ライフサイエンスコーパス: diastolic pressure

1 = 0.037 for systolic pressure; P = 0.019 for diastolic pressure).

2 ge occurrence of a sympathetic burst against diastolic pressure.

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

4 peak pressure and a dramatic increase in end diastolic pressure.

5 ystolic pressure conferred greater risk than diastolic pressure.

6 ure and -0.2 (95% CI: -4.1, 3.7) mmHg/kg for diastolic pressure.

7 more rapid increase in left ventricular end-diastolic pressure.

8 Relationships were smaller for diastolic pressure.

9 dge pressure (PCWP) and left ventricular end-diastolic pressure.

10 s include LA dP/dt, LA relaxation and LV end-diastolic pressure.

11 kg/m2 for body mass index, and 0.48 mmHg for diastolic pressure.

12 the cuff technique in predicting the aortic diastolic pressure.

13 e systolic pressure without greatly reducing diastolic pressure.

14 intracellular calcium, but did not decrease diastolic pressure.

15 er than physical dilation from increased end-diastolic pressure.

16 beneficial effects and further increased LV diastolic pressure.

17 left ventricular developed pressure and end diastolic pressure.

18 fibrosis, and decreased left ventricular end-diastolic pressure.

19 reduced rate pressure product and increased diastolic pressure.

20 nd maximum LV dP/dt, as well as lower LV end-diastolic pressure.

21 mean arterial pressure than for systolic or diastolic pressure.

22 r estimates of pulmonary artery systolic and diastolic pressures.

23 of pulse pressure above that of systolic and diastolic pressures.

24 ic LV diameter was smaller at matched LV end-diastolic pressures.

25 tion at rest and on exercise, and higher end-diastolic pressures.

26 sure, -0.7 mm Hg (CI, -0.6 to -0.9 mm Hg) in diastolic pressure, -0.17 mmol/L (CI, -0.09 to -0.25 mmo

27 A were inversely related to small changes in diastolic pressure (1 to 3 mm Hg), suggesting that respi

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

29 y artery pressure (25+/-10 mm Hg) and LV end-diastolic pressure (11+/-5 mm Hg; P<0.001 for both compa

30 ss (70 +/- 2 vs. 63 +/- 1%), enhanced LV end-diastolic pressure (14 +/- 2 vs. 8 +/- 1 mmHg) and these

31 8+/-5 mm Hg, P=0.04), lower pulmonary artery diastolic pressures (14+/-9 versus 21+/-9 mm Hg, P=0.01)

32 an pressure, 39+/-12 mm Hg), elevated LV end-diastolic pressure (19+/-5 mm Hg), and reduced stroke vo

33 P-induced cardiac function (left ventricular diastolic pressure, 20 +/- 5.9%; +/- dP/dt, 5.2 +/- 4.5%

34 ents revealed similar reductions in systolic/diastolic pressure (-22/12 versus -21/13 mm Hg) and LV m

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

36 ities, including higher left ventricular end-diastolic pressures (24.3+/-4.6 versus 12.9+/-5.5 mm Hg)

37 +/-SD: LV ejection fraction, 19+/-7%; LV end-diastolic pressure, 25+/-8 mm Hg; QRS duration, 157+/-36

38 n reduced cardiac function (left ventricular diastolic pressure, 39 +/- 3.8%; +/- dP/dt, 32 +/- 4.4%,

39 ) and kappa(e) with the relationship: LV end-diastolic pressure=-4.73+0.27 tau(ln)+0.54 kappa(e) (r=0

40 eperfusion increased left ventricle (LV) end diastolic pressure (450% vs. 33%, p < 0.01) and reduced

41 artery conduit group having a higher aortic diastolic pressure (55 versus 42 mm Hg), a narrowed syst

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

43 /s, p < 0.0001), and elevated in vivo LV end-diastolic pressure (7 +/- 6 vs. 2 +/- 1 mm Hg, p = 0.04)

44 traction 24%, and mean right ventricular end-diastolic pressure 9 mm Hg.

45 patients with elevated left ventricular end-diastolic pressure, a finding largely attributed to the

46 End diastolic pressure, a negative index of myocardial perfo

47 ed neither the elevated left ventricular end-diastolic pressures, a measure of diastolic function, no

48 he combination of a high systolic and normal diastolic pressure-a widened pulse pressure-seems to be

49 Systolic and diastolic pressures among control and VVS were the same,

50 s >35% had an increased left ventricular end-diastolic pressure and a marked increase in heart weight

51 An inverse relationship between diastolic pressure and adverse cardiac ischemic events (

52 End-diastolic pressure and chamber diastolic stiffness did n

53 Indeed, a J-shaped relationship between diastolic pressure and coronary events was documented in

54 Partial to complete recovery of diastolic pressure and developed pressure was seen irres

55 fractional shortening, and increased LV end-diastolic pressure and fibrosis (P<0.05 versus control w

56 An interaction between decreased diastolic pressure and history of revascularization was

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

58 olic function, lowering left ventricular end-diastolic pressure and increasing the filling rate.

59 evidenced by increased left ventricular end-diastolic pressure and left ventricular volume indexes.

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

61 ed HF, CXL-1020 reduced left ventricular end-diastolic pressure and myocardial oxygen consumption whi

62 the J-shaped relationship persisted between diastolic pressure and primary outcome.

63 <.01 for difference between pulmonary artery diastolic pressure and pulmonary artery occlusion pressu

64 son, the regression between pulmonary artery diastolic pressure and pulmonary artery occlusion pressu

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

66 beat-to-beat changes in left ventricular end-diastolic pressure and SV was used as an index of the dy

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

68 offset the pacing-induced increase in LV end-diastolic pressure and the time constant of isovolumic r

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

70 of early pregnancy in humans despite reduced diastolic pressure and total peripheral resistance.

71 oconstriction from ET-1 led to higher aortic diastolic pressure and very narrow pulse pressure after

72 ding heart rate, peak-systolic pressure, end-diastolic pressure and volume, end-systolic pressure and

73 myocardium, as demonstrated by elevated end-diastolic pressures and decreased percent recovery of de

74 Similarly, left ventricular diastolic pressures and diastolic stiffness were elevate

75 ts, the pathophysiological cause of elevated diastolic pressures and heart failure is abnormal diasto

76 n Fontan, manifested by high ventricular end-diastolic pressures and pulmonary arterial wedge pressur

77 n, which subsequently led to elevated LV end-diastolic pressures and pulmonary hypertension.

78 remained in failure with similarly elevated diastolic pressures and reduced dP/dtmax.

79 , its association with increasing left heart diastolic pressures and systemic vascular stiffening, an

80 Systolic and diastolic pressures and their low- and respiratory-frequ

81 tolic pressure, 1.27 (95% CI, 1.01-1.60) for diastolic pressure, and 1.30 (95% CI, 1.05-1.61) for mea

82 e increase at 40 mm Hg, left ventricular end-diastolic pressure, and cardiac index, was significantly

83 de, left ventricular developed pressure, end-diastolic pressure, and coronary flow were significantly

84 aturation, elevated systemic ventricular end-diastolic pressure, and elevated main pulmonary artery p

85 lated with PH severity, left ventricular end-diastolic pressure, and left ventricular dilatation.

86 inephrine levels, lower left ventricular end-diastolic pressure, and lower right ventricle/body weigh

87 Left ventricular volumes, diastolic pressures, and diastolic stiffness were higher

88 vels, baseline and in-treatment systolic and diastolic pressures, and for diuretic therapy, losartan-

89 ed LV mass, posterior wall thickness and end diastolic pressures, and increased fractional shortening

90 d albuminuria, similar baseline systolic and diastolic pressures, and reductions in diastolic pressur

91 Elevation in right ventricular end-diastolic pressure appeared to predict poor vasodilatory

92 At similar left ventricular volumes, their diastolic pressures are more than twice as high as in co

93 Additionally, the end-diastolic pressure-area curves shifted to the left in al

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

95 l hearts had similar cardiac outputs and end-diastolic pressures as WT or transgenic hearts.

96 sure from randomization showed a benefit for diastolic pressure at month 12 (P = 0.039) but not at mo

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

98 based not only on the height of systolic and diastolic pressure but also on the presence of target or

99 a function of elevated left ventricular end diastolic pressure but was associated with increased per

100 rd, decreasing cardiac output at matched end-diastolic pressure by 44%.

101 e (75 to 100 mmol/d) will, on average, lower diastolic pressure by approximately 1 mmHg and systolic

102 n resistance (homeostasis model assessment), diastolic pressure, C-reactive protein, and the number o

103 ng diastole; hence, an excessive decrease in diastolic pressure can significantly hamper perfusion.

104 trolled delivery group (left ventricular end-diastolic pressure, cardiac index, +dP/dt, -dP/dt, and t

105 Left ventricular diastolic pressure, cardiac index, dP/dt40 and negative

106 nt parameters, including RV systolic and end-diastolic pressures, cardiac output, RV size, and morbid

107 was proportional to the magnitude of the end-diastolic pressure change.

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

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

110 End-diastolic pressure correlated significantly with tissue

111 Although left ventricular end-diastolic pressure decreased in 45/10, it increased in 4

112 r time constant of isovolumic relaxation and diastolic pressure (Delta +29+/-9% and +38+/-12%) and a

113 CPA produced improvement in postischemic end-diastolic pressure, developed pressure, and rate-pressur

114 In contrast, changes in end-diastolic pressure did induce vasodilatation that, altho

115 ed (n=49) subgroups according to whether the diastolic pressure difference (diastolic pulmonary arter

116 The diastolic pressure difference (DPD) is recommended to di

117 trol for 15 variables plus proline, systolic/diastolic pressure differences were -2.7/-2.0 mm Hg (z s

118 emic O(2) delivery, and (4) elevated cardiac diastolic pressures do not represent systolic dysfunctio

119 ive ethnic differences in either systolic or diastolic pressure during childhood and adolescence.

120 e of the linear correlation between MSNA and diastolic pressure during spontaneous breathing.

121 velop increases in left ventricular (LV) end-diastolic pressures during exercise that contribute to d

122 astolic volume (EDV) and Doppler-derived end-diastolic pressure (EDP) were used to derive the diastol

123 t ventricular developed pressure (LVDP), end diastolic pressure (EDP), and ATP were measured througho

124 q, even with marked reduction of volume (end-diastolic pressure [EDP], 1 to 2 mm Hg), whereas in cont

125 -derived baseline estimated pulmonary artery diastolic pressure (ePAD) and change from baseline ePAD

126 +/-10 mm, estimated resting pulmonary artery diastolic pressure (ePAD) of 16+/-9 mm Hg, and diastolic

127 Median estimated pulmonary artery diastolic pressures (ePAD) were calculated every 24 hour

128 The pulmonary artery diastolic pressure estimate of pulmonary artery occlusio

129 ion coefficient between the pulmonary artery diastolic pressure estimate of pulmonary artery occlusio

130 contrast, the bias for the pulmonary artery diastolic pressure estimate significantly increased with

131 be at increased risk for coronary events if diastolic pressure falls below critical levels.

132 stolic pressure declined in both groups, but diastolic pressure fell less with ALT-711 (P=0.056).

133 dP/dt max, -dP/dt min, and left ventricular diastolic pressure followed injection of MSCs before ind

134 index, LV dP/dt40, LV negative dP/dt, and LV diastolic pressure followed injection of MSCs, regardles

135 d protocol based on the left ventricular end-diastolic pressure for the prevention of contrast-induce

136 unloading manifested by a decrease in LV end-diastolic pressure from 11.4 +/- 9.0 mm Hg to 8.8 +/- 5.

137 e in intracellular calcium, but it decreased diastolic pressure from 19.7+/-3.5 to 17.5+/-3.7 mm Hg (

138 dardized measurements of seated systolic and diastolic pressures from eight large epidemiologic studi

139 to 1.35; p = 0.15) when defined according to diastolic pressure gradient.

140 tension (systolic pressure > or =140 mmHg or diastolic pressure > or = 90 mmHg) across quintiles of B

141 a systolic blood pressure > or =140 mm Hg or diastolic pressure > or =90 mm Hg at any FHS cycle exami

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

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

144 ure into postcapillary (left ventricular end-diastolic pressure, >15 mm Hg; n=269) and precapillary g

145 Left ventricular end-diastolic pressure-guided fluid administration seems to

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

147 cated in a 1:1 ratio to left ventricular end-diastolic pressure-guided volume expansion (n=196) or th

148 Interventions were performed after LV end-diastolic pressure had increased approximately 7 mm Hg.

149 after 45 minutes of low-flow ischemia, after diastolic pressure had increased from 8.5+/-0.6 to 19.7+

150 pressure, without associated changes in end-diastolic pressure, had no significant effect on vascula

151 demonstrated significant increases in LV end-diastolic pressure, heart and body weight, and LV chambe

152 ut (57%) and significant decreases in LV end-diastolic pressure, heart rate, and systemic vascular re

153 n, in-treatment use of digoxin, systolic and diastolic pressure, heart rate, QRS duration, Cornell vo

154 Right ventricular systolic and diastolic pressures, heart rate, and pressure derivative

155 The isovolumic end-diastolic pressure, however, remained elevated throughou

156 =0.02) and more likely to have higher RV end-diastolic pressure (HR, 1.07; 95% CI, 1.00-1.15; P=0.057

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

158 ic measures of diastolic function and LV end-diastolic pressure improve in most patients.

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

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

161 r the improvement in left ventricle (LV) end-diastolic pressure in cardiomyopathy patients treated wi

162 all subjects with a significant reduction in diastolic pressure in the HYL group (P = 0.008) but not

163 Diastolic pressure increased by 6+/-2 mm Hg (P:<0.05), a

164 Although central diastolic pressure increased significantly with pacing,

165 Diastolic pressures increased dramatically in response t

166 further dichotomized by left ventricular end-diastolic pressure into postcapillary (left ventricular

167 N(+)HFpEF had increased left ventricular end-diastolic pressure, left atrial volume, N-terminal prope

168 pertension (systolic pressure 160-200 mm Hg; diastolic pressure <110 mm Hg) who were aged 80 years or

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

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

171 fraction) and hemodynamic variables (LV end-diastolic pressure, LV dP/dtmax, preload adjusted maxima

172 of a noninvasive measure of left ventricular diastolic pressure (LVDP) early after acute myocardial i

173 paradoxically decreased left ventricular end-diastolic pressure (LVEDP) and left ventricular end-dias

174 t led to an increase of left ventricular end-diastolic pressure (LVEDP) by > or =20 mm Hg (ie, cardia

175 astolic volumes with little effect on LV end-diastolic pressure (LVEDP) or the end-diastolic P-V rela

176 lood pressure (DBP) and left ventricular end-diastolic pressure (LVEDP) to systolic blood pressure (S

177 ary enalaprilat reduced left ventricular end-diastolic pressure (LVEDP), but not left ventricular end

178 asurements, including cardiac output, LV end-diastolic pressure (LVEDP), rate of pressure rise at LV

179 onal marker of elevated left ventricular end-diastolic pressure (LVEDP), which adds prognostic value

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

181 creased DCS (isovolumic left ventricular end-diastolic pressure [LVEDP] increased 10 mm Hg, P<0.001,

182 omanometer-tipped catheters, and the mean LV diastolic pressure (M-LVDP) was used as a surrogate for

183 es, SMV activation increased the mean aortic diastolic pressure (MADP) by 26.5+/-3.5%, the mean diast

184 ew noninvasive methods to predict the aortic diastolic pressure may help in the future.

185 Ventricular end-diastolic pressure, mean PA pressure, and ventricular fu

186 ore defibrillation: 1) right atrial systolic/diastolic pressures (mm Hg) were lower (85 +/- 19, 4 +/-

187 stolic and diastolic function, higher LV end-diastolic pressure, more cardiomyocyte hypertrophy, and

188 )HFpEF had no change in left ventricular end-diastolic pressure, myocardial passive stiffness, collag

189 rformance with elevated left ventricular end-diastolic pressure, not seen in the wild-type.

190 early rapid filling and equalization of end-diastolic pressures obtained by cardiac catheterization

191 n, cardiac systolic pressure generation at a diastolic pressure of 15 mm Hg averaged 110 +/- 11, 66 +

192 end-diastolic volume at an idealized LV end-diastolic pressure of 20 mm Hg (EDV20), and RV remodelin

193 sure (systolic pressure of 130 to 139 mm Hg, diastolic pressure of 85 to 89 mm Hg, or both).

194 systolic pressure of 139 mm Hg or lower and diastolic pressure of 85 to 89 mm Hg, were randomly assi

195 of systolic pressure of 130 to 139 mm Hg and diastolic pressure of 89 mm Hg or lower, or systolic pre

196 vation in the systolic blood pressure with a diastolic pressure of less than 90 mm Hg.

197 pedance threshold valve results in sustained diastolic pressures of >55 mm Hg in patients in cardiac

198 r systolic pressures of 110 to 130 mm Hg and diastolic pressures of 70 to 90 mm Hg, which suggests th

199 r systolic pressures of 110 to 130 mm Hg and diastolic pressures of 70 to 90 mm Hg.

200 This adverse effect of too low a diastolic pressure on coronary heart disease leaves the

201 es, the end-diastolic volume at a common end-diastolic pressure on the sequential end-diastolic press

202 , increasing cardiac work while reducing the diastolic pressure, on which coronary flow is dependent.

203 th respect to time but did not change LV end-diastolic pressure or improve LV regional function.

204 function with elevated left ventricular (LV) diastolic pressure or may be merely a manifestation of a

205 tolic pressure without an increase in LV end-diastolic pressure, or decrease in LV dP/dt or LV wall t

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

207 d ejection fraction and left ventricular end-diastolic pressure (P<0.05).

208 ular pressure by micromanometer provided end-diastolic pressure (P) area (A) relations during initiat

209 f renal-cell cancer (P for trend, <0.001 for diastolic pressure; P for trend, 0.007 for systolic pres

210 Her systolic/diastolic pressure peaked at 23 min to reach 123/70 mmHg

211 Her systolic/diastolic pressure peaked at 7 min to reach 144/78 mmHg

212 th SHF and those with DHF; however, elevated diastolic pressures play a pivotal role in the underlyin

213 s in blood pressure and left ventricular end-diastolic pressure produced by GTN in vivo.

214 0.01) but an inverse correlation with LV end-diastolic pressure (r = -0.53, p = 0.01).

215 the time required for reaching the lowest LV diastolic pressure (r = 0.70, p = 0.04).

216 versely associated with left ventricular end-diastolic pressure (r=-0.728; P<0.001), resulting in a b

217 as SR(E) was significantly related to LV end-diastolic pressure (r=0.52, P=0.005) in the experimental

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

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

220 olow-Lyon voltage, in-treatment systolic and diastolic pressure, randomized treatment, and standard c

221 sympathetic response divided by the maximum diastolic pressure reduction during straining, was the s

222 and sympathetic baroreflex sensitivity (MSNA-diastolic pressure relation) were measured.

223 p but has no effect on the stroke volume/end-diastolic pressure relationship.

224 ft ventricular (LV) function measured by end-diastolic pressure response to preload augmentation, con

225 effect on heart rate, LV relaxation, LV end-diastolic pressure, right atrial pressure, or pulmonary

226 section again blunted the increase in LV end-diastolic pressure secondary to volume expansion (+4+/-3

227 Excessive reduction in diastolic pressure should be avoided in patients with CA

228 ; however, there was no increase in ischemic diastolic pressure, slowing of the calcium transient dec

229 HF, in-treatment differences in systolic and diastolic pressures, Sokolow-Lyon voltage, and Cornell p

230 osis and left atrium diameter (marker of end-diastolic pressure), suggesting an improvement in diasto

231 there was no alteration in left ventricular diastolic pressure, suggesting that ischemic diastolic d

232 elated cardiac dysfunction, including LV end-diastolic pressure, systolic performance, and chamber st

233 the pulse pressure index ([systolic pressure-diastolic pressure]/systolic pressure) in the range of 0

234 The peak diastolic pressure tended to be higher post- than pre-fl

235 e LV contractile function, and higher LV end-diastolic pressure than Ptges(+/+) mice after myocardial

236 , Whites have more hypertension (systolic or diastolic pressure) than do Blacks.

237 proach would mitigate the increase in LV end-diastolic pressure that develops during volume loading i

238 However, it is a normal diastolic pressure that separates patients with isolated

239 cardiac ischemic events (i.e., the lower the diastolic pressure the greater the risk of coronary hear

240 citation cardiac index, left ventricular end-diastolic pressure, the rate of left ventricular pressur

241 e relations of total and LDL cholesterol and diastolic pressure to distensibility had been present at

242 relaxation and lowering left ventricular end diastolic pressure to facilitate ventricular filling, th

243 Resting diastolic pressure trended lower (P = 0.09), heart rate

244 mia, cardiac output decreased by 41% and end diastolic pressure tripled for CD36-null hearts, with no

245 omitantly lowered cardiac preload volume and diastolic pressure (venodilation) without a change in ar

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

247 n fraction, end-systolic volume, and the end-diastolic pressure volume relationship by Ang-(1-9) trea

248 .9+/-5.5 mm Hg), caused by an upward-shifted diastolic pressure-volume curve.

249 LV diastolic pressure-volume curves confirmed a substantial

250 A left shift of the diastolic pressure-volume curves without changes in thei

251 nction and prompt leftward shifts of the end-diastolic pressure-volume curves.

252 oke work relation were measured from the end-diastolic pressure-volume relation before and during del

253 -volume curve and a reduced slope of the end-diastolic pressure-volume relation in the myoblast-trans

254 The diastolic pressure-volume relation was shifted up and to

255 ntricle, and induced a downward shift of the diastolic pressure-volume relation.

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

257 /leftward shift in the left ventricular (LV) diastolic pressure-volume relationship (P = 0.001), a gr

258 normal dogs underwent measurement of the end-diastolic pressure-volume relationship during caval occl

259 on (p = 0.014) and improvement of the RV end-diastolic pressure-volume relationship in PH pigs treate

260 The LV end-diastolic pressure-volume relationship measured by the i

261 The end-diastolic pressure-volume relationship slope was elevate

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

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

264 end-diastolic pressure on the sequential end-diastolic pressure-volume relationships was measured (le

265 ers assessed changes in end-systolic and end-diastolic pressure-volume relationships, and microsphere

266 Stiffness coefficient of exponential diastolic pressure-wall thickness relation was higher fo

267 Myocardial stiffness was estimated from diastolic pressure-wall thickness relationship obtained

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

269 on hemodynamics over time, mean right atrial diastolic pressure was 9 +/- 0.6 mm Hg with no lean, 10

270 t; 95% CI, 1.04-1.25; P = .006); however, if diastolic pressure was added, model fit improved and the

271 ral venous pressure nor left ventricular end diastolic pressure was altered by thapsigargin.

272 story of revascularization was observed; low diastolic pressure was associated with a relatively lowe

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

274 Left ventricular diastolic pressure was estimated with Doppler echocardio

275 LV end-diastolic pressure was increased with CIH (CIH, 13.7+/-5

276 nalysis revealed that the decrease in LV end-diastolic pressure was indicative of significant improve

277 LV end-diastolic pressure was measured by micromanometer.

278 Diastolic pressure was reduced in young old participants

279 In the treated hearts, the increase in end-diastolic pressure was significantly attenuated at the e

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

281 ction fraction [EF] and left ventricular end-diastolic pressure) was assessed at days 28 and 56.

282 lmonary artery pressure-left ventricular end-diastolic pressure) was normal (<7 mm Hg) or elevated (>

283 dP/dt min (-dP/dt min), and left ventricular diastolic pressure, was measured before inducing VF and

284 ht ventricular mass and left ventricular end diastolic pressure were increased and left ventricular s

285 tricle/body weight, and left ventricular end-diastolic pressure were increased and maximal left ventr

286 index, LV dP/dt40, LV negative dP/dt, and LV diastolic pressure were measured 4 wks after administeri

287 entricle weight/body weight ratio and LV end-diastolic pressure were significantly higher in hearts w

288 ulmonary capillary wedge pressure and LV end-diastolic pressure were significantly increased after th

289 for 38,184 children on 52,053 occasions for diastolic pressure were used; 51 percent (24,048 childre

290 LV diastolic pressures were lower during CHF exercise after

291 Left ventricular end-diastolic pressures were significantly elevated 4 weeks

292 Baseline mean systolic and diastolic pressures were similar in both groups.

293 ure and -0.4 (95% CI: -2.9, 2.2) mmHg/kg for diastolic pressure, while in within-pair analysis the va

294 The potential harm of further reducing the diastolic pressure with antihypertensive therapy, especi

295 ericardiotomy blunted the increase in LV end-diastolic pressure with saline infusion, while enhancing

296 c and diastolic pressures, and reductions in diastolic pressure with treatment but greater reductions

297 and total MI was J-shaped, particularly for diastolic pressure, with a nadir at 119/84 mm Hg.

298 measurements at 6 months showed lower LV end-diastolic pressures, with enhanced LV function (contract

299 Furthermore, at any given diastolic pressure, within-breath MSNA varied inversely

300 ary effect of this kind of therapy on LV end-diastolic pressure would be indicative of an improvement