ライフサイエンスコーパス: PWV

1 PWV and AGI decreased to a nadir at 6 weeks [PWV to 74.2

2 PWV and AI are deeply modified in SCD patients in compar

3 PWV was determined between the mid-ascending and -descen

4 PWV was higher (i.e., increased aortic stiffness) in HCM

5 PWV was not associated with the child's current oily fis

6 PWV was significantly associated with adulthood systolic

7 PWV was significantly higher in HCM patients compared wi

8 l (P = 0.30), C-reactive protein (P = 0.10), PWV (P = 0.30), or AI (P = 0.84).

9 s (<30 ng/mL) for changes in FMD (p = 0.65), PWV (p = 0.93), AIx (p = 0.97), or CRP (p = 0.26).

10 n FMD (0.3 [3.4] vs. 0.3 [2.6] %, p = 0.77), PWV (0.00 [1.06] vs. 0.05 [0.92] m/s, p = 0.65), AIx (2.

11 ity and cardiovascular confounders [adjusted PWV 7.52 (95% CI 7.09; 7.96) vs. 7.13 (95% CI 6.67; 7.59

12 ho restored normal total FMI in adolescence (PWV 5.8 m/s [5.7-5.9] for metabolically healthy and 5.9

13 al to the common iliac artery did not affect PWV.

14 iliac artery (via the sheath) did not affect PWV.

15 After PWV was added to a standard risk factor model, integrate

16 though aortic PWV rose similarly with aging, PWV had more of an influence on PP in women than did mea

17 here were no significant differences in AIx, PWV, or BP between treatments over time.

18 In subjects with active disease, the AIx, PWV, and level of CRP were elevated compared with that i

19 antisense miR-92a (LNA-miR-92a) ameliorated PWV, SBP, DBP, and impaired vasodilation induced by Ang

20 CIMT (r = 0.188 [0.02-0.354], p = 0.03), and PWV (r = 0.235 [0.159-0.310], p < 0.00001).

21 mpared with quintile 1; P-trend = 0.04), and PWV (-0.4 +/- 0.2 m/s for quintile 5 compared with quint

22 ard, whereas the Einc versus TP (P<0.05) and PWV versus TP (P<0.01) curves were shifted downward.

23 outcome) and DBP, 24-hour ambulatory BP, and PWV were assessed by blinded technicians at baseline and

24 No association was noted between HDL-C and PWV.

25 At week 96, IMT decreased and PWV increased in the PHIV group (P <= .03); IMT increase

26 (E') varied inversely with Zc, SVRI, Ea, and PWV (r = -0.4 to 0.5; beta = 1.0 to 1.2; p < or = 0.004)

27 V and mortality showed a ceiling effect, and PWV was truncated at 12 m/sec.

28 c compliance and decreases isobaric Einc and PWV in the human brachial artery.

29 FMD and PWV were direct physiological measurements, and VEGF-sti

30 t-test, and potential predictors of IMT and PWV were assessed using quantile regression.

31 Circulating serum miR-92a level and PWV were correlated in these mice.

32 We measured blood pressure and PWV photoplethysmographically at a median corrected post

33 in diastolic BP, mean arterial pressure, and PWV (-2.24 +/- 1.31 mm Hg, -1.24 +/- 1.30 mm Hg, and -0.

34 clarifying association between standing and PWV in opposite directions for work and nonwork time.

35 bility can be achieved for aortic strain and PWV measurements in a multicenter trial setting using st

36 Brachial-ankle PWV was significantly higher among Abeta-positive partic

37 emoral-ankle PWV), and mixed (brachial-ankle PWV) vascular beds.

38 Femoral-ankle PWV was only higher among Abeta-positive participants at

39 eart-femoral PWV), peripheral (femoral-ankle PWV), and mixed (brachial-ankle PWV) vascular beds.

40 s with lower, below median GFR had higher Ao-PWV than those with GFR above the median (P = 0.043).

41 ent, raised ACR is associated with higher Ao-PWV, a relationship most likely mediated by raised BP.

42 with raised ACR (>/=3 mg/mmol) had higher Ao-PWV, poorer diabetic control, and higher pulse pressure

43 n analysis, the significant predictors of Ao-PWV were age, SBP or PP, duration of diabetes, gender, n

44 The closest univariate associations of Ao-PWV were positively with age, duration of diabetes, SBP,

45 The association of Ao-PWV with reduced GFR suggests that even modest renal dys

46 ACR emerged as a significant predictor of Ao-PWV.

47 together explained 55% of the variance of Ao-PWV.

48 Aortic pulse wave velocity (Ao-PWV) and albumin creatinine ratio (ACR) were measured in

49 omen's Survey), the child's descending aorta PWV was measured at the age of 9 years using velocity-en

50 Aortic PWV improves risk prediction when added to standard risk

51 Aortic PWV is a powerful independent predictor of mortality in

52 1.01 and -0.67 +/- 0.91; p = 0.002), aortic PWV (-0.69 +/- 1.15 m/s and -0.71 +/- 0.71 m/s; p = 0.00

53 scular mortality associated with age, aortic PWV, and aortic bifurcation diameter with high specifici

54 Although aortic PWV rose similarly with aging, PWV had more of an influe

55 r, the age-related changes in AIx and aortic PWV were non-linear, with AIx increasing more in younger

56 g and risk in younger individuals but aortic PWV is likely to be a better measure in older individual

57 y was associated with lower childhood aortic PWV (sex-adjusted beta=-0.084 m/s per portion per week;

58 l blood pressures and Doppler-derived aortic PWV were measured.

59 isplacing SBP as a prognostic factor, aortic PWV is probably further along the causal pathway for art

60 bPP; and 0.867, 0.851, and 0.825 for aortic PWV, aoPP, and Pb, respectively.

61 presence of diabetes mellitus, higher aortic PWV was associated with a 48% increase in cardiovascular

62 ted with the corresponding changes in aortic PWV (r = 0.53 to 0.61, p < 0.01).

63 iated with a concomitant reduction in aortic PWV and improvement in endothelial function.

64 The age-associated increase in aortic PWV was higher in patients (P<0.001).

65 locity (PWV) was measured invasively (aortic PWV).

66 was associated with an increased mean aortic PWV of 0.19 m/sec (95% CI: 0.03, 0.36) in total and an i

67 0.36) in total and an increased mean aortic PWV of 0.42 m/sec (95% CI: 0.03, 0.81) in the abdominal

68 ril 2011 to 6 November 2012 by way of aortic PWV (aPWV), estimated carotid-femoral PWV (ePWV) and aor

69 the stiffness gradient [(brachial PWV/aortic PWV)(0.5)] and ascending aortic and aortic bifurcation d

70 eride content with total and regional aortic PWV and carotid IMT while adjusting for several possible

71 vel of systolic blood pressure (SBP), aortic PWV was greater in subjects with diabetes than in contro

72 Results Total aortic PWV (mean difference, 0.5 m/sec; 95% confidence interval

73 We tested whether aortic PWV predicts cardiovascular and all-cause mortality in t

74 estimated that a 1% increase in aortic arch PWV (in meters per second) is related to a 0.3% increase

75 aortic distensibility, increased aortic arch PWV (p < 0.001), and increased central blood pressures (

76 Aortic arch PWV helped predict WMH volume independent of the other d

77 Aortic arch PWV measured with phase-contrast MR imaging is a highly

78 However, effects of aortic arch PWV on the transmission of harmful excessive pulsatile e

79 model of subsequent WMH burden, aortic arch PWV provides a distinct contribution along with systolic

80 Aortic arch PWV was measured with phase-contrast magnetic resonance

81 ar regression was conducted with aortic arch PWV, 15 other cardiovascular risk factors, and age, sex,

82 d for sex and ethnicity included aortic arch PWV, age, systolic blood pressure, hypertension treatmen

83 Central (carotid-femoral artery PWV, PWV(CF) ) and peripheral (carotid-radial artery PWV

84 1 production directly regulates large artery PWV in vivo.

85 (CF) ) and peripheral (carotid-radial artery PWV, PWV(CR) ) arterial stiffness was measured by pulse-

86 The association between PWV and mortality showed a ceiling effect, and PWV was t

87 The association between PWV and mortality was assessed in a Cox regression analy

88 analysis to assess the relationship between PWV and exposure to adiposity, and tested for linear tre

89 RP level was positively correlated with both PWV and the AIx.

90 e pressure, AP, AIx, and aortic and brachial PWV all increased significantly with age; however, the a

91 ortic pulse wave velocity (PWV) and brachial PWV to evaluate the stiffness gradient [(brachial PWV/ao

92 Aortic and brachial PWV were also determined in a subset of 998 subjects.

93 o evaluate the stiffness gradient [(brachial PWV/aortic PWV)(0.5)] and ascending aortic and aortic bi

94 pectively; P=0.046) and higher brachioradial PWV (9.17+/-3.1 versus 8.06+/-1.9 m/s, respectively; P=0

95 time of repair was related to brachioradial PWV (r=0.42, P=0.002) but not to brachial FMD or NTG.

96 Higher aortic stiffness assessed by PWV is associated with increased risk for a first cardio

97 A decrease in PWV(CF) , PWV(CR) , SBP and DBP (-25%, -17%, -4% and -8%, respecti

98 cf-PWV and AI were independently associated with age, sex,

99 CF-PWV was a significant independent predictor of incident

100 ral pulse pressure multivariable-adjusted CF-PWV hazard ratio, 1.26 [95% CI, 1.08-1.48]; P=0.004).

101 (per SD increase, multivariable-adjusted CF-PWV hazard ratio, 1.36 [95% CI, 1.03-1.76]; P=0.030; cen

102 pulmonary hypertension, and priapism, and cf-PWV was associated with microalbuminuria.

103 02 m/s (95% CI: - 0.08, 0.04) in baseline cf-PWV and 0.06 m/s (95% CI: - 0.02, 0.14), 0.05 m/s (95% C

104 en the greenspace indicators and baseline cf-PWV and 4-year progression of cf-PWV was assessed using

105 The association between CF-PWV and incident HF persisted after adjustment for systo

106 After adjustment for these correlates, cf-PWV and AI were associated with the glomerular filtratio

107 % CI: - 0.09, 0.09) in 4-y progression in cf-PWV, respectively.

108 Mean cf-PWV was lower in SCD patients (7.5+/-2.0 m/s) than in co

109 The clinical and biological correlates of cf-PWV and AI were investigated by using a multivariable mu

110 baseline cf-PWV and 4-year progression of cf-PWV was assessed using linear mixed-effects models with

111 nspace and baseline or 4-y progression of cf-PWV; interquartile range (IQR) increases in NDVI, EVI, a

112 the hazard ratios for the middle and top CF-PWV tertiles were 1.95 (95% confidence interval, 0.92-4.

113 tios among subjects in the middle and top CF-PWV tertiles were 2.33 (95% confidence interval, 1.37-3.

114 e of carotid-femoral pulse wave velocity (cf-PWV) and augmentation index (AI) at a steady state.

115 Carotid-femoral pulse wave velocity (CF-PWV) and brachial and central pulse pressure were measur

116 ure, carotid-femoral pulse wave velocity (cf-PWV), lipids/lipoproteins, and glycemic control were mea

117 the carotid-femoral pulse wave velocity (cf-PWV).

118 Carotid-femoral pulse wave velocity (CF-PWV; the gold standard index of large artery stiffness),

119 After a median follow-up of 7 years, CF-PWV and central pulse pressure were associated with an i

120 ly infused ET-1 did not significantly change PWV compared with infusion of saline (change of -0.08 +/

121 for metabolically unhealthy) had comparable PWV to those who had normal FMI throughout (5.7 m/s [5.7

122 < .001, P = .001 and P = .003) vs. controls [PWV 7.53 (7.09; 7.97) m/s adjusted mean (95% CI)].

123 Estimates of heritability (h(2)) of cPP, PWV, P1, and DeltaP(aug) were 0.43, 0.34, 0.31, and 0.62

124 validation, TONO was performed to determine PWV between the carotid and femoral artery.

125 ween carotid and femoral points to determine PWV.

126 For this purpose, carotid-distal PWV was measured twice in 497 European American (EA) and

127 tient groups, the focus on a proxy endpoint (PWV), and the high risk of bias.

128 re utilized in clinical practice to estimate PWV.

129 Estimated PWV mainly reflects the entered age rather than true vas

130 Estimated PWV values were located on the same regression line like

131 stiffness was estimated via carotid-femoral PWV (cfPWV).

132 aortic PWV (aPWV), estimated carotid-femoral PWV (ePWV) and aortic PP (aPP).

133 re favorably associated with carotid-femoral PWV (r=-0.14, P=0.038).

134 Carotid-femoral PWV was measured using the same system.

135 Brachial artery FMD, carotid-femoral PWV, central AIx, and blood pressure (BP) were measured

136 crease in central stiffness (carotid-femoral PWV, P = .001; heart-femoral PWV, P = .004) was linked w

137 ith unfavorable increases in carotid-femoral PWV.

138 e central (carotid-femoral and heart-femoral PWV), peripheral (femoral-ankle PWV), and mixed (brachia

139 carotid-femoral PWV, P = .001; heart-femoral PWV, P = .004) was linked with increases in Abeta deposi

140 ns in the shape of flow waveforms on 4D flow PWV measurements remains unclear.

141 ly estimate potential differences of 4D flow PWV using known values of PWV and the used iT.

142 e imaging-based pulse wave velocity (4D flow PWV) estimation is a promising tool for measuring region

143 Blood pressure, FMD, PWV, markers of inflammation, oxidative stress, and meta

144 meters (P = .45 for diameter and P = .55 for PWV) between stable aneurysms (n = 12) and unstable aneu

145 mental influences become larger with age for PWV.

146 According to VA derived from PWV, most patients exhibited values below chronological

147 resence of the metabolic cluster had greater PWV (b = 0.20, 95% confidence interval [CI] 0.01 to 0.38

148 ages 9 and 17 years were related to greater PWV (0.15 m/s per kg/m(2), 0.05-0.24; p=0.0044 and 0.15

149 Here, PWV in children with kidney failure undergoing kidney re

150 Higher PWV was associated with male sex, longer time since LTx,

151 , all COVID-19-positive groups showed higher PWV (+0.41, +0.37, and +0.40 m/s for groups 2-4, P < .00

152 rol subjects (heavier individual with higher PWV), whereas group 1 showed the opposite (negative) int

153 sistent symptoms were associated with higher PWV, regardless of disease severity and cardiovascular c

154 A 4-kg/year higher PWV was associated with a 1.87-cm (95% confidence interv

155 However, PWV and the AIx were not significantly different between

156 fusion of ET-1 significantly increased iliac PWV by 12 +/- 5% (mean +/- STD; p < 0.001), whereas infu

157 nomethyl-L-arginine (L-NMMA) increased iliac PWV significantly, by 3+/-2% (P<0.01).

158 A stable or improved PWV after 12 months was found in the COVID+ groups, wher

159 the HIV- group (P = .03), with no change in PWV (P = .92).

160 he 12-month follow-up, the average change in PWV was 7.1+/-10.7% in the placebo group and 0.87+/-10.0

161 younger individuals, whereas the changes in PWV were more prominent in older individuals.

162 A decrease in PWV(CF) , PWV(CR) , SBP and DBP (-25%, -17%, -4% and -8%

163 ding diabetes accentuated the differences in PWV seen between groups (controls vs. CKDu vs. CKD: 6.7

164 crease in AoD (P < .0001) and an increase in PWV (P < .0001).

165 fine particles and PM2.5, and an increase in PWV and augmentation index with NO2 and ultrafine partic

166 sult in an age-related, regional increase in PWV primarily affecting the proximal aorta.

167 ion (hazard ratio 1.10 per 1 m/s increase in PWV, 95% confidence interval 1.00 to 1.30, p = 0.03) in

168 Each 1 m/sec increase in PWV, up to 12 m/sec, was associated with mortality, haza

169 aortic stiffness, as indicated by increased PWV, is evident in HCM patients, and is more pronounced

170 sk" metabolic cluster did not have increased PWV or AI@75.

171 At inclusion, increased PWV and IMT were detected in 13% and 30%, respectively,

172 lder group displayed significantly increased PWV in the region spanning the ascending and proximal de

173 In addition, exogenous ET-1 increases PWV, and this can be blunted by ET(A) receptor blockade.

174 Both TTTS groups showed marked intertwin PWV discordance, unlike MCDA control subjects.

175 t, posterior tibial FMD, NTG, and lower limb PWV were comparable.

176 r flavone intake was associated with a lower PWV (-0.4 +/- 0.2 m/s for quintile 5 compared with quint

177 Controls had a lower PWV compared to subjects with CKDu and CKD.

178 renal dysfunction, CKDu subjects had a lower PWV than those with CKD (8.7 +/- 1.5 vs. 9.9 +/- 2.2 m/s

179 and berry intake was associated with a lower PWV, no associations were observed for total and other f

180 nges in any of the primary outcome measures (PWV changed by +9.5% and +6.0%, F2-isoprostanes changed

181 DAPT prevented such increase in MILD, PWV and MEAD (P < 0.01).

182 By stepwise Cox proportional hazards models, PWV was an independent predictor of incident hypertensio

183 Moreover, PWV and AI are associated with several SCD clinical comp

184 MI in adolescence was associated with normal PWV, suggesting adolescence as an important period for i

185 aorto-femoral tapering (p < 0.0001) but not PWV.

186 and SBP predicted mortality; the addition of PWV independently predicted all-cause and cardiovascular

187 In-plane PCMRI permits determination of PWV in multiple aortic locations in a single acquisition

188 te HNBC smoking caused a smaller increase of PWV than Tcig (change 1.1 vs 0.54 m/s, p < 0.05) without

189 imal arterial diameters, and, independent of PWV, is a major determinant of cPP.

190 ilation of muscular arteries, independent of PWV.

191 erences of 4D flow PWV using known values of PWV and the used iT.

192 Variability of PWV was low: 0.7% for intraobserver variability, 1.5% fo

193 but not with other cardiac measures, cIMT or PWV.

194 e in AP, with no significant change in P1 or PWV but an increase in large artery diameters of 4% to 1

195 The PCMRI PWV was measured in three aortic segments.

196 When PCMRI PWV was averaged over the three locations, it was not di

197 Previously, PWV has been measured at a single aortic location, or ha

198 ea (P = .073), and sex (P = .005), pulmonary PWV demonstrated an independent positive association wit

199 Conclusion Pulmonary PWV is reliably assessed with cardiac MR imaging.

200 The repeatability coefficient for pulmonary PWV was 0.96.

201 Increases in pulmonary PWV and RVEF were associated with increases in age (r =

202 The association of pulmonary PWV with RV function and mass was quantified with univar

203 Central (carotid-femoral artery PWV, PWV(CF) ) and peripheral (carotid-radial artery PWV, PWV

204 ) and peripheral (carotid-radial artery PWV, PWV(CR) ) arterial stiffness was measured by pulse-wave

205 ual endothelin-A/B receptor blockade reduced PWV and increased tPA release in AAV in the crossover st

206 ptor antagonist BQ-123 significantly reduced PWV by 12 +/- 4% (p < 0.001).

207 cetylcholine and glyceryl trinitrate reduced PWV significantly, by 6+/-4% (P=0.03) and 5+/-2% (P<0.01

208 he standard deviation of the high-resolution PWV was significantly higher (P < .001/12) in unstable a

209 nt was independently associated with child's PWV.

210 FMS was calculated from the manufacturer's PWV beta formulas.

211 S reference diet, the geometric mean (+/-SD) PWV was 7.67 +/- 1.62 m/s, and mean percentages of chang

212 years old, the younger group showed similar PWV at each aortic location.

213 ease in E/A, and increased aortic stiffness (PWV: 6.36 +/- 0.47 vs.4.89 +/- 0.41, OSED vs. YSED, P <

214 ect of high total FMI on arterial stiffness (PWV 6.0 m/s [95% CI 5.9-6.0] for metabolically healthy p

215 mixed effects regression models showed that PWV was an independent determinant of the longitudinal i

216 This suggests that PWV could help identify normotensive individuals who sho

217 The PWV discordance seen in laser treated twin pairs resembl

218 The PWV improved model discrimination with an increase in Ha

219 The PWV is a strong risk factor for mortality in KTRs.

220 1 was significantly positively correlated to PWV (p < 0.0001); AP was correlated to aorto-femoral tap

221 (MAP), and CRP were independently related to PWV, and that age, MAP, CRP, sex, and heart rate were as

222 Of 1497 KTRs, 1040 (69%) had a valid PWV measurement.

223 shift in the resonant Peak Wavelength Value (PWV) that is detectable with <10 pm wavelength resolutio

224 s where the column precipitable water vapor (PWV) is less than 1 mm.

225 e of 54.9% +/- 2.5) and pulse wave velocity (PWV) (decrease of 1.3 m/sec +/- 0.8).

226 c resonance measures of pulse wave velocity (PWV) and aortic distensibility (AoD) in the thoracic aor

227 s indices [i.e., aortic pulse wave velocity (PWV) and augmentation (AGI) of carotid arterial pressure

228 ic blood pressure (BP), pulse wave velocity (PWV) and augmentation index (AIx) were assessed in 130 s

229 FVC]) and a decrease in pulse wave velocity (PWV) and augmentation index up to 26 h after the walk.

230 We measured aortic pulse wave velocity (PWV) and brachial PWV to evaluate the stiffness gradient

231 ffness [carotid-femoral pulse wave velocity (PWV) and carotid augmentation index (AI)].

232 Aortic pulse wave velocity (PWV) and carotid augmentation index were reduced only wi

233 ce as assessed by using pulse wave velocity (PWV) and central augmentation index (AIx).

234 n the aortic arch using pulse wave velocity (PWV) and have found a stronger association with cerebrov

235 s in carotid to femoral pulse wave velocity (PWV) and plasma 8-isoprostane F2alpha-III concentrations

236 Pulse wave velocity (PWV) and the augmentation index (AIx) were assessed noni

237 ured by carotid-femoral pulse wave velocity (PWV) and total arterial compliance.

238 Arterial pulse wave velocity (PWV) correlates with the level of stiffness and can be d

239 fness, as calculated by pulse wave velocity (PWV) for large-, medium- and small-sized arteries, showe

240 ested this by examining pulse wave velocity (PWV) in brachial arteries of twin survivors of TTTS trea

241 suggested that AIx and pulse wave velocity (PWV) increase linearly with age, yet epidemiological dat

242 resonance imaging (MRI) pulse wave velocity (PWV) measurements.

243 fness was determined by pulse-wave velocity (PWV) of the brachioradial and femoral-dorsalis pedis tra

244 Higher pulse wave velocity (PWV) reflects increased arterial stiffness and is an est

245 Pulse wave velocity (PWV) was assessed three times by five readers as Deltax/

246 Pulse wave velocity (PWV) was calculated by the foot-to-foot methodology from

247 Pulse wave velocity (PWV) was calculated using the foot-to-foot methodology f

248 Aortic pulse wave velocity (PWV) was calculated.

249 Pulmonary pulse wave velocity (PWV) was determined by the interval between arterial sys

250 Aortic pulse wave velocity (PWV) was measured in 2007-2009 (Phase 9) and at a 4-year

251 Pulse wave velocity (PWV) was measured in the central (carotid-femoral and he

252 Pulse wave velocity (PWV) was measured invasively (aortic PWV).

253 MD), blood pressure and pulse wave velocity (PWV) were assessed as secondary outcomes, while markers

254 dia thickness (IMT) and pulse wave velocity (PWV) were evaluated in 101 PHIV and 96 HIV negative chil

255 dia thickness (IMT) and pulse-wave velocity (PWV) were evaluated in 101 PHIV and 96 HIV-negative (HIV

256 tic modulus (Einc), and pulse wave velocity (PWV) were measured over a TP range from 0 to 100 mm Hg.

257 detect and measure the pulse wave velocity (PWV) when skin mounted.

258 sive increase in aortic pulse wave velocity (PWV) with age.

259 media thickness (cIMT), pulse wave velocity (PWV)) and cardiac (left ventricular (LV) structure and f

260 ness measured by aortic pulse wave velocity (PWV), 2) oxidative stress assessed by total plasma F2-is

261 ght to evaluate whether pulse wave velocity (PWV), a noninvasive index of arterial stiffness, is a pr

262 (FMD), carotid-femoral pulse wave velocity (PWV), and aortic augmentation index (AIx).

263 P), augmentation index, pulse wave velocity (PWV), and intima-media thickness.

264 yceride content, aortic pulse wave velocity (PWV), and visceral fat.

265 easures, generally from pulse-wave velocity (PWV), are widely used with little knowledge of relations

266 rotid artery (CCA-IMT), pulse wave velocity (PWV), augmentation index, blood pressure (BP), and vascu

267 d pressure (BP), aortic pulse wave velocity (PWV), B-mode ultrasonography and wave form analysis of t

268 blood pressure, aortic pulse wave velocity (PWV), brachial artery flow-mediated dilation (FMD), and

269 g the impact of NSPT on pulse wave velocity (PWV), carotid intima-media thickness (CIMT), and flow-me

270 d carbon monoxide (CO), pulse wave velocity (PWV), malondialdehyde (MDA) and thromboxane B2 (TxB2) we

271 Progressive increase in pulse wave velocity (PWV), maximal intra-luminal diameter (MILD) and maximal

272 a thickness (CIMT), and pulse wave velocity (PWV), respectively.

273 itively correlated with pulse wave velocity (PWV), systolic blood pressure (SBP), diastolic blood pre

274 iffness was measured by pulse-wave velocity (PWV), together with systolic (SBP) and diastolic (DBP) b

275 ness was assessed using pulse wave velocity (PWV).

276 r fibrosis and elevated pulse wave velocity (PWV).

277 flected by increases in pulse wave velocity (PWV; indicating arteriosclerosis), intima-media thicknes

278 easured carotid-femoral pulse wave velocity (PWV; SphygmoCor apparatus) 8 weeks after transplantation

279 ght velocity (PHV) and peak weight velocity (PWV) in infancy were derived from parametric growth curv

280 tile range increase in peak weight velocity (PWV), the risk of asthma increased significantly (adjHR:

281 of arterial stiffness (pulse wave velocity [PWV] and augmentation index corrected for heart rate [AI

282 terial stiffness (using pulse wave velocity [PWV]) and arterial diameters (using ultrasonography) wer

283 ral arterial stiffness (pulse wave velocity [PWV]) and arterial diameters, and their respective herit

284 ess (carotid to femoral pulse wave velocity [PWV]) measured at age 17 years.

285 ess (carotid to femoral pulse wave velocity [PWV]) was measured and peripheral blood CD4+CD28- T cell

286 distensibility and arch pulse wave velocity [PWV]), and LV volumes and mass.

287 to arterial stiffness (pulse wave velocity [PWV]), wave reflection (augmentation index, carotid-brac

288 ) and aortic stiffness (pulse wave velocity; PWV) were evaluated before and after exercise training o

289 In healthy volunteers, PWV and augmentation index were associated both with bla

290 PWV and AGI decreased to a nadir at 6 weeks [PWV to 74.2 +/- 4.4% of baseline (B), P = 0.007; AGI to

291 1.25 vs 1.21 mm for max IMT; P < .05), while PWV did not differ between groups (P = .06).

292 1.25 vs 1.21 mm for max IMT; p<0.05), while PWV did not differ between groups (p=0.06).

293 particles that was inversely associated with PWV (P < 0.001).

294 otal fat mass was positively associated with PWV at age 17 years (0.004 m/s per kg, 95% CI 0.001-0.00

295 ndrome (inverse) displayed associations with PWV only after BMI was accounted for.

296 aP(aug) did not independently correlate with PWV but independently negatively correlated with the rat

297 portion of CD4+CD28- T cells correlated with PWV (r=0.408, p=0.035).

298 gly independently positively correlated with PWV (standardized regression coefficient, beta = 0.4, p

299 ot significantly associated with PHV or with PWV (adjOR: 1.07; CI: 0.64-1.77 and adjOR: 1.11; CI: 0.6

300 In a subgroup with PWV data, net improvements were observed [flavonoid (n =