ライフサイエンスコーパス: mitral valve disease

1 sural prolapse, as well as a mixed cause for mitral valve disease.

2 o promote the development of AF in rheumatic mitral valve disease.

3 prove outcomes in patients with degenerative mitral valve disease.

4 trial fibrillation or flutter or significant mitral valve disease.

5 ntional surgical approaches for degenerative mitral valve disease.

6 n selected patients with combined aortic and mitral valve disease.

7 al valve repair or from organ donors without mitral valve disease.

8 s for the treatment of aortic, pulmonic, and mitral valve disease.

9 n in part the pathophysiology of Fen-related mitral valve disease.

10 fibrillation, particularly in patients with mitral valve disease.

11 roaches for treatment of isolated aortic and mitral valve disease.

12 perhaps more common nonsyndromic variants of mitral valve disease.

13 oronary artery disease (CAD) without primary mitral valve disease.

14 6.6%), ischemic (4.6%), and traumatic (0.3%) mitral valve disease.

15 n of atrial arrhythmias and in patients with mitral valve disease.

16 the diagnosis and treatment of patients with mitral valve disease.

17 cognized as an important anatomic feature of mitral valve disease.

18 gated aortic valve disease and the remainder mitral valve disease.

19 nce (CMR) imaging in assessing patients with mitral valve disease.

20 escribed the use of ultrasound for assessing mitral-valve disease.

21 with increased repair rates of degenerative mitral valve disease (adjusted odds ratio [OR]: 1.13 for

22 Mitral valve diseases affect ~3% of the population and a

23 gy VHD II registry, 470 had severe rheumatic mitral valve disease and 332 had previous rheumatic mitr

24 e cellular mechanisms involved in myxomatous mitral valve disease and calcific aortic valve disease a

25 ation (SMR) occurs in the absence of organic mitral valve disease and may develop as the left ventric

26 s versus valves from patients with rheumatic mitral valve disease and nondiseased aortic valves versu

27 ommon to valves from patients with rheumatic mitral valve disease and valves from patients with rheum

28 to pathological stimuli (e.g., hypertension, mitral valve disease) and physiological stimuli (exercis

29 ated cardiomyopathy, 10 dogs with myxomatous mitral valve disease, and 7 healthy non-Boxer dogs) were

30 on, the management of rheumatic, aortic, and mitral valve disease, and the application of balloon com

31 elopments in the management of patients with mitral valve disease are reviewed.

32 orifice area, prolapse height and volume in mitral valve disease, area of the left ventricular outfl

33 creased incidence of cardiovascular disease, mitral valve disease, arrhythmias, and mortality.

34 ater understanding of the pathophysiology of mitral valve disease as well as the improved outcome rel

35 ents with failing bioprostheses and rings or mitral valve disease associated with severe mitral annul

36 predispositions for certain diseases (i.e., mitral valve disease, atrial fibrillation and osteosarco

37 bserved the expected breed associations with mitral valve disease, atrial fibrillation, and osteosarc

38 preoperative differentiation of degenerative mitral valve disease based on etiology (predominantly Ba

39 ir was the preferred option for degenerative mitral valve disease but was only slightly more commonly

40 t outcomes in patients with heart failure or mitral valve disease, but their impact on outcomes in pa

41 l assessment, and haemodynamic assessment of mitral valve disease by CMR.

42 of mitral valve repair techniques to address mitral valve disease can be related to increased surgica

43 learly shown that patients with degenerative mitral valve disease can expect very durable repairs, an

44 Forty-nine patients with degenerative mitral valve disease classified as FED (n=31) and DMD (n

45 eration (DMD) are phenotypes of degenerative mitral valve disease defined morphologically.

46 The field of mitral valve disease diagnosis and management is rapidly

47 with Tendyne led to successful treatment of mitral valve disease due to MAC and significant improvem

48 g left ventricular dysfunction and aortic or mitral valve disease; FoCUS-assisted examination may hel

49 will surgeons, who have led the treatment of mitral valve disease for the past 30 years, have a role

50 aortic regurgitation and without associated mitral valve disease) from 3 different medical centers (

51 dramatic changes in the course of myxomatous mitral valve disease in both dogs and humans.

52 ial tissues from the patients with rheumatic mitral valve disease in either sinus rhythm or persisten

53 close to 60% of patients having surgery for mitral valve disease in the US.

54 omen) consecutive patients with degenerative mitral valve disease, in whom LAVI was prospectively mea

55 of calcific aortic stenosis and degenerative mitral valve disease is 9 and 24 million people, respect

56 The etiology of mitral valve disease is changing.

57 he value of robotically assisted surgery for mitral valve disease is questioned because the high cost

58 ing dedicated devices in native noncalcified mitral valve diseases is beyond the scope of the article

59 Because up to 6% of PSRA patients develop mitral valve disease, it is recommended that antistrepto

60 ten localized (for example, to the aortic or mitral valve), disease manifestations are regularly obse

61 Patients with significant mitral valve disease (mitral stenosis or > or = moderate

62 Patients were divided into the mitral valve disease (MVD) category (ie, those with mitr

63 left atrial pressure (LAP) in patients with mitral valve disease (MVD), given the confounding effect

64 worsened in 65.4% of patients with intrinsic mitral valve disease (myxomatous, calcific, or ischemic

65 tic stenosis (n=20), arch obstruction (n=7), mitral valve disease (n=5), apical aortic conduit stenos

66 ase, and valves from patients with rheumatic mitral valve disease; n=30) followed by system biology a

67 prolapse [MVP] and 202 with nondegenerative mitral valve disease [non-MVP]) were phenotyped for the

68 ssisted examination for diagnosing aortic or mitral valve disease (of at least moderate severity) wer

69 For patients with mitral valve disease, options for tissue valve replaceme

70 ons from patients aged over 70 years who had mitral valve disease or atrial fibrillation when compare

71 pid regurgitation, whether in the context of mitral valve disease or heart failure, should no longer

72 ventricular systolic dysfunction, aortic or mitral valve disease, or pericardial effusion; and used

73 cant left-sided valve disease [predominantly mitral valve disease]), previous documented episodes of

74 ower the incidence of clinically significant mitral valve disease requires further study.

75 Therefore, patients with intrinsic mitral valve disease should be considered for concomitan

76 a repair, valve replacement for degenerative mitral valve disease should be infrequent.

77 AC, a risk factor for clinically significant mitral valve disease, suggesting a causal association.

78 also develop aortic root aneurism and aorto-mitral valve disease that can be fatal depending on the

79 timate goal of preventing the progression of mitral valve disease to the stage of clinical expression

80 heumatic heart disease, atrial ablation, and mitral valve disease was compared, and odds ratios were

81 Patients with intrinsic mitral valve disease were excluded.

82 t surgical approaches to treat patients with mitral valve disease who may also concurrently suffer fr

83 ents (median age 10 months) with symptomatic mitral valve disease who underwent placement of a supraa

84 Children with symptomatic mitral valve disease whose annulus is too small for the