ライフサイエンスコーパス: ventricular dilatation

1 with PD98059 delayed the development of left ventricular dilatation.

2 ventricular end-diastolic pressure, and left ventricular dilatation.

3 ion, fibrosis, and decompensated right-sided ventricular dilatation.

4 of the ventricular myocardium and resultant ventricular dilatation.

5 processes which occur with acute and chronic ventricular dilatation.

6 leads to a significant elevation of VEGF and ventricular dilatation.

7 hypertrophy and associated with the onset of ventricular dilatation.

8 y as measured by dimensional indexes of left ventricular dilatation.

9 ion analysis to determine predictors of left ventricular dilatation.

10 ventricular dilatation and 20% having right ventricular dilatation.

11 djusted odds ratio 2.2; P<0.0001), and right ventricular dilatation (adjusted odds ratio 2.2; P<0.000

12 T and leads to impaired cardiac function and ventricular dilatation after cardiac injury.

13 pectively), with 26% of patients having left ventricular dilatation and 20% having right ventricular

14 ecause the GSK-3beta knockouts had less left ventricular dilatation and better-preserved left ventric

15 ced hypertrophy that rapidly transitioned to ventricular dilatation and contractile dysfunction.

16 (H222P/H222P) mice after they developed left ventricular dilatation and decreased ejection fraction.

17 38alpha inhibitor ARRY-371797 prevented left ventricular dilatation and deterioration of fractional s

18 ation, inhibit apoptosis, and attenuate left ventricular dilatation and disease progression.

19 ment of older patients with less severe left ventricular dilatation and dysfunction during the years.

20 e mice that survived the first 10 days, left ventricular dilatation and dysfunction remained worse in

21 post-MI, KO mice had significantly more left ventricular dilatation and dysfunction than WT mice.

22 seline evaluation, patients had marked right ventricular dilatation and dysfunction, abnormal septal

23 auses significant morbidity, producing right ventricular dilatation and dysfunction, exercise intoler

24 initial clinical status and the severity of ventricular dilatation and dysfunction.

25 arrhythmia, and right and occasionally left ventricular dilatation and dysfunction.

26 larly prevalent in families with early-onset ventricular dilatation and dysfunction.

27 eased in the late stages of hypertrophy when ventricular dilatation and failure are present.

28 Before onset of ventricular dilatation and heart failure (determined by

29 D4(+) T cells and prevented progressive left ventricular dilatation and hypertrophy, whereas adoptive

30 primary myocardial disorder characterized by ventricular dilatation and impaired systolic function.

31 after acute myocardial infarction can reduce ventricular dilatation and improve patient survival.

32 It has been proposed that ventricular dilatation and neurohormonal activation duri

33 cardial infarction (AMI) is characterized by ventricular dilatation and regional akinesis.

34 ardiomyopathy (IDC) is characterized by left ventricular dilatation and systolic dysfunction after kn

35 predominantly in coronary heart disease with ventricular dilatation and systolic dysfunction.

36 ngs in Dhcr7(T93M/Delta3-5) mice include CNS ventricular dilatation and two to three syndactyly.

37 perior preservation of LV geometry with less ventricular dilatation and wall thinning.

38 oinciding with severe hypertrophy, preceding ventricular dilatation, and glucose transporter protein

39 ventricular diastolic dysfunction and right ventricular dilatation are the echocardiographic variabl

40 troponin T (deltaLys210) caused early-onset ventricular dilatation (average age at diagnosis, 24 yea

41 c left ventricular remodeling, greater right ventricular dilatation (base, 34+/-7 versus 31+/-6 and 3

42 minent in animals that had more initial left ventricular dilatation (both P<0.05).

43 sation in most animals characterized by left ventricular dilatation, depressed systolic function, and

44 TnI1-193) in the heart were found to develop ventricular dilatation, diminished contractility, and re

45 omed to the heart and induced long-term left ventricular dilatation, dysfunction, and fibrosis in nai

46 in dyssynchrony >200 ms, lack of severe left ventricular dilatation (end-systolic dimension index <29

47 ructural remodeling is characterized by left ventricular dilatation, fibrosis, and hypertrophy of the

48 monary hypertension is associated with right ventricular dilatation, high right-sided filling pressur

49 iASPP deficiency specifically induces right ventricular dilatation in mouse embryos at embryonic day

50 centric left ventricular remodeling and less ventricular dilatation in response to arterial hypertens

51 experienced periventricular haemorrhage and ventricular dilatation in the neonatal period showed the

52 mber per heart, contractile dysfunction, and ventricular dilatation in zebrafish.

53 mitral E-to-strain-rate e'-wave ratio, right ventricular dilatation (increased right ventricular end-

54 Left ventricular dilatation is a well-recognized precursor of

55 At both ages, lateral ventricular dilatation, necrotic foci, periventricular c

56 isease, before fixed atrial fibrillation and ventricular dilatation occur.

57 ic volumes revealed that the least amount of ventricular dilatation occurred in the MN group (P<0.05)

58 evidence of periventricular haemorrhage and ventricular dilatation on neonatal ultrasound exhibited

59 tudy establishes the role of very early left ventricular dilatation on outcome in MI and may be usefu

60 curs soon after MI, the effect of early left ventricular dilatation on outcome is not established and

61 The effect of left ventricular dilatation on the risk of heart failure in p

62 e findings challenge the paradigm that right ventricular dilatation on ultrasound during cardiopulmon

63 3-4, i.e., intraventricular hemorrhage with ventricular dilatation or intraparenchymal involvement).

64 The magnitude of elevation predicted left ventricular dilatation (r=.80 when variables were treate

65 hages or intraventricular hemorrhage without ventricular dilatation, respectively); and 3) severe int

66 Neonatal periventricular haemorrhage with ventricular dilatation revealed by ultrasound may be ass

67 on secondary to increased afterload and left ventricular dilatation secondary to volume overload.

68 The marked ventricular dilatation seen in the untreated fistula gro

69 onses culminate in diminished pump function, ventricular dilatation, wall thinning, and fibrosis, and

70 tion, left ventricular hypertrophy, and left ventricular dilatation were associated with the developm