is frequently an antecedent to aortic valve stenosis or insufficiency and is often associated

141 pathophysiological conditions such as aortic valve stenosis or insufficiency, making it possible to p

142 brillation without moderate or severe mitral valve stenosis or prosthetic mechanical heart valves, tr

143 dings were mild and were not associated with valve stenosis or regurgitation.

144 tation was associated with lesser degrees of valve stenosis or regurgitation.

145 04 [95% CI, 0.77-1.39]; P=0.810), and aortic valve stenosis (OR, 1.03 [95% CI, 0.56-1.90]; P=0.926).

146 h CAD (OR, 1.25 [95% CI, 1.12-1.40]), aortic valve stenosis (OR, 1.29 [95% CI, 1.04-1.61]), and hyper

147 sm (OR, 1.75 [95% CI, 1.40-2.17]) and aortic valve stenosis (OR, 1.46 [95% CI, 1.25-1.70]).

148 lts without hematologic malignancies, mitral valve stenosis, or previous mitral valve procedure from

149 for PALMD's contribution to calcific aortic valve stenosis pathology.

150 asurements were performed in HOCM and aortic valve stenosis patients 4 months after surgery.

151 h is associated with both the risk of native valve stenosis progression and bioprosthetic valve degen

152 omising pharmaceutical target to slow aortic valve stenosis progression.

153 ofibroblast activation and subsequent aortic valve stenosis progression.

154 ic cardiovascular disease (ASCVD) and aortic valve stenosis, provides clinical guidance for testing a

155 roke, ischaemic stroke, hypertension, aortic valve stenosis, pulmonary embolism, and venous thrombo-e

156 e valve for the treatment of bicuspid aortic valve stenosis) registry included 353 consecutive patien

157 valves (BAVs) are associated with premature valve stenosis, regurgitation, and ascending aortic aneu

158 Neonates with critical aortic valve stenosis remain a particularly high-risk group.

159 subjects with a medical diagnosis of aortic valve stenosis (remaining n=308 683 individuals), phenom

160 gnostic value of the mPAP/CO slope in aortic valve stenosis remains unknown.

161 values was found before and after the aortic valve stenosis removal (0.89+/-0.10 versus 0.89+/-0.13;

162 ronary hemodynamics are influenced by aortic valve stenosis removal.

163 AI accurately classified aortic valve stenosis severity in 85.8% of patients (302 of 352

164 Aortic valve stenosis severity was assessed by a core lab with

165 diseases such as atherosclerosis and aortic valve stenosis, since it strongly suggests a genetic bas

166 ation: no cardiac damage associated with the valve stenosis (Stage 0), left ventricular damage (Stage

167 ndomize all-comers with severe native aortic valve stenosis to either transcatheter aortic valve repl

168 (Bicuspid Aortic Valve Stenosis Transcatheter Aortic Valve Replacement Re

169 ransplant recipients (KT) with severe aortic valve stenosis underwent transfemoral TAVI.

170 age and sex-adjusted hazard ratio for aortic valve stenosis was 1.3 (95% confidence interval [CI]: 1.

171 ty for the treatment of aortic and pulmonary valve stenosis was first described nearly 40 years ago.

172 Tricuspid valve stenosis was not documented in any of the patients

173 e right sinus of Valsalva, congenital aortic valve stenosis (with bicuspid valve) and myocarditis.

174 Aortic valve stenosis (with or without aortic regurgitation and

175 rosthetic valve regurgitation, or prosthetic valve stenosis within 30 days of the procedure.

176 the hypothesis that calcification and aortic valve stenosis would develop in genetically hypercholest