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1 carotid and femoral arteries as a measure of aortic stiffness.
2 ident stroke independently of CV factors and aortic stiffness.
3 stroke risk prediction beyond Framingham and aortic stiffness.
4 n is predominantly correlated with increased aortic stiffness.
5 se wave velocity (aPWV), a robust measure of aortic stiffness.
6 this effect correlates with the decrease in aortic stiffness.
7 s likely account for the greater increase in aortic stiffness.
8 cancer therapy adversely increases thoracic aortic stiffness, a known independent predictor of adver
11 content and improved its solubility, reduced aortic stiffness, ameliorated diabetic nephrosclerosis,
15 (PMAP), peripheral vascular resistance, AIx, aortic stiffness and central pulse pressure, but only an
16 ur results suggest that associations between aortic stiffness and CVD events are mediated by pathways
17 analyses, 8% to 13% of the relation between aortic stiffness and CVD events was mediated by hyperemi
19 onsistent with the hypothesis that increased aortic stiffness and excessive flow pulsatility damage t
20 ysis showed that 34% of the relation between aortic stiffness and GFR was mediated by pulsatility ind
21 for pulsatility index, the relation between aortic stiffness and GFR was no longer significant (P=0.
25 and determine their relationship to central aortic stiffness and left ventricular (LV) remodeling.
29 arable with EDS patients, they had decreased aortic stiffness and tensile strength and hyperextensibl
31 ators of vascular phenotype severity such as aortic stiffness and vertebral tortuosity index have bee
32 ining reversed the reduction in E/A, reduced aortic stiffness, and eliminated impairment of coronary
36 nd without myocardial fibrosis, have altered aortic stiffness as assessed by magnetic resonance imagi
37 d whether this association is independent of aortic stiffness as estimated by carotid-femoral pulse w
41 creased filling pressures were correlated to aortic stiffness (augmentation pressure and index, P<0.0
42 terial tonometry, we evaluated 3 measures of aortic stiffness: brachial pulse pressure; carotid-femor
44 P amplification, mainly related to increased aortic stiffness, contributes to the significant increas
46 al pulse wave velocity, a measure of central aortic stiffness, decreased after cranberry juice (8.3 +
48 inear relationship of PMAP with both AIx and aortic stiffness did not differ significantly between dr
50 ansplant recipients (KTRs) is uncertain, and aortic stiffness has not yet been incorporated into risk
52 of microvascular structure and function, and aortic stiffness in 2045 participants (1107 women, mean
53 aortic arch is related to increased proximal aortic stiffness in individuals without cardiovascular d
54 elationship between telomere length (TL) and aortic stiffness in well-characterized, younger and olde
56 nt for age, important correlates of abnormal aortic stiffness included higher mean arterial pressure,
57 n the participants receiving anthracyclines, aortic stiffness increased markedly (relative to baselin
61 Increased pulse pressure, a reflection of aortic stiffness, increases cardiac load and may increas
62 - 1.6 x 10(-3) mm Hg, p < 0.001) and greater aortic stiffness index (26.7 +/- 25.8 and 55.9 +/- 76.8
66 t that the burden of disease attributable to aortic stiffness is likely to increase considerably over
67 atrilat compared with enalapril suggest that aortic stiffness is maintained by specific, partially re
69 ese analyses provide the first evidence that aortic stiffness may contribute to lower GFR by transfer
70 dation of the role this novel locus plays in aortic stiffness may facilitate development of therapeut
71 ch as renal dysfunction and enhanced central aortic stiffness may play an important role in the devel
73 ng adults with a CTD was performed to derive aortic stiffness measures (strain, distensibility, and b
75 erations in left ventricular function and in aortic stiffness occur during the early phase of aneurys
78 individuals (<50 years), whereas changes in aortic stiffness per se are more marked in older individ
81 E/A), myocardial performance index (MPI) and aortic stiffness (pulse wave velocity; PWV) were evaluat
82 n IVRT, a 64% decrease in E/A, and increased aortic stiffness (PWV: 6.36 +/- 0.47 vs.4.89 +/- 0.41, O
83 ral hemodynamic parameters involve increased aortic stiffness, reduced wave reflections, and increase
88 were independently associated with increased aortic stiffness, renal injury, and incident cardiovascu
89 lying clinical conditions known to influence aortic stiffness, such as hypertension or diabetes (P <
90 st, however, after additional adjustment for aortic stiffness, suggesting a shared causal pathway.
93 h IFG to prevent LV hypertrophy and abnormal aortic stiffness that is observed in middle-aged and old
94 e velocity (CFPWV) is a heritable measure of aortic stiffness that is strongly associated with increa
95 ected five highly significant QTLs affecting aortic stiffness: two interacting QTLs (AS-m1 on chromos
98 cardiovascular disease risk factors, higher aortic stiffness was associated with increased LV mass (
100 for mean arterial pressure, each measure of aortic stiffness was associated with reduced hyperemic f
103 modify arterial stiffness, proximal thoracic aortic stiffness was not increased in those with IFG com
104 ted for age, sex, heart rate, and body size, aortic stiffness was related to GFR (Slope of regression
105 pulse wave velocity, which reflects central aortic stiffness, was statistically significantly lower
106 in which factors known to influence thoracic aortic stiffness were included as covariates in the mode
108 trophy, diastolic dysfunction, and increased aortic stiffness, which are independent predictors of ca
109 rmal (9.2 +/- 2.2 m/s), indicating increased aortic stiffness, which strongly correlated with NT-proB
110 H patients have increased apparent ascending aortic stiffness, which was strongly associated with the
111 anges in vascular properties responsible for aortic stiffness with aging would be greater in old male
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