ライフサイエンスコーパス: end-systolic

1 astolic (175 mL +/- 35 to 201 mL +/- 40) and end-systolic (100 mL +/- 24 to 115 mL +/- 29) volumes (P

2 mm Hg, p = 0.01), increased left ventricular end-systolic (51 +/- 13 vs 50 +/- 14 mm, p = 0.05) and e

3 aries followed by model-based calculation of end-systolic and end-diastolic LV volumes.

4 From standard cine and CP-BOLD images, end-systolic and end-diastolic myocardium was segmented.

5 Both end-systolic and end-diastolic RV volumes increased in S

6 c-to-diastolic ratio (S/D), quotient of mean end-systolic and end-diastolic signal intensities (on CP

7 Subsequently, RV end-systolic and end-diastolic volume increased more in

8 elocity, mitral E/e' ratio, left ventricular end-systolic and end-diastolic volume indexes (LVESVI an

9 End-systolic and end-diastolic volumes were calculated u

10 left ventricular (LV) ejection fraction, LV end-systolic and end-diastolic volumes, infarct size, an

11 meters (infarct wall thickening fraction, LV end-systolic and end-diastolic volumes, LV ejection frac

12 Systolic function (EF, end-systolic and end-diastolic volumes, stroke volumes)

13 Both the LV and RV end-systolic and LV end-diastolic volumes were increased

14 sed by echocardiographic end-diastolic area, end-systolic area, fractional area change, tricuspid ann

15 ted with a significant increase in dp/dtmax, end-systolic blood pressure, and systemic vascular resis

16 consistent with increased end-diastolic and end-systolic chamber elastance, as well as diastolic dys

17 Within the test set, myocardial end-systolic circumferential Green strain errors were -0

18 m [95% CI: -4.09 to -0.90; p = 0.002] and LV end systolic diameter -2.09 mm [95% CI: -4.11 to -0.06 p

19 soon as ejection fraction (EF) </=60% or LV end-systolic diameter >/=40 mm.

20 nal hazard model identified left ventricular end-systolic diameter >61 mm as an independent predictor

21 Those with left ventricular end-systolic diameter >61 mm had a 51% 3-year incidence

22 th CRT and a defibrillator, left ventricular end-systolic diameter >61 mm is a powerful predictor of

23 Among patients with left ventricular end-systolic diameter </=61 mm, multivariate predictors

24 2 +/- 5.5% to 32.7 +/- 6.7 %, p < 0.001), LV end-systolic diameter (5.93 +/- 0.55 cm to 5.62 +/- 0.32

25 al effective regurgitant orifice, indexed LV end-systolic diameter (LVESD), and right ventricular sys

26 3.6 mL (0.5-6.7, p=0.0217), left ventricular end-systolic diameter -1.8 mm (-2.9 to -0.6, p=0.0027),

27 Higher LV end-systolic diameter and symptoms correlate with less L

28 ; independent correlates included smaller LV end-systolic diameter in patients with aortic stenosis a

29 ameter was 48.6 +/- 5.7 mm, left ventricular end-systolic diameter was 32.3 +/- 5.7 mm, mV(O(2)) was

30 , end-diastolic diameter was 7.33+/-0.89 cm, end-systolic diameter was 6.74+/-0.88 cm, pulmonary arte

31 -8%; end-diastolic diameter, 4.81+/-0.58 cm; end-systolic diameter, 3.53+/-0.51 cm; pulmonary capilla

32 ), a larger left atrium and left ventricular end-systolic diameter, and T-wave inversion/ST-segment d

33 eft ventricular ejection fraction (LVEF), LV end-systolic diameter-index (LVESDi), DBP, and RHR were

34 ealed behind preoperative normal LVEF and LV end-systolic diameter.

35 EI) using following formula: LVEI=indexed LV end-systolic diameter/LV outflow tract time-velocity int

36 ence in change in LVEF, LV end diastolic and end systolic diameters between the 2 groups.

37 50%, LV end-diastolic dimension </=70 mm, LV end-systolic dimension </=50 mm or </=25 mm/m(2)) in who

38 tomatic, and 93 patients (7%) had indexed LV end-systolic dimension (iLVESD) >/=2.5 cm/m(2).

39 ssessed by LV end-diastolic dimension and LV end-systolic dimension (LVESd).

40 ejection time (p < 0.0001) and decreases in end-systolic dimension (p < 0.05).

41 T exposure was negatively associated with LV end-systolic dimension and heart rate (z-score differenc

42 action (59%, 58%, and 46%, respectively), LV end-systolic dimension and volume index, >= moderate tri

43 rtic valve surgery, LV ejection fraction, LV end-systolic dimension and volume index, presence of FMR

44 lack of severe left ventricular dilatation (end-systolic dimension index <29 mm/m(2)), and lack of e

45 ssion to stage C/D AR was associated with LV end-systolic dimension index (adjusted p = 0.02).

46 orbidities, baseline symptoms, and higher LV end-systolic dimension index (LVESDi) were associated wi

47 (LV) ejection fraction (p <= 0.003), not LV end-systolic dimension index.

48 igated whether an internally scaled index of end-systolic dimension is incremental to well-validated

49 z scores; all P = .001) and an increased LV end-systolic dimension z score (all P < .03).

50 et all these criteria: left ventricular (LV) end-systolic dimension z-score >2.6, age at diagnosis yo

51 eart failure, and increased left ventricular end-systolic dimension zscore at diagnosis were independ

52 V-GLS to STS, resting RVSP, left ventricular end-systolic dimension, and mitral effective regurgitant

53 Mean LV ejection fraction, indexed LV end-systolic dimension, resting right ventricular systol

54 change in pressure over time (dp/dt) and the end-systolic dimension-pressure relation.

55 Right ventricular (RV) end-systolic dimensions provide information on both size

56 The outcomes included RV end-diastolic and end-systolic dimensions, RV ejection fraction, functiona

57 End-systolic EI of 1.16 best identified the presence of

58 -independent parameter of systolic function, end systolic elastance (Ees), requires invasive catheter

59 LV systolic properties, namely EF, end systolic elastance, stroke work, and preload recruit

60 ; p < 0.001) and increased right ventricular end-systolic elastance (+0.72 +/- 0.2 mm Hg/mL; p < 0.00

61 -126 versus 555+/-122 mm Hg/s, P=0.006), and end-systolic elastance (1.03+/-0.57 versus 0.89+/-0.38 m

62 Effective arterial elastance (Ea) end-systolic elastance (Ees) and ventricular-arterial co

63 Ea, total arterial compliance (TAC), and end-systolic elastance (Ees) were calculated at baseline

64 V instantaneous peak pressure (dP/dtmax) and end-systolic elastance (Ees) were preserved in both grou

65 cts had adequate paired data to determine LV end-systolic elastance (Ees), end-diastolic elastance (E

66 and tonometry: left ventricular volumes and end-systolic elastance (Ees), peripheral resistance, art

67 ssociated with prognosis in systolic HF, but end-systolic elastance (Eessb) is not.

68 ffective arterial elastance/left ventricular end-systolic elastance [Ea/Ees]) after adjustment for po

69 hout PH (n=7) to derive contractile indexes (end-systolic elastance [Ees] and preload recruitable str

70 rterial coupling, defined by the quotient of end-systolic elastance and effective arterial elastance,

71 CXL-1020 increased contractility assessed by end-systolic elastance and provided venoarterial dilatio

72 cular coupling was worse in Cpc-PH patients (end-systolic elastance to effective arterial elastance [

73 -PAH patients did not augment contractility (end-systolic elastance) whereas IPAH did (P<0.001).

74 LV dP/dtmax, preload adjusted maximal power, end-systolic elastance, preload recruitable stroke work)

75 sed compliance of myocytes, but it depresses end-systolic elastance; under conditions of exercise, th

76 End-systolic fiber stress was elevated in 45 of 46 subje

77 ndocardial surfaces at the end-diastolic and end-systolic frames for rest-stress studies were registe

78 =0.0114), reduced left ventricular dilation (end-systolic inner left ventricular diameter, 3.59 versu

79 d left ventricular end-systolic volume at an end-systolic left ventricular pressure of 100 mm Hg.

80 egurgitation (MR) when left ventricular (LV) end-systolic (LVES) dimension is >40 mm, LV ejection fra

81 terload as expressed by the left ventricular end-systolic meridional wall stress (35 +/- 13 to 18 +/-

82 nction (median: 4.8 versus 1.8 mm; P<0.001), end-systolic mitral annular diameters (median: 41.2 vers

83 r pressure (dp/dtmax ), and the slope of the end-systolic P-V relationship (ESPVR), suggesting that a

84 volume relationship during systole (Sslope); end-systolic peak (peak ); and diastolic uncoupling (sys

85 essure exerted by the contracting ventricle (end systolic pressure) to its volume (end systolic volum

86 O; P<0.05) and induced systolic dysfunction (end systolic pressure-volume relationship =24.86+/-2.46

87 ases >= 15%), fluid administration increased end-systolic pressure and decreased effective arterial e

88 pressure, end-diastolic pressure and volume, end-systolic pressure and volume, and ratio of systole t

89 In the 15 fluid nonresponders, end-systolic pressure increased (p < 0.05), whereas effe

90 123 +/- 18 mm Hg; both P=0.02), and central end-systolic pressure trended lower (116 +/- 18 to 111 +

91 The slope of the end-systolic pressure volume relationship (i.e., contrac

92 lic volume [EDV]); contractile function (the end-systolic pressure volume relationship slope [Eessb]

93 End-systolic pressure was calculated as 0.9 x systolic a

94 According to the "cardiocentric" view, end-systolic pressure was considered the classic index o

95 end-diastolic LV volume, augmentation index, end-systolic pressure, and cardiovascular disease risk f

96 easurements revealed complete restoration of end-systolic pressure, ejection fraction, end-systolic v

97 d administration increased stroke volume and end-systolic pressure, whereas effective arterial elasta

98 t effect on systolic function, improving the end-systolic pressure-volume relation (+0.98 +/- 0.41 mm

99 derzone (P<0.01), and a steeper slope of the end-systolic pressure-volume relationship (P=0.01).

100 Ischemia shifted the end-systolic pressure-volume relationship and cardiac ou

101 7% (p < .05), and significantly improved the end-systolic pressure-volume relationship and preload re

102 terval, 13-24]% versus 12 [10-14]%, P=0.008; end-systolic pressure-volume relationship slope 2.4 [1.9

103 Hg [IQR, 21-46 mm Hg]; P=0.005), whereas the end-systolic pressure-volume relationship was not signif

104 estimates of effective arterial elastance = end-systolic pressure/stroke volume in critically ill pa

105 accompanying echocardiographic criteria: (1) end-systolic ratio of noncompacted layer to compacted la

106 RV end-systolic remodeling index (RVESRI) was defined by la

107 diomyocytes exhibit higher end-diastolic and end-systolic stiffness than +/+ cardiomyocytes, whereas

108 arterial coupling) is defined by a ratio of end-systolic to arterial elastances (Ees/Ea).

109 /-7.32 mL; P=0.03), a trend toward decreased end systolic volume (142.4+/-16.5 versus 107.6+/-7.4 mL;

110 positively associated with end diastolic and end systolic volume and inversely related to ejection fr

111 FF (P=0.06) and significant reductions in LV end systolic volume index (-6.7 +/- 21.1 versus 2.1 +/-

112 ation, and smaller baseline left ventricular end systolic volume index also were also associated with

113 LV end systolic volume index is a significant predictor of

114 LV end systolic volume index was also evaluated as a predic

115 LV end systolic volume index was predictive of mortality/mo

116 e clinical composite score, left ventricular end systolic volume index, 6-minute walk time, and quali

117 up to 1% for every 1 mL/m(2) increase in LV end systolic volume index.

118 ygenic score of MRI-derived left ventricular end systolic volume strongly associates with incident DC

119 Resting end systolic volume was 129+/-60 mL at rest and increase

120 ricle (end systolic pressure) to its volume (end systolic volume).

121 We estimated 95th weighted percentiles of LV end systolic volume, LV end diastolic volume, relative w

122 nal treatment in end diastolic volume (EDV), end systolic volume, stroke volume (SV), cardiac output

123 onse to CRT was defined as a reduction in LV end-systolic volume >/=15% at 6 months.

124 as defined as a decrease in left ventricular end-systolic volume >15% at follow-up echocardiography c

125 .01 mm/mL; P<0.01), a lower left ventricular end-systolic volume (-0.01 mm/mL; P=0.01), and lower lef

126 r end-diastolic volume (-18 mL; P=0.009) and end-systolic volume (-14 mL; P=0.005) occurred at end in

127 ociated with a reduction in left ventricular end-systolic volume (-24.8 +/- 3.0 ml vs. -8.8 +/- 3.9 m

128 vs. placebo, respectively; p < 0.001) and LV end-systolic volume (-26.6 +/- 20.5 ml vs. -0.5 +/- 21.9

129 ith controls, evoked by a preservation of LV end-systolic volume (-4.05 mL; 95% CI, -6.91 to -1.18; P

130 e interval, -3.55 to -0.95; P=0.0007) and LV end-systolic volume (-6.37 mL; 95% confidence interval,

131 nce interval, -5.47 to -2.59; P<0.00001), LV end-systolic volume (-8.91 mL; 95% confidence interval,

132 nction (bias +/- 95% confidence) in terms of end-systolic volume (0 +/- 3.3 ml), end-diastolic volume

133 0.83 cm to 6.51 +/- 0.91 cm, p < 0.001), LV end-systolic volume (178 +/- 72 to 145 +/- 23 ml, p < 0.

134 -16 mL/m(2); P<0.05), and greater indexed LV end-systolic volume (41+/-11 versus 31+/-7 and 30+/-8 mL

135 .4 vs. 94.1 +/- 21.1 mmHg, P < 0.001) and LV end-systolic volume (44.2 +/- 7.8 vs. 50.5 +/- 10.8 ml,

136 rease of indexed RV end-diastolic volume and end-systolic volume (98 ml/m(2) to 87 ml/m(2) and 50 ml/

137 Allopurinol also reduced LV end-systolic volume (allopurinol -2.81 +/- 7.8 mls vs. p

138 eta=0.01/mL; P<0.0001), and left ventricular end-systolic volume (beta=0.01/mL; P<0.001) were associa

139 me (beta=0.811; adjusted P=0.007), higher LV end-systolic volume (beta=0.350; adjusted P=0.048), high

140 s associated with significant decrease in LV end-systolic volume (DeltaLV end-systolic volume -28.2+/

141 . 1.8 +/- 7.9; P < 0.05), difference between end-systolic volume (ESV) at rest and stress (DeltaESV[s

142 l coupling ratio using stroke volume (SV) to end-systolic volume (ESV) has been shown to be an indepe

143 agreement of LV end-diastolic volume (EDV), end-systolic volume (ESV), and EF measured by 3DE and 2D

144 by measuring LV end-diastolic volume (EDV), end-systolic volume (ESV), and ejection fraction (EF).

145 rence limits for end-diastolic volume (EDV), end-systolic volume (ESV), ejection fraction, and region

146 Cardiac function parameters, including the end-systolic volume (ESV), end-diastolic volume (EDV), s

147 End-diastolic volume (EDV), end-systolic volume (ESV), stroke volume (SV), ejection

148 ricular volumes were strongly correlated for end-systolic volume (ESV: Pearson r = 0.99, P < .001), e

149 efined as reduction in both left ventricular end-systolic volume (LVESV) and left atrial volume (LAV)

150 tricular end-diastolic volume (LVEDV) and LV end-systolic volume (LVESV) by cardiovascular magnetic r

151 mary endpoint was change in left ventricular end-systolic volume (LVESV) on cardiac magnetic resonanc

152 jection fraction (LVEF) and left ventricular end-systolic volume (LVESV) relative to baseline measure

153 ce area [BSA], 25 mL/m(2)); left ventricular end-systolic volume (LVSV), 21 mL (LVSV/BSA, 13 mL/m(2))

154 erence: 43+/-22.5 mL), higher left ventricle end-systolic volume (mean difference: 34+/-20.5 mL), and

155 tion fraction (P < 0.0001) and a decrease in end-systolic volume (P = 0.0002) were observed, which al

156 tion, while the RVPAS group had increased RV end-systolic volume (p = 0.004) and decreased right vent

157 elastance (p = 0.003), and right ventricular end-systolic volume (p = 0.020) while right ventricular

158 4 +/- 7% (P<0.001) because of an increase in end-systolic volume (P<0.05).

159 ex, and body surface area, right ventricular end-systolic volume (P=0.004) strongly predicted mortali

160 n fraction (P<0.001) because of an increased end-systolic volume (P=0.015).

161 = 0.14, respectively, for PRF and PRV) or RV end-systolic volume (r = 0.2; p = 0.42 and r = 0.19; p =

162 relations were found for LV mass (r = 0.95), end-systolic volume (r = 0.93), and end-diastolic volume

163 nd related to the change in left ventricular end-systolic volume (r=-0.53; P<0.001).

164 L (RVDV/BSA, 164 mL/m(2)); right ventricular end-systolic volume (RVSV), 198 mL (RVSV/BSA, 124 mL/m(2

165 decrease in LV end-systolic volume (DeltaLV end-systolic volume -28.2+/-38.9 versus -4.9+/-33.8 mL,

166 olic volume 106 +/- 15 versus 110 +/- 22 mL; end-systolic volume 35 +/- 6 versus 36 +/- 6 mL) or incr

167 [milliliters]/body surface area [BSA](1.3), end-systolic volume [milliliters]/BSA(1.3), and mass [gr

168 In control animals, LV end-systolic volume and end-diastolic volume increased f

169 use mortality and change in left ventricular end-systolic volume and end-diastolic volume.

170 End-systolic volume and end-diastolic volume/body surfac

171 stress, reduced LV end-diastolic volume, LV end-systolic volume and increase in LV ejection fraction

172 In multivariate analysis, LV end-systolic volume and mitral annulus area most strongl

173 c infarction resulted in less increase in LV end-systolic volume and preservation of LV ejection frac

174 ined as >/=15% reduction in left ventricular end-systolic volume at 1-year of follow-up) among 612 pa

175 those demonstrating a >/=15% reduction in LV end-systolic volume at 6 months.

176 efined as >15% reduction in left ventricular end-systolic volume at 6 months.

177 rimary endpoint was a >/=15% reduction in LV end-systolic volume at 6 months.

178 The effect of cooling on left ventricular end-systolic volume at a pressure of 100 mm Hg (hyperthe

179 ar contractility increased (left ventricular end-systolic volume at a pressure of 100 mm Hg: 74 +/- 5

180 assessed by the calculated left ventricular end-systolic volume at an end-systolic left ventricular

181 ocardiography compared with left ventricular end-systolic volume at baseline.

182 Adjustment for 3-month DeltaLV end-systolic volume attenuated the association between Q

183 analyses, female sex was associated with LV end-systolic volume change (beta=0.12; P=0.003) and a lo

184 on between sex and LV reverse remodeling (LV end-systolic volume change) and sex and the composite ou

185 increase at post (39+/-2%; P<0.05), whereas end-systolic volume decreased.

186 This was accompanied by a reduction in LV end-systolic volume from 122.7 to 89.0 mL (difference, 3

187 noncontrast 3D EF, end-diastolic volume, and end-systolic volume had significantly lower temporal var

188 ic volume improved from 172 ml to 140 ml and end-systolic volume improved from 82 ml to 73 ml (both p

189 o 143 +/- 53 ml (n = 203; p < 0.0001) and LV end-systolic volume improved from 87 +/- 47 ml to 79 +/-

190 e right atrial volume than right ventricular end-systolic volume in AF-TR (P<0.001).

191 e of 6.7 mL/m(2) in the change of indexed LV end-systolic volume in favor of G-CSF group (P=0.02).

192 In addition, LV end-systolic volume increased by 108% in controls versus

193 up; p = 0.0012), as did the left ventricular end-systolic volume index (48.4 +/- 19.7 ml/m(2) vs. 43.

194 3-vessel CAD, EF below the median (27%), and end-systolic volume index (ESVI) above the median (79 ml

195 controls with 3D wall motion tracking for RV end-systolic volume index (ESVi), RV ejection fraction (

196 scularization outcomes could be modulated by end-systolic volume index (ESVi).

197 The left atrial end-systolic volume index (LAESVI) is a predictor of car

198 e primary end point was the left ventricular end-systolic volume index (LVESVI) at 12 months, as asse

199 fined as a decrease in left ventricular (LV) end-systolic volume index (LVESVI) of more than 10% from

200 gnificant difference in the left ventricular end-systolic volume index (LVESVI) or survival after 1 y

201 Temporal changes in MR severity and LV end-systolic volume index (LVESVi) were evaluated by lin

202 e primary end point was the left ventricular end-systolic volume index (LVESVI), a measure of left ve

203 , LV end-diastolic volume index (LVEDVI), LV end-systolic volume index (LVESVI), left atrial volume i

204 gnificant difference in the left ventricular end-systolic volume index (LVESVI), survival, or adverse

205 3-mL/m(2) mean reduction in left ventricular end-systolic volume index (P<0.0001), whereas non-LBBB p

206 s associated with increased left ventricular end-systolic volume index (r=0.62, P<0.01), left atrial

207 ctors of death (P < 0.01): right ventricular end-systolic volume index adjusted for age and sex, and

208 nary anatomy, and left ventricular function, end-systolic volume index and B-type natriuretic peptide

209 ivariable regression model, left ventricular end-systolic volume index and left atrial volume index w

210 Right ventricular end-systolic volume index and left ventricular strain-ra

211 ences in mean LV end-diastolic volume index, end-systolic volume index and LVEF between diabetic pati

212 but not when combined with right ventricular end-systolic volume index and strain-rate e'-wave in the

213 rison with placebo, empagliflozin reduced LV end-systolic volume index by 6.0 (95% CI, -10.8 to -1.2)

214 Percentage-predicted right ventricular end-systolic volume index can identify a high percentage

215 Percentage-predicted right ventricular end-systolic volume index independently predicted outcom

216 , defined as an increase in left ventricular end-systolic volume index of >15% at 24 months.

217 arly in patients with increased preoperative end-systolic volume index or B-type natriuretic peptide.

218 End-systolic volume index remained unchanged (P=0.8).

219 ts: A percentage-predicted right ventricular end-systolic volume index threshold of 227% or a left ve

220 cted by VNS (p < 0.05), but left ventricular end-systolic volume index was not different (p = 0.49).

221 ues for LV end-diastolic volume index and LV end-systolic volume index were negligible (g<0.10).

222 eft ventricle end-diastolic volume index and end-systolic volume index were reduced from 128.4+/-22.1

223 rong predictor of change in left ventricular end-systolic volume index with monotonic increases as QR

224 ular dilatation (increased right ventricular end-systolic volume index), high Acute Physiology and Ch

225 ventricular ejection fraction, 23+/-9%; mean end-systolic volume index, 113+/-48 mL; mean total myoca

226 n after adjusting for clinical risk factors, end-systolic volume index, mitral regurgitation, incompl

227 mpared with the CABG group: left ventricular end-systolic volume index, MR volume, and plasma B-type

228 ow-up (end-diastolic volume index, P=0.0056; end-systolic volume index, P=0.4719).

229 n analyses, the MRI-derived left ventricular end-systolic volume index, RV, and OMR category (severe

230 15% or more increase in the left ventricular end-systolic volume index.

231 LV remodeling was defined as change in LV end-systolic volume index.

232 ction, LV end-diastolic volume index, and LV end-systolic volume index.

233 (9.5 years between examinations 1 and 5) in end-systolic volume indexed (ESVi) to body surface area.

234 were change from baseline to 36 weeks in LV end-systolic volume indexed to body surface area and LV

235 her right ventricular (RV) end-diastolic and end-systolic volume indices accompanied by lower RV ejec

236 Corrected right ventricular end-systolic volume is a strong prognostic marker in idi

237 (74%) met standard criteria for response (LV end-systolic volume reduction >/= 15%), 18 patients (58%

238 %), 18 patients (58%) for super-response (LV end-systolic volume reduction >/= 30%).

239 Echocardiographic left ventricular end-systolic volume reduction >=15% after 6 months was d

240 uintile versus the bottom quintile of the LV end-systolic volume risk score).

241 RV volumes (end-diastolic volume and end-systolic volume), stroke volume, and EF were measure

242 eling (defined as >/=15% reduction in the LV end-systolic volume).

243 volumes (end-diastolic volume, -5 mLdecade; end-systolic volume, -3 mL/decade; EF, -2 mL/decade) and

244 ate adverse LV remodeling was attenuated (LV end-systolic volume, 42.6 mL [38.5-50.5] to 56.1 mL [50.

245 olic volume, LV wall stress, no change in LV end-systolic volume, and a fall in LV ejection fraction.

246 ts included changes in end-diastolic volume, end-systolic volume, and ejection fraction, analyzed wit

247 h-dose allopurinol regresses LVH, reduces LV end-systolic volume, and improves endothelial function i

248 ntricle end-diastolic volume, left ventricle end-systolic volume, and left ventricle ejection fractio

249 end-diastolic volume, higher left ventricle end-systolic volume, and lower LVEF with both imaging mo

250 lar (LV) ejection fraction, infarct size, LV end-systolic volume, and LV end-diastolic volume were an

251 lar (LV) ejection fraction, infarct size, LV end-systolic volume, and LV end-diastolic volume were es

252 (3 loci each for LV end-diastolic volume, LV end-systolic volume, and LV mass to end-diastolic volume

253 However, changes in end-diastolic volume, end-systolic volume, and LVEF did not differ between gro

254 of end-systolic pressure, ejection fraction, end-systolic volume, and the end-diastolic pressure volu

255 es of left ventricular ejection fraction and end-systolic volume, but not with the severity of brain

256 eft ventricular dilation compared with sham (end-systolic volume, day 2: 40.6 +/- 10.2 muL vs. 23.8 +

257 ft ventricular (LV) end-diastolic volume, LV end-systolic volume, LV ejection fraction, left atrial v

258 en comorbidity burden and improvements in LV end-systolic volume, LV end-diastolic volume, left ventr

259 s of 6 LV traits-LV end-diastolic volume, LV end-systolic volume, LV stroke volume, LV ejection fract

260 or volumes (end-diastolic volume, R(2)=0.43; end-systolic volume, R(2)=0.35; stroke volume, R(2)=0.30

261 to LV global functional parameters (indexed end-systolic volume, r=0.47, P<0.001; ejection fraction,

262 t predictor of survival, independent of age, end-systolic volume, sex, mitral regurgitation, diabetes

263 Biventricular end-diastolic volume, end-systolic volume, stroke volume, and ejection fractio

264 here LA emptying fraction was defined as (LA end-systolic volume--LA end-diastolic volume) / LA end-s

265 fined as a 15% reduction in left ventricular end-systolic volume.

266 ecause of a preservation of left ventricular end-systolic volume.

267 s quantified as 6-month percent change of LV end-systolic volume.

268 stolic volume--LA end-diastolic volume) / LA end-systolic volume.

269 erioration in LV end-diastolic volume and LV end-systolic volume.

270 reased LV ejection fraction and decreased LV end-systolic volume.

271 V ED 3-dimensional radius/wall thickness; LV end-systolic volume/body surface area, LV longitudinal s

272 by 14 months (end-diastolic volume/BSA(1.3), end-systolic volume/BSA(1.3), and mass/BSA(1.3) mean dif

273 icant reduction of left ventricular volumes (end-systolic volume: -4.3 [11.3] versus 7.4 [11.8], P=0.

274 4, Delta end-diastolic volume: P<0.02, Delta end-systolic volume: P<0.005).

275 tract-velocity time integral] / [indexed LA end-systolic volume]), where LA emptying fraction was de

276 dysfunction preceded LV dysfunction, with RV end systolic volumes increased and RV ejection fractions

277 ifferences were observed in left ventricular end-systolic volumes (-6.4 mL [95% CI, -18.8 to 5.9] ver

278 .2 +/- 0.7 versus 1.59 +/- 0.6 mL; P<0.001), end-systolic volumes (0.72 +/- 0.42 versus 0.40 +/- 0.19

279 71+/-4% versus 69+/-4%; P=0.03), and smaller end-systolic volumes (38+/-9 versus 43+/-12 mL; P=0.03).

280 versus 69%), higher indexed left ventricular end-systolic volumes (96 versus 40 mL), and greater inde

281 6; 95% CI, 0.8-2.5; P<0.001), and smaller LV end-systolic volumes (beta=1.4; 95% CI, 0.5-2.3; P=0.001

282 as reductions in atrial and left ventricular end-systolic volumes (LVESV) at 1 year.

283 =0.016), end-diastolic volume (P=0.029), and end-systolic volumes (P=0.021).

284 th crypts had lower indexed left ventricular end-systolic volumes (P=0.042) and higher indexed left a

285 s in indexed RV end-diastolic volumes and RV end-systolic volumes (RVESVi) (indexed RV end-diastolic

286 Fallot in women had larger right ventricular end-systolic volumes (standard deviation scores: women,

287 LV end-diastolic and end-systolic volumes and diastolic function were signifi

288 The LV end-diastolic and end-systolic volumes and LV ejection fraction were not s

289 LV end-diastolic and end-systolic volumes decreased as early as 30 days after

290 In controls, end-diastolic and end-systolic volumes increased and ejection fraction dec

291 ft ventricular end-diastolic and left atrial end-systolic volumes increased by 3.63 ml/m(2) (P = 0.00

292 ther BiVP or HisBP, the LV end-diastolic and end-systolic volumes were significantly lower (mean dura

293 ther BiVP or HisBP, the LV end-diastolic and end-systolic volumes were significantly lower (mean dura

294 nt decreases in LV end-diastolic volumes, LV end-systolic volumes, cardiac output, cardiac index, atr

295 LV end-diastolic and end-systolic volumes, ejection fraction, plasma norepine

296 icant treatment effects found on LV ED or LV end-systolic volumes, LV ED mass/LV ED volume or LV ED 3

297 sing left ventricular end-diastolic volumes, end-systolic volumes, stroke volumes, and masses with in

298 etic peptide (NT-proBNP) and circumferential end-systolic wall stress (cESS) on echocardiography are

299 increased in both groups (P < 0.001), as was end-systolic wall stress (P < 0.001).

300 Percutaneous mitral valve repair increased end-systolic wall stress (WSES; from [median] 184 mm Hg