ライフサイエンスコーパス: ventricular dilation

1 Only L-NAME caused right ventricular dilation.

2 ogressive symptomatic heart failure and left ventricular dilation.

3 ic regurgitation complicated by extreme left ventricular dilation.

4 ile function, decreased work capability, and ventricular dilation.

5 art from catastrophic rupture and attenuates ventricular dilation.

6 h, associated with eccentric hypertrophy and ventricular dilation.

7 However, MMPi reduced ventricular dilation.

8 city and contractile function and attenuated ventricular dilation.

9 racterized by impaired systolic function and ventricular dilation.

10 er (91% vs. 65%, p = 0.04), and severe right ventricular dilation (39% vs. 0%, p = 0.013).

11 was 41% (n = 70): 49% in patients with right ventricular dilation, 53% in right ventricular systolic

12 The phenotype consisted of left ventricular dilation (68%), systolic dysfunction (46%),

13 Mitral regurgitation (MR) causes ventricular dilation, a blunted myocardial force-frequen

14 on of an MMP inhibitor attenuates early left ventricular dilation after experimental MI in mice.

15 ized mice to cardiac decompensation and left ventricular dilation after long-term stimulation by pres

16 Cardiac rupture is preceded by left ventricular dilation and a severe decrease in cardiac co

17 ed the clinical manifestation of human ARVC: ventricular dilation and aneurysm, cardiac fibrosis, car

18 ultiple cardiac phenotypic defects including ventricular dilation and cardiac dysfunction.

19 ed CD34+ cells (CD34(Shh)) protected against ventricular dilation and cardiac functional declines ass

20 Echocardiography revealed ventricular dilation and decreased cardiac function, whi

21 ar (LV) fractional shortening accompanied by ventricular dilation and decreased phosphocreatine to AT

22 c analysis demonstrated the presence of left ventricular dilation and decreased systolic function in

23 al CaMKII inhibition are protected from left ventricular dilation and dysfunction after MI.

24 n Medicine Study included patients with left ventricular dilation and dysfunction attributed to idiop

25 ion with 3 months follow-up resulted in left ventricular dilation and dysfunction in both wild-type a

26 elopment of regurgitation resulting in right ventricular dilation and dysfunction necessitating pulmo

27 systole, left ventricular dysfunction, right ventricular dilation and dysfunction, and a large perica

28 ardial iNOS expression, cardiac hypertrophy, ventricular dilation and dysfunction, and fibrosis, wher

29 regurgitation, pulmonary hypertension, right ventricular dilation and dysfunction, and tricuspid regu

30 c echocardiography demonstrated severe right ventricular dilation and dysfunction, raising the suspic

31 tion and angiogenesis, thereby limiting left ventricular dilation and dysfunction.

32 to CD8KO mice, MHCIIKO mice did not develop ventricular dilation and dysfunction.

33 e receptor (AR) pathways in hearts with left ventricular dilation and dysfunction.

34 ion of recombinant GDF15 protein, attenuated ventricular dilation and heart failure in muscle lim pro

35 ac filling pressures may lead to progressive ventricular dilation and heart failure progression.

36 lly followed by scar formation with eventual ventricular dilation and heart failure.

37 farction (MI) is associated with progressive ventricular dilation and heart failure.

38 re 85+/-1 versus 66+/-2 mm Hg; P<0.01), left ventricular dilation and hypertrophy (mass/body weight 4

39 iotensin-converting enzyme inhibition limits ventricular dilation and hypertrophy and improves surviv

40 Ventricular dilation and hypertrophy in addition to dete

41 mmunocomplexes followed by cardiomegaly with ventricular dilation and hypertrophy, ultimately succumb

42 athic dilated cardiomyopathy had evidence of ventricular dilation and hypokinesis, with a left ventri

43 adverse functional consequences of TAC, left ventricular dilation and impaired ejection fraction.

44 Mutant G202R and A592E mice exhibited left ventricular dilation and impaired function with specific

45 ation of the heart, as well as in attenuated ventricular dilation and improved cardiac function.

46 more than wild type, along with greater left ventricular dilation and increased fibrosis, apoptosis,

47 y 14, echocardiography showed increased left ventricular dilation and infarct expansion.

48 nges were associated with reductions in left ventricular dilation and left ventricular mass measured

49 Left ventricular dilation and loss of heart function was prec

50 during atrial arrhythmia are those with left ventricular dilation and low atrial ejection fraction ac

51 ejection fraction (HFrEF) is associated with ventricular dilation and markedly reduced systolic funct

52 ially with an epicardial patch to limit left ventricular dilation and mitral regurgitation.

53 3+, fibrillation (vs. type I flutter), left ventricular dilation and mitral valve area < 2.0 cm2.

54 hat IL-1beta and TNF-alpha may contribute to ventricular dilation and myocardial failure by promoting

55 Left ventricular dilation and myocardial fibrosis are associa

56 hallium lung-to-myocardial ratio (L/M), left ventricular dilation and perfusion defect site were comp

57 Lung uptake, left ventricular dilation and perfusion defect size show good

58 The engrafted human myocardium attenuated ventricular dilation and preserved regional and global c

59 car with newly formed myocardium, attenuated ventricular dilation and prevented the chronic decline i

60 s remodeling of the myocardium, resulting in ventricular dilation and pump dysfunction.

61 In mice with left ventricular dilation and pump failure attributable to pr

62 graphy of homozygous mutant mice showed left ventricular dilation and reduced contractile function at

63 Systolic heart failure is characterized by ventricular dilation and reduced ejection fraction, and

64 ted myocytes was depressed and preceded left ventricular dilation and reduced fractional shortening.

65 +cell hearts exhibited attenuation of global ventricular dilation and reduced septum-to-free wall dia

66 lso enhance late survival by preventing left ventricular dilation and reducing arrhythmias, independe

67 ath and low rate of reintervention for right ventricular dilation and residual outflow tract obstruct

68 Proapoptotic Nix caused ventricular dilation and severe contractile depression i

69 s of afterload reduction for preventing left ventricular dilation and symptom onset in aortic regurgi

70 ilated cardiomyopathy, characterized by left ventricular dilation and systolic dysfunction with signs

71 Left ventricular dilation and the presence of late gadolinium

72 Heterozygous patients exhibit left ventricular dilation and ventricular arrhythmias.

73 Patients with both ventricular dilation and worse GCS were at highest risk.

74 endent increase in cardiac hypertrophy, left ventricular dilation, and adverse left ventricular remod

75 g arrhythmia or conduction disease, isolated ventricular dilation, and hypokinetic nondilated cardiom

76 pertrophy of unaffected cardiomyocytes, left ventricular dilation, and impaired contractile function.

77 st results in persistent truncus arteriosus, ventricular dilation, and impaired ventricular contracti

78 entricular ejection fraction <40%, mild left ventricular dilation, and no symptoms of heart failure (

79 developed greater cardiac hypertrophy, left ventricular dilation, and reduced contractile function.

80 eccentric hypertrophy, substantial fibrosis, ventricular dilation, and reduced fractional shortening,

81 r rates of cardiac rupture, more severe left ventricular dilation, and suppressed ejection fraction c

82 d late activated regions and (2) Global left ventricular dilation as measured in experiments.

83 ascular-specific expression (vGOF) show left ventricular dilation as well as less-markedly increased

84 db/db animals, dbTSP mice had increased left ventricular dilation associated with mild nonprogressive

85 Untreated sheep developed left ventricular dilation at 3 months, with global dysfunctio

86 , congestive heart failure, and greater left ventricular dilation at diagnosis were independently ass

87 uld not be attributed to differences in left ventricular dilation because end-diastolic volumes incre

88 sion maintenance and increased resistance to ventricular dilation) but also for a potentially deleter

89 Both NOS inhibitors led to left ventricular dilation, but PE did not.

90 ice, loss of cMyBP-C has been linked to left ventricular dilation, cardiac hypertrophy, and systolic

91 Results: Pressure overload evoked rapid left ventricular dilation compared with sham (end-systolic vo

92 ed an increase in myocyte width without left ventricular dilation (concentric hypertrophy) and preser

93 age, heterozygous individuals developed left ventricular dilation, contractile dysfunction, and episo

94 ith pulmonary pathophysiology, whereas right ventricular dilation correlated with renal dysfunction.

95 decline in cardiac function, attenuated left ventricular dilation, decreased infarct size, and reduce

96 exacerbated, as indicated by increased left ventricular dilation, decreased ventricular function, in

97 h adverse outcomes are characterized by left ventricular dilation despite CRT.

98 ed in aortic regurgitation with extreme left ventricular dilation (diastolic dimension >/= 80 mm), bu

99 Extreme left ventricular dilation due to aortic regurgitation is obse

100 egurgitation (AR) focus on symptoms and left ventricular dilation/dysfunction.

101 (40% higher after 30 days) and stronger left ventricular dilation early after MI.

102 ventricular power, P=0.0002), and increased ventricular dilation (end-diastolic volume, P=0.01).

103 28.4% versus 18.8%; P=0.0114), reduced left ventricular dilation (end-systolic inner left ventricula

104 ks of pressure-overload stimulation, reduced ventricular dilation, enhanced ventricular performance,

105 KOs developed severe heart failure with left ventricular dilation, impaired cardiomyocyte growth acco

106 erload developed less hypertrophy and showed ventricular dilation, impaired contractile function, inc

107 orsened systolic dysfunction, increased left ventricular dilation, impaired scar maturation, and decr

108 Trpc6 deletion also ameliorated left ventricular dilation, improved cardiac function, and ten

109 eart failure therapy indexed by reduced left ventricular dilation, improved left ventricular ejection

110 p to day 56 after MI revealed increased left ventricular dilation in CD4 KO compared with WT mice.

111 iction (TAC) for 6 weeks caused greater left ventricular dilation in G6PDX mice than wild-type mice.

112 iography showed significantly increased left ventricular dilation in male IL-13(-/-) compared with WT

113 dulin kinase II (CaMKII) activation and left ventricular dilation in mice one week after myocardial i

114 ography at day 1 demonstrated increased left ventricular dilation in OIM/OIM animals.

115 Advanced age is a predictor of death and ventricular dilation in patients with MI; however, the c

116 -/-) animals lack a corpus callosum and show ventricular dilation indicating early hydrocephalus.

117 Therefore, extreme left ventricular dilation is not a contraindication to operat

118 severe cardiac abnormalities, including left ventricular dilation, left ventricular mass reduction, a

119 Left ventricular dilation may predispose to alterations of re

120 viable myocardium after infarction, limiting ventricular dilation, myocardial loading, and cardiac hy

121 These factors limit ventricular dilation, myocardial loading, cardiac hypert

122 However, ventricular dilation, myocyte hypertrophy and death, and

123 Ultimately, a phase develops where ventricular dilation occurs in an attempt to limit the r

124 ess increase, decreased tension (0-20%), and ventricular dilation (of order 10-30%).

125 muscle disorder characterized by atrial and ventricular dilation often with relative wall thinning,

126 gurgitation is indicated if symptoms or left ventricular dilation or dysfunction occur.

127 th arrhythmias in the absence of substantial ventricular dilation or dysfunction.

128 It can be associated with left ventricular dilation or hypertrophy, systolic or diastol

129 ntriculomegaly due to either posthemorrhagic ventricular dilation or periventricular white matter los

130 of increased wall thickness, local or global ventricular dilation, or dysfunction also involved the R

131 P < 0.0001; right, P = 0.0037) and less left ventricular dilation (P < 0.0179).

132 cular ejection fraction (p = 0.006) and left ventricular dilation (p = 0.015) at the follow-up evalua

133 isease, there was weak correlation with left ventricular dilation (r = 0.423, p = 0.020) but not left

134 tolic dimension >/= 80 mm), but extreme left ventricular dilation raises concern about irreversible l

135 protein composition, loss of cardiomyocytes, ventricular dilation, reduced pump function, and ultimat

136 particularly severe myocardial fibrosis with ventricular dilation, reminiscent of the dilated cardiom

137 ions in ventricular performance, and greater ventricular dilation than alpha1C(+)/(+) controls.

138 ated cardiomyopathy is characterised by left ventricular dilation that is associated with systolic dy

139 d cellular hypertrophy, are concomitant with ventricular dilation, thinning of the wall and cardiac d

140 nd indicates severe symptoms (hydrocephalus, ventricular dilation), treatment is continued until deli

141 rapidly progressive cardiomyopathy with left ventricular dilation, wall thinning, and reduced systoli

142 Left ventricular dilation was associated with hemodynamic cha

143 Ventricular dilation was associated with marked reductio

144 Right ventricular dilation was defined as right ventricular:le

145 Right ventricular dilation was noted in 40 subjects (74.1%), w

146 Ventricular dilation was observed in all BSN-dosed mice.

147 Left ventricular dilation was reduced in the GH-treated versu

148 Preoperatively, extreme left ventricular dilation was seen only in male patients and

149 ients late after Fontan operation, increased ventricular dilation was the strongest independent predi

150 rity of preoperative cardiac dysfunction and ventricular dilation were not.

151 sis of embryos revealed evidence of profound ventricular dilation, which likely resulted in embryonic

152 l infarction (MI) developed progressive left ventricular dilation with dysfunction and HF at 4 wk pos

153 roduced spontaneous eccentric remodeling and ventricular dilation with heart failure.

154 infarction and exhibit significantly limited ventricular dilation with sustained and remarkably enhan

155 potentially induce a reversible form of left ventricular dilation with systolic dysfunction, known as

156 The right ventricular dilation with systolic impairment phenotype

157 Right ventricular dilation with systolic impairment was the on

158 icular systolic impairment, and 72% in right ventricular dilation with systolic impairment.