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

4 the sarcomeric protein titin, which adjusts ventricular filling.

5 become progressively rigid, thereby impeding ventricular filling.

6 er techniques are most useful for evaluating ventricular filling.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

38 Increased left ventricular filling pressure and the resultant increase

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

73 Left ventricular filling pressures were altered during differ

74 Left ventricular filling pressures were reduced to a similar

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

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

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

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

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

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

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

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

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

84 ably distinguished normal from elevated left ventricular filling pressures.

85 in distinguishing normal from elevated left ventricular filling pressures.

86 re consistent with chronically elevated left ventricular filling pressures.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

106 Ventricular filling was controlled by adjusting the rate

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

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

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

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