ライフサイエンスコーパス: aortic valve stenosis

1 s causally associated with increased risk of aortic valve stenosis.

2 lerotic cardiovascular disease, and calcific aortic valve stenosis.

3 atherosclerotic cardiovascular disease, and aortic valve stenosis.

4 >=20% PESP has a 100% sensitivity for severe aortic valve stenosis.

5 posits, calcification and the development of aortic valve stenosis.

6 samples derived from patients with calcific aortic valve stenosis.

7 myocardial infarction, ischaemic stroke, and aortic valve stenosis.

8 nd predicted risk undergoing TAVR for native aortic valve stenosis.

9 aortic valve replacement in the treatment of aortic valve stenosis.

10 equently in patients with symptomatic severe aortic valve stenosis.

11 nical benefit for cardiovascular disease and aortic valve stenosis.

12 ll shear stress (WSS), and classification of aortic valve stenosis.

13 ted tomography in patients with low-gradient aortic valve stenosis.

14 h efficacy) trials in patients with moderate aortic valve stenosis.

15 tionized the treatment of symptomatic severe aortic valve stenosis.

16 ients 70 years or older with isolated severe aortic valve stenosis.

17 increased risk of myocardial infarction and aortic valve stenosis.

18 ed treatment option for patients with severe aortic valve stenosis.

19 uding ascending aortic dilation and calcific aortic valve stenosis.

20 existing cardiovascular disease or calcific aortic valve stenosis.

21 tain high-risk surgical patients with severe aortic valve stenosis.

22 ctor for cardiovascular disease and calcific aortic valve stenosis.

23 mic and functional characteristics of severe aortic valve stenosis.

24 functional properties of severe degenerative aortic valve stenosis.

25 or cardiovascular disease (CVD) and calcific aortic valve stenosis.

26 for treatment of severe symptomatic calcific aortic valve stenosis.

27 e best approach to treat neonatal congenital aortic valve stenosis.

28 PPM and regression of SMR following AVR for aortic valve stenosis.

29 alve thickening to severe calcification with aortic valve stenosis.

30 enic signaling, and halts the progression of aortic valve stenosis.

31 entify therapeutic targets for prevention of aortic valve stenosis.

32 ative predictive value for diagnosing severe aortic valve stenosis.

33 italization, and aortic valve replacement in aortic valve stenosis.

34 in low-surgical risk patients with bicuspid aortic valve stenosis achieved favorable 30-day results,

35 gh shear stress, as present in patients with aortic valve stenosis, activates multiple monocyte funct

36 rdiographic findings in patients with severe aortic valve stenosis after transcatheter aortic valve r

37 as generally been the first-line therapy for aortic valve stenosis, although some contemporary studie

38 prospective study, participants with severe aortic valve stenosis and clinically indicated CT for tr

39 egies aiming to prevent PPM in patients with aortic valve stenosis and concomitant SMR.

40 will effectively reduce the risk of calcific aortic valve stenosis and CVD.

41 ies unique drivers of atherosclerosis versus aortic valve stenosis and implicates EVs in advanced car

42 Aortic valve stenosis and insufficiency develop over tim

43 Eligible patients had severe bicuspid aortic valve stenosis and met American Heart Association

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

45 ong risk factors for development of calcific aortic valve stenosis and predict severity of the diseas

46 ies that highlight Lp(a) in CVD and calcific aortic valve stenosis and propose pathways to clinical r

47 x was associated with causal risk ratios for aortic valve stenosis and replacement, respectively, of

48 was causally associated with higher risk of aortic valve stenosis and replacement.

49 ss index is causally associated with risk of aortic valve stenosis and replacement.

50 d Lp(a) is causally associated with calcific aortic valve stenosis and the need for aortic valve repl

51 le to understand the molecular mechanisms of aortic valve stenosis and to help guide sex-based precis

52 Thirty-five patients with aortic-valve stenosis and 10 healthy controls underwent

53 tive cardiomyopathy (HOCM), 10 patients with aortic valve stenosis, and 14 healthy individuals using

54 nvasive diagnostic tool in the assessment of aortic valve stenosis, and how the results compare with

55 are clinical risk factors for development of aortic valve stenosis, and hypercholesterolemia is a put

56 lacement in patients with symptomatic severe aortic valve stenosis; and antiplatelet agents vorapaxar

57 Causal risk factors for aortic valve stenosis are poorly understood, limiting th

58 option for patients with severe symptomatic aortic valve stenosis (AS) across the whole spectrum of

59 nto the haemodynamic cardiac consequences of aortic valve stenosis (AS) and aortic valve regurgitatio

60 Whether aortic valve stenosis (AS) can adversely affect systemic

61 Aortic valve stenosis (AS) can cause angina despite unob

62 athophysiological shear rates as observed in aortic valve stenosis (AS) can influence protein conform

63 vere pulmonary hypertension (PHT) and severe aortic valve stenosis (AS) from 1987 to 1999.

64 Aortic valve stenosis (AS) induces compensatory alterati

65 Calcific aortic valve stenosis (AS) is a life-threatening disease

66 Aortic valve stenosis (AS) is the most common manifestat

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

68 (AT)/ejection time (ET) ratio is a marker of aortic valve stenosis (AS) severity and predicts outcome

69 the value of stress FR for the detection of aortic valve stenosis (AS) severity and the prediction o

70 In aortic valve stenosis (AS), the occurrence of heart fail

71 treatment can modify the natural history of aortic valve stenosis (AS).

72 nd obesity impacted outcome in patients with aortic valve stenosis (AS).

73 The use of TAVI in severe bicuspid aortic valve stenosis, asymptomatic severe aortic stenos

74 In patients with severe aortic valve stenosis at intermediate surgical risk, tra

75 Aortic valve stenosis (AVS) is a progressive disease, wh

76 Aortic valve stenosis (AVS) is a sexually dimorphic dise

77 Accurate quantification of aortic valve stenosis (AVS) is needed for relevant manag

78 Aortic valve stenosis (AVS) patients experience pathogen

79 Congenital aortic valve stenosis (AVS), coarctation of the aorta (C

80 A region was associated with the presence of aortic valve stenosis (AVS), no prospective study has su

81 Aortic valve stenosis (AVS), which is the most common va

82 rity of aortic valve regurgitation (AVR) and aortic valve stenosis (AVS).

83 ospectively associate with increased risk of aortic valve stenosis (AVS).

84 the severity and hemodynamic consequences of aortic valve stenosis (AVS).

85 s assessed by FFR in 54 patients with severe aortic valve stenosis before and after transcatheter aor

86 g triglycerides is likely to prevent CAD and aortic valve stenosis but may increase thromboembolic ri

87 ctor for cardiovascular disease and calcific aortic valve stenosis, but no approved specific therapy

88 er aortic valve replacement (AVR) for severe aortic valve stenosis, but whether or not frail patients

89 In patients with low-gradient aortic valve stenosis, catheter-induced premature ventri

90 Congenital aortic valve stenosis (CAVS) affects up to 10% of the wo

91 Calcific aortic valve stenosis (CAVS) is a frequent and life-thre

92 Calcific aortic valve stenosis (CAVS) is a major health problem f

93 to cardiovascular disease (CVD) and calcific aortic valve stenosis (CAVS) is substantial.

94 Calcific aortic valve stenosis (CAVS) is the most frequent valve

95 se (CAD), ischemic stroke (IS), and calcific aortic valve stenosis (CAVS).

96 ently no medical therapy to prevent calcific aortic valve stenosis (CAVS).

97 Patients with severe aortic valve stenosis deemed to be at intermediate or in

98 Patients with severe aortic valve stenosis deemed to be at intermediate risk

99 As aortic valve stenosis develops, valve tissue becomes sti

100 f hypertrophy was also seen in patients with aortic valve stenosis: ERK(Thr188) phosphorylation was i

101 Pharmacological treatments for fibrocalcific aortic valve stenosis (FCAVS) have been elusive for >50

102 nderwent TAVR for treatment of severe native aortic valve stenosis from June 2010 to May 2021 across

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

104 nts, and risk factors described for critical aortic valve stenosis have been shown to be inapplicable

105 nt (TAVR) in low-risk patients with bicuspid aortic valve stenosis have not been studied in a large s

106 ly with CAD risk, peripheral artery disease, aortic valve stenosis, heart failure, and lifespan.

107 en have a better prognosis when experiencing aortic valve stenosis, hypertrophic cardiomyopathy, or h

108 ortic valve sclerosis was present in 26% and aortic valve stenosis in 2% of the entire study cohort;

109 risk of cardiovascular disease and calcific aortic valve stenosis in patients with elevated Lp(a) co

110 Aortic valve stenosis is a sexually dimorphic disease, w

111 Whether aortic valve stenosis is accelerated by inflammation and

112 Aortic valve stenosis is an increasingly prevalent degen

113 ructure of myofibroblasts from patients with aortic valve stenosis is more condensed than that of myo

114 g hypertension in patients with asymptomatic aortic valve stenosis is scarce.

115 Aortic valve stenosis is the most common type of congeni

116 Although aortic-valve stenosis is clearly associated with adverse

117 Aortic valve stenosis may influence fractional flow rese

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

119 Atrial fibrillation, calcific aortic valve stenosis, mitral regurgitation, and left at

120 ion, diabetes, atrial fibrillation, calcific aortic valve stenosis, mitral regurgitation, and left at

121 In moderate and severe aortic valve stenosis, mPAP/CO slope and percent-predict

122 tional associations of obesity with incident aortic valve stenosis (n = 1,215) and replacement (n = 4

123 or redo TAVR were moderate-severe prosthetic aortic valve stenosis (n=10, 21.7%), moderate-severe cen

124 Patients with severe aortic valve stenosis (n=161) undergoing aortic valve re

125 aortic valve is frequently an antecedent to aortic valve stenosis or insufficiency and is often asso

126 ion of pathophysiological conditions such as aortic valve stenosis or insufficiency, making it possib

127 (OR, 1.04 [95% CI, 0.77-1.39]; P=0.810), and aortic valve stenosis (OR, 1.03 [95% CI, 0.56-1.90]; P=0

128 ted with CAD (OR, 1.25 [95% CI, 1.12-1.40]), aortic valve stenosis (OR, 1.29 [95% CI, 1.04-1.61]), an

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

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

131 w-up measurements were performed in HOCM and aortic valve stenosis patients 4 months after surgery.

132 s in myofibroblast activation and subsequent aortic valve stenosis progression.

133 as a promising pharmaceutical target to slow aortic valve stenosis progression.

134 sclerotic cardiovascular disease (ASCVD) and aortic valve stenosis, provides clinical guidance for te

135 agic stroke, ischaemic stroke, hypertension, aortic valve stenosis, pulmonary embolism, and venous th

136 pandable valve for the treatment of bicuspid aortic valve stenosis) registry included 353 consecutive

137 Neonates with critical aortic valve stenosis remain a particularly high-risk gr

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

139 The prognostic value of the mPAP/CO slope in aortic valve stenosis remains unknown.

140 in FFR values was found before and after the aortic valve stenosis removal (0.89+/-0.10 versus 0.89+/

141 Coronary hemodynamics are influenced by aortic valve stenosis removal.

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

143 Aortic valve stenosis severity was assessed by a core la

144 ons for diseases such as atherosclerosis and aortic valve stenosis, since it strongly suggests a gene

145 t to randomize all-comers with severe native aortic valve stenosis to either transcatheter aortic val

146 (Bicuspid Aortic Valve Stenosis Transcatheter Aortic Valve Replace

147 idney transplant recipients (KT) with severe aortic valve stenosis underwent transfemoral TAVI.

148 nd the age and sex-adjusted hazard ratio for aortic valve stenosis was 1.3 (95% confidence interval [

149 from the right sinus of Valsalva, congenital aortic valve stenosis (with bicuspid valve) and myocardi

150 Aortic valve stenosis (with or without aortic regurgitat

151 tested the hypothesis that calcification and aortic valve stenosis would develop in genetically hyper