ライフサイエンスコーパス: left ventricular wall

1 al infarction (>75% transmural extent of the left-ventricular wall).

2 nd 41+/-1% of the inner circumference of the left ventricular wall.

3 in the anterior and lateral portions of the left ventricular wall.

4 n delivery and stimulate angiogenesis in the left ventricular wall.

5 ation of cardiomyocytes within the embryonic left ventricular wall.

6 ort-term effect of injecting material to the left ventricular wall.

7 demonstrated re-entry involving the inferior left ventricular wall.

8 reversing the direction of activation of the left ventricular wall.

9 reversing the direction of activation of the left ventricular wall.

10 t two of the three standard segments in each left ventricular wall.

11 roperties of Ca2+ channels across the canine left ventricular wall.

12 interventricular septum than in the right or left ventricular walls.

13 s exhibited a nonprogressive thinning of the left ventricular wall and a concomitant decrease in card

14 argeted large-scale support of the infarcted left ventricular wall and improvement of heart function.

15 varying degrees was observed in the anterior left ventricular wall and septum.

16 severe dilated cardiomyopathy with thickened left ventricular walls and profound impairment of systol

17 Dispersion of APD90 across the left ventricular wall averaged 51+/-19 and 64+/-25 ms at

18 smural stress and strain distribution in the left ventricular wall considering it to be made of homog

19 Tissue samples isolated from the left ventricular wall demonstrate that sarcoplasmic reti

20 assess systolic and diastolic function, and left ventricular wall dimensions.

21 Surgical restoration of the left ventricular wall (Dor procedure) has been advocated

22 ent of a signaling pathway in the control of left ventricular wall edema during sepsis.

23 Interestingly, exaggerated left ventricular wall edema was not coupled with aggrava

24 ith a contrast of 0.25 were simulated in the left ventricular wall for 6 locations.

25 tion of noncontractile material to a damaged left ventricular wall has important effects on cardiac m

26 ity of repolarization that exists across the left ventricular wall, how this dispersion of repolariza

27 que were implanted into the anterior-lateral left ventricular wall in C57BL/6J (allogeneic model, n =

28 gene construct subepicardially in the canine left ventricular wall in situ.

29 eight closed-chest dogs with acute posterior left ventricular wall ischemia either with (MR) or witho

30 ith borderline increases in thickness of the left ventricular wall, mild morphologic expression of hy

31 l pattern that involves the proximal lateral left ventricular wall most severely, with relative spari

32 Left ventricular wall motion (WM) abnormalities have rec

33 A new regional left ventricular wall motion abnormality occurred more f

34 Patients (n = 119) with abnormal left ventricular wall motion and a left ventricular ejec

35 ntraoperative TEE for assessment of regional left ventricular wall motion and measurement of hemodyna

36 logy for the echocardiographic assessment of left ventricular wall motion based on acoustic quantific

37 heart disease or hypertension, Killip class, left ventricular wall motion index, and sex.

38 ted to estimated glomerular filtration rate, left ventricular wall motion index, sex, blood pressure,

39 lide MPI and two supplementary codes (add-on left ventricular wall motion or left ventricular ejectio

40 Left ventricular wall motion score (LVWMS) increased sig

41 y artery disease (P < .0001), global resting left ventricular wall motion score index (P < .0001), in

42 ess echocardiography underwent DCMR in which left ventricular wall motion score index (WMSI), defined

43 Large MIs (based on echocardiographic left ventricular wall motion score index) were created b

44 Left ventricular wall motion scores were similar at base

45 In 78 women (85%), left ventricular wall motion was normal at baseline and

46 re used to reconstruct the three-dimensional left ventricular wall motion.

47 using small-angle x-ray diffraction of mouse left ventricular wall muscle.

48 ed infarcts greater than at least 35% of the left ventricular wall (n = 8).

49 iated cardiac-enriched hESC progeny into the left ventricular wall of athymic rats.

50 d by planar wavefronts on the surface of the left ventricular wall of Langendorff-perfused isolated r

51 rified miRNAs were injected in vivo into the left ventricular wall of mice, and, 48 hours later, the

52 ns (each 0.15 mL, 5 mg.mL-1 saline) into the left ventricular wall of rat hearts before a 60-minute o

53 t of proximal flow constraint induced by the left ventricular wall on the accuracy of calculated flow

54 art uptake allowing clear delineation of the left ventricular wall over 60 min after tracer administr

55 siological properties of myocytes across the left ventricular wall play an important role in both the

56 es and cells are maintained in intact canine left ventricular wall preparations in which the myocardi

57 Nonfailing left ventricular wall samples procured from explanted he

58 ely determine whether mechanical behavior of left ventricular wall segments that contain different de

59 Compared with baseline, mean left ventricular wall stress and stroke work were not ch

60 End-systolic left ventricular wall stress was calculated by finite el

61 End-systolic left ventricular wall stress was significantly higher wh

62 ial injury and NT-proBNP levels as marker of left ventricular wall stress were determined.

63 We tested the hypothesis that reducing left ventricular wall stress with a percutaneous left at

64 ter reperfusion in the MI+unload group (mean left ventricular wall stress, 44 658 versus 22 963 dynes

65 nges in left ventricular loading conditions, left ventricular wall stress, desensitization of proinfl

66 ndpoint was change in NT-proBNP, a marker of left ventricular wall stress, from baseline to 12 weeks;

67 ors potentially related to chronic increased left ventricular wall stress, including age, hypertensio

68 al probrain natriuretic peptide, a marker of left ventricular wall stress.

69 sis of the papillary muscles and inferobasal left ventricular wall, suggesting a myocardial stretch b

70 onomicrometric crystals in the region of the left ventricular wall supplied by the occluded left ante

71 emodynamic function, pulmonary gas exchange, left ventricular wall thickening and myocardial blood fl

72 hemodynamic function, myocardial blood flow, left ventricular wall thickening and pulmonary gas excha

73 With LAD constriction, left ventricular wall thickening fell 45+/-8% (P<0.01).

74 The mean percentages of left ventricular wall thickening in infarcted, stunned,

75 phic identification of otherwise unexplained left ventricular wall thickening in the presence of a no

76 e was substantiated by localized patterns of left ventricular wall thickening occurring more commonly

77 hemodynamic function, myocardial blood flow, left ventricular wall thickening or pulmonary gas exchan

78 ere-measured regional myocardial blood flow, left ventricular wall thickening or pulmonary gas exchan

79 However, left ventricular wall thickening was not reversed.

80 ntation, five patients showed progression of left ventricular wall thickening with increased left ven

81 Young female transgenic mice exhibited left ventricular wall thickening without dilatation, whe

82 characterize microstructural dynamics during left ventricular wall thickening, and apply the techniqu

83 Risk factors for SCD were left ventricular wall thickness >/=30 mm (20%), family h

84 nger HCM patients and compared with ATH with left ventricular wall thickness >13 mm.

85 and prehypertensive participants had higher left ventricular wall thickness (0.83 and 0.78 versus 0.

86 versus 0.85+/-0.13 cm, P:<0.005), posterior left ventricular wall thickness (1.00+/-0.24 versus 0.88

87 Patients in the DE group (n=35) had greater left ventricular wall thickness (2.09+/-0.44 versus 1.78

88 xrazoxane, relative to doxorubicin alone, on left ventricular wall thickness (difference between grou

89 tly related to NYHA class as well as age and left ventricular wall thickness (each with a value of P=

90 At 4 weeks after MI, left ventricular wall thickness (echocardiography; 0.89+

91 pathies, but their contribution to increased left ventricular wall thickness (LVWT) in the community

92 ), family history of sudden death (FHSD) and left ventricular wall thickness (LVWT).

93 Left ventricular wall thickness (mean 16+/-6 mm) and dis

94 farcted or had infarction comprising <25% of left ventricular wall thickness (P<0.005 for ejection fr

95 01), end-diastolic diameter (r2=.32, P<.05), left ventricular wall thickness (r2=.38, P<.01), left at

96 al HCM; n=36), mutation carriers with normal left ventricular wall thickness (subclinical HCM; n=28),

97 severity as well as confounding variables of left ventricular wall thickness and age.

98 ardiography showed a significantly increased left ventricular wall thickness and decreased fractional

99 netic analyses of 24 subjects with increased left ventricular wall thickness and electrocardiograms s

100 f left ventricular hypertrophy, with reduced left ventricular wall thickness and heart weight/body we

101 monstrate that LHFS of the MI region altered left ventricular wall thickness and material properties,

102 ined ventricular tachycardia (nsVT), maximum left ventricular wall thickness and obstruction were sig

103 Left ventricular wall thickness and postinfarct scar thi

104 iovascular magnetic resonance to investigate left ventricular wall thickness and the presence of asym

105 cludes T2-weighted imaging and assessment of left ventricular wall thickness in detecting patients wi

106 Left ventricular wall thickness increased from 10 to 14

107 ntiating features from normal pregnancy were left ventricular wall thickness of >/=1.0 cm, exaggerate

108 Echocardiography demonstrated maximal left ventricular wall thickness of 19.9+/-3.8 mm, systol

109 .7 years, p = 0.0002), had more hypertrophy (left ventricular wall thickness of 24.2 vs. 21.1 mm, p =

110 obstruction of at least 30 mm Hg, and marked left ventricular wall thickness of more than 25 mm-were

111 If left ventricular wall thickness seemed nonuniform, the s

112 The mean maximal left ventricular wall thickness was 21 mm.

113 Left ventricular wall thickness was also measured.

114 Using cardiovascular magnetic resonance, the left ventricular wall thickness was measured in all 17 s

115 was good (90%), although CMR measurements of left ventricular wall thickness were approximately 19% l

116 reased left ventricular dimension and normal left ventricular wall thickness) and dilated cardiomyopa

117 otocol (with the addition of T2-weighted and left ventricular wall thickness) increased the specifici

118 logic phenotype (by virtue of showing normal left ventricular wall thickness).

119 hortening [FS]), end-diastolic diameter, and left ventricular wall thickness).

120 ses of 20 subjects with massive hypertrophy (left ventricular wall thickness, > or =30 mm) but withou

121 t weight, enlarged cardiomyocytes, increased left ventricular wall thickness, and decreased fractiona

122 nance imaging reveals a dramatic increase in left ventricular wall thickness, as compared with Cav-1-

123 imilar increases in systolic blood pressure, left ventricular wall thickness, left ventricular mass,

124 the rest of the cohort in age at diagnosis, left ventricular wall thickness, left ventricular outflo

125 ent, revealed significant associations among left ventricular wall thickness, postinfarct scar thickn

126 ventricular function and a partial rescue of left ventricular wall thickness.

127 in RTRs regardless of BP, mainly by reducing left ventricular wall thickness.

128 tolic contractile function and reductions in left ventricular wall thickness.

129 agnetic resonance imaging, and assessment of left ventricular wall thickness.

130 ined by confounding due to changes in BSA or left ventricular wall thickness.

131 ecedent cardiac hypertrophy (average maximal left-ventricular-wall thickness, 8.5 mm) nor histopathol

132 Left ventricular wall thicknesses in the overall study g

133 These mice develop left ventricular wall thinning and chamber dilation, wit

134 hin a myocardial infarct (MI) contributes to left ventricular wall thinning and changes in regional s

135 LV left ventricular wall thinning with LV left ventricular

136 At 60 min, the uptake ratios of left ventricular wall to blood, lung, and liver (mean of

137 f the papillary muscle still attached to the left ventricular wall was also noted but was less sensit

138 Reduction of the akinetic left ventricular wall was observed in BMCeP-treated hear

139 Myocardial blood flow of the anterior left ventricular wall was reduced from 1.00 +/- 0.18 to

140 The left ventricular wall was segmented and characterized us

141 al infarction (<50% transmural extent of the left-ventricular wall), whereas SPECT identified only 31

142 EPCM was sutured to the anterolateral left ventricular wall, which included the region of isch

143 ents by advancing the fiberoptic through the left ventricular wall with the laser inactivated.