ライフサイエンスコーパス: ventricular filling

1 P) to Doppler parameters of right atrial and ventricular filling.

2 g for elastic diastolic recoil and aiding in ventricular filling.

3 d mechanism by which HDAC inhibitors improve ventricular filling.

4 nts and >50% in 16; all had restrictive left ventricular filling.

5 the sarcomeric protein titin, which adjusts ventricular filling.

6 become progressively rigid, thereby impeding ventricular filling.

7 er techniques are most useful for evaluating ventricular filling.

8 and 4.7+/-0.8 s(-1), respectively) and rapid ventricular filling (1.9+/-0.8 versus 8.7+/-1.7 and 3.7+

9 during both isovolumic relaxation and rapid ventricular filling, allows for the discrimination of RC

10 echocardiographic evidence of impaired left ventricular filling and biatrial enlargement, but preser

11 rough the pulmonary circulation, restricting ventricular filling and cardiac output.

12 ts on atrial contractility which facilitates ventricular filling and contributes to maintaining cardi

13 roduces reciprocal changes in right and left ventricular filling and ejection dynamics during the res

14 able linear regressions were used to compare ventricular filling and ejection measures between groups

15 e are of primary importance for optimal left ventricular filling and emptying but are incompletely ch

16 n increase in heart rate with both increased ventricular filling and emptying.

17 Furthermore, the combined effects of reduced ventricular filling and increased inotropic state were a

18 s (obliteration during inspiration) in right ventricular filling and pulmonary perfusion, ultimately

19 stores arterial oxygen content, whereas left ventricular filling and stroke volume are lowered as a r

20 This is also associated with a better left ventricular filling and systolic function after surgery.

21 des atrial cells with a mechanism to improve ventricular filling and to maintain cardiac output, but

22 res which, in turn, determine left and right ventricular fillings and regulates cardiac output via th

23 s including increased cardiac size, enhanced ventricular filling, and augmentation of stroke volume e

24 oint 4, earliest left atrial pressure during ventricular filling; and the line between points 5 and 6

25 1) display a significant improvement in left ventricular filling as shown by increased E-wave velocit

26 t function is associated with impaired early ventricular filling, as potential mechanism leading to i

27 ransients that would result in a decrease in ventricular filling (diastolic dysfunction); and (2) the

28 Doppler-derived indexes of ventricular filling do not provide specific information

29 there would be an increase in resistance to ventricular filling during diastole resulting from the p

30 efore the action potential, corresponding to ventricular filling during diastole, increases the magni

31 Keywords: Diastolic Function, Left Ventricular Filling, Hypertrophic Cardiomyopathy, Cardia

32 lation is usually ascribed to time-dependent ventricular filling, implying a single positive relation

33 e also provided better understanding of left ventricular filling in hypertension.

34 ith ivabradine on exercise capacity and left ventricular filling in patients with heart failure with

35 showed decreased atrial contribution to left ventricular filling in the control group (P<0.05).

36 ring exercise, consistent with impaired left ventricular filling, in 36% of patients with severe pulm

37 ated and have normal contractility, but left ventricular filling is impaired.

38 ves for total and early (1/3) diastolic left ventricular filling, left atrial (LA) emptying, and left

39 relations, but there was failure to augment ventricular filling manifest by absence of change in dV/

40 d that relief of external constraint to left ventricular filling may also play a role.

41 Measures designed to increase ventricular filling may improve quality of life of these

42 r exertional limitation due to impairment of ventricular filling or ejection of blood or both.

43 s the left atrium (without compromising left ventricular filling or forward cardiac output) is a rati

44 onary artery VWT and both E/A (ratio of left ventricular-filling peak blood flow velocity in early di

45 nfidence interval, 1.16-2.00), elevated left ventricular filling pressure (E/E'; adjusted hazard rati

46 y in identifying patients with elevated left ventricular filling pressure (sensitivity 6%, specificit

47 at initial sarcomere length is a function of ventricular filling pressure and that this relation expl

48 Increased left ventricular filling pressure and the resultant increase

49 CKD is often associated with elevated left ventricular filling pressure and volume overload, which

50 stroke volume (SV), (2) the upper limits to ventricular filling pressure and volume, and (3) the nor

51 al conditions, CVP appropriately tracks left ventricular filling pressure as indexed by PCWP.

52 er suggests the implication of elevated left ventricular filling pressure in MAC initiation.

53 f E/e' to estimate and track changes of left ventricular filling pressure in patients with unexplaine

54 Elevated left ventricular filling pressure is a cardinal feature of he

55 few varieties of pulmonary edema where left ventricular filling pressure is normal.

56 essed whether exercise training reduces left ventricular filling pressure measured during exercise in

57 ocardiographic measurements to estimate left ventricular filling pressure or to monitor treatment.

58 city, with a contribution from improved left ventricular filling pressure response to exercise as ref

59 g elevated blood pressure, and reducing left ventricular filling pressure without reducing cardiac ou

60 T, left ventricular hypertrophy, higher left ventricular filling pressure, and higher pulmonary arter

61 is that changes in CVP reflect those in left ventricular filling pressure, as expressed by pulmonary

62 e (CVP) provides information regarding right ventricular filling pressure, but is often assumed to re

63 stroke volume (SV) for a similar decrease in ventricular filling pressure, compared to normothermia,

64 A measure of left ventricular filling pressure, E/E', and BNP were signifi

65 (LAV), a marker of chronically elevated left ventricular filling pressure, is a predictor of atrial f

66 en proposed as a noninvasive measure of left ventricular filling pressure.

67 essure, but is often assumed to reflect left ventricular filling pressure.

68 ity and intensity of the burden of increased ventricular filling pressure.

69 s repeated after an attempt to decrease left ventricular filling pressure.

70 and prognostic implications of elevated left ventricular filling pressures (LVFP) in CTEPH.

71 chocardiography can be used to estimate left ventricular filling pressures (LVFPs) in patients in sin

72 l heart disease are characterized by reduced ventricular filling pressures and decreased systemic oxy

73 This was directly correlated with higher ventricular filling pressures and depressed cardiac outp

74 r NO signaling, as during exercise when left ventricular filling pressures and pulmonary artery press

75 t can be applied clinically to estimate left ventricular filling pressures and to predict prognosis i

76 d the correlation between these estimates of ventricular filling pressures and ventricular end-diasto

77 se training program resulted in reduced left ventricular filling pressures at mild exertion and impro

78 d indicated when HFpEF is suspected but left ventricular filling pressures at rest are normal.

79 HFpEF based on the presence of elevated left ventricular filling pressures at rest or during exercise

80 lmonary artery pressures, and left and right ventricular filling pressures can be obtained with reaso

81 are no data on how these 2 estimates of left ventricular filling pressures compare.

82 are useful in predicting and estimating left ventricular filling pressures in patients with left vent

83 Nitroprusside reduces afterload and left ventricular filling pressures in patients with LGSAS and

84 n of the mitral flow velocity curves to left ventricular filling pressures in patients with two diffe

85 velocity curves can be used to predict left ventricular filling pressures in specific disease entiti

86 Left ventricular filling pressures measured by resting E/e' o

87 ral inflow velocities, used to estimate left ventricular filling pressures noninvasively, are limited

88 pture), which leads to an acute rise in left-ventricular filling pressures resulting in pulmonary ede

89 ve at a clinically useful assessment of left ventricular filling pressures using a comprehensive appr

90 Left ventricular filling pressures were altered during differ

91 Left ventricular filling pressures were reduced to a similar

92 diastolic function are associated with left ventricular filling pressures with exercise and could be

93 ess of preload alterations in assessing left ventricular filling pressures with transmitral Doppler v

94 ients, nitroprusside reduced elastance, left ventricular filling pressures, and pulmonary artery pres

95 ms including extracellular fluids, increased ventricular filling pressures, and/or auto-transfusion o

96 Despite high left ventricular filling pressures, E/E' (mean, 9+/-4) was <1

97 oninvasively, are limited in predicting left ventricular filling pressures, especially in patients wi

98 y catheter; b) continuous monitoring of left ventricular filling pressures, pulmonary vascular pressu

99 er imaging provide measures of elevated left ventricular filling pressures, which are associated with

100 peptide (BNP) have been correlated with left ventricular filling pressures, yet there are no data on

101 ed without an increase in heart rate or left ventricular filling pressures.

102 pEF), even in the presence of increased left ventricular filling pressures.

103 pEF who had objective signs of elevated left ventricular filling pressures.

104 sed E/e' ratio as a marker of increased left ventricular filling pressures.

105 ably distinguished normal from elevated left ventricular filling pressures.

106 in distinguishing normal from elevated left ventricular filling pressures.

107 re consistent with chronically elevated left ventricular filling pressures.

108 aphy have been proposed to reflect left (LV) ventricular filling pressures.

109 g application is to use pulsed-TDE to assess ventricular filling pressures.

110 ay be useful in noninvasively assessing left ventricular filling pressures.

111 ventricular dysfunction and restrictive left ventricular filling, provides incremental prognostic val

112 t strain correlated with the volume of early ventricular filling (r=0.67; P<0.01), but not LV stiffne

113 also observed, with a reduction in peak left ventricular filling rates and mitral inflow E/A, by 17%

114 This is due to failure to augment right ventricular filling rates during tachycardia, presumably

115 n the early ventricular filling velocity and ventricular filling ratio (E/A), indicative of grade 1 d

116 The early-to-late ventricular filling ratio (E:A) is widely used to index

117 ction were linearly related to impaired left ventricular filling, reduced stroke volume, and lower ca

118 resistance and secondary reductions in left ventricular filling, stroke volume, and cardiac output.

119 With aging, left ventricular filling tends to decrease in early diastole,

120 ricular end diastolic pressure to facilitate ventricular filling, thus resulting in better utilizatio

121 ed to assess changes in cardiac output, left ventricular filling time, ejection time, total isovolumi

122 ion of electromechanical synchronization and ventricular filling to the optimal hemodynamic effect in

123 ding loss of the atrial contribution to left ventricular filling, valvular regurgitation, increased v

124 including mitral ratio of the early to late ventricular filling velocities >2, RAP >10 mm Hg, sPAP >

125 regression analysis, early transmitral left ventricular filling velocity (E)/septal Ea ratio predict

126 We assessed the ratio of early to late ventricular filling velocity (E/A), ratio of early mitra

127 of AC9(-/-) displays a decrease in the early ventricular filling velocity and ventricular filling rat

128 Ventricular filling was controlled by adjusting the rate

129 c assessment of myocardial function and left ventricular filling were undertaken at rest and after ex

130 main contributor to the disease is impaired ventricular filling, which we improved with antisense ol

131 ) caused by beat-to-beat alterations in left ventricular filling, which we propose reflects the compl

132 sfunction and a diminished ability to couple ventricular filling with cardiac output on a beat-to-bea

133 is a rare disorder characterized by impaired ventricular filling with decreased diastolic volume.