ライフサイエンスコーパス: LV dilation

1 rtrophy), and tall R waves in V4 through V6 (LV dilation).

2 fter MI and be associated with the degree of LV dilation.

3 emodeling, leading to myocardial rupture and LV dilation.

4 rnal validation (AUROC: LV dysfunction 0.89; LV dilation 0.83; RV dysfunction 0.82; RV dilation 0.80)

5 nternal testing (AUROC: LV dysfunction 0.87; LV dilation 0.86; RV dysfunction 0.88; RV dilation 0.81)

6 after myocardial infarction (MI) results in LV dilation, a major cause of congestive heart failure a

7 lsartan and valsartan attenuated progressive LV dilation after 1 and 5 weeks treatment.

8 protects against contractile dysfunction and LV dilation after chronic pressure overload.

9 argeted deletion of the MMP9 gene attenuates LV dilation after experimental MI in mice.

10 lure may be caused by late left ventricular (LV) dilation after anterior infarction.

11 deletion of MMP9 have less left ventricular (LV) dilation after experimental MI than do sibling wild-

12 O-null mice experienced 35.1% (P<0.001) less LV dilation and a 52.2% (P<0.0001) improvement in LV fun

13 ilure model, TG hearts displayed accelerated LV dilation and a faster decline of shortening fraction.

14 Despite marked LV dilation and depressed function initially, children w

15 P<0.001), causing lethal cardiomyopathy with LV dilation and depressed systolic function (percent fra

16 osis in unstressed mice, causing progressive LV dilation and diminished systolic function.

17 When associated with LV dilation and dysfunction, hypertrophy, or congenital

18 urred with the initiation and progression of LV dilation and dysfunction.

19 entricles (LVs) and is often associated with LV dilation and dysfunction.

20 The degree of LV dilation and enhanced function did not significantly

21 MMPi attenuated the degree of post-MI LV dilation and expansion of the infarct during the late

22 ed with saline control, would result in less LV dilation and fewer adverse clinical events between ba

23 CMR predictors of CEs were LV dilation and LGE.

24 MMP activity contributes to LV dilation and progression to LV dysfunction in a roden

25 concomitant MMPi with developing CHF limited LV dilation and reduced wall stress.

26 esent project tested the hypothesis that the LV dilation and remodeling during the progression of CHF

27 to non-CIMR, CIMR animals exhibited greater LV dilation and significant reductions in posterior maxi

28 The results suggest that preventing LV dilation and stretch with the CSD promotes downregula

29 iated with increased LV function and reduced LV dilation and that end-systolic wall stress was reduce

30 lude alternative causes of left ventricular (LV) dilation and dysfunction, identify etiologies that m

31 rm administration prevents left ventricular (LV) dilation and infarct expansion.

32 ure (CHF) is associated with left ventricle (LV) dilation and myocardial remodeling.

33 e (CHF) is associated with left ventricular (LV) dilation and myocardial remodeling.

34 ute MI improves global LV function, prevents LV dilation, and blunts the increase in constitutive mic

35 reserved LV systolic performance, diminished LV dilation, and decreased ventricular sphericalization.

36 iographically defined stage (LV hypertrophy, LV dilation, and LV failure).

37 ed age at diagnosis younger than 14.3 years, LV dilation, and LV posterior wall thinning.

38 ocyte infiltration, significant reduction in LV dilation, and marked preservation of LV function.

39 ortic constriction caused myocyte apoptosis, LV dilation, and systolic failure, all of which were inh

40 Echocardiograms revealed LV dilation, as well as decreased LV fractional shorteni

41 arly post-MI treatment with p1158/59 reduced LV dilation at day 7 post-MI by preserving LV structure

42 on, particularly those younger and with less LV dilation at diagnosis.

43 metric distortion of the mitral apparatus by LV dilation (augmented leaflet tethering).

44 2; LV hypertrophy: AUROC, 0.84, AUPRC, 0.25; LV dilation: AUROC, 0.87, AUPRC, 0.33), with composite o

45 3; LV hypertrophy: AUROC, 0.88, AUPRC, 0.28; LV dilation: AUROC, 0.91, AUPRC, 0.47) and external vali

46 +/- 8%, MR was initially trace with limited LV dilation, but it became moderate with subsequent prom

47 ic constriction developed significantly less LV dilation by echocardiography and magnetic resonance i

48 eks after MI, untreated rats had significant LV dilation compared with sham-operated rats (LV diastol

49 -/-) mice developed a faster and more severe LV dilation compared with WT mice (P<0.05 for both end-s

50 Chronic AR causes left ventricular (LV) dilation, creating the potential for FMR.

51 s isolated NCCM, NCCM with left ventricular (LV) dilation (DCM), and NCCM with LV hypertrophy (HCM).

52 AAP LV hypertrophy was driven by LV dilation (DeltaLV end-diastolic volume, 9+/-3 mL/m(2)

53 tening or ejection fraction z-score <-2) and LV dilation (end-diastolic dimension [LVEDD] z-score >2)

54 Left ventricular (LV) dilation from days 1 to 90 was used as a measure of

55 5%; and 3% (n = 7) had frank DCM, defined as LV dilation, impaired contractile performance and LVEDD

56 LV dilation, impaired LV ejection fraction, and LV-ncMM

57 These perturbations may be linked to more LV dilation in CIMR, which possibly reduced the effectiv

58 evice (CSD) was shown to prevent progressive LV dilation in dogs with heart failure (HF) and increase

59 Transdermal NTG patches prevent LV dilation in patients surviving AMI.

60 Four weeks of TACE inhibition abrogated the LV dilation in the MHCsTNF mice and resulted in an incre

61 matrix metalloproteinase inhibitor prevented LV dilation in the MHCsTNF2 mice.

62 g at 2 weeks after MI, reduced the extent of LV dilation, infarct expansion, and EF decline.

63 Longer durations of SVT caused progressive LV dilation, LV pump failure, and myocyte contractile dy

64 to have no prognostic impact over and above LV dilation, LV systolic dysfunction, and presence of LG

65 nical CHF while the remaining 12 animals had LV dilation (LVR) without CHF.

66 Left ventricular (LV) dilation, mitral regurgitation, elevated central ven

67 dil for 6 days before imaging did not reduce LV dilation or improve function compared with those in c

68 control mice; however, AC(VI) mice had less LV dilation (P < 0.001) and increased ejection fractions

69 r (RV) apical dilation and left ventricular (LV) dilation (p < 0.01), RV basal bulging and LV conicit

70 We conclude that in the adult heart, LV dilation produced stretch-mediated activation of phos

71 erexpression of TNF that develop progressive LV dilation/remodeling from 4 to 12 weeks of age.

72 bilateral ARVD had greater LV mass index and LV dilation than patients with unilateral disease.

73 LV function, cardiac myocyte shortening, and LV dilation that were at least partially reversible by r

74 concentric hypertrophy to left ventricular (LV) dilation that occurs in this line of transgenic mice

75 ) dysfunction versus geometric distortion by LV dilation, using models of acute and chronic segmental

76 lar collagen weave in the MHCsTNF2 mice with LV dilation was characterized by a diminished collagen c

77 However, LV dilation was reduced by approximately 50% in both the

78 l arteriovenous fistula, volume overload and LV dilation were detected.

79 myocardial infarction, BM(-/-) mice had more LV dilation, worse LV systolic and diastolic function, h

80 Ptges(-/-) mice develop more left ventricle (LV) dilation, worse LV contractile function, and higher