ライフサイエンスコーパス: systolic pressure

1 lse pressure and 1.42 [CI, 1.14 to 1.76] for systolic pressure).

2 y vascular remodeling, and right ventricular systolic pressure.

3 elated with an increase in right ventricular systolic pressure.

4 200 mug/kg) decreased right ventricular peak systolic pressure.

5 A secondary endpoint was nocturnal dip in systolic pressure.

6 h reversible increments of right ventricular systolic pressure.

7 PAH as judged by elevated right ventricular systolic pressure.

8 enous iloprost in reducing right ventricular systolic pressure.

9 ure with treatment but greater reductions in systolic pressure.

10 rate lowering consistently increases central systolic pressure.

11 tio of right ventricular (RV) to aortic (Ao) systolic pressure.

12 ontrol were unchanged after adjusting for RV systolic pressure.

13 than or equal to two-thirds of the systemic systolic pressure.

14 ic dimension, LV mass, and right ventricular systolic pressure.

15 ht ventricular afterload by pulmonary artery systolic pressure.

16 Sildenafil had no effect on pulmonary artery systolic pressure.

17 on abdominal aortic aneurysm than did raised systolic pressure.

18 ely 60% of the increase in right ventricular systolic pressure.

19 rmined between the predicted and measured PA systolic pressures.

20 -MI in vivo exercise capacity and ex vivo LV systolic pressures.

21 fference between the left and right brachial systolic pressures.

22 -16 mm Hg; +16%; P=0.006) with a decrease in systolic pressure (116+/-20 to 99+/-26 mm Hg; -15%; P=0.

23 Estrogen therapy did not change systolic pressure (128+/-2 versus 123+/-2 mm Hg) or card

24 0.4 to 23.6 + or - 0.4 kg), left ventricular systolic pressure (137.0 + or - 3.4 to 124.0 + or - 6.7

25 DASH/SRD reduced clinic and 24-hour brachial systolic pressure (155 +/- 35 to 138 +/- 30 and 130 +/-

26 Patients with hypertension (systolic pressure 160-200 mm Hg; diastolic pressure <110

27 ne, patients had severe hypertension (aortic systolic pressure, 176+/-26 mm Hg), pulmonary hypertensi

28 th a 46% reduction in right ventricular peak systolic pressure (38 mm Hg), suggesting significant pul

29 were associated with higher pulmonary artery systolic pressure: 39 +/- 9 mm Hg with thrombi versus 33

30 olume index (44 mL/m2), and pulmonary artery systolic pressure (41 mm Hg) were consistent with chroni

31 with control intake, peripheral and central systolic pressures [-5.7 mm Hg (P = 0.007) and -5.4 mm H

32 mean reduction in estimated pulmonary artery systolic pressure (63.9 +/- 13 to 54.2 +/- 12 mm Hg, p =

33 2 men; mean, 77 years; mean pulmonary artery systolic pressure, 69.4+/-10.5 mm Hg), of which PH was l

34 ary hypertension (estimated pulmonary artery systolic pressure, 71+/-23 mm Hg) and in 44 age- and gen

35 o 21.7 mm Hg, P<0.001) and right ventricular systolic pressure (72.8 to 47.3 mm Hg, P<0.001) at cathe

36 stenting included significantly decreased RV systolic pressure (89+/-18 to 65+/-20 mm Hg, P<0.001) an

37 putamen radioactivity correlated with supine systolic pressure across all subjects and among PD patie

38 Systolic pressure also fell in the latter group (133.1 [

39 es were -0.9 (95% CI: -6.4, 4.6) mmHg/kg for systolic pressure and -0.2 (95% CI: -4.1, 3.7) mmHg/kg f

40 es were -0.1 (95% CI: -4.0, 3.8) mmHg/kg for systolic pressure and -0.4 (95% CI: -2.9, 2.2) mmHg/kg f

41 monotonically decreasing association between systolic pressure and adjusted probability of death acro

42 ompared with control, right ventricular (RV) systolic pressure and arterial elastance (measure of vas

43 Low LV systolic pressure and deterioration in LV relaxation wer

44 ne acetate mice had similar left ventricular systolic pressure and fractional shortening but more hyp

45 n, judged by regression of right ventricular systolic pressure and hypertrophy and pulmonary artery o

46 ea (1.5 mg/kg IC) increased left ventricular systolic pressure and left ventricular dP/dt and caused

47 At 17 weeks postinfection, right ventricular systolic pressure and liver and lung egg counts were mea

48 ral wall CS correlated with pulmonary artery systolic pressure and LV eccentricity index, after adjus

49 iography-estimated elevated pulmonary artery systolic pressure and LV lateral E/e' ratio were indepen

50 the same relative fatiguing force, the peak systolic pressure and mean arterial pressure during stat

51 statistically supportable threshold between systolic pressure and mortality emerges from the data a

52 Left ventricular systolic pressure and positive and negative maximal valu

53 re used to determine the association between systolic pressure and probability of death, adjusting fo

54 estimated vagal baroreflex sensitivity with systolic pressure and R-R interval cross-spectra measure

55 The strong correlation between systolic pressure and R-R intervals at respiratory frequ

56 ed modest increases in the right ventricular systolic pressure and right ventricle hypertrophy.

57 ly attenuated elevation of right ventricular systolic pressure and right ventricular hypertrophy and

58 00A4/Mts1 mice had greater right ventricular systolic pressure and right ventricular hypertrophy at b

59 acute hypoxia (10% O2) or the increase in RV systolic pressure and RV hypertrophy following 3 weeks i

60 ced PH, including attenuated increases in RV systolic pressure and RV hypertrophy, decreased platelet

61 The similar elevation in RV systolic pressure and RV hypertrophy, despite the attenu

62 termined by measuring right ventricular (RV) systolic pressure and RV hypertrophy.

63 nol on relaxation velocity, left ventricular systolic pressure and stroke volume were blunted in dysf

64 ed significantly increased right ventricular systolic pressure and substantial pulmonary vascular rem

65 eatment with candesartan lowered (P<0.05) LV systolic pressure and the first derivative of LV pressur

66 nt significantly decreased right ventricular systolic pressure and total pulmonary vascular resistanc

67 sure, end-diastolic pressure and volume, end-systolic pressure and volume, and ratio of systole to di

68 characteristics caused a decrease in aortic systolic pressure and wasted LV pressure energy.

69 +) mice exhibited elevated right ventricular systolic pressures and right ventricular hypertrophy wit

70 n fraction, LV dimensions, right ventricular systolic pressure) and exercise variables (metabolic equ

71 del, A-17 and A-21 reduced right ventricular systolic pressure, and all antagomirs decreased pulmonar

72 ence, association with high pulmonary artery systolic pressure, and attributable mortality remain unk

73 diastolic LV volume, augmentation index, end-systolic pressure, and cardiovascular disease risk facto

74 er adjustment for age, sex, pulmonary artery systolic pressure, and comorbidities, the presence of an

75 The TRI, calculated from baseline age, systolic pressure, and heart rate, was established in pa

76 and cardiac output, higher pulmonary artery systolic pressure, and more severe RV enlargement and tr

77 ed pulmonary hypertension (right ventricular systolic pressure approximately 100 mm Hg) and severe pu

78 diponectin, and had higher right ventricular systolic pressure associated with right ventricular hype

79 at peak exercise and higher pulmonary artery systolic pressure at rest and at peak exercise, and lowe

80 the abdominal vasculature is associated with systolic pressure augmentation in the ascending aorta an

81 ading conditions in the ascending aorta, and systolic pressure augmentation may be a more useful guid

82 Wave-reflection-induced systolic pressure augmentation was determined using the

83 Keeping systolic pressure below 120 mm Hg before age 35 years ma

84 (beta=-0.22, P=0.002), and pulmonary artery systolic pressure (beta=-0.14, P=0.047).

85 ity score of 3 or greater) and a prehospital systolic pressure between 40 and 119 mm Hg were included

86 (30%) and depends weakly on pulmonary artery systolic pressure but mainly on left ventricular remodel

87 attenuated the increase in right ventricular systolic pressure but without a significant effect on ri

88 oximately 118% increase in right ventricular systolic pressure) but not polycythemia and was associat

89 2) Egtazic acid reduced LV systolic pressure by 30% (p < 0.001), indicating reduced

90 dose of norepinephrine necessary to increase systolic pressure by 33 and 100 mm Hg (pressor dose 33 a

91 0 mm Hg were associated with larger falls in systolic pressure by 4.3/2.9 mm Hg in Gabon/Bastrop per

92 cium chloride, 5 and 14 mmol/L, increased LV systolic pressure by 42% and 70%, respectively (p < 0.00

93 o 27 mL/min), causing right ventricular peak systolic pressure/cardiac output to increase from 0.6 co

94 bited significantly higher right ventricular systolic pressure compared with wild-type littermates un

95 A 1-SD (20 mm Hg) increment in systolic pressure conferred a 56% increased risk for CHF

96 was associated with risk for CHF, pulse and systolic pressure conferred greater risk than diastolic

97 sing doses of norepinephrine (norepinephrine-systolic pressure curve) were assessed during a baseline

98 ith LV hypertrophy were older and had higher systolic pressure, damage index scores, C-reactive prote

99 Systolic pressure declined in both groups, but diastolic

100 er independent correlates were adipose mass, systolic pressure, diabetes, age, and use of digoxin and

101 The slope of the LV end-systolic pressure-diameter relationship was increased at

102 Subclavian stenosis, diagnosed by a brachial systolic pressure difference (BSPD) > or =15 mm Hg, is a

103 Pulmonary artery systolic pressure dropped more in HFpEF than in HFrEF de

104 rements revealed complete restoration of end-systolic pressure, ejection fraction, end-systolic volum

105 th heart function including heart rate, peak-systolic pressure, end-diastolic pressure and volume, en

106 stroke volume index, ejection fraction, peak systolic pressure/end-systolic volume ratio) to endotoxi

107 The estimated pulmonary artery systolic pressure (ePASP) was >30 mm Hg in 4 participant

108 eters, including estimated right ventricular systolic pressure (ERVSP), and a full review of medical

109 An increase in pulmonary artery systolic pressure, estimated noninvasively by echocardio

110 For systolic pressure, estimates were -12.7 mm Hg (95% confi

111 end-systolic pressure/SVI, and E(LV)I = end-systolic pressure/ESVI, at rest and during exercise in 2

112 Systolic pressure exhibited similar relationships with A

113 nalyses, adjusting for BMI, age, height, and systolic pressure, fasting insulin was independently cor

114 7 mm Hg (P<0.001), and the right ventricular systolic pressure fell from 71.6 +/- 21.7 to 46.7 +/- 15

115 re was a 0.2-mm Hg reduction (0.0 to 0.3) in systolic pressure for each 3 months of breast-feeding.

116 ry embolism increased right ventricular peak systolic pressure (from 28 to 47 mm Hg) and decreased ca

117 In addition, cardiac systolic pressure generation at a diastolic pressure of

118 Successful outcome was defined as peak systolic pressure gradient after stent implantation < 20

119 ak longitudinal global systolic strain rate, systolic pressure gradient between RV and right atrium (

120 Peak systolic pressure gradient decreased from 32 +/- 12 mm H

121 Preoperative transvalvular peak systolic pressure gradients across stenotic aortic valve

122 1 g to >6 g), the average transvalvular peak systolic pressure gradients progressively increased.

123 data, pHTN was defined as right ventricular systolic pressure greater than or equal to two-thirds of

124 uncomplicated systolic hypertension (supine systolic pressure > or =140 mm Hg off medication) and 30

125 ine blood pressure in patients with PD + SH (systolic pressure >/= 180 mm Hg, n = 8), patients with P

126 an SVEF </= 40%, a subpulmonary ventricular systolic pressure >/= 50 mm Hg, atrial fibrillation, and

127 Doppler-echocardiography estimated pulmonary systolic pressure >/=45 mm Hg (n=692) and those without

128 erate PH, defined here as a pulmonary artery systolic pressure >/=60 mm Hg detected echocardiographic

129 mptomatic patients with hypertension (aortic systolic pressure >140 mm Hg) and low-gradient (mean gra

130 A subset of mice with right ventricular systolic pressure >30 mm Hg exhibited right ventricular

131 ion (defined as an elevated pulmonary artery systolic pressure >40 mm Hg on echocardiogram).

132 mean transaortic gradient, pulmonary artery systolic pressure >60 mm Hg; p < 0.05 for all) and 2 pro

133 patients with an estimated right ventricular systolic pressure>35 mm Hg, suggestive of pulmonary vasc

134 tio 1.55), higher baseline right ventricular systolic pressure (hazard ratio 1.11), more abnormal LV-

135 17-0.50; P<0.001), resting right ventricular systolic pressure (hazard ratio, 1.03; 95% confidence in

136 d ratio, 1.29), and higher right ventricular systolic pressure (hazard ratio, 1.3) were associated wi

137 Baseline systolic pressures higher by 10 mm Hg were associated wi

138 Association class IV (HR: 5.88), and aortic systolic pressure (HR: 0.99) as independent correlates f

139 ardiographic assessments of pulmonary-artery systolic pressure in 195 consecutive patients (82 men an

140 e found in 78% and elevated pulmonary artery systolic pressure in 67%.

141 ypoxia-induced increase in right ventricular systolic pressure in anesthetized mice.

142 0.05), despite a significantly lower LV peak systolic pressure in AT(1)RB dogs.

143 ique, this method was used to predict the PA systolic pressure in cases on which the ANN had not been

144 udil also markedly reduced right ventricular systolic pressure in late-stage rats.

145 c profile except for a marginal reduction in systolic pressure in old carrier mice.

146 thrombi and to measure the pulmonary artery systolic pressure in patients with a cardiovascular impl

147 a significant increase in right ventricular systolic pressure in Prkg1(-/-) mice in the absence of s

148 d DBL(PKA-) mice displayed depressed maximum systolic pressure in response to dobutamine as measured

149 m) did not rise directly in proportion to RV systolic pressure in Rosa26(R899X) but did in Sm22(R899X

150 ses diastolic and mean pressures and reduces systolic pressure in the central aorta and the coronary

151 resence of SS, easily diagnosed by comparing systolic pressures in the left and right arm, predicts t

152 to a reduction of RV volume by 54% and an RV systolic pressure increase of 58%.

153 and a significantly increased LV afterload (systolic pressure increase, P<0.001).

154 ne) attenuated MCT-induced right ventricular systolic pressure increase, right ventricular hypertroph

155 Systolic pressure increased by 1.3 mm Hg (95% CI, 0.3 to

156 During 36 volume-overload events, RV systolic pressures increased by 25 +/- 4% (p < 0.05) and

157 aortic regurgitation, and right ventricular systolic pressure), increased the c-statistic from 0.57

158 prorenalase becomes maximally activated when systolic pressure increases by >5 mm Hg.

159 his improved function, with left ventricular systolic pressure increasing from 103 +/- 4 mm Hg to 137

160 on in patients in whom the right ventricular systolic pressure is calculated to be 50 mmHg or greater

161 tension, but estimation of right ventricular systolic pressure is often inaccurate.

162 Consistently, ejection duration and aortic systolic pressure load were significantly diminished, in

163 Participants were exposed to intensive (goal systolic pressure < 120 mm Hg) versus standard (<140 mm

164 Controls had a right ventricular systolic pressure < 40 mm Hg (if estimable) and normal r

165 .009), while in those with right ventricular systolic pressure<35 mm Hg, a lower value for the percen

166 ardiography with estimated right ventricular systolic pressure, <35 mm Hg; n = 122).

167 =692) and those without PH (n=692; pulmonary systolic pressure, <45 mm Hg) for age, sex, LV ejection

168 increased heart rate (HR), left ventricular systolic pressure (LVSP), the maximum first derivative o

169 n injury, cardiac function (left ventricular systolic pressure, maximum dP/dt, minimum dP/dt, and cor

170 intraperitoneally) to mice, left ventricular systolic pressure, maximum first derivative of ventricul

171 ces in age, country, hospital location, era, systolic pressure, mean arterial pressure, lactate, bund

172 olic pressure, peak stress right ventricular systolic pressure, metabolic equivalents achieved, and h

173 0 ng/kg) titrated to a rise in radial artery systolic pressure of > or =20 mm Hg.

174 Participants with repeated measurements of systolic pressure of 130 to 139 mm Hg and diastolic pres

175 in persons with high-normal blood pressure (systolic pressure of 130 to 139 mm Hg, diastolic pressur

176 diastolic pressure of 89 mm Hg or lower, or systolic pressure of 139 mm Hg or lower and diastolic pr

177 an, 10% lean, or 20% lean to maintain aortic systolic pressure of 80-90 mm Hg.

178 Perfusion was maintained at an average systolic pressure of 93 +/- 2 mm Hg, flow 310 +/- 20 mL/

179 Hg diastolic and a relatively flat curve for systolic pressures of 110 to 130 mm Hg and diastolic pre

180 The curve was relatively flat for systolic pressures of 110 to 130 mm Hg and diastolic pre

181 veloped PH with respective right ventricular systolic pressures of 40.2 +/- 1.5 and 39.6 +/- 1.5 mm H

182 heral atherosclerosis was assessed using the systolic pressures of the dorsal pedal, posterior tibial

183 associated with an elevated pulmonary artery systolic pressure on echocardiogram, may identify an at-

184 at 6 months was defined by right ventricular systolic pressure or MPAP as significant (<35 mm Hg), pa

185 t of PH because we found no difference in RV systolic pressure or RV hypertrophy in wild-type versus

186 y increased cardiac output, pulmonary artery systolic pressure or sympathetic nervous system activity

187 y valve leaflet, calculated pulmonary artery systolic pressure, or left ventricular ejection fraction

188 n fraction (p = 0.013), and pulmonary artery systolic pressure (p = 0.047) were associated with in-ho

189 retinopathy and hypertension (P = 0.037 for systolic pressure; P = 0.019 for diastolic pressure).

190 orse renal function, higher pulmonary artery systolic pressure (PAP), abnormal left ventricular (LV)

191 s the presence of estimated pulmonary artery systolic pressure (PASP) >35 mmHg and/or tricuspid regur

192 about age-related change in pulmonary artery systolic pressure (PASP) and its prognostic impact in th

193 for Doppler measurement of pulmonary artery systolic pressure (PASP) and the mechanism of enhancemen

194 imary outcome measures were pulmonary artery systolic pressure (PASP) and the PASP response to acute

195 ts on the factors affecting pulmonary artery systolic pressure (PASP) are limited.

196 heart failure (HF) whether pulmonary artery systolic pressure (PASP) assessed by Doppler echocardiog

197 urements of ventilation and pulmonary artery systolic pressure (PASP) assessed by Doppler echocardiog

198 esised that the increase in pulmonary artery systolic pressure (PASP) at HA would be associated with

199 able echocardiogram-derived pulmonary artery systolic pressure (PASP) from the Jackson Heart Study (N

200 to assess exercise-induced pulmonary artery systolic pressure (PASP) increase by means of stress Dop

201 Although elevated pulmonary artery systolic pressure (PASP) is associated with heart failur

202 t failure who have elevated pulmonary artery systolic pressure (PASP) on echocardiography.

203 Pulmonary artery systolic pressure (PASP) was derived from the tricuspid

204 Pulmonary artery systolic pressure (PASP) was serially assessed with Dopp

205 ADR cardiac output (QT) and pulmonary artery systolic pressure (PASP) were significantly increased; h

206 lation and dysfunction, and pulmonary artery systolic pressure (PASP).

207 n fraction) with PH (HF-PH; pulmonary artery systolic pressure [PASP] >/=40 mm Hg) were compared to n

208 elicit a change of 20 mm Hg in radial artery systolic pressure (PD20) defined the vasopressor respons

209 ak oxygen uptake, resting pulmonary arterial systolic pressure, peak exercise heart rate, and quality

210 ystolic dimension, resting right ventricular systolic pressure, peak stress right ventricular systoli

211 es were observed in LV end-diastolic or peak systolic pressures, peak positive or negative LV dP/dt,

212 a significant reduction in right ventricular systolic pressure (placebo versus sildenafil: 43.3+/-9.9

213 fraction, and high resting right ventricular systolic pressure predicted worse outcomes.

214 urgeons score and baseline right ventricular systolic pressure) provided incremental prognostic utili

215 +/- 3 mm Hg) (p < 0.001), right ventricular systolic pressures (Prv,s = 45 +/- 2 mm Hg) (p < 0.01),

216 Dynamic changes in systolic pressure, pulse pressure, and stroke volume in

217 n inversely correlated with pulmonary artery systolic pressure (r=-0.39, P<0.01) and LV eccentricity

218 al wall LS, correlated with pulmonary artery systolic pressure (r=0.56, P<0.01; r=0.32, P<0.01) and L

219 edictions correlated with measured pulmonary systolic pressures (r = 0.846, P <.001).

220 The median ventricular-to-aortic systolic pressure ratio decreased from 1.7 (1.3-2.6) to

221 y associated with the TAPSE/pulmonary artery systolic pressure ratio.

222 nt in RV-PA coupling (TAPSE/pulmonary artery systolic pressure) ratio.

223 as evidenced by decreased right ventricular systolic pressure, ratio of right ventricular weight to

224 This group had a more effective PA systolic pressure reduction after PTE (49 +/- 20 mm Hg v

225 For example, the average systolic pressure reduction during 30 mmHg straining was

226 d) were identified based on the RVESRI to RV systolic pressure relationship.

227 multivariable analysis, age, sex, pulmonary systolic pressure, right atrial minimal volume, as well

228 with no differences in right ventricular end-systolic pressure, right ventricular dP/dt, bromodeoxyur

229 ension, judged by elevated right ventricular systolic pressure, right ventricular hypertrophy, and lo

230 in prevention of increased right ventricular systolic pressure, right ventricular hypertrophy, as wel

231 th established PH improved right ventricular systolic pressures, right ventricular function, and surv

232 s below 40% and the subpulmonary ventricular systolic pressure rises above 50 mm Hg.

233 y developed PAH, as indicated by elevated RV systolic pressure, RV hypertrophy, and increased muscula

234 Right ventricular systolic pressure (RVSP) (mean +/- SD) on the two-dimens

235 atio for prediction of the right ventricular systolic pressure (RVSP) in patients clinically known to

236 The rise in right ventricular systolic pressure (RVSP) normally observed following chr

237 olic diameter (LVESD), and right ventricular systolic pressure (RVSP) were 62 +/- 2%, 0.56 +/- 0.30 c

238 o have the same life span, right ventricular systolic pressure (RVSP), and lung histology as those of

239 gurgitant orifice, resting right ventricular systolic pressure (RVSP), exercise metabolic equivalents

240 graphy and measurements of right ventricular systolic pressure (RVSP).

241 ocardiography to determine right ventricular systolic pressure (RVSP).

242 (PHT) (RVEF 31.4 +/- 9.6%, right ventricular systolic pressure [RVSP] 76.5 +/- 26.2 mm Hg) and 60 hea

243 When differences in gender, race, diabetes, systolic pressure, serum creatinine and high density lip

244 h exaggerated elevation of right ventricular systolic pressure, significant right ventricular hypertr

245 lowering of systemic arterial elastance (end-systolic pressure/stroke volume) and systemic vascular r

246 The LV end systolic pressure/SV(index), an estimate of total LV vas

247 dex (SVI) and its two determinants EaI = end-systolic pressure/SVI, and E(LV)I = end-systolic pressur

248 Baseline systolic pressures tended to be higher in space than on

249 gs of these mice with high right ventricular systolic pressure, the expression of proteins involved i

250 ciated with an increase in right ventricular systolic pressure, thickening of the pulmonary artery me

251 of the right ventricular to left ventricular systolic pressure-time area during inspiration versus ex

252 ding aorta to increase left ventricular (LV) systolic pressure to 214+/-5 mm Hg for 30 minutes, the v

253 significantly reduced the right ventricular systolic pressure to 30.1 +/- 1.3 mm Hg.

254 re exerted by the contracting ventricle (end systolic pressure) to its volume (end systolic volume).

255 +/- 18 mm Hg; both P=0.02), and central end-systolic pressure trended lower (116 +/- 18 to 111 +/- 1

256 pressure variation, stroke volume variation, systolic pressure variation, and the change in stroke/ca

257 perating characteristic between the baseline systolic pressure variation, stroke volume variation, an

258 pleural pressure; pulse pressure variations, systolic pressure variations, and stroke volume variatio

259 tility (the slope of the relationship of end-systolic pressure versus end-systolic volume [Emax] and

260 The slope of the end-systolic pressure volume relationship (i.e., contractili

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

262 fect on systolic function, improving the end-systolic pressure-volume relation (+0.98 +/- 0.41 mm Hg/

263 nce was measured by the slopes of the LV end-systolic pressure-volume relation (E(ES)) and stroke wor

264 tively (both p < 0.0001) and shifted the end-systolic pressure-volume relation to the left (p < 0.01)

265 The end-systolic pressure-volume relation was increased by isopr

266 ad-independent indexes of contractility (end-systolic pressure-volume relation, preload-recruitable s

267 mined by hemodynamic measurements and by end-systolic pressure-volume relations.

268 lopment (p = 0.002), and slope of the LV end-systolic pressure-volume relationship (p = 0.04).

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

270 Ischemia shifted the end-systolic pressure-volume relationship and cardiac output

271 p < .05), and significantly improved the end-systolic pressure-volume relationship and preload recrui

272 al, 13-24]% versus 12 [10-14]%, P=0.008; end-systolic pressure-volume relationship slope 2.4 [1.9-3.2

273 e measurements a regression slope of the end-systolic pressure-volume relationship was determined to

274 The end-systolic pressure-volume relationship was increased in D

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

276 systolic stress-shortening relationship, end-systolic pressure-volume relationship, and peak (+)dP/dt

277 ce (Emax) was determined as the slope of end-systolic pressure-volume relationships during caval occl

278 Mean systolic pressure was 100 versus 107 mm Hg in those not

279 Each 10-point increase of systolic pressure was associated with a decrease in the

280 ications 1 to 2 weeks before enrollment, and systolic pressure was confirmed to be > or =160 mm Hg.

281 Pulmonary artery systolic pressure was higher in AF.

282 At the end of the feeding period, tail systolic pressure was higher in the high salt than in lo

283 Systolic pressure was not a useful metric in the vasopre

284 Systolic pressure was related to AF (HR, 1.14 per 20-mm

285 aortic regurgitation, and right ventricular systolic pressure) was 0.64 (95% confidence interval 0.5

286 of heart rate or R-R interval to changes in systolic pressure, was diminished in the EX-DEH conditio

287 regurgitant velocity, a measure of pulmonary systolic pressure, was predictive of events in a multiva

288 dence interval, 1.4-2.3), pulmonary arterial systolic pressure (weighted mean difference, -3.7 mm Hg;

289 horacic Surgeons score and right ventricular systolic pressure were 2+/-3 and 15+/-16 mm Hg, respecti

290 horacic Surgeons score and right ventricular systolic pressure were 3.3+/-3 and 31+/-7 mm Hg, respect

291 end-diastolic volume, and right ventricular systolic pressure were 4+/-1%, 62+/-3%, 0.55+/-0.2 cm(2)

292 ortic valve gradients, and right ventricular systolic pressure were 7+/-6, 58+/-6%, 54+/-10 mm Hg and

293 ment of leaflet coaptation, and estimated PA systolic pressure were determined on pre- and post-PTE e

294 ge, renal dysfunction, and right ventricular systolic pressure were independently associated with the

295 Wide ranges of right ventricular systolic pressure were observed in mice with heterozygou

296 for sham; P<0.001), whereas left ventricular systolic pressures were significantly reduced (ligated 8

297 Despite higher right ventricular systolic pressures with chronic hypoxia, S100A4/Mts1 mic

298 The LV was able to generate twice the LV systolic pressure without an increase in LV end-diastoli

299 Changes in ventricular peak systolic pressure, without associated changes in end-dia

300 re (PCWP) derived as: PCWP(Doppler) = LV(end-systolic pressure) x e(-IVRT/(T(Ea-E))), where IVRT is i