(Circulation. 1999;99:2434-2439.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Impact of Aortic Stiffness on Survival in End-Stage Renal Disease
From the Service de Médecine, Hôpital Broussais, Paris (J.B., M.E.S.), and the Hôpital F.H. Manhès, Fleury-Mérogis (A.P.G., B.P., S.J.M., G.M.L.), France.
Correspondence to Dr Gérard London, CH Manhès, 8, Grande Rue, Fleury-Mérogis, 91712 Ste/Geneviève des Bois, France.
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Background—Damage to large arteries is a major factor in the high cardiovascular morbidity and mortality of patients with end-stage renal disease (ESRD). Increased arterial stiffness and intima-media thickness, together with increased pulse pressure, are the principal arterial alterations. Whether increased aortic pulse-wave velocity (PWV), a classic marker of increased arterial stiffness, may predict all-cause and/or cardiovascular mortality has never been investigated.
Methods and Results—A cohort of 241 patients with ESRD undergoing hemodialysis was studied between April 1987 and April 1998. The mean duration of follow-up was 72±41 months (mean±SD). Mean age at entry was 51.5±16.3 years. Seventy-three deaths occurred, including 48 cardiovascular and 25 noncardiovascular fatal events. At entry, together with standard clinical and biochemical analyses, patients underwent echocardiography and aortic PWV measured by Doppler ultrasonography. On the basis of Cox analyses, 2 factors emerged as predictors of all-cause and cardiovascular mortality: age and aortic PWV. Hemoglobin and low diastolic pressure interfered to a smaller extent. After adjustment for all the confounding factors, an OR for PWV >12.0 versus <9.4 m/s was 5.4 (95% CI, 2.4 to 11.9) for all-cause mortality and 5.9 (95% CI, 2.3 to 15.5) for cardiovascular mortality. For each PWV increase of 1 m/s in our study population, all-cause mortality–adjusted OR was 1.39 (95% CI, 1.19 to 1.62).
Conclusions—These results provide the first direct evidence that in patients with ESRD, increased aortic stiffness determined by measurement of aortic PWV is a strong independent predictor of all-cause and mainly cardiovascular mortality.
Key Words: aorta • survival • kidney
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Introduction |
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Patients with end-stage renal disease (ESRD) are at increased risk of cardiovascular disease. Epidemiological and clinical studies have shown that damage of large arteries is a major contributory factor to the high cardiovascular morbidity and mortality of ESRD patients.1 Macrovascular disease develops rapidly in uremic patients and is responsible for the high incidence of ischemic heart disease, left ventricular (LV) hypertrophy, congestive heart failure, sudden death, and stroke.1 Many complications arise in ESRD patients in the absence of clinically significant atherosclerotic disease.2 The principal arterial alteration in this latter situation consists of arterial stiffening associated with arterial enlargement and hypertrophy.3 Arterial stiffening occurs normally with aging4 but also correlates with the prevalence of atherosclerosis. The most obvious consequences of arterial stiffening are higher systolic blood pressure (SBP) and lower diastolic blood pressure (DBP), thereby causing increased LV afterload and altering coronary perfusion.4 The principal outcomes of these changes are LV hypertrophy, aggravation of coronary ischemia, and increased fatigue of arterial wall tissues. Higher SBP and pulse pressure, lower DBP, and LV hypertrophy have been identified as independent factors of cardiovascular morbidity and mortality in the general population5 6 as well as in ESRD patients.7 8 9
Arterial stiffness can be assessed noninvasively by measurement of pulse-wave velocity (PWV).10 11 According to the Moens-Korteweg equation,4 the PWV, which is related to the square root of the elasticity modulus, rises in stiffer arteries. The elastic properties of the aorta and central arteries are important determinants of cardiovascular coupling, and the PWV measured along the aortic or aortoiliac pathway is the most clinically relevant.4 Nevertheless, whether aortic stiffening is predictive of clinical outcome or death has never been established. To identify the impact of aortic stiffening on cardiovascular and all-cause mortality in hemodialyzed ESRD patients, we conducted a prospective study on a cohort of 241 patients followed up for a period of up to 11 years.
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Methods |
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Patients
This prospective cohort study was started at the F.H. Manhès Hospital, Fleury-Mérogis (in the Paris/Ile de France area), in April 1987. Patients were eligible for entry into the study when (1) they had been on hemodialysis for
3 months (48±51 months,
mean±SD) and (2) they had had no clinical
cardiovascular disease during 6 months preceding entry.
Patient recruitment was closed in October 1996, and follow-up ended in
April 1998. In all, 241 patients fulfilled the entry criteria. Patients
who underwent renal transplantation (n=28) and patients who moved away
(n=7) were censored at transplantation or departure to another unit.
All but 6 patients were white. The mean patient follow-up was 72±41
months. Data on mortality were obtained for the entire cohort. The mean
age of the cohort was 51.5±16.3 years; 61% were male; 7% had
insulin-dependent diabetes mellitus; and 48% were treated with
different antihypertensive drugs. Of these patients, 126 received
recombinant human erythropoietin at some time during follow-up. During
the follow-up, all patients were dialyzed by the same unique
standardized technique, including synthetic membrane hemodialyzers
(AN69 and polysulfone) matched for the subject's body surface area
(1.36 to 2.0 m2), bicarbonate dialysate, and
controlled ultrafiltration rate. The duration of dialysis sessions was
tailored (4 to 6 hours, 3 times weekly) to achieve a total dialysis
dose (Kt/V) 1.2 (1.38±0.17). Each subject provided informed
written consent to participate in the study, which was approved by our
institutional review board.
Data Collection
Information compiled from the questionnaire filled out at entry
into the study included personal and family histories, smoking habits
(126 patients were current or former smokers), and previous history of
cardiovascular disease, including coronary
artery disease, angina pectoris, cardiac failure,
peripheral vascular disease, and cerebrovascular disease.
Causes of death (WHO International Classification of Disease, ninth
revision) were obtained from death certificates, hospital record
forms, and autopsy data reviewed by the authors. Sudden death was
defined as a witnessed death that occurred within 1 hour after the
onset of acute symptoms, with no evidence that violence or accident
played any role in the fatal outcome. During the mean follow-up period,
we recorded 73 deaths, including 48 fatal
cardiovascular events: 15 deaths attributed to
coronary heart disease, 12 to cerebrovascular and/or aortic
disease, 12 to sudden death, 6 to congestive heart failure, and 3 to
pulmonary embolism. The 25 fatal
noncardiovascular events were 12 deaths due to cancer,
6 to infectious disease, 5 by withdrawal from dialysis, and 2
suicides.
The measurements were performed during the 2 weeks after inclusion, on the morning before the midweek hemodialysis. Blood chemistry was measured at baseline and at monthly intervals. BP was measured with a mercury sphygmomanometer after 15 minutes of recumbency. Phases I and V of the Korotkoff sounds were taken as the SBP and DBP, respectively. Five measurements determined at 2-minute intervals were averaged.
Baseline echocardiography was performed with a Hewlett-Packard Sonos 100 device equipped with a 2.25-MHz probe allowing M-mode, 2-dimensional, and pulsed Doppler measurements. Measurements were made according to the recommendations of the American Society of Echocardiography.12 LV mass was calculated according to the Penn convention.13 Adequate echocardiographic tracings were obtained for 214 subjects. LV hypertrophy (LV mass index >132 g/m2 in men and >110 g/m2 in women) was present in 81% of the patients.
Baseline aortic PWV was determined from transcutaneous Doppler flow recordings and the foot-to-foot method.3 10 Two simultaneous Doppler flow tracings were taken at the aortic arch and the femoral artery in the groin with a nondirectional Doppler unit (SEGA M842, 10 MHz) with a handheld probe and recorded on a Gould 8188 recorder (Gould Electronique) at a speed of 100 to 200 mm/s. For aortic flow, the transducer was placed in the suprasternal notch. When a good-quality high-frequency signal could not be recorded in this location, the transducer was placed laterally at the base of the neck, and the signal from the common carotid artery opposite to the site of arteriovenous fistula was recorded. The time delay (t) was measured between the bases of the flow waves recorded at these different points and was averaged over 10 beats. The distance (D) traveled by the pulse wave was measured over the body surface as the distance between the 2 recording sites, and when measured from the carotid artery, the distance from the suprasternal notch to the carotid was subtracted. PWV was calculated as PWV=D/t. All measurements were done by the same observer (G.M.L.), and the intraobserver repeatability of the aortic PWV measurement was 5.8±1%.14 The heart period was determined from the 3-lead orthogonal ECG.
Analysis
The outcome events studied were cardiovascular
mortality and all-cause mortality. Survival curves were estimated by
the Kaplan-Meier product-limit method and compared by the Mantel
(log-rank) test. Prognostic factors of survival were identified by use
of logistic regression analysis and the Cox proportional
hazards regression model. The assumption of proportional hazards over
time was verified before the analyses were performed and was
met by all covariates. The assumption concerning linearity of
continuous covariates was also verified before analysis. All
analyses, including echocardiographic LV mass
among the covariates, were limited to the subset with adequate
echocardiographic tracings. The cohort was divided into
3 groups (80 or 81 patients per group) according to the PWV <9.4 m/s
in the lower third, between 9.4 and 12.0 in the second third, and
>12.0 in the upper third. Variables were considered to be
prognostic when they were found to be statistically significant
(P<0.05) in the logistic regression or the Cox proportional
hazards regression models of all-cause or
cardiovascular mortality. The adjusted relative risk of
experiencing an outcome event during follow-up for the patients in the
second or in the upper third of any prognostic variable compared
with the risk of the patients in the lower third was estimated as the
OR. Adjusted ORs were calculated as the antilogarithm of the ß
coefficient of the logistic regression of the outcome events with all
the prognostic variables, considered as continuous variables in
the model (PWV, age, time on dialysis before inclusion, DBP, and
hemoglobin). The 95% CIs around the adjusted OR estimates were
obtained with the formula antilogarithm(ß±1.96 SE), where SE is
the standard error of ß.
Data are expressed as mean±SD. ANOVA was used for comparison of
normally distributed continuous variables. Differences in frequency
were tested by 
2 analysis. Sex (1,
male; 2, female), previous history of cardiovascular
disease (1, no; 2, yes), and antihypertensive drug therapy (1, no; 2,
yes) were used as dummy variables. Statistical analysis was
performed with NCSS 6.0.21 software. Repeatability and reproducibility
of the methods were defined as recommended by the British Standards
Institution.15 A value of P<0.05 was
considered significant. All tests were 2-sided.
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Results |
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Patient Characteristics
The characteristics of the cohort at the time of inclusion are shown in Table 1
. The
characteristics of patients as a function of their PWV values are shown
in Table 2. Comparing the different
subgroups, age, age at the initiation of dialysis, SBP, mean BP, pulse
pressure, LV mass index, tobacco lifelong dose, and incidence of
diabetes and previous cardiovascular events increased
from the lower to the upper third, whereas DBP and serum
albumin decreased. Serum albumin levels were negatively
associated with age (P<0.001), and in the subsequent
analysis, the role of the albumin level could not be
differentiated from the influence of aging.
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Outcome and Prognostic Impact of Aortic PWV
During the follow-up period, 73 deaths were recorded.
According to the Cox analysis, the significant covariates
retained by the model were only age, PWV, and DBP (negative
association) (Table 3). Smoking, heart
rate, hemoglobin, serum albumin, LV hypertrophy,
antihypertensive drug therapy, sex, parathyroid hormone, and
previous cardiovascular events did not reach
statistical significance in multivariate
analysis. After adjustments for all the prognostic
variables (PWV, age, time on dialysis before inclusion, DBP, and
hemoglobin), PWV was the strongest predictor of mortality, followed by
the duration of hemodialysis before inclusion and the patient's age at
inclusion (Table 4). Duration of
hemodialysis before inclusion was inversely correlated with the
patient's age at start of hemodialysis (P<0.001) and at
inclusion (P=0.05). Compared with patients in the lower
third of PWV, patients in the upper third had a 5.4-fold adjusted risk
of all-cause mortality (95% CI, 2.4 to 11.9). For each PWV increase of
1 m/s in our study population, all-cause mortality relative risk was
1.39 (95% CI, 1.19 to 1.62).
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Forty-eight cardiovascular deaths were documented
during the follow-up period. According to the Cox analysis, the
significant covariates entering the model were age, PWV, hemoglobin,
and DBP (Table 3
). Serum lipids, smoking, heart rate, LV
hypertrophy, antihypertensive therapy, sex, and parathyroid
hormone did not reach statistical significance in
multivariate analysis. After adjustment for all
the prognostic variables, PWV was again the strongest predictor of
cardiovascular mortality (Table 4). Compared
with patients in the lower third of PWV, patients in the upper third
had a 5.9-fold adjusted risk of cardiovascular
mortality (95% CI, 2.3 to 15.5). Duration of hemodialysis before
inclusion predicted cardiovascular mortality but to a
lesser degree. The Figure shows the
probabilities of all-cause (A) and event-free (B,
cardiovascular) survival as a function of PWV values.
Comparisons between survival curves were highly significant.
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Considering 3 tertile groups according to age at initiation of dialysis, we found that PWV, in univariate analysis, was strongly related to mortality in the 3 subsets (r=0.44, P<0.0001 for the lower tertile; r=0.40, P=0.0016 for the second tertile; and r=0.47, P<0.0001 for the upper tertile). Differences in mortality for the 3 aortic stiffness categories persisted after stratification by age and time since initiation of dialysis (data not shown).
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Discussion |
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Arterial stiffness increases with age,4 10 hypertension,16 diabetes mellitus,17 atherosclerosis,18 and ESRD.3 In ESRD patients, the increased arterial stiffness is associated with acceleration of the arterial aging process, namely dilatation and increased wall thickness of major arteries. In this study, we found that arterial stiffness in patients who require hemodialysis was a major predictor of all-cause and cardiovascular mortality. The role of arterial stiffening was independent of other factors known to affect the outcome of uremic patients, namely age, overall duration of ESRD, preexisting cardiovascular disease, degree of LV hypertrophy, BP, and serum albumin and hemoglobin levels. Furthermore, PWV was a better predictor of mortality than age or number of years on hemodialysis.
PWV measurement offers a simple, reproducible, indirect, and noninvasive evaluation of regional arterial stiffness.14 The PWV determined from foot-to-foot transit time in the aorta eliminates the influence of wave reflections and is close to the characteristic PWV determined from phase velocities.4 The critical factors are the precise measurements of this transit time and the length of the vascular segments. Transcutaneous determination of the vessel length is an approximation that might underestimate the vascular length, an error that might arise especially in elderly patients with unfolded tortuous aorta. Despite these limitations, measurement of PWV is strongly correlated to direct measurements of arterial distensibility and can be considered a good surrogate to evaluation of arterial stiffness by phase-locked echo-tracking systems.3 Several clinical cross-sectional studies have found an association between atherosclerosis and abnormal arterial stiffness, especially an association between aortic stiffness and coronary artery disease.19 Studies in ESRD patients have shown that arterial stiffness is enhanced independently of age and BP,3 making these patients an appropriate test population to analyze the impact of arterial stiffness on mortality.
Whether enhanced arterial stiffness is a risk factor contributing to the development of cardiovascular disease or is a marker of established cardiovascular disease is a matter of debate.20 A study in Chinese and Australians21 has suggested that morphological and structural alterations of the aorta may be influenced by both environmental and mostly genetic factors, suggesting that changes of biomechanical properties of major arteries may precede the development of clinically overt disease. Although data reported in the literature indicate that LV hypertrophy is an independent factor of overall mortality in ESRD,7 we did not find an independent association between LV hypertrophy and death. As a determinant of pressure load, aortic stiffness correlates with LV mass and ratio of LV wall thickness to radius in ESRD patients3 as well as in those with essential hypertension.22 The collinearity between aortic stiffness and LV hypertrophy in the present study (r=0.23, P=0.0007) is the most probable cause for the absence of independent association between mortality and LV mass.
Arterial stiffness is associated with increased SBP and decreased DBP. In ESRD patients, enhanced SBP has been shown to be associated with the development of ischemic heart disease,8 and a relationship between low DBP and mortality was found in these patients9 as well as in the general population.23 Contrary to the observation made by Charra et al24 but in agreement with others,25 26 we did not find an independent relationship between hypertension and patient survival. Confirming data reported in the literature, the present study indicates that other factors associated with survival are patient age and the number of years on dialysis.27 However, in the present population, PWV measurement persisted as a strong predictor of mortality whatever the age of the patient and even if this measurement was made (long) after the initiation of dialysis.
In the present study, there was a weak inverse relationship between the hemoglobin level and cardiovascular mortality. In the general population, an association between increased risks of all-cause and cardiovascular mortality and higher hematocrit values was observed.28 In ESRD, anemia is considered an independent risk factor for cardiovascular disease and mortality.29 Data by Besarab et al30 show that in ESRD, the normalization of hemoglobin level in patients with compromised cardiovascular function was not associated with favorable improvement in survival. The possibility that excessive correction of anemia and increased blood viscosity is deleterious for microcirculation in patients with damaged arterial function cannot be ruled out and was also suggested by Iseki et al.31
The ability to generalize the results of the present study may be limited because the demographics and characteristics of the ESRD patients reported were significantly different from those of ESRD patients in North America and in northern Europe.32 The proportion of diabetics among ESRD patients, while steadily increasing in France, remains low; diabetic patients represented 6.9% of ESRD patients in 1989.33 Survival on hemodialysis is superior in France and southern Europe to that in northern Europe or North America,32 the salient difference being the death rate due to myocardial ischemia and infarction, which is greater in northern Europe.34 The overall annual mortality rate in ESRD patients in France was 13.3% in 199532 and 6% in the Paris area and the Ile de France.35 Therefore, the impact of aortic PWV on mortality in the present relatively "low-risk" population of ESRD patients possibly underlines the pathological role of aortic stiffening. In addition, it is important to consider 2 other influences that the relatively lower mortality rates might have on our final results. First, the substantially lower cardiovascular mortality rates might result in an underestimate of the true impact of aortic stiffness on overall mortality in ESRD populations in North America and Europe. Second, in populations with much higher undifferentiated mortality rates, the predictive value of aortic PWV might be altered substantially.
To qualify as a risk factor, increased aortic stiffness must raise the probability of an adverse outcome. The results of the present analysis suggest that this is indeed the case. Although correlation does not imply causation, aortic PWV is a strong independent predictor of cardiovascular and all-cause mortality in patients with ESRD on hemodialysis. In addition, aortic stiffness measurements could serve as an important tool in identifying patients at risk of cardiovascular disease. The ability to identify these patients would lead to better risk stratification and earlier and more cost-effective preventive therapy.
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Acknowledgments |
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This work was supported by the Société Française d'Hypertension Artérielle, the Groupe d'Etude de Pathophysiologie de l'Insuffisance Rénale, Daniel Brun for Organica Association, the Groupe de Pharmacologie et d'Hémodynamique Cardio-vasculaire, and the Union des Mutuelles de l'Ile de France.
Received October 7, 1998; revision received February 2, 1999; accepted February 16, 1999.
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A. LeBeouf, F. Mac-Way, M. S. Utescu, N. Chbinou, P. Douville, S. Desmeules, and M. Agharazii Effects of acute variation of dialysate calcium concentrations on arterial stiffness and aortic pressure waveform Nephrol. Dial. Transplant., December 1, 2009; 24(12): 3788 - 3794. [Abstract] [Full Text] [PDF]
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 M. J. Blaha, M. J. Budoff, J. J. Rivera, R. Katz, D. H. O'Leary, J. F. Polak, J. Takasu, R. S. Blumenthal, and K. Nasir Relationship of Carotid Distensibility and Thoracic Aorta Calcification: Multi-Ethnic Study of Atherosclerosis Hypertension, December 1, 2009; 54(6): 1408 - 1415. [Abstract] [Full Text] [PDF]
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M. Cecelja and P. Chowienczyk Dissociation of Aortic Pulse Wave Velocity With Risk Factors for Cardiovascular Disease Other Than Hypertension: A Systematic Review Hypertension, December 1, 2009; 54(6): 1328 - 1336. [Abstract] [Full Text] [PDF]
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M. S. Utescu, A. LeBoeuf, N. Chbinou, S. Desmeules, M. Lebel, and M. Agharazii The impact of arteriovenous fistulas on aortic stiffness in patients with chronic kidney disease Nephrol. Dial. Transplant., November 1, 2009; 24(11): 3441 - 3446. [Abstract] [Full Text] [PDF]
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D. Sengstock, R. L. Sands, B. W. Gillespie, X. Zhang, M. Kiser, G. Eisele, P. Vaitkevicius, M. Kuhlmann, N. W. Levin, A. Hinderliter, et al. Dominance of traditional cardiovascular risk factors over renal function in predicting arterial stiffness in subjects with chronic kidney disease Nephrol. Dial. Transplant., October 23, 2009; (2009) gfp559v1. [Abstract] [Full Text] [PDF]
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M. Hornum, P. Clausen, J. Kjaergaard, J. M. Hansen, E. R. Mathiesen, and B. Feldt-Rasmussen Pre-diabetes and arterial stiffness in uraemic patients Nephrol. Dial. Transplant., October 21, 2009; (2009) gfp558v1. [Abstract] [Full Text] [PDF]
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 A. Upadhyay, S.-J. Hwang, G. F. Mitchell, R. S. Vasan, J. A. Vita, P. I. Stantchev, J. B. Meigs, M. G. Larson, D. Levy, E. J. Benjamin, et al. Arterial Stiffness in Mild-to-Moderate CKD J. Am. Soc. Nephrol., September 1, 2009; 20(9): 2044 - 2053. [Abstract] [Full Text] [PDF]
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 A. W.Y. Chung, H.H. C. Yang, J. M. Kim, M. K. Sigrist, E. Chum, W. A. Gourlay, and A. Levin Upregulation of Matrix Metalloproteinase-2 in the Arterial Vasculature Contributes to Stiffening and Vasomotor Dysfunction in Patients With Chronic Kidney Disease Circulation, September 1, 2009; 120(9): 792 - 801. [Abstract] [Full Text] [PDF]
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 N. C. Edwards, R. P. Steeds, P. M. Stewart, C. J. Ferro, and J. N. Townend Effect of spironolactone on left ventricular mass and aortic stiffness in early-stage chronic kidney disease: a randomized controlled trial. J. Am. Coll. Cardiol., August 4, 2009; 54(6): 505 - 512. [Abstract] [Full Text] [PDF]
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I. Dursun, H. M Poyrazoglu, Z. Gunduz, H. Ulger, A. Yykylmaz, R. Dusunsel, T. Patyroglu, and M. Gurgoze The relationship between circulating endothelial microparticles and arterial stiffness and atherosclerosis in children with chronic kidney disease Nephrol. Dial. Transplant., August 1, 2009; 24(8): 2511 - 2518. [Abstract] [Full Text] [PDF]
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 H. Eddington and J. G. Heaf Clinical management of disturbances of calcium and phosphate metabolism in dialysis patients NDT Plus, August 1, 2009; 2(4): 267 - 272. [Abstract] [Full Text] [PDF]
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H. P. Kuhl Hypertrophic cardiomyopathy, fibrosis, and aortic stiffness an unidentified association unraveled by magnetic resonance imaging. J. Am. Coll. Cardiol., July 14, 2009; 54(3): 263 - 264. [Full Text] [PDF]
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N. Dhaun, I. M. MacIntyre, V. Melville, P. Lilitkarntakul, N. R. Johnston, J. Goddard, and D. J. Webb Blood Pressure-Independent Reduction in Proteinuria and Arterial Stiffness After Acute Endothelin-A Receptor Antagonism in Chronic Kidney Disease Hypertension, July 1, 2009; 54(1): 113 - 119. [Abstract] [Full Text] [PDF]
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 C. E Bolton, J. R Cockcroft, R. Sabit, M. Munnery, C. M McEniery, I. B Wilkinson, S. Ebrahim, J. E Gallacher, D. J Shale, and Y. Ben-Shlomo Lung function in mid-life compared with later life is a stronger predictor of arterial stiffness in men: The Caerphilly Prospective Study Int. J. Epidemiol., June 1, 2009; 38(3): 867 - 876. [Abstract] [Full Text] [PDF]
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 K. V. Tarasov, S. Sanna, A. Scuteri, J. B. Strait, M. Orru, A. Parsa, P.-I Lin, A. Maschio, S. Lai, M. G. Piras, et al. COL4A1 Is Associated With Arterial Stiffness by Genome-Wide Association Scan Circ Cardiovasc Genet, April 1, 2009; 2(2): 151 - 158. [Abstract] [Full Text] [PDF]
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 J. A. Chirinos, S. S. Franklin, R. R. Townsend, and L. Raij Body Mass Index and Hypertension Hemodynamic Subtypes in the Adult US Population Arch Intern Med, March 23, 2009; 169(6): 580 - 586. [Abstract] [Full Text] [PDF]
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T. Adragao, A. Pires, R. Birne, J. D. Curto, C. Lucas, M. Goncalves, and A. P. Negrao A plain X-ray vascular calcification score is associated with arterial stiffness and mortality in dialysis patients Nephrol. Dial. Transplant., March 1, 2009; 24(3): 997 - 1002. [Abstract] [Full Text] [PDF]
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J. Maizel, I. Six, M. Slama, C. Tribouilloy, H. Sevestre, S. Poirot, P. Giummelly, J. Atkinson, G. Choukroun, M. Andrejak, et al. Mechanisms of Aortic and Cardiac Dysfunction in Uremic Mice With Aortic Calcification Circulation, January 20, 2009; 119(2): 306 - 313. [Abstract] [Full Text] [PDF]
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M. Rodriguez-Garcia, C. Gomez-Alonso, M. Naves-Diaz, J. B. Diaz-Lopez, C. Diaz-Corte, J. B. Cannata-Andia, and the Asturias Study Group Vascular calcifications, vertebral fractures and mortality in haemodialysis patients Nephrol. Dial. Transplant., January 1, 2009; 24(1): 239 - 246. [Abstract] [Full Text] [PDF]
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O. Cseprekal, E. Kis, P. Schaffer, T. E. H. Othmane, B. Cs. Fekete, A. Vannay, A. J. Szabo, A. Remport, A. Szabo, T. Tulassay, et al. Pulse wave velocity in children following renal transplantation Nephrol. Dial. Transplant., January 1, 2009; 24(1): 309 - 315. [Abstract] [Full Text] [PDF]
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A. Hiukka, J. Westerbacka, E. S. Leinonen, H. Watanabe, O. Wiklund, L. M. Hulten, J. T. Salonen, T.-P. Tuomainen, H. Yki-Jarvinen, A. C. Keech, et al. Long-Term Effects of Fenofibrate on Carotid Intima-Media Thickness and Augmentation Index in Subjects With Type 2 Diabetes Mellitus J. Am. Coll. Cardiol., December 16, 2008; 52(25): 2190 - 2197. [Abstract] [Full Text] [PDF]
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 S. R. Lammers, P. H. Kao, H. J. Qi, K. Hunter, C. Lanning, J. Albietz, S. Hofmeister, R. Mecham, K. R. Stenmark, and R. Shandas Changes in the structure-function relationship of elastin and its impact on the proximal pulmonary arterial mechanics of hypertensive calves Am J Physiol Heart Circ Physiol, October 1, 2008; 295(4): H1451 - H1459. [Abstract] [Full Text] [PDF]
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J. Karalliedde, A. Smith, L. DeAngelis, V. Mirenda, A. Kandra, J. Botha, P. Ferber, and G. Viberti Valsartan Improves Arterial Stiffness in Type 2 Diabetes Independently of Blood Pressure Lowering Hypertension, June 1, 2008; 51(6): 1617 - 1623. [Abstract] [Full Text] [PDF]
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B. Dursun, E. Dursun, G. Suleymanlar, B. Ozben, I. Capraz, A. Apaydin, and T. Ozben Carotid artery intima-media thickness correlates with oxidative stress in chronic haemodialysis patients with accelerated atherosclerosis Nephrol. Dial. Transplant., May 1, 2008; 23(5): 1697 - 1703. [Abstract] [Full Text] [PDF]
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S. S. Najjar, A. Scuteri, V. Shetty, J. G. Wright, D. C. Muller, J. L. Fleg, H. P. Spurgeon, L. Ferrucci, and E. G. Lakatta Pulse Wave Velocity Is an Independent Predictor of the Longitudinal Increase in Systolic Blood Pressure and of Incident Hypertension in the Baltimore Longitudinal Study of Aging J. Am. Coll. Cardiol., April 8, 2008; 51(14): 1377 - 1383. [Abstract] [Full Text] [PDF]
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F. A. Benedetto, G. Tripepi, F. Mallamaci, and C. Zoccali Rate of Atherosclerotic Plaque Formation Predicts Cardiovascular Events in ESRD J. Am. Soc. Nephrol., April 1, 2008; 19(4): 757 - 763. [Abstract] [Full Text] [PDF]
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M. Delahousse, M. Chaignon, L. Mesnard, P. Boutouyrie, M. E. Safar, T. Lebret, M. Pastural-Thaunat, L. Tricot, A. Kolko-Labadens, A. Karras, et al. Aortic Stiffness of Kidney Transplant Recipients Correlates with Donor Age J. Am. Soc. Nephrol., April 1, 2008; 19(4): 798 - 805. [Abstract] [Full Text] [PDF]
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P. Stenvinkel, J. J. Carrero, J. Axelsson, B. Lindholm, O. Heimburger, and Z. Massy Emerging Biomarkers for Evaluating Cardiovascular Risk in the Chronic Kidney Disease Patient: How Do New Pieces Fit into the Uremic Puzzle? Clin. J. Am. Soc. Nephrol., March 1, 2008; 3(2): 505 - 521. [Abstract] [Full Text] [PDF]
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M. Frimodt-Moller, A. H. Nielsen, A.-L. Kamper, and S. Strandgaard Reproducibility of pulse-wave analysis and pulse-wave velocity determination in chronic kidney disease Nephrol. Dial. Transplant., February 1, 2008; 23(2): 594 - 600. [Abstract] [Full Text] [PDF]
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M. Essig, B. Escoubet, D. de Zuttere, F. Blanchet, F. Arnoult, E. Dupuis, C. Michel, F. Mignon, F. Mentre, C. Clerici, et al. Cardiovascular remodelling and extracellular fluid excess in early stages of chronic kidney disease Nephrol. Dial. Transplant., January 1, 2008; 23(1): 239 - 248. [Abstract] [Full Text] [PDF]
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P. Eller, K. Hochegger, G. M. Feuchtner, E. Zitt, I. Tancevski, A. Ritsch, F. Kronenberg, A. R. Rosenkranz, J. R. Patsch, and G. Mayer Impact of ENPP1 genotype on arterial calcification in patients with end-stage renal failure Nephrol. Dial. Transplant., January 1, 2008; 23(1): 321 - 327. [Abstract] [Full Text] [PDF]
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S. S. DeLoach and R. R. Townsend Vascular Stiffness: Its Measurement and Significance for Epidemiologic and Outcome Studies Clin. J. Am. Soc. Nephrol., January 1, 2008; 3(1): 184 - 192. [Abstract] [Full Text] [PDF]
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M. M. Lemos, A. D. B. Jancikic, F. M. R. Sanches, D. M. Christofalo, S. A. Ajzen, M. H. Miname, R. D. Santos, F. C. Fachini, A. B. Carvalho, S. A. Draibe, et al. Pulse wave velocity a useful tool for cardiovascular surveillance in pre-dialysis patients Nephrol. Dial. Transplant., December 1, 2007; 22(12): 3527 - 3532. [Abstract] [Full Text] [PDF]
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M. Yoshida, H. Tomiyama, J. Yamada, Y. Koji, K. Shiina, M. Nagata, and A. Yamashina Relationships among Renal Function Loss within the Normal to Mildly Impaired Range, Arterial Stiffness, Inflammation, and Oxidative Stress Clin. J. Am. Soc. Nephrol., November 1, 2007; 2(6): 1118 - 1124. [Abstract] [Full Text] [PDF]
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F. Verbeke, W. Van Biesen, P. Peeters, L. M. Van Bortel, and R. C. Vanholder Arterial stiffness and wave reflections in renal transplant recipients Nephrol. Dial. Transplant., October 1, 2007; 22(10): 3021 - 3027. [Abstract] [Full Text] [PDF]
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N. Cheung, A. R. Sharrett, R. Klein, M. H. Criqui, F.M. A. Islam, K. J. Macura, M. F. Cotch, B. E.K. Klein, and T. Y. Wong Aortic Distensibility and Retinal Arteriolar Narrowing: The Multi-Ethnic Study of Atherosclerosis Hypertension, October 1, 2007; 50(4): 617 - 622. [Abstract] [Full Text] [PDF]
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A. Benjo, R. E. Thompson, D. Fine, C. W. Hogue, D. Alejo, A. Kaw, G. Gerstenblith, A. Shah, D. E. Berkowitz, and D. Nyhan Pulse Pressure Is an Age-Independent Predictor of Stroke Development After Cardiac Surgery Hypertension, October 1, 2007; 50(4): 630 - 635. [Abstract] [Full Text] [PDF]
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K. M. Maki-Petaja, A. D. Booth, F. C. Hall, S. M.L. Wallace, J. Brown, C. M. McEniery, and I. B. Wilkinson Ezetimibe and Simvastatin Reduce Inflammation, Disease Activity, and Aortic Stiffness and Improve Endothelial Function in Rheumatoid Arthritis J. Am. Coll. Cardiol., August 28, 2007; 50(9): 852 - 858. [Abstract] [Full Text] [PDF]
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M. F. O'Rourke and J. Hashimoto Mechanical Factors in Arterial Aging: A Clinical Perspective J. Am. Coll. Cardiol., July 3, 2007; 50(1): 1 - 13. [Abstract] [Full Text] [PDF]
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J. Ajiro, B. Alchi, I. Narita, K. Omori, D. Kondo, M. Sakatsume, J. J. Kazama, K. Akazawa, and F. Gejyo Mortality Predictors after 10 Years of Dialysis: A Prospective Study of Japanese Hemodialysis Patients Clin. J. Am. Soc. Nephrol., July 1, 2007; 2(4): 653 - 660. [Abstract] [Full Text] [PDF]
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J. Nogueira and M. Weir The Unique Character of Cardiovascular Disease in Chronic Kidney Disease and Its Implications for Treatment with Lipid-Lowering Drugs Clin. J. Am. Soc. Nephrol., July 1, 2007; 2(4): 766 - 785. [Abstract] [Full Text] [PDF]
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M. J. Roman, R. B. Devereux, J. R. Kizer, E. T. Lee, J. M. Galloway, T. Ali, J. G. Umans, and B. V. Howard Central Pressure More Strongly Relates to Vascular Disease and Outcome Than Does Brachial Pressure: The Strong Heart Study Hypertension, July 1, 2007; 50(1): 197 - 203. [Abstract] [Full Text] [PDF]
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A. D. Protogerou, M. E. Safar, P. Iaria, H. Safar, K. Le Dudal, J. Filipovsky, O. Henry, P. Ducimetiere, and J. Blacher Diastolic Blood Pressure and Mortality in the Elderly With Cardiovascular Disease Hypertension, July 1, 2007; 50(1): 172 - 180. [Abstract] [Full Text] [PDF]
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R. Sabit, C. E. Bolton, P. H. Edwards, R. J. Pettit, W. D. Evans, C. M. McEniery, I. B. Wilkinson, J. R. Cockcroft, and D. J. Shale Arterial Stiffness and Osteoporosis in Chronic Obstructive Pulmonary Disease Am. J. Respir. Crit. Care Med., June 15, 2007; 175(12): 1259 - 1265. [Abstract] [Full Text] [PDF]
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P. Raggi, A. Bellasi, E. Ferramosca, G. A. Block, and P. Muntner Pulse Wave Velocity Is Inversely Related to Vertebral Bone Density in Hemodialysis Patients Hypertension, June 1, 2007; 49(6): 1278 - 1284. [Abstract] [Full Text] [PDF]
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I. J. Kullo and A. R. Malik Arterial Ultrasonography and Tonometry as Adjuncts to Cardiovascular Risk Stratification J. Am. Coll. Cardiol., April 3, 2007; 49(13): 1413 - 1426. [Abstract] [Full Text] [PDF]
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K. Noma, C. Goto, K. Nishioka, D. Jitsuiki, T. Umemura, K. Ueda, M. Kimura, K. Nakagawa, T. Oshima, K. Chayama, et al. Roles of Rho-Associated Kinase and Oxidative Stress in the Pathogenesis of Aortic Stiffness J. Am. Coll. Cardiol., February 13, 2007; 49(6): 698 - 705. [Abstract] [Full Text] [PDF]
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G. Fernandez-Fresnedo, E. Rodrigo, A. L. M. de Francisco, S. S. de Castro, O. Castaneda, and M. Arias Role of Pulse Pressure on Cardiovascular Risk in Chronic Kidney Disease Patients J. Am. Soc. Nephrol., December 1, 2006; 17(12_suppl_3): S246 - S249. [Abstract] [Full Text] [PDF]
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N.C. Edwards, R.P. Steeds, C.J. Ferro, and J.N. Townend The treatment of coronary artery disease in patients with chronic kidney disease QJM, November 1, 2006; 99(11): 723 - 736. [Abstract] [Full Text] [PDF]
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C Vlachopoulos, K Aznaouridis, and C Stefanadis Clinical appraisal of arterial stiffness: the Argonauts in front of the Golden Fleece Heart, November 1, 2006; 92(11): 1544 - 1550. [Abstract] [Full Text] [PDF]
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A. Covic, N. Mardare, P. Gusbeth-Tatomir, O. Prisada, R. Sascau, and D. J. A. Goldsmith Arterial wave reflections and mortality in haemodialysis patients--only relevant in elderly, cardiovascularly compromised? Nephrol. Dial. Transplant., October 1, 2006; 21(10): 2859 - 2866. [Abstract] [Full Text] [PDF]
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