ライフサイエンスコーパス: pulse pressure

1 fening was assessed from the brachial artery pulse pressure.

2 lus high-density lipoprotein cholesterol and pulse pressure.

3 with forward and reflected wave and carotid pulse pressure.

4 onger predictor of ESRD than diastolic BP or pulse pressure.

5 en in the absence of increases in arteriolar pulse pressure.

6 the relation was strongest for systolic and pulse pressure.

7 ongly related to cardiovascular disease than pulse pressure.

8 onsistent for systolic BP, diastolic BP, and pulse pressure.

9 h advancing age and increase with increasing pulse pressure.

10 thesis that OPG is associated with increased pulse pressure.

11 n long-term average systolic, diastolic, and pulse pressure.

12 .4-mmHg (95% CI: 0.2, 0.6; p < 0.001) higher pulse pressure.

13 r results were obtained for diastolic BP and pulse pressure.

14 analysis with systolic BP or diastolic BP or pulse pressure.

15 left ventricular dysfunction, and increased pulse pressure.

16 and intraventricular hemorrhage volume, and pulse pressure.

17 cturnal drop in blood pressure (dipping) and pulse pressure.

18 % of the variability in central systolic and pulse pressures.

19 5% confidence interval (CI): 0.25, 1.62] and pulse pressure (0.76 mmHg; 95% CI: 0.22, 1.30).

20 .095 +/- 0.043 SD/SD, P = 0.028) and carotid pulse pressure (-0.114 +/- 0.045 SD/SD, P = 0.013) were

21 CI, -1.8 to 1.6], P=0.9; change in brachial pulse pressure, -0.02 mm Hg [95% CI, -1.6 to 1.6], P=0.9

22 5% CI, -2.3 to 1.2], P=0.5; change in aortic pulse pressure, -0.4 mm Hg [95% CI, -1.9 to 1.0], P=0.6)

23 cPP increased more than peripheral pulse pressure (10.3 and 9.2 mm Hg, respectively; p < 0.

24 14 mm, p = 0.003) dimensions, and decreased pulse pressure (15 +/- 13 vs 29 +/- 22 mm Hg, p = 0.02).

25 re (55 versus 42 mm Hg), a narrowed systemic pulse pressure (43 versus 64 mm Hg), a lower Qp:Qs (0.92

26 /-12.7 vs. 98.2+/-13.0 mmHg, P=0.002), lower pulse pressure (51.6+/-15.1 vs. 61.4+/-15.6 mmHg, P=0.00

27 pressure (135 +/- 1 to 127 +/- 1 mm Hg) and pulse pressure (54 +/- 1 to 48 +/- 1 mm Hg) (both P < 0.

28 5% CI: 0.6, 2.3; p < 0.001), 1.0-mmHg higher pulse pressure (95% CI: 0.4, 1.7; p = 0.001), 0.8-mmHg h

29 otensive participants, elevation of arterial pulse pressure (a surrogate of arterial stiffness) was l

30 Increased pulse pressure, a reflection of aortic stiffness, increa

31 sent recent data unveiling the importance of pulse pressure above that of systolic and diastolic pres

32 er aortic diastolic pressure and very narrow pulse pressure after resuscitation.

33 ic blood pressure, diastolic blood pressure, pulse pressure, age, chronic hypertension, and medicatio

34 sympathetic nerve activity and directly with pulse pressure (all amalgamated R2 > .88, all p < or = .

35 (P <.001) but not by systolic, diastolic, or pulse pressure (all P values were >.13).

36 tion of blood pressure (systolic, diastolic, pulse pressure) among UK Biobank participants of Europea

37 dex ([Second/First systolic peak] x 100) and pulse pressure amplification ([Radial/aortic pulse press

38 Central (carotid) to peripheral (brachial) pulse pressure amplification (PPA) was calculated with t

39 ssess the effect of vasoconstrictor drugs on pulse pressure amplification and arterial stiffness in v

40 , which also produced a greater reduction in pulse pressure amplification than angiotensin II.

41 mentation index, central pulse pressure, and pulse pressure amplification were not related to cardiov

42 pulse wave velocity, augmentation index, and pulse pressure amplification) are intrinsically limited

43 predictive value of blood pressure (BP) and pulse pressure amplification, a marker of arterial funct

44 ent effects on peripheral pulse pressure and pulse pressure amplification.

45 Pulse pressure, an index of vascular aging, was associat

46 Increased pulse pressure, an indicator of conduit vessel stiffness

47 n (hazard ratio, 1.41 [CI, 1.18 to 1.69] for pulse pressure and 1.42 [CI, 1.14 to 1.76] for systolic

48 ardiographic images, the association between pulse pressure and AF persisted in models that adjusted

49 X) for CbTX greatly diminished inhibition of pulse pressure and agonist flow responses (with or witho

50 essure waveform allows assessment of central pulse pressure and arterial stiffness.

51 We assessed changes in pulse pressure and conduit vessel stiffness in a 12-week

52 analyses investigated relationships between pulse pressure and distinct cerebral spinal fluid biomar

53 e compared the accuracy of measured arterial pulse pressure and estimated left ventricular stroke vol

54 o perfuse arterial segments at physiological pulse pressure and flow.

55 To examine relations between pulse pressure and incident AF.

56 d progressive reductions of R-R interval and pulse pressure and progressive increases of muscle sympa

57 wo drugs had divergent effects on peripheral pulse pressure and pulse pressure amplification.

58 ation because larger (max) and smaller (min) pulse pressure and stroke volume may occur.

59 Greater reductions in pulse pressure and Z(c) in hypertensive subjects treated

60 0.2+/-16.2 versus -3.2+/-16.9 mm Hg, P<0.01) pulse pressures and Z(c) (237+/-83 to 208+/-70 versus 22

61 ender, prior coronary artery disease, higher pulse pressure, and diabetes were significant cardiovasc

62 e and sex, diabetics had higher systolic BP, pulse pressure, and heart rate; lower diastolic BP; and

63 and 4 BP traits: systolic BP, diastolic BP, pulse pressure, and mean arterial pressure.

64 Independent predictors of PASP were age, pulse pressure, and mitral E/e' (all P< or =0.003).

65 In contrast, augmentation index, central pulse pressure, and pulse pressure amplification were no

66 ht atrial pressure, reduced pulmonary artery pulse pressure, and reduced stroke volume.

67 diastolic BP (DBP), mean arterial BP (MAP), pulse pressure, and renal function during the first year

68 Dynamic changes in systolic pressure, pulse pressure, and stroke volume in patients undergoing

69 dominant species involved in modulating both pulse pressure- and bradykinin-induced in vivo coronary

70 Aortic pulse pressure (aoPP) and its components (incident press

71 Peripheral and central pulse pressure, AP, AIx, and aortic and brachial PWV all

72 Reduced arterial compliance and increased pulse pressure are common and major risk factors for car

73 Systolic blood pressure and pulse pressure are substantially higher in older adults.

74 predictive power of systolic, diastolic, and pulse pressure, are described.

75 ere performed, with systolic, diastolic, and pulse pressures as quantitative traits, adjusting for ag

76 Arterial pulse pressure, as well as, left ventricular stroke volu

77 ticipants (13.1%) a median of 12 years after pulse pressure assessment.

78 Increased pulse pressure associated with age-related arterial stif

79 Pulse pressure associations were inverse for abdominal a

80 Higher pulse pressure at any age and higher pulse pressure with

81 ty, forward pressure wave amplitude, central pulse pressure, augmentation pressure, augmentation inde

82 was to explore whether the brachial/carotid pulse pressure (B/C-PP) ratio selectively predicts the s

83 ith the normal subjects, after adjusting for pulse pressure, baPWV in the BRVO patients was significa

84 hod yielded central systolic, diastolic, and pulse pressure bias and precision errors of -0.6 to 2.6

85 diabetes, MI during follow-up, hypertension, pulse pressure, body mass index, and current smoking, th

86 Brachial pulse pressure (bPP), aoPP, and all measures of arterial

87 LBNP decreased pulse pressure, but did not change mean arterial pressur

88 esistance, AIx, aortic stiffness and central pulse pressure, but only angiotensin II reduced cardiac

89 g (95% confidence interval: -1.2, -0.2), and pulse pressure by 1.2 mmHg (95% confidence interval: -1.

90 fice diastolic BP by 8.9/9.5/11.7 mm Hg, and pulse pressure by 13.4/14.2/14.9 mm Hg (n=245/236/90; P

91 itamins and folate, the odds ratios for high pulse pressure by increasing TWA quintiles were 1.00 (re

92 ne) to 5 vascular function measures (central pulse pressure, carotid-femoral pulse-wave velocity, mea

93 ted 3 measures of aortic stiffness: brachial pulse pressure; carotid-femoral pulse wave velocity (CFP

94 ascular disease risk factors, local brachial pulse pressure, CFPWV, and Pf, considered separately, we

95 iables-age, gender, systolic blood pressure, pulse pressure, cholesterol, smoking, ejection fraction,

96 Dynamic changes in arterial pulse pressure closely tracked left ventricular stroke v

97 s (eg, 25% increase in dP/dt(max) and aortic pulse pressure) compared with atrial pacing-LBBB, and th

98 ); similarly, a 1-SD (16 mm Hg) increment in pulse pressure conferred a 55% increased risk for CHF (h

99 stolic blood pressure (SBP and DBP), central pulse pressure (cPP) and flow-mediated dilatation (FMD).

100 examine the progression of central arterial pulse pressure (cPP) in women and the degree to which th

101 gmentation pressure (DeltaP(aug)) to central pulse pressure (cPP), their relation to central arterial

102 Aortic pulse pressure decreased from 76.2 +/- 23.3 mm Hg to 61.

103 After ganglion blockade, systolic and pulse pressure decreased significantly by 13% and 26%, r

104 was associated with lower blood pressure and pulse pressure, decreased systemic vascular resistance,

105 95% CI, 3.3 to 5.4; P<0.0001; central aortic pulse pressure, Delta3.0 mm Hg; 95% CI, 2.1 to 3.9; P<0.

106 otid ligation normalized cerebral arteriolar pulse pressure did not prevent increases in CSA in homoz

107 ulse pressure were associated with childhood pulse pressure (difference per additional average risk a

108 se data reveal that assessment of peripheral pulse pressure does not always reliably predict changes

109 % CI, 0.78-0.96; P = .01), consistent with a pulse pressure effect.

110 Pulse pressure, especially in central arteries, is an in

111 Central pulse pressure, forward pressure wave, reflected pressur

112 m Hg or less (25th percentile) and 23.3% for pulse pressure greater than 61 mm Hg (75th percentile).

113 t for every additional 20-mm Hg increment in pulse pressure >40 mm Hg, there was an OR of 1.49 (CI, 1

114 omly assigned subjects with resting arterial pulse pressures >60 mm Hg and systolic pressures >140 mm

115 Odds ratios for high pulse pressure (> or = 55 mmHg) by increasing TWA quinti

116 Pulse pressure had neither a linear nor nonlinear associ

117 n adolescents, cIMT was associated with SBP, pulse pressure, heart rate, BMI, and waist/hip ratio.

118 Reductions in pump speed led to increases in pulse pressure (high versus low speed: 17 +/- 7 versus 2

119 Pulse pressure, however, was lower in young women and hi

120 was no impact of HR on brachial systolic or pulse pressures; however, there was a highly significant

121 Patients with pulse pressure hypertension >80 mm Hg were 3 times more

122 mic view of the syndrome of systolic or wide pulse pressure hypertension and its hallmark abnormality

123 review the risk of systolic hypertension and pulse pressure hypertension independent of elevated dias

124 The evidence is compelling that wide pulse pressure hypertension is a strong and an independe

125 linkage analyses of log serum creatinine and pulse pressure (i.e., systolic-diastolic BP) provided "s

126 rachial pressure amplification), and central pulse pressure in 2232 participants (mean age, 63 years;

127 s based on SNPs for aortic root diameter and pulse pressure in adults are associated with the same ou

128 t serum OPG is independently associated with pulse pressure in kidney transplant recipients.

129 vely improves arterial compliance and lowers pulse pressure in older individuals with vascular stiffe

130 c arteries is the primary cause of increased pulse pressure in subjects with degeneration and hyperpl

131 tral) and 66 (peripheral) of the variance in pulse pressure in younger participants (<50 years) and 9

132 (PAC, ratio of stroke volume over pulmonary pulse pressure), in relation to pulmonary vascular resis

133 ie, augmentation index = (augmented pressure/pulse pressure) increases].

134 rning Score (2.6 vs 3.3; p<0.001) and higher pulse pressure index (0.45 vs 0.41; p<0.001) and tempera

135 Arterial stiffening with increased pulse pressure is a leading risk factor for cardiovascul

136 Pulse pressure is an important risk factor for incident

137 Beside established risk factors, pulse pressure is independently and significantly associ

138 diastolic diameter, systolic blood pressure, pulse pressure (linear and squared), ethnicity, gender,

139 with an SBP >/=120 mm Hg, and thus elevated pulse pressure, low DBP was associated with subclinical

140 ghest quartile of IMT were older age, higher pulse pressure, lower levels of albumin, elevated C-reac

141 >/=90 mm Hg (HR, 1.8; 95% CI, 1.1-2.9), and pulse pressure <50 mm Hg (HR, 1.8; 95% CI, 1.1-2.9), wit

142 measured LVSV, ventriculovascular stiffness (pulse pressure/LVSV(index)), and aortic distensibility a

143 Pulse pressure may also be a valuable risk assessment to

144 Moreover, central aortic pulse pressure may be a determinant of clinical outcomes

145 Increased pulse pressure may help identify hypertensive patients a

146 k factors include prehypertension, increased pulse pressure, obstructive sleep apnea, high-level phys

147 ive 20-year AF incidence rates were 5.6% for pulse pressure of 40 mm Hg or less (25th percentile) and

148 9 mm Hg, diastolic BP of 70 to 79 mm Hg, and pulse pressure of 60 to 69 mm Hg taken as reference.

149 The predictive value of a change in pulse pressure on passive leg raising is inferior to a p

150 The use of changes in pulse pressure on passive leg raising showed a lower dia

151 val analysis examined the effect of baseline pulse pressure on progression to dementia.

152 impact of achieved systolic, diastolic, and pulse pressures on CV outcomes in 1590 adults who had ov

153 t always reliably predict changes in central pulse pressure or arterial stiffness.

154 Age, body mass index and pulse pressure (OR: 1.21 per 10 mm Hg; CI: 1.00 to 1.46)

155 ard brachial artery blood pressure, brachial pulse pressure, or mean arterial pressure are inadequate

156 rease in systolic blood pressure (P = .005), pulse pressure (P = .02), and mean arterial pressure (P

157 .3 mmHg in CT and TT combined; P = 0.04) and pulse pressure (P = 0.04) at baseline; this association

158 09), diastolic blood pressure (P =.003), and pulse pressure (P =.017) but not history of hypertension

159 emoral pulse wave velocity (P=0.02), central pulse pressure (P<0.0001), mean arterial pressure (P=0.0

160 lood pressure, diastolic blood pressure, and pulse pressure (p<or=0.01 for all).

161 th mean arterial pressure (P=0.003), central pulse pressure (P=0.001), and forward pressure wave (P=0

162 terial pressure and was inversely related to pulse pressure (P=0.037).

163 p between HR and central aortic systolic and pulse pressures (p < 0.001).

164 (95% CI: 0.02, 0.25; p = 0.021) increase in pulse pressure per month over the course of pregnancy.

165 lure have resolved, and continuous decreased pulse-pressure perfusion has had no adverse effects in t

166 BP) (p < 0.001) or each 15 mmHg increment in pulse pressure (PP) (p < 0.001).

167 and therefore may not adapt to variations in pulse pressure (PP) amplification (ratio of radial to ce

168 tolic BP (SBP) and diastolic BP (DBP) versus pulse pressure (PP) and mean arterial pressure (MAP) com

169 ow report genome-wide association studies of pulse pressure (PP) and mean arterial pressure (MAP).

170 Ao-PWV, poorer diabetic control, and higher pulse pressure (PP) and systolic BP (SBP) (all P < 0.05)

171 tervals (RR), systolic blood pressure (SBP), pulse pressure (PP) and their coefficients of variation

172 tance of diastolic (DBP), systolic (SBP) and pulse pressure (PP) as predictors of coronary heart dise

173 BP (DBP), mean arterial pressure (MAP), and pulse pressure (PP) averaged over multiple years in 46,6

174 r reducing systolic blood pressure (SBP) and pulse pressure (PP) in postmenopausal women with elevate

175 Elevated pulse pressure (PP) is associated with increased cardiov

176 Pulse pressure (PP) provides valuable prognostic informa

177 Pulse pressure (PP) reflects increased large artery stif

178 05, 2010 and 2014; each 1-mm Hg increment in pulse pressure (PP) was associated with 1.6% (95% CI: 0.

179 We sought to determine whether pulse pressure (PP), a measure of arterial stiffness, is

180 ssure (SBP), diastolic blood pressure (DBP), pulse pressure (PP), and traditional cardiac risk factor

181 rences in arterial stiffness could influence pulse pressure (PP), now recognized as a cardiovascular

182 uate the effects of MetS on brachial central pulse pressure (PP), PP amplification, aortic stiffness,

183 c BP (DBP), mean arterial pressure (MAP) and pulse pressure (PP), we genotyped approximately 50 000 s

184 BP (DBP), mean arterial pressure (MAP), and pulse pressure (PP), we genotyped ~50,000 SNPs in up to

185 signed to facilitate clinical use of central pulse pressure (PP).

186 er aortic pressure wave pulsatility (central pulse pressure [PP], reflected pressure wave, and reserv

187 Increased pulse pressure predicted increased all-cause mortality,

188 Those with higher baseline pulse pressure progressed to dementia more rapidly (95%

189 Peripheral pulse pressure provides a surrogate measure of arterial

190 Carotid pulse pressure, pulsatility index and carotid-femoral pu

191 pressure (r = 0.079, P = 0.02), and central pulse pressure (r = 0.072, P = 0.035).

192 cluded systolic BP (r = 0.16; p = 0.006) and pulse pressure (r = 0.14; p = 0.02).

193 ) and to a lesser extent with changes in the pulse pressure (r = 0.18) and heart rate (r = 0.09).

194 provements in median stroke volume/pulmonary pulse pressure ratio (2.6 ml/mm Hg [IQR, 1.8-3.5] vs. 1.

195 Arterial compliance (stroke volume/pulse pressure ratio) was reduced in the lean hypertensi

196 rimary endpoints and stroke volume/pulmonary pulse pressure ratio, tricuspid annular plane systolic e

197 ssure measurements (systolic, diastolic, and pulse pressure) recorded during pregnancy.

198 und that an analytical method using arterial pulse pressure recording (pressure recording analytical

199 omarker profile exhibited mean (SD) elevated pulse pressure regardless of age (62.0 [15.6] mm Hg for

200 In a stepwise model that evaluated age-pulse pressure relations in the full sample, the late ac

201 er arrival of the reflected wave to elevated pulse pressure remain controversial.

202 .1% of variation in systolic, diastolic, and pulse pressure, respectively, in GERA non-Hispanic white

203 olic and normal diastolic pressure-a widened pulse pressure-seems to be the best predictor of cardiov

204 to loss of arterial compliance and increased pulse pressure seen with age, diabetes, and renal insuff

205 ring both SBP and DBP, not just SBP, DBP, or pulse pressure separately.

206 STdep was associated with older age, greater pulse pressure, serum fibrinogen levels and urinary albu

207 ension also were associated with higher mean pulse pressure/stroke volume index (1.24 and 1.15 versus

208 CI, 1.15 to 2.74; P=0.01), and preoperative pulse pressure such that for every additional 20-mm Hg i

209 ith age, yet epidemiological data concerning pulse pressure suggest that large artery stiffening pred

210 index of stroke volume divided by pulmonary pulse pressure (SV/PP) and prospectively gathered data o

211 ALT-711 netted a greater decline in pulse pressures than placebo (-5.3 versus -0.6 mm Hg at

212 ized change in central arterial systolic and pulse pressure that is not detected by cuff pressure mea

213 riation in forward wave amplitude paralleled pulse pressure throughout adulthood.

214 This measure was related to their pulse pressure to assess arterial distensibility.

215 Relationships of SBP, DBP, and pulse pressure to cardiovascular disease-related mortali

216 ) values at or above the 75th percentile and pulse pressure values below the 75th percentile (P < 0.0

217 ange CCA-IMT, augmentation index, or BP, but pulse pressure variability improved (flavonoid: -0.11 +/

218 Multiple systolic and pulse pressure variables (office and ambulatory), but no

219 Preload responsiveness (pulse pressure variation >13%) was observed in 48% of do

220 luded stroke volume variation (nine trials), pulse pressure variation (one trial), and stroke volume

221 dds ratio were 0.89, 0.88, and 59.86 for the pulse pressure variation and 0.82, 0.86, and 27.34 for t

222 threshold values were 12.5 +/- 1.6% for the pulse pressure variation and 11.6 +/- 1.9% for the strok

223 Measures of arterial pulse pressure variation and left ventricular stroke vol

224 The absolute change in pulse pressure variation and stroke volume variation aft

225 best cutoff values of the absolute change in pulse pressure variation and stroke volume variation aft

226 Esmolol infusion decreased both pulse pressure variation and stroke volume variation as

227 r of breaths sampled may increase calculated pulse pressure variation and stroke volume variation bec

228 Both pulse pressure variation and stroke volume variation dur

229 ta-adrenergic blockade differentially alters pulse pressure variation and stroke volume variation dur

230 ume (tidal volume challenge) are superior to pulse pressure variation and stroke volume variation in

231 e validation is required to define threshold pulse pressure variation and stroke volume variation val

232 is, "tidal volume challenge," the changes in pulse pressure variation and stroke volume variation wil

233 and contractility would independently alter pulse pressure variation and stroke volume variation.

234 idal volume and contractility may also alter pulse pressure variation and stroke volume variation.

235 e variation, stroke volume variation, and/or pulse pressure variation and the change in stroke index/

236 Before fluid administration, we recorded pulse pressure variation and the changes in pulse contou

237 g fluid responsiveness was not different for pulse pressure variation and the passive leg-raising and

238 d-expiratory occlusion test were better than pulse pressure variation at predicting fluid responsiven

239 espiratory system was </= 30 mL/cm H2O, then pulse pressure variation became less accurate for predic

240 Stroke volume variation and pulse pressure variation do not reliably predict fluid r

241 Pulse pressure variation increased progressively with in

242 The changes in pulse pressure variation or stroke volume variation obta

243 However, dobutamine did not alter either pulse pressure variation or stroke volume variation.

244 cteristics curve was significantly lower for pulse pressure variation than for the passive leg-raisin

245 A 10% pulse pressure variation threshold discriminated between

246 The ability of pulse pressure variation to predict fluid responsiveness

247 riminating patients regarding the ability of pulse pressure variation to predict fluid responsiveness

248 We tested whether the poor ability of pulse pressure variation to predict fluid responsiveness

249 Pulse pressure variation was calculated as 100 x (PPmax

250 ex >/= 15% (44% +/- 39%) in 30 "responders." Pulse pressure variation was significantly correlated wi

251 We hypothesized that the magnitude of pulse pressure variation would increase with sampling du

252 ) was observed in 48% of donors (mean +/- sd pulse pressure variation, 19.2% +/- 4.8%).

253 association between stroke volume variation, pulse pressure variation, and/or stroke volume variation

254 The pulse pressure variation, stroke volume variation, and c

255 The pulse pressure variation, stroke volume variation, centr

256 orrelation coefficients between the baseline pulse pressure variation, stroke volume variation, systo

257 er the prediction of fluid responsiveness by pulse pressure variation.

258 characteristic curves was different between pulse pressure variations (0.95; 95% confidence interval

259 (VmaxAo) measured using either approach, and pulse pressure variations (PP) were recorded with the pa

260 onders (10% [8-16] vs. 14% [12-16]), whereas pulse pressure variations were significantly higher in r

261 ial pressure, cardiac index, heart rate, and pulse pressure variations) was observed.

262 d with a pressure recording analytic method, pulse pressure variations, and cardiac output estimated

263 pericardial pressure, and pleural pressure; pulse pressure variations, systolic pressure variations,

264 asuring radial artery augmentation index and pulse pressure velocity.

265 Among those with more advanced age, higher pulse pressure was also associated with cerebral amyloid

266 Low pulse pressure was associated with increased mortality.

267 ent myocardial infarction or heart failure), pulse pressure was associated with increased risk for AF

268 Pulse pressure was calculated from the arterial pressure

269 1 hypertension, stage 2-3 hypertension), and pulse pressure was calculated.

270 dvancing age, whereas in older participants, pulse pressure was higher and wave reflection was lower

271 Pulse pressure was increased after the removal of all da

272 systole, nondipping was more prevalent, and pulse pressure was increased compared with -CAN.

273 t across adulthood: In younger participants, pulse pressure was lower and wave reflection was higher

274 ave reflection on age-related differences in pulse pressure was minor.

275 very old participants, a further increase in pulse pressure was observed in those exhibiting both P-t

276 Each 10-mm Hg increase in pulse pressure was related to a smaller aortic root (by

277 rtional-hazards modeling showed that central pulse pressure was significantly associated with a post

278 Furthermore, increased pulse pressure was strongly associated with increased me

279 Peripheral pulse pressure was unaffected by infusion of angiotensin

280 Arterial pulse pressure was unaffected in both groups.

281 aortic augmentation index from radial artery pulse pressure waveforms.

282 Brachial systolic and pulse pressure were also independently associated with i

283 Weighted and unweighted risk scores for pulse pressure were associated with childhood pulse pres

284 In contrast, wave reflection and pulse pressure were divergent across adulthood: In young

285 Systolic BP, diastolic BP, or pulse pressure were either not associated or inversely c

286 elerated increases in central and peripheral pulse pressure were markedly attenuated when variation i

287 Systolic blood pressure and pulse pressure were significantly reduced by 6 and 3 mm

288 blood pressure, mean arterial pressure, and pulse pressure were weaker predictors of CVD risk in thi

289 mentation index, mean arterial pressure, and pulse pressure) were determined at baseline.

290 index, waist circumference, systolic BP, and pulse pressure, were identified, suggesting that the gen

291 oking, high density lipoprotein cholesterol, pulse pressure, white blood cell count, and fibrinogen.

292 determine whether interventions that reduce pulse pressure will limit the growing incidence of AF.

293 Higher pulse pressure at any age and higher pulse pressure with advancing age is associated predomin

294 the empirically observed chronic changes in pulse pressure with age and the impaired capacity of hyp

295 parate relations of systolic, diastolic, and pulse pressure with risk for heart failure have not been

296 ciation of baseline systolic, diastolic, and pulse pressure with risk for incident CHF was examined i

297 for mean arterial pressure, and 10 SNPs for pulse pressure) with the same outcomes in children (medi

298 55-79 years of age) on clinical measures and pulse pressure x age group interactions were investigate

299 area at diastole)/(lumen area at diastole x pulse pressure)] x 1000, was compared between patients w

300 pulse pressure amplification ([Radial/aortic pulse pressure] x 100) were assessed as predictors of CV