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 sis ( G(~ATP)) and elevated left ventricular end diastolic pressure.

3 (DeltaG(~ATP)) and elevated left ventricular end diastolic pressure.

4 ased left ventricular developed pressure and end diastolic pressure.

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

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

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

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

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

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

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

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

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

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

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

16 LV global longitudinal strain (LVGLS) and LV end-diastolic pressure.

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

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

19 5 vs. 28+/-10 mmHg, P<0.001), and lowered LV end diastolic pressure (10+/-1 vs. 86+/-13 mmHg, P<0.001

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

21 ere RV dysfunction was indicated by elevated end-diastolic pressure (11.3+/-2.5 versus 5.7+/-2.0 mm H

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

23 +/- 15 mm Hg (p = 0.07) and left ventricular end-diastolic pressure 14 +/- 5 versus 16 +/- 4 mm Hg (p

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

25 90+/-80 versus 165+/-71 mL, P<0.0001) and LV end-diastolic pressure (14.3+/-10.2 versus 9.9+/-9.3 mm

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

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

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

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

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

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

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

33 /- 3%; p < 0.05], and lower left ventricular end-diastolic pressure [3 +/- 1 vs 8 +/- 2 mm Hg; p < 0.

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

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

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

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

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

39 08 m/s, p < 0.0001), and elevated in vivo LV end-diastolic pressure (7 +/- 6 vs. 2 +/- 1 mm Hg, p = 0

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

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

42 2 extraction 24%, and mean right ventricular end-diastolic pressure 9 mm Hg.

43 End diastolic pressure, a negative index of myocardial p

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

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

46 nd sgridAND correlated with left ventricular end-diastolic pressure across both groups (average R(2)

47 t risk factors for elevated left ventricular end-diastolic pressure after AoV surgery, while concomit

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

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

50 onary artery pressure, high left ventricular end-diastolic pressure and a normal ejection fraction, s

51 End-diastolic pressure and chamber diastolic stiffness d

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

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

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

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

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

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

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

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

60 tudinal strain (PALS) is strongly related to end-diastolic pressure and prognosis, but it is still no

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

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

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

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

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

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

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

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

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

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

71 cardial restraint contributes to elevated LV end-diastolic pressure, and acute studies have shown tha

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

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

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

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

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

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

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

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

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

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

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

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

84 8 of the 63 patients; thus, 92% had elevated end-diastolic pressure (average, 24+/-8 mm Hg).

85 27 +/- 0.06 (n = 724); left ventricular (LV) end-diastolic pressure averaged 22 +/- 12 mm Hg (n = 548

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

87 P=0.0056), 34% reduction in left ventricular end-diastolic pressure by -7 mm Hg ([95% CI, -10 to -5]

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

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

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

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

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

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

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

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

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

97 End-diastolic pressure correlated significantly with tis

98 Baseline noninvasive LV end-diastolic pressure correlated with invasive pulmonar

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

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

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

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

103 The derived left ventricular end-diastolic pressure (dLVEDP), estimated by device alg

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

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

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

107 t ventricular mass, relative wall thickness, end-diastolic pressure (EDP), end-diastolic pressure/end

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

109 all thickness, end-diastolic pressure (EDP), end-diastolic pressure/end-diastolic volume (EDP/EDV) ra

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

125 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

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

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

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

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

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

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

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

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

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

135 8 mm Hg) and was similar to left ventricular end-diastolic pressure in the sham-operated rats (P = NS

136 trophy, reduced stroke volume, and increased end-diastolic pressure, in association with increased my

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

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

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

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

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

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

143 state of chronically elevated left ventricle end diastolic pressure (LVEDP > 20mmHg).

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

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

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

147 infarct-related artery and left ventricular end-diastolic pressure (LVEDP) are acute, prognostic bio

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

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

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

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

152 LV end-diastolic pressure (LVEDP) was unchanged following P

153 wedge pressure (mPAWP) and left ventricular end-diastolic pressure (LVEDP) were utilized for assessm

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

155 10 to 20 cm H2O increased cardiac output, LV end-diastolic pressure (LVEDP), and peak LV pressure (LV

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

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

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

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

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

161 diac output) and diastolic (left ventricular end-diastolic pressure, mitral valve deceleration time a

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

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

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

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

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

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

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

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

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

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

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

173 essure (3.7 +/- 3.3 to 6.5 +/- 3.5 mmHg) and end diastolic pressure or EDP (11.5 +/- 4 to 18 +/- 3.8

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

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

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

177 CRD-733 prevented elevations in LV end diastolic pressures (P=0.037) compared with vehicle,

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

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

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

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

182 t any effect on heart rate, left ventricular end diastolic pressure, phosphocreatine/ATP ratio, or De

183 t any effect on heart rate, left ventricular end diastolic pressure, phosphocreatine/ATP ratio, or G(

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

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

186 nt [r(s) ]= -0.42, P = .005) and ventricular end diastolic pressure (r(s) = -0.33, P = .04) and posit

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

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

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

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

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

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

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

194 igated by 41% (95% CI, 27%-45%, P<0.0001; LV end-diastolic pressure reduced from +9 3 mm Hg to +5 3 m

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

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

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

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

199 or RV systolic, LV minimum diastolic, and LV end-diastolic pressures, respectively.

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

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

202 RV end-diastolic pressure (RVEDP) decreased after PAB defla

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

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

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

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

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

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

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

210 th diastolic dysfunction or left ventricular end-diastolic pressure thresholds.

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

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

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

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

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

216 ons revealed significant improvements in the end-diastolic pressure volume relationship, relaxation k

217 d an empirical single-beat estimation of the end-diastolic pressure volume relationship.

218 cardiac hypertrophy, diastolic dysfunction (end diastolic pressure-volume relationship =0.051+/-0.00

219 mulation, exacerbated diastolic dysfunction (end diastolic pressure-volume relationship =0.11+/-0.004

220 ected against cardiac diastolic dysfunction (end diastolic pressure-volume relationship =0.110+/-0.00

221 ation and exacerbated diastolic dysfunction (end diastolic pressure-volume relationship =0.124+/-0.00

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

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

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

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

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

227 The end-diastolic pressure-volume relationship (EDPVR), whic

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

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

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

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

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

233 KE right-shifted the left ventricular end-diastolic pressure-volume relationship, suggestive o

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

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

236 howed impaired relaxation and upward-shifted end-diastolic pressure-volume relationships despite pres

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

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

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

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

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

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

243 Left ventricular end-diastolic pressure was determined.

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

245 , beat-to-beat variation in left ventricular end-diastolic pressure was found to have a greater influ

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

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

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

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

250 LV end-diastolic pressure was measured by micromanometer.

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

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

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

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

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

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

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

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

259 e mean errors in LV minimum diastolic and LV end-diastolic pressures were 7.2 mm Hg +/- 4.5 and 6.8 m

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

261 Postreperfusion end-diastolic pressures were significantly increased in

262 ise, RT was responsible for 64% (53%-76%) of end-diastolic pressure, whereas incomplete relaxation an

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

264 The increase in LV end-diastolic pressure with volume loading was mitigated

265 hat pericardiotomy attenuates the rise in LV end-diastolic pressure with volume loading.

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

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