ライフサイエンスコーパス: aortic valve disease

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

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

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

4 utic candidates targeting the progression of aortic valve disease.

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

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

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

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

9 history of combined stenotic and regurgitant aortic valve disease.

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

11 e mineralised material produced in calcified aortic valve disease.

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

13 patients with ascending aortic aneurysms and aortic valve disease.

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

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

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

17 f calcium deposition that causes progressive aortic valve disease.

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

19 atients with comparable degrees of tricuspid aortic valve disease.

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

21 linical factors associated with degenerative aortic valve disease.

22 rence, reoperation and secondary progressive aortic valve disease.

23 underwent 17 reoperations for recurrence or aortic valve disease.

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

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

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

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

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

29 /- 8 years of age, 68% men) with and without aortic valve disease and measured their coronary calcium

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

69 Calcific aortic valve disease is characterized by an abnormal min

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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