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1 ts were change in flow-mediated dilation and augmentation index.
2 ere seen in either flow-mediated dilation or augmentation index.
3 n independent predictor of higher hs-CRP and augmentation index.
4 o influence on augmentation index (change in augmentation index, -0.4%; 95% CI, -1.7 to 0.8; P=0.5) o
6 ry flow reserve, (3) pulse wave velocity and augmentation index, (4) circulating NT-proBNP (N-termina
7 +/- 1.0 m/s vs. -0.1 +/- 0.9 m/s, p < 0.01), augmentation index (-5.2 +/- 6.1% vs. -1.4 +/- 5.9%, p <
8 orearm mitochondrial oxidative function, and augmentation index (a marker of arterial wave reflection
9 sterone, and endothelin (ET)-1 together with augmentation index, a measure of arterial stiffness, wer
11 01), AI d (r = -0.17, P = 0.06), the central augmentation index (AI c ) (r = 0.61, P < 0.001) or AI c
12 AI rd , a combination of AI r and diastolic augmentation index (AI d ) with a weight alpha, to achie
17 t the hypothesis that age-related changes in augmentation index (AIx) are more prominent in younger i
20 pressure (BP), pulse wave velocity (PWV) and augmentation index (AIx) were assessed in 130 subjects (
23 s, LV wall thickness and dimensions, central augmentation index (AIx), aortic pulse wave velocity (aP
24 Pulse wave analysis was used to determine augmentation index (AIx), which provides a measure of sy
27 % vs. placebo -0.69 +/- 2.8%; p = 0.017) and augmentation index (allopurinol -2.8 +/- 5.1% vs. placeb
28 hanges in air pollution were associated with augmentation index and augmentation pressure at several
29 t-term exposure to air pollution and central augmentation index and augmentation pressure, correlates
31 elocity and radial tonometry-derived central augmentation index and subendocardial viability ratio we
32 arterial stiffness (pulse wave velocity and augmentation index) and blood pressure were also not sig
34 tic modulus, impedance, pulse wave velocity, augmentation index, and pulse pressure amplification) ar
35 6 mm Hg (95% confidence interval, 2.4-20.7), augmentation index, and pulse wave velocity without chan
37 -femoral pulse wave velocity (cfPWV), aortic augmentation index, and systemic arterial compliance.
39 n of either meal significantly decreased the augmentation index at 2 and 4 h (P < 0.002) and signific
40 a and augments pressure in late systole [ie, augmentation index = (augmented pressure/pulse pressure)
41 mpliance estimates but may underestimate the augmentation index because the latter requires greater f
42 ulse wave velocity (beta = -0.09, p = 0.04), augmentation index (beta = -0.11, p = 0.03), and subendo
43 artery (CCA-IMT), pulse wave velocity (PWV), augmentation index, blood pressure (BP), and vascular bi
44 arkedly change wave reflection amplitude and augmentation index by altering stiffness of the muscular
45 tic impedance [Zc]) and late-systolic loads (augmentation index [cAI]; late pressure-time integral [P
46 y arterial pulse-wave velocity (Doppler) and augmentation index (carotid tonometry) declined with ver
48 pulse wave velocity [PWV]), wave reflection (augmentation index, carotid-brachial pressure amplificat
49 tion, carotid artery intima-media thickness, augmentation index, central blood pressure, subendocardi
51 -1.9 to 1.0], P=0.6) and had no influence on augmentation index (change in augmentation index, -0.4%;
53 ial stiffness (pulse wave velocity [PWV] and augmentation index corrected for heart rate [AI@75]) wer
55 ex, height, weight, end-diastolic LV volume, augmentation index, end-systolic pressure, and cardiovas
56 oCor Mx system was used to derive the aortic augmentation index from radial artery pulse pressure wav
58 sodilatation was calculated as the change in augmentation index in response to an endothelium-depende
59 essure augmentation was determined using the augmentation index in the ascending aorta (AIaa) and dis
60 arterial stiffness (pulse wave velocity and augmentation index) in 20 adult patients with hypertensi
62 a strong inverse relationship between HR and augmentation index, indicative of increased wave reflect
63 levels and 3 measures of vascular function (augmentation index, mean arterial pressure, and pulse pr
64 , 1.6 [95% CI, 1.3-2.0] per 1 SD; P < .001), augmentation index (OR, 1.7 [95% CI, 1.4-2.0] per 1 SD;
65 ention did not significantly change CCA-IMT, augmentation index, or BP, but pulse pressure variabilit
66 eactive protein (P(interaction) < 0.001) and augmentation index (P = 0.06) values at or above the 75t
67 had higher hs-CRP (P=0.014), higher central augmentation index (P=0.015), and lower glutathione leve
69 lood pressure, mean arterial pressure (MAP), augmentation index, pulse wave velocity (PWV), and intim
70 = [Reflected/Forward wave amplitude] x 100), augmentation index ([Second/First systolic peak] x 100)
71 rterial compliance to 6 +/- 7% accuracy, and augmentation index to within -7% points (30 +/- 45% accu
73 nts/cm(3) IQR increase) were associated with augmentation index values that were 0.8% (95% confidence
75 is cohort, higher aortic stiffness, FWA, and augmentation index were associated with higher risk of i
77 Aortic pulse wave velocity (PWV) and carotid augmentation index were reduced only with SR (p < 0.05).
78 Six months after RD aortic augmentation and augmentation index were significantly reduced by -11 mm
79 y [CFPWV], forward wave amplitude [FWA], and augmentation index) were examined over a 7-year period i
80 ticles and PM2.5, and an increase in PWV and augmentation index with NO2 and ultrafine particles.
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