ライフサイエンスコーパス: end-diastolic pressure

1 to peak pressure and a dramatic increase in end diastolic pressure.

2 ased left ventricular developed pressure and end diastolic pressure.

3 fraction, and an increased left ventricular end-diastolic pressure.

4 and more rapid increase in left ventricular end-diastolic pressure.

5 y wedge pressure (PCWP) and left ventricular end-diastolic pressure.

6 nants include LA dP/dt, LA relaxation and LV end-diastolic pressure.

7 rather than physical dilation from increased end-diastolic pressure.

8 but a significantly higher left ventricular end-diastolic pressure.

9 viscoelasticity, with larger net effects on end-diastolic pressure.

10 (LV) systolic function and an increase in LV end-diastolic pressure.

11 ft ventricular relaxation and an increase in end-diastolic pressure.

12 ced fibrosis, and decreased left ventricular end-diastolic pressure.

13 l, and maximum LV dP/dt, as well as lower LV end-diastolic pressure.

14 stolic LV diameter was smaller at matched LV end-diastolic pressures.

15 suction at rest and on exercise, and higher end-diastolic pressures.

16 5 vs. 28+/-10 mmHg, P<0.001), and lowered LV end diastolic pressure (10+/-1 vs. 86+/-13 mmHg, P<0.001

17 onary artery pressure (25+/-10 mm Hg) and LV end-diastolic pressure (11+/-5 mm Hg; P<0.001 for both c

18 ), and increased transmural left ventricular end-diastolic pressure (139 +/- 6%).

19 +/- 15 mm Hg (p = 0.07) and left ventricular end-diastolic pressure 14 +/- 5 versus 16 +/- 4 mm Hg (p

20 ) mass (70 +/- 2 vs. 63 +/- 1%), enhanced LV end-diastolic pressure (14 +/- 2 vs. 8 +/- 1 mmHg) and t

21 At 60 minutes, bosentan reduced LV end-diastolic pressure (17 +/- 2 versus 11 +/- 2 mm Hg;

22 (mean pressure, 39+/-12 mm Hg), elevated LV end-diastolic pressure (19+/-5 mm Hg), and reduced strok

23 ular stiffness (110+/-26% over baseline) and end-diastolic pressure (22+/-1.7 mm Hg).

24 and diastolic function (eg, left ventricular end-diastolic pressure 23+/-9 in WT and 51+/-5 mm Hg in

25 heart failure had elevated left ventricular end-diastolic pressures (24.1 +/- 2.6 mm Hg) and a mean

26 rmalities, including higher left ventricular end-diastolic pressures (24.3+/-4.6 versus 12.9+/-5.5 mm

27 mean+/-SD: LV ejection fraction, 19+/-7%; LV end-diastolic pressure, 25+/-8 mm Hg; QRS duration, 157+

28 mpanied by global LV dysfunction (in vivo LV end-diastolic pressure, 4+/-1 versus 23+/-1.6 mm Hg; Lan

29 u(ln) and kappa(e) with the relationship: LV end-diastolic pressure=-4.73+0.27 tau(ln)+0.54 kappa(e)

30 ia-reperfusion increased left ventricle (LV) end diastolic pressure (450% vs. 33%, p < 0.01) and redu

31 versus IPC, P<.05) and contractile recovery (end-diastolic pressure, 52+/-5 versus 29+/-5 mm Hg, P<.0

32 n in NTg (53 versus 38%, P<0.01), whereas LV end-diastolic pressure (6 versus 12 mm Hg, P<0.05) and l

33 08 m/s, p < 0.0001), and elevated in vivo LV end-diastolic pressure (7 +/- 6 vs. 2 +/- 1 mm Hg, p = 0

34 onary arteries and elevated left ventricular end-diastolic pressure (7.7+/-0.3 to 19+/-3.4 mm Hg, P<.

35 better recovery than Con (%PCr, 56+/-6% and end-diastolic pressure, 72+/-6 mm Hg).

36 2 extraction 24%, and mean right ventricular end-diastolic pressure 9 mm Hg.

37 End diastolic pressure, a negative index of myocardial p

38 t in patients with elevated left ventricular end-diastolic pressure, a finding largely attributed to

39 locked neither the elevated left ventricular end-diastolic pressures, a measure of diastolic function

40 nary perfusion pressure and left ventricular end-diastolic pressure and a decrease in developed left

41 arcts >35% had an increased left ventricular end-diastolic pressure and a marked increase in heart we

42 End-diastolic pressure and chamber diastolic stiffness d

43 th 80 micromol/L diazoxide, left ventricular end-diastolic pressure and coronary flow were significan

44 ased fractional shortening, and increased LV end-diastolic pressure and fibrosis (P<0.05 versus contr

45 ary cardiospheres decreased left ventricular end-diastolic pressure and increased cardiac output.

46 iastolic function, lowering left ventricular end-diastolic pressure and increasing the filling rate.

47 nt inverse relationships to left ventricular end-diastolic pressure and infarct size.

48 F as evidenced by increased left ventricular end-diastolic pressure and left ventricular volume index

49 ved between the plasma DPPIV activity and LV end-diastolic pressure and lung congestion.

50 nduced HF, CXL-1020 reduced left ventricular end-diastolic pressure and myocardial oxygen consumption

51 Improvement in postischemic recovery of end-diastolic pressure and reduction in infarct size was

52 een beat-to-beat changes in left ventricular end-diastolic pressure and SV was used as an index of th

53 iac output and decreases in left ventricular end-diastolic pressure and systemic vascular resistance.

54 and offset the pacing-induced increase in LV end-diastolic pressure and the time constant of isovolum

55 lic dysfunction became manifest as increased end-diastolic pressure and time to 90% relaxation.

56 ncluding heart rate, peak-systolic pressure, end-diastolic pressure and volume, end-systolic pressure

57 def) myocardium, as demonstrated by elevated end-diastolic pressures and decreased percent recovery o

58 ad in Fontan, manifested by high ventricular end-diastolic pressures and pulmonary arterial wedge pre

59 ction, which subsequently led to elevated LV end-diastolic pressures and pulmonary hypertension.

60 educed LV mass, posterior wall thickness and end diastolic pressures, and increased fractional shorte

61 ssure increase at 40 mm Hg, left ventricular end-diastolic pressure, and cardiac index, was significa

62 poride, left ventricular developed pressure, end-diastolic pressure, and coronary flow were significa

63 us saturation, elevated systemic ventricular end-diastolic pressure, and elevated main pulmonary arte

64 orrelated with PH severity, left ventricular end-diastolic pressure, and left ventricular dilatation.

65 orepinephrine levels, lower left ventricular end-diastolic pressure, and lower right ventricle/body w

66 pulmonary artery pressure, left ventricular end-diastolic pressure, and lower thoracic aortic flow b

67 in systolic and mean arterial pressures, LV end-diastolic pressure, and LV end-systolic volume, as w

68 Elevation in right ventricular end-diastolic pressure appeared to predict poor vasodila

69 Additionally, the end-diastolic pressure-area curves shifted to the left i

70 Compliance was assessed by end-diastolic pressure-area curves.

71 -null hearts had similar cardiac outputs and end-diastolic pressures as WT or transgenic hearts.

72 urthermore, E:A=3:1 yielded 37% to 50% lower end-diastolic pressures at similar volumes (versus E:A=1

73 8 of the 63 patients; thus, 92% had elevated end-diastolic pressure (average, 24+/-8 mm Hg).

74 27 +/- 0.06 (n = 724); left ventricular (LV) end-diastolic pressure averaged 22 +/- 12 mm Hg (n = 548

75 not a function of elevated left ventricular end diastolic pressure but was associated with increased

76 .05) attenuated transmural left ventricular end-diastolic pressure by 30% to 40%, left ventricular e

77 mode) decreased transmural left ventricular end-diastolic pressure by 40% to 60% (p < .05), left ven

78 htward, decreasing cardiac output at matched end-diastolic pressure by 44%.

79 controlled delivery group (left ventricular end-diastolic pressure, cardiac index, +dP/dt, -dP/dt, a

80 At week 8, differences in LV end-diastolic pressure, cardiac output, end-diastolic an

81 levant parameters, including RV systolic and end-diastolic pressures, cardiac output, RV size, and mo

82 ll, was proportional to the magnitude of the end-diastolic pressure change.

83 ate of relaxation and lower left ventricular end diastolic pressure compared with controls.

84 olic volume in IPAH (+7%; P < 0.05), whereas end-diastolic pressure continuously dropped.

85 End-diastolic pressure correlated significantly with tis

86 In those receiving metoprolol, LV end-diastolic pressure decreased (P=0.001).

87 Although left ventricular end-diastolic pressure decreased in 45/10, it increased

88 CCPA produced improvement in postischemic end-diastolic pressure, developed pressure, and rate-pre

89 In contrast, changes in end-diastolic pressure did induce vasodilatation that, a

90 n develop increases in left ventricular (LV) end-diastolic pressures during exercise that contribute

91 left ventricular developed pressure (LVDP), end diastolic pressure (EDP), and ATP were measured thro

92 d-diastolic volume (EDV) and Doppler-derived end-diastolic pressure (EDP) were used to derive the dia

93 w Veq, even with marked reduction of volume (end-diastolic pressure [EDP], 1 to 2 mm Hg), whereas in

94 fluid protocol based on the left ventricular end-diastolic pressure for the prevention of contrast-in

95 LV) unloading manifested by a decrease in LV end-diastolic pressure from 11.4 +/- 9.0 mm Hg to 8.8 +/

96 ere as follows: "a" wave to left ventricular end-diastolic pressure gradient 17 +/- 5 versus 4 +/- 4

97 fined by clinical signs and left ventricular end diastolic pressures > 25 mm Hg.

98 All CHF rats had left ventricular end-diastolic pressure >10 mm Hg, and heart weight/body

99 -1) IV) more than doubled chamber stiffness (end-diastolic pressure >25 mm Hg, P<0.001), whereas stif

100 ressure into postcapillary (left ventricular end-diastolic pressure, >15 mm Hg; n=269) and precapilla

101 Left ventricular end-diastolic pressure-guided fluid administration seems

102 equently in patients in the left ventricular end-diastolic pressure-guided group (6.7% [12/178]) than

103 allocated in a 1:1 ratio to left ventricular end-diastolic pressure-guided volume expansion (n=196) o

104 Interventions were performed after LV end-diastolic pressure had increased approximately 7 mm

105 olic pressure, without associated changes in end-diastolic pressure, had no significant effect on vas

106 als demonstrated significant increases in LV end-diastolic pressure, heart and body weight, and LV ch

107 output (57%) and significant decreases in LV end-diastolic pressure, heart rate, and systemic vascula

108 The isovolumic end-diastolic pressure, however, remained elevated throu

109 5; P=0.02) and more likely to have higher RV end-diastolic pressure (HR, 1.07; 95% CI, 1.00-1.15; P=0

110 ction of I79N hearts significantly worsened (end-diastolic pressure: I79N 20 +/- 4 mmHg versus CON 13

111 raphic measures of diastolic function and LV end-diastolic pressure improve in most patients.

112 Left ventricular (LV) end-diastolic pressure in AAV-VEGF-B and AAV-control was

113 amlodipine improved in vivo left ventricular end-diastolic pressure in association with the normaliza

114 of increases in transmural left ventricular end-diastolic pressure in both heart conditions, and als

115 decreased tau (P<0.001) and left ventricular end-diastolic pressure in both old and young hearts.

116 m for the improvement in left ventricle (LV) end-diastolic pressure in cardiomyopathy patients treate

117 We conclude that the decrease in LV end-diastolic pressure in cardiomyopathy patients treate

118 in detecting increased left ventricular (LV) end-diastolic pressure in patients with coronary artery

119 8 mm Hg) and was similar to left ventricular end-diastolic pressure in the sham-operated rats (P = NS

120 Left ventricular end-diastolic pressure increased significantly in the po

121 ere further dichotomized by left ventricular end-diastolic pressure into postcapillary (left ventricu

122 h HTN(+)HFpEF had increased left ventricular end-diastolic pressure, left atrial volume, N-terminal p

123 9) and precapillary groups (left ventricular end-diastolic pressure, </=15 mm Hg; n=56).

124 axation (tau), left atrial (LA) pre-A and LV end-diastolic pressures (LV-EDP) were measured.

125 tion fraction) and hemodynamic variables (LV end-diastolic pressure, LV dP/dtmax, preload adjusted ma

126 ately threefold increase in left ventricular end diastolic pressure (LVEDP) and 38% increase in the t

127 In healthy and CHF (left ventricular end diastolic pressure (LVEDP): 6 +/- 1 versus 14 +/- 1

128 ine paradoxically decreased left ventricular end-diastolic pressure (LVEDP) and left ventricular end-

129 rrest led to an increase of left ventricular end-diastolic pressure (LVEDP) by > or =20 mm Hg (ie, ca

130 und a threefold increase of left ventricular end-diastolic pressure (LVEDP) in LVH during 2DG perfusi

131 d diastolic volumes with little effect on LV end-diastolic pressure (LVEDP) or the end-diastolic P-V

132 ic blood pressure (DBP) and left ventricular end-diastolic pressure (LVEDP) to systolic blood pressur

133 y perfusion pressure (CPP), left ventricular end-diastolic pressure (LVEDP), and developed left ventr

134 10 to 20 cm H2O increased cardiac output, LV end-diastolic pressure (LVEDP), and peak LV pressure (LV

135 oronary enalaprilat reduced left ventricular end-diastolic pressure (LVEDP), but not left ventricular

136 n measurements, including cardiac output, LV end-diastolic pressure (LVEDP), rate of pressure rise at

137 ditional marker of elevated left ventricular end-diastolic pressure (LVEDP), which adds prognostic va

138 n increased DCS (isovolumic left ventricular end-diastolic pressure [LVEDP] increased 10 mm Hg, P<0.0

139 Ventricular end-diastolic pressure, mean PA pressure, and ventricula

140 V systolic and diastolic function, higher LV end-diastolic pressure, more cardiomyocyte hypertrophy,

141 , indicated by an increased left ventricular end diastolic pressure, myocardial creatine kinase relea

142 TN(-)HFpEF had no change in left ventricular end-diastolic pressure, myocardial passive stiffness, co

143 l performance with elevated left ventricular end-diastolic pressure, not seen in the wild-type.

144 g of early rapid filling and equalization of end-diastolic pressures obtained by cardiac catheterizat

145 No significant changes in left ventricular end-diastolic pressure occurred in response to stimulati

146 through the mitral valve and distended to an end-diastolic pressure of 10 mm Hg.

147 d LV end-diastolic volume at an idealized LV end-diastolic pressure of 20 mm Hg (EDV20), and RV remod

148 of left ventricular (LV) pacing produced LV end-diastolic pressures of 15+/-1.7 mm Hg, whereas overt

149 t CHF at 4 to 5 weeks was associated with LV end-diastolic pressures of 24+/-1.7 mm Hg; prepacing val

150 forces, the end-diastolic volume at a common end-diastolic pressure on the sequential end-diastolic p

151 e with respect to time but did not change LV end-diastolic pressure or improve LV regional function.

152 s observed among groups for left ventricular end-diastolic pressures or dimensions, or catecholamine

153 systolic pressure without an increase in LV end-diastolic pressure, or decrease in LV dP/dt or LV wa

154 tion was seen for stiffness with ventricular end-diastolic pressure (P = 0.001) and pulmonary artery

155 roved ejection fraction and left ventricular end-diastolic pressure (P<0.05).

156 tricular pressure by micromanometer provided end-diastolic pressure (P) area (A) relations during ini

157 lmonary artery systolic and left ventricular end-diastolic pressures (p < 0.01).

158 dence of diabetes, ejection fraction < 0.25, end-diastolic pressure, prior myocardial infarction, or

159 lines in blood pressure and left ventricular end-diastolic pressure produced by GTN in vivo.

160 p < 0.01) but an inverse correlation with LV end-diastolic pressure (r = -0.53, p = 0.01).

161 s inversely associated with left ventricular end-diastolic pressure (r=-0.728; P<0.001), resulting in

162 hereas SR(E) was significantly related to LV end-diastolic pressure (r=0.52, P=0.005) in the experime

163 diastolic velocity (E/E ) correlated with LV end-diastolic pressure (r=0.52, P=0.007).

164 The delay related well with LV end-diastolic pressure (r=0.76) and volume (r=-0.73), an

165 d and the heart paced until left ventricular end-diastolic pressure reached 25 mm Hg and clinical sig

166 icular dilitation, elevated left ventricular end-diastolic pressure, redo coronary surgery, depressed

167 immediate peak gradient and left ventricular end-diastolic pressure reductions were 54% and 20%, resp

168 nship but has no effect on the stroke volume/end-diastolic pressure relationship.

169 d to baseline values, whereas the isovolumic end-diastolic pressure remained elevated for 20 mins.

170 large increases in end-diastolic volume, the end-diastolic pressure remained unchanged.

171 Left ventricular (LV) function measured by end-diastolic pressure response to preload augmentation,

172 d no effect on heart rate, LV relaxation, LV end-diastolic pressure, right atrial pressure, or pulmon

173 l resection again blunted the increase in LV end-diastolic pressure secondary to volume expansion (+4

174 , diastolic relaxation, and left ventricular end-diastolic pressures stabilized in the cardiomyoplast

175 fibrosis and left atrium diameter (marker of end-diastolic pressure), suggesting an improvement in di

176 HF-related cardiac dysfunction, including LV end-diastolic pressure, systolic performance, and chambe

177 worse LV contractile function, and higher LV end-diastolic pressure than Ptges(+/+) mice after myocar

178 l approach would mitigate the increase in LV end-diastolic pressure that develops during volume loadi

179 esuscitation cardiac index, left ventricular end-diastolic pressure, the rate of left ventricular pre

180 ial relaxation and lowering left ventricular end diastolic pressure to facilitate ventricular filling

181 schemia, cardiac output decreased by 41% and end diastolic pressure tripled for CD36-null hearts, wit

182 tion fraction or stroke volume and decreased end diastolic pressure versus controls.

183 nd the "stiffness" coefficient (beta) of the end-diastolic pressure volume relation.

184 ction fraction, end-systolic volume, and the end-diastolic pressure volume relationship by Ang-(1-9)

185 c function and prompt leftward shifts of the end-diastolic pressure-volume curves.

186 ese curves deviate markedly from the passive end-diastolic pressure-volume relation (EDPVR) and explo

187 stroke work relation were measured from the end-diastolic pressure-volume relation before and during

188 sure-volume curve and a reduced slope of the end-diastolic pressure-volume relation in the myoblast-t

189 There were no changes observed in end-diastolic pressure-volume relations, but there was f

190 lic properties were quantified by use of the end-diastolic pressure-volume relationship and the time

191 ung normal dogs underwent measurement of the end-diastolic pressure-volume relationship during caval

192 action (p = 0.014) and improvement of the RV end-diastolic pressure-volume relationship in PH pigs tr

193 The LV end-diastolic pressure-volume relationship measured by t

194 The end-diastolic pressure-volume relationship slope was ele

195 ment in left ventricular chamber compliance (end-diastolic pressure-volume relationship; P<0.01) and

196 In both models, isolated, perfused heart end-diastolic pressure-volume relationships and passive

197 Both the end-systolic and end-diastolic pressure-volume relationships shifted fart

198 mon end-diastolic pressure on the sequential end-diastolic pressure-volume relationships was measured

199 theters assessed changes in end-systolic and end-diastolic pressure-volume relationships, and microsp

200 central venous pressure nor left ventricular end diastolic pressure was altered by thapsigargin.

201 The LV end-diastolic pressure was >16 mm Hg in 58 of the 63 pat

202 occurring at 29+/-1.6 days, left ventricular end-diastolic pressure was 25+/-1 mm Hg, left ventricula

203 Left ventricular end-diastolic pressure was determined.

204 LV end-diastolic pressure was elevated (>/=15 mm Hg) in 72%

205 In vivo left ventricular end-diastolic pressure was higher in the untreated LVH t

206 LV end-diastolic pressure was increased with CIH (CIH, 13.7

207 on analysis revealed that the decrease in LV end-diastolic pressure was indicative of significant imp

208 Left ventricular end-diastolic pressure was lower in the AT1-blocker-trea

209 LV end-diastolic pressure was measured by micromanometer.

210 In the treated hearts, the increase in end-diastolic pressure was significantly attenuated at t

211 -1) versus 0.05+/-0.03 after MI, P=0.06), LV end-diastolic pressure was unchanged as MR resolved.

212 (ejection fraction [EF] and left ventricular end-diastolic pressure) was assessed at days 28 and 56.

213 c pulmonary artery pressure-left ventricular end-diastolic pressure) was normal (<7 mm Hg) or elevate

214 right ventricular mass and left ventricular end diastolic pressure were increased and left ventricul

215 ventricle/body weight, and left ventricular end-diastolic pressure were increased and maximal left v

216 ht ventricle weight/body weight ratio and LV end-diastolic pressure were significantly higher in hear

217 Pulmonary capillary wedge pressure and LV end-diastolic pressure were significantly increased afte

218 Left ventricular end-diastolic pressures were significantly elevated 4 we

219 Postreperfusion end-diastolic pressures were significantly increased in

220 s, pericardiotomy blunted the increase in LV end-diastolic pressure with saline infusion, while enhan

221 mic measurements at 6 months showed lower LV end-diastolic pressures, with enhanced LV function (cont

222 alutary effect of this kind of therapy on LV end-diastolic pressure would be indicative of an improve