ライフサイエンスコーパス: aortic valve disease

1 linical factors associated with degenerative aortic valve disease.

2 rence, reoperation and secondary progressive aortic valve disease.

3 underwent 17 reoperations for recurrence or aortic valve disease.

4 rocedure of choice for elderly patients with aortic valve disease.

5 gether conferred a 3.5-fold risk of calcific aortic valve disease.

6 way as a potential pharmaceutical target for aortic valve disease.

7 d high body mass index with risk of calcific aortic valve disease.

8 ex are both causal risk factors for calcific aortic valve disease.

9 t of aortic arch architecture and functional aortic valve disease.

10 ease and valves from patients with rheumatic aortic valve disease.

11 ss >=13 mm and no history of hypertension or aortic valve disease.

12 is in mice causes accelerated progression of aortic valve disease.

13 utic candidates targeting the progression of aortic valve disease.

14 regurgitation, and in patients with bicuspid aortic valve disease.

15 in the context of both moderate and advanced aortic valve disease.

16 and the DNA methylation pattern in calcific aortic valve disease.

17 t lncRNA H19 (H19) was increased in calcific aortic valve disease.

18 ve of a causal association between LDL-C and aortic valve disease.

19 dies for plasma lipids, were associated with aortic valve disease.

20 olic dysfunction in patients with mitral and aortic valve disease.

21 verity, allows diagnosis of severe calcified aortic valve disease.

22 history of combined stenotic and regurgitant aortic valve disease.

23 e mineralised material produced in calcified aortic valve disease.

24 role of this operation for the management of aortic valve disease.

25 patients with ascending aortic aneurysms and aortic valve disease.

26 rkers as potential risk factors for calcific aortic valve disease.

27 ic signaling, and retards the progression of aortic valve disease.

28 ison with Marfan-like syndromes and isolated aortic valve disease.

29 f calcium deposition that causes progressive aortic valve disease.

30 ing in vivo, and provide an animal model for aortic valve disease.

31 atients with comparable degrees of tricuspid aortic valve disease.

32 ment option in young patients suffering from aortic-valve disease.

33 be a poor predictor of subclinical calcific aortic-valve disease.

34 We aimed to assess native aortic valve disease activity and bioprosthetic valve du

35 ssions Database, we identified patients with aortic valve disease admitted 2012 to 2016 for SAVR, TAV

36 ase the risk of atherosclerosis and calcific aortic valve disease, affecting millions of patients wor

37 and potentially causal mediators of calcific aortic valve disease allows opportunities for therapies

38 secutive, nonrandomized patients treated for aortic valve disease and ascending aortic aneurysm (n=27

39 edure and to compare early outcome in simple aortic valve disease and complex left heart disease.

40 tify the Eln(+/-) mouse as a model of latent aortic valve disease and establish a role for elastin dy

41 ltiple links between the polygenic score for aortic valve disease and key health-related comorbiditie

42 /- 8 years of age, 68% men) with and without aortic valve disease and measured their coronary calcium

43 fundamentally differ from those observed in aortic valve disease and open novel avenues guiding futu

44 Of these trials, 103 (74%) investigated aortic valve disease and the remainder mitral valve dise

45 myxomatous mitral valve disease and calcific aortic valve disease and to redefine the term degenerati

46 hate may be a novel risk factor for calcific aortic valve disease and warrants further study.

47 sorders, including mitral valve prolapse and aortic valve disease, and describe findings that implica

48 isease such as the Marfan syndrome, bicuspid aortic valve disease, and hereditary aortic aneurysm and

49 uring hyperlipidemia, leading to early-stage aortic valve disease, and PPARgamma activation protects

50 ses (vs. mechanical prostheses) for treating aortic valve disease, and this tendency is likely to con

51 [NDMVs], valves from patients with rheumatic aortic valve disease, and valves from patients with rheu

52 Human control and calcific aortic valve disease aortic valve leaflets and patient-s

53 tions of aortic 4D flow MRI in patients with aortic valve disease, aortopathy, coarctation, dissectio

54 Complications from congenital aortic valve disease are a major source of premature mor

55 ggest that the processes leading to calcific aortic valve disease are metabolically active for many y

56 n outcome and prognostic factors in combined aortic valve disease are scarce.

57 KEY POINTS: Severe aortic valve diseases are common cardiac abnormalities t

58 Subjects with severe native or bioprosthetic aortic valve disease at high or extreme risk for surgery

59 ons of HF (including ischemic heart disease, aortic valve disease, atrial fibrillation, congenital he

60 Ross procedure as treatment for adults with aortic valve disease (AVD) has been the subject of renew

61 Aortic valve disease (AVD) is a growing public health pr

62 Aortic valve disease (AVD) is associated with high morta

63 d a set of 25 chest radiographs (15 cases of aortic valve disease [AVD], 10 control cases without AVD

64 importance of operating on the elderly with aortic valve disease; both long-term survival and functi

65 bicuspid aortic valve formation and calcific aortic valve disease, but knowledge is very limited abou

66 Ten-year absolute risk of calcific aortic valve disease by categories of lipoprotein(a) lev

67 MI registry (n=403).Compared with tricuspid aortic valve disease, CAE occurred more than twice as fr

68 Asymptomatic patients with combined aortic valve disease can be safely followed until surgic

69 cularly dire clinical relevance, as calcific aortic valve disease can progress rapidly to aortic sten

70 uses on technologies at the core of calcific aortic valve disease (CAVD) and drug target research adv

71 Calcific aortic valve disease (CAVD) and stenosis have a complex

72 Calcific aortic valve disease (CAVD) increasingly afflicts our ag

73 Calcific aortic valve disease (CAVD) is a highly prevalent condit

74 Calcific aortic valve disease (CAVD) is a prevailing disease with

75 Calcific aortic valve disease (CAVD) is a prevalent valvular diso

76 Calcific aortic valve disease (CAVD) is a widely prevalent heart

77 Calcific aortic valve disease (CAVD) is an increasingly prevalent

78 Calcific aortic valve disease (CAVD) is characterized by a phenot

79 Calcific aortic valve disease (CAVD) is common in people over the

80 Calcific aortic valve disease (CAVD) is the most common cause of

81 Calcific aortic valve disease (CAVD) is the most common form of v

82 Calcific aortic valve disease (CAVD) is the most common heart dis

83 Calcific aortic valve disease (CAVD) is the most common valve dis

84 Calcific aortic valve disease (CAVD) occurs when subpopulations o

85 An insufficient understanding of calcific aortic valve disease (CAVD) pathogenesis remains a major

86 he morbidity and mortality rates of calcific aortic valve disease (CAVD) remain high while treatment

87 Calcific aortic valve disease (CAVD) resulting in aortic stenosis

88 In calcific aortic valve disease (CAVD), activated T lymphocytes loc

89 athways constituting biomarkers for calcific aortic valve disease (CAVD), including extra-cellular ma

90 In calcific aortic valve disease (CAVD), mechanosensitive valvular c

91 and Lp(a) have been associated with calcific aortic valve disease (CAVD).

92 tein(a) [Lp(a)] was associated with calcific aortic valve disease (CAVD).

93 iated phospholipase A2 (Lp-PLA2) in calcific aortic valve disease (CAVD).

94 A large family with autosomal-dominant aortic valve disease consisting of bicuspid aortic valve

95 Calcific aortic valve disease currently lacks effective treatment

96 Degenerative aortic valve disease (DAVD) has become the most common c

97 pies that impact the progression of calcific aortic valve disease do not currently exist.

98 eavy AVC-load reflective of severe calcified aortic valve disease, emphasizing the clinical yield of

99 ed mechanisms leading to overt fibrocalcific aortic valve disease (FCAVD).

100 The management of aortic valve disease has been improved by accurate diagn

101 (vi) The incidence of calcific aortic valve disease has increased seven-fold during the

102 Progressive aortic valve disease has remained a persistent cause of

103 ase, peripheral artery disease, and bicuspid aortic valve disease have been updated with new evidence

104 ase, peripheral artery disease, and bicuspid aortic valve disease have been updated with new evidence

105 Deciphering which patients with low-gradient aortic valve disease have severe stenosis can be difficu

106 onsidered as an important initial process of aortic valve disease; however, cellular and molecular ev

107 e for the treatment of operable, symptomatic aortic valve disease; however, to date, there are limite

108 s versus valves from patients with rheumatic aortic valve disease identified 213 proteins enriched in

109 etween C-reactive protein (CRP) and calcific aortic valve disease in a large, randomly selected, popu

110 The management of severe aortic valve disease in adults younger than 65 years is

111 rocedure has been used increasingly to treat aortic valve disease in children and young adults.

112 ermine the prevalence and characteristics of aortic valve disease in girls and women with monosomy fo

113 The optimal management of aortic valve disease in patients >80 years old depends o

114 The Ross procedure is commonly used to treat aortic valve disease in pediatric and adult patients.

115 The number of patients treated for aortic valve disease in the United States is increasing

116 nto the haemodynamic cardiac consequences of aortic valve diseases in those with preserved LV ejectio

117 Treatment of aortic-valve disease in young patients still poses chall

118 linical factors associated with degenerative aortic valve disease included age (twofold increased ris

119 The management of aortic valve disease, including aortic stenosis and aort

120 ect in vivo the key cellular events in early aortic valve disease, including endothelial cell and mac

121 The 10-year absolute risk of calcific aortic valve disease increased with higher lipoprotein(a

122 g of the complex mechanisms driving calcific aortic valve disease initiation and progression towards

123 w the role of hemodynamic forces in calcific aortic valve disease initiation and progression, with fo

124 patients were identified as severe calcified aortic valve disease, irrespective of flow.

125 RATIONALE: Aortic valve disease is a cell-mediated process without

126 Calcific aortic valve disease is a common condition and is associ

127 ation in the promoter of H19 during calcific aortic valve disease is associated with a higher express

128 Calcific aortic valve disease is characterized by an abnormal min

129 Calcific aortic valve disease is common in the elderly, is correl

130 aneurysm surgery in the setting of bicuspid aortic valve disease is complex, with multiple factors i

131 Calcific aortic valve disease is dramatically increasing in globa

132 , in AS with discordant MG, severe calcified aortic valve disease is generally detected.

133 The prevalence of calcific aortic valve disease is increasing with aging of the pop

134 lines of evidence suggest that degenerative aortic valve disease is not an inevitable consequence of

135 or aortic valve replacement in patients with aortic valve disease is not known.

136 rtopathy after AVR in patients with bicuspid aortic valve disease is substantially different from tha

137 to test the hypothesis that risk of calcific aortic valve disease is the highest when both plasma lip

138 Calcific aortic valve disease is the most common indication for s

139 Calcific aortic valve disease is the pathological remodeling of v

140 d aortic regurgitation (AR) (n = 554), mixed aortic valve disease (MAVD) (n = 190), or no significant

141 omparison of outcomes between moderate mixed aortic valve disease (MAVD) and isolated aortic stenosis

142 se for elucidation of the pathophysiology of aortic valve disease mechanisms and for the design of ef

143 r intervention to reduce LDL-C could prevent aortic valve disease merits further investigation.

144 rd/Senning (n=2), tetralogy of Fallot (n=2), aortic valve disease (n=2), and other biventricular surg

145 undred seventy-seven patients with suspected aortic valve disease (n=94 BAV, n=83 tricuspid aortic va

146 gene in hypercholesterolemic mice with early aortic valve disease normalizes oxidative stress, reduce

147 lve area is predictive of increased risk for aortic valve disease (odds ratio, 1.14; P=2.3x10(-6)).

148 ndle branch block may also develop following aortic valve disease or cardiac procedures.

149 ween CRP levels and the presence of calcific aortic-valve disease or incident aortic stenosis.

150 significant advances in our understanding of aortic valve disease over the past year.

151 ation to investigate the genetic etiology of aortic valve disease, perform clinical prediction, and u

152 e disease that encompass the entire range of aortic valve disease progression from initial cellular c

153 herapy has proven effective to halt calcific aortic valve disease progression, with invasive and cost

154 therapeutics to alleviate or delay calcific aortic valve disease progression.

155 verload, commonly caused by hypertension and aortic valve disease, promotes remodelling of the myocar

156 ver, its specific role in the development of aortic valve disease remains poorly understood.

157 Calcific aortic valve disease sits at the confluence of multiple

158 sex, hypertension, carotid artery stenosis, aortic valve disease, smoking, and alcohol dependence or

159 ry of hypertension, carotid artery stenosis, aortic valve disease, smoking, or alcohol abuse.

160 mutation in an unrelated family with similar aortic valve disease, suggesting that NOTCH1 haploinsuff

161 This review highlights aspects of calcific aortic valve disease that encompass the entire range of

162 Among 190 563 patients with aortic valve disease, the average aggregate 6-month inpa

163 In calcific aortic valve disease, the valve cusps undergo retraction

164 (age 72+/-8 years, 30% women) with calcific aortic valve disease, therefore predisposed to MAC, unde

165 are upregulated and colocalized in calcific aortic valve disease tissue compared with control tissue

166 olecular imaging can detect early changes in aortic valve disease, we used in vivo a panel of near-in

167 the multivariable adjusted HRs for calcific aortic valve disease were 1.6 (95% CI: 1.3-1.9) for the

168 gone cardiac transplantation, and those with aortic valve disease were better characterized by invest

169 hese do not reduce Lp(a) or risk of calcific aortic valve disease, which has no available drug therap

170 e, and 11,053 control patients with acquired aortic valve disease) who underwent primary AVR without

171 umber of admissions associated with treating aortic valve disease with SAVR, TAVR, or MT.

172 chanical haemodynamic consequences of severe aortic valve diseases (with preserved LV ejection fracti

173 lion people are living with either mitral or aortic valve disease worldwide, and more than 180 000 he