(Circulation. 2001;103:987.)
© 2001 American Heart Association, Inc.
Clinical Investigation and Reports |
Impact of Aortic Stiffness Attenuation on Survival of Patients in End-Stage Renal Failure
From Service d’Hémodialyse (A.P.G., B.P., S.J.M., G.M.L.), Hôpital F.H. Manhès, Fleury-Mérogis, and Service de Médecine Interne (J.B., M.E.S.), Hôpital Broussais, Paris, France.
Correspondence to Dr G.M. London, Hôpital F.H. Manhès, 8, Grande Rue, Fleury-Mérogis, 91712 Ste-Geneviève-des-Bois, Cedex, France. E-mail glondon{at}club-internet.fr
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Abstract |
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Background—Aortic pulse wave velocity (PWV) is a predictor of mortality in patients with end-stage renal failure (ESRF). The PWV is partly dependent on blood pressure (BP), and a decrease in BP can attenuate the stiffness. Whether the changes in PWV in response to decreases in BP can predict mortality in ESRF patients has never been investigated.
Methods and Results—One hundred fifty ESRF patients (aged 52±16 years) were monitored for 51±38 months. From entry until the end of follow-up, the changes of PWV in response to decreased BP were measured ultrasonographically. BP was controlled by adjustment of "dry weight" and, when necessary, with ACE inhibitors, calcium antagonists, and/or ß-blockers, in combination if necessary. Fifty-nine deaths occurred, including 40 cardiovascular and 19 noncardiovascular events. Cox analyses demonstrated that independent of BP changes, the predictors of all-cause and cardiovascular mortality were as follows: absence of PWV decrease in response to BP decrease, increased left ventricular mass, age, and preexisting cardiovascular disease. Survival was positively associated with ACE inhibitor use. After adjustment for all confounding factors, the risk ratio for the absence of PWV decrease was 2.59 (95% CI 1.51 to 4.43) for all-cause mortality and 2.35 (95% CI 1.23 to 4.41) for cardiovascular mortality. The risk ratio for ACE inhibitor use was 0.19 (95% CI 0.14 to 0.43) for all-cause mortality and 0.18 (95% CI 0.06 to 0.55) for cardiovascular mortality.
Conclusions—These results indicate that in ESRF patients, the insensitivity of PWV to decreased BP is an independent predictor of mortality and that use of ACE inhibitors has a favorable effect on survival that is independent of BP changes.
Key Words: kidney • waves • mortality • hypertension
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Introduction |
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Epidemiological and clinical studies have shown that increased aortic stiffness, determined by the measurement of aortic pulse wave velocity (PWV), is an independent marker of cardiovascular risk in the general population1 and a major contributor to the mortality of end-stage renal failure (ESRF) and that each aortic PWV increase of 1 m/s increased the all-cause mortality by 39%.2 PWV depends on the arterial wall structure and function but is mainly influenced by age-associated alterations and blood pressure (BP).3 4 Clinical studies involving essential hypertension and ESRF patients have shown that ACE inhibitors and calcium antagonists decreased aortic PWV to a large extent in response to BP lowering.5 6 Nevertheless, whether the attenuation of aortic stiffening in response to BP decrease is predictive of clinical outcome has not been established. To determine the impact of the aortic stiffening response to sustained decreased BP on all-cause and cardiovascular mortality, we conducted a prospective study on a cohort of 150 ESRF patients followed for up to 136 months. The results indicate that independent of BP changes, survival was substantially better for those subjects whose aortic PWV declined in response to decreased BP.
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Methods |
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Patients
Patients were eligible for inclusion when (1) they had been on hemodialysis at least for 3 months (67±62 months, mean±SD), (2) they had no clinical cardiovascular disease during the 6 months preceding entry, and (3) they agreed to participate in the follow-up study, which was approved by our Institutional Review Board. The study began in September 1988, recruitment was closed in April 1998, and follow-up ended December 31, 1999. In all, 150 patients fulfilled the entry criteria. Patients who underwent renal transplantation and patients who moved were censored on the day of transplantation or departure. All but 12 patients were white, 60% were males, and 8% had diabetes mellitus. The mean±SD follow-up was 51±38 months (median 46 months, range 4 to 136 months). Data on mortality were obtained for the entire cohort. The mean±SD age of the cohort at inclusion was 52±16 years. During follow-up, all patients were dialyzed by use of the same techniques as previously detailed.1 Patient "dry weight" is defined as the body weight below which a normal albuminemic patient experiences hypotension or muscle cramps and postural hypotension is clinically manifest.
Data Collection
Information compiled from the questionnaire filled
out at inclusion included personal and family histories, smoking
habits, and prior history of cardiovascular disease, including coronary
artery disease, angina pectoris, cardiac insufficiency, peripheral
vascular disease, and cerebrovascular disease. The baseline
measurements were made during the 2 weeks after inclusion, on the
morning before the midweek hemodialysis. Blood chemistry analyses at
baseline and at monthly intervals included blood urea, hemoglobin,
serum albumin, blood lipids, parathyroid hormone, serum calcium,
and serum phosphate. BP was measured after 15 minutes of recumbency in
the arm contralateral to the arteriovenous shunt with a mercury
sphygmomanometer and a cuff of appropriate size. Phases I and V of the
Korotkoff sounds were taken as the systolic BP (SBP) and diastolic BP
(DBP), respectively. The mean BP (MBP) was calculated as follows:
MBP=DBP+[(SBP-DBP)/3]. Five measurements were made at 2-minute
intervals; the last 3 were averaged and considered to be
representative. The heart rate was determined from the 3-lead
orthogonal ECG. Echocardiography was performed by using a
Hewlett-Packard Sonos 100 equipped with a 2.25-MHz probe. Measurements
were made according to the recommendations of the American Society of
Echocardiography.7 Left
ventricular (LV) mass was calculated according to the Penn convention
and expressed as LV mass
index.8
Baseline aortic PWV was determined by using transcutaneous
Doppler flow recordings and the foot-to-foot
method.1 3 Two
simultaneous Doppler flow tracings were taken from the common carotid
artery opposite the side of the arteriovenous fistula and the femoral
artery in the groin. Flow waves were measured with a nondirectional
Doppler unit (SEGA M842, 10 MHz) and recorded on a Gould 8188 recorder
(Gould Electronique) at a speed of 100 or 200 mm/s. The time interval
(t) was measured between the feet of the flow waves and was averaged
over 10 beats. The distance (D) traveled by the flow wave was measured
over the body surface as the distance between the 2 recording sites,
and the distance from the suprasternal notch to the carotid was
subtracted. PWV was calculated as PWV=D/t. The mean±SD intraobserver
repeatability of aortic PWV measurements was
5.8±1%.6 The PWV was
measured at inclusion, after reaching the target BP (see below), and
quarterly thereafter until the end of follow-up. The change of aortic
PWV (
PWV, in meters per second), used as a prognostic variable, was
quantified as follows: PWV=(PWV at inclusion)-(PWV at target
BP).
Therapeutic Strategy
Under physiological conditions, arterial stiffness
indexes are BP dependent, and a pressure decrease could be followed by
a parallel decrease of stiffness. Therefore, to analyze the aortic PWV
response to BP changes, the first step was aimed at obtaining a
long-term and stable normal BP or a 15 mm Hg decrease of SBP.
According to the definition of hypertension proposed in the 1980s,
normotension was defined as predialysis BP <160/90 mm Hg. The first
step for all patients was an attempt to achieve a dry weight. For
ethical reasons, a placebo-controlled study was not feasible, and when
this attempt failed, antihypertensive drug therapy was initiated.
Experimental and clinical studies have shown that ACE inhibitors,
calcium antagonists, and (to a lesser degree) selective or nonselective
ß-blockers decrease arterial
stiffness.5 6 9 10
Patients were randomly assigned to receive the ACE inhibitor
perindopril or the dihydropyridine calcium antagonist nitrendipine. The
pharmacokinetic study in hemodialyzed patients showed that 2 to 4 mg
perindopril given every 48 hours produced a significant long-standing
antihypertensive effect.11
Nitrendipine lowered BP in hemodialyzed patients for 24 hours, and its
pharmacokinetics were unaltered in ESRF
patients.12 13
Perindopril was administered at a dose of 4 to 8 mg every 48 hours, and
nitrendipine was administered at a dose of 10 to 20 mg/d. If the drug
was not well tolerated (intradialytic hypotension, ankle edema, flush,
and/or cough), the drugs were interchanged. If the target BP was still
not achieved, the ß-blocker atenolol was prescribed at a dose of 25
to 50 mg/d. Finally, if this combined bitherapy did not achieve the
target BP, a combination of ACE inhibitor, calcium antagonist, and
ß-blocker was prescribed. The target BP was achieved after 3 to 16
weeks (median 8 weeks).
Analyses
The outcome events studied were all-cause and
cardiovascular mortality. The primary analysis concerned the survival
curves and Cox proportional hazards model. Survival was estimated by
the Kaplan-Meier product-limit method and compared by the Mantel
(log-rank) test. Factors prognostic of survival were identified with
use of the Cox proportional hazards regression model. The assumption of
proportional hazards over time was verified before the analyses and was
met by all covariates. The assumption concerning linearity of
continuous covariates was also verified before analysis. Stepwise,
multivariate Cox modeling was the primary statistical analysis used to
determine the independent relationship of PWV changes and other
baseline characteristics to survival. Each significant predictor
(P<0.05) identified by this
analysis was subsequently tested in a backward selection process with
all candidate variables forced into the model. The following variables
were considered along with sex, age, smoking, and diabetes in the
modeling procedures: PWV; duration of dialysis before inclusion;
baseline, target, and follow-up BP; type of antihypertensive treatment;
preexisting cardiovascular disease; LV mass index; and blood lipids,
Kt/V (product of dialyzer urea clearance [K] and treatment
time [t] normalized to urea distribution volume [V]), and changes
in blood chemistries. Variables were considered to be prognostic when
they were found to be statistically significant in the Cox proportional
hazards regression model
(P<0.05, adjusted for all
variables retained in the final model). Adjusted hazard rate ratios
(RRs) were calculated as the antilogarithm of the ß coefficient of
the Cox proportional hazards regression of the outcome events with all
the prognostic variables entered in the models. The 95% CI for the
adjusted RR estimates were obtained with the following formula:
antilogarithm (ß±1.96SE), where SE is the standard error of ß. To
assess PWV as a prognostic variable test with the use of receiver
operating characteristic (ROC) curves, we calculated sensitivities,
specificities, positive predictive values, and negative predictive
values to predict mortality at different cutoff values. Optimal PWV
cutoff values were defined as the maximization of the sum of
sensitivity and
specificity.14 Data are
expressed as mean±SD, unless otherwise specified. ANOVA was used for
comparison of normally distributed variables. Differences in frequency
were tested by 
2 analysis. Sex (0, male;
1, female), history of cardiovascular disease (0, no; 1, yes), ACE
inhibitor (0, no; 1, yes), ß-blocker (0, no; 1, yes), nitrendipine
(0, no; 1,yes), and PWV (0, negative PWV; 1, positive PWV)
were used as dummy variables. All tests were 2-sided, and analyses were
performed with NCSS 6.0.21 software. Reproducibility of the methods was
defined by the British Standards
Institution.15 A value of
P<0.05 was considered
significant.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Patient Characteristics
The characteristics of the cohort at inclusion are shown in Table 1
. The BP and aortic PWV changes from
inclusion to target BP and at the end of follow-up are reported in
Table 2. Target BP was obtained by adjustment of dry weight
in only 44 (29%) patients; antihypertensive drugs alone or in
combination were prescribed to 106 patients. Among patients receiving
antihypertensive drugs, 49 (46%) took perindopril, 56 (53%) took
atenolol, and 83 (78%) took nitrendipine. The patients received an
average of 1.7±0.7 antihypertensive drugs. At target BP, SBP and DBP
had decreased significantly in the entire cohort
(Table 2). During follow-up, BP remained stable
(Table 2), and at the end of follow-up, 48 (46%) patients
were taking an ACE inhibitor, 50 (47%) were taking a ß-blocker, and
79 (74%) were taking a calcium antagonist. At target BP, the aortic
PWV decreased in 100 patients (-1.32±0.98 m/s) but increased or was
unchanged in 50 patients (0.95±0.91 m/s). After adjustment for age and
prior cardiovascular disease, the PWV was correlated with changes in
SBP (r=0.538,
P<0.0001) but not to the type
of antihypertensive medication (ACE inhibitor -1.02±1.40 m/s,
calcium blocker -0.62±1.66 m/s;
P=NS).
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Outcome and Prognostic Impact of PWV
During the follow-up period, 59 deaths were
recorded. Forty patients died from cardiovascular complications, and 19
died from noncardiovascular events. Absence of PWV decrease (positive
PWV) was a predictor associated with all-cause and cardiovascular
mortality
(Table 3). When in the Cox model the PWV was expressed in
meters per second, the adjusted RR for a PWV decrease of 1 m/s was 0.71
(95% CI 0.60 to 0.86) for all-cause mortality and 0.79 (95% CI 0.69
to 0.93) for cardiovascular mortality. Increased LV mass index had a
negative impact on all-cause and cardiovascular mortality. Age had a
negative impact on overall survival but not on cardiovascular
mortality, which was positively associated with a history of prior
cardiovascular diseases. Use of an ACE inhibitor, either alone or in
combination, had a favorable impact on all-cause and cardiovascular
mortality. The prescription of atenolol or nitrendipine was not
predictive of outcome. The adjusted RRs for baseline SBP and DBP were
not significant; their respective values were 1.1 (95% CI 0.97 to
1.22) and 0.9 (95% CI 0.64 to 1.18) for overall mortality, and they
were similar for cardiovascular mortality (not shown). The adjusted RRs
for SBP and DBP were 0.98 (95% CI 0.79 to 1.17) and 1.15 (95%
CI 0.75 to 1.56), respectively, and were not significant for overall
mortality or cardiovascular mortality. The role of factors such as sex,
smoking, time on dialysis, and blood chemistry abnormalities were not
significant.
Figure 1 shows the ROC curve; the cutoff value for PWV
was 0.04 m/s (ie, 
0). The negative predictive value of PWV was
70% (70% of patients with positive PWV died during follow-up), and
the positive predictive value was 74% (74% of patients with negative
PWV survived during follow-up). The sensitivity of PWV was 56%,
and its specificity was 84%.
Figure 2 shows the probabilities of survival of patients
with negative PWV or positive PWV.
Figure 3 shows the MBP and aortic PWV changes measured
during follow-up of survivors and nonsurvivors. In survivors, the
aortic PWV changes initially paralleled BP changes and remained stable
despite aging. Although BP changes were similar in nonsurvivors, their
aortic PWV steadily increased until the end of
follow-up.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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PWV measurement offers a simple and reproducible evaluation of regional arterial stiffness.1 3 Recent studies have shown that aortic PWV is a marker of cardiovascular risk in essential hypertension2 and an independent predictor of mortality of ESRF patients.1 Arterial stiffness depends on the geometry and structure of the arterial wall and is influenced by BP. Aortic stiffening can be functional, resulting from high BP without structural changes of the artery, and can be reversed with BP lowering.3 4 5 Arterial stiffness may also increase because of disease-induced structural changes of the artery. In the presence of structural changes, the stiffening is less dependent on BP.16 The results of the present study showed that survival of ESRF patients was significantly better for patients whose aortic PWV declined in response to BP lowering. The adjusted RRs for all-cause and cardiovascular mortality in those whose PWV did not decline in response to BP changes were 2.59 (95% CI 1.51 to 4.43) and 2.35 (95% CI 1.23 to 4.51), respectively (P<0.01). The prognostic value of PWV sensitivity to BP lowering on survival was independent of age, BP changes including pulse pressure, and blood chemistry abnormalities. The findings reported in the present study indicate that arterial stiffness is not only a risk factor contributing to the development of cardiovascular disease but also a marker of established, more advanced, less reversible arterial changes. This concept is supported by the loss of aortic PWV sensitivity to BP lowering in nonsurvivors compared with survivors in whom arterial stiffness remained pressure sensitive (Figure 3
). As shown by Cox analysis, the outcome was not
affected by BP changes per se. Lower BPs were observed in patients
regardless of whether their aortic PWV decreased or increased during
the course of the study, and BP changes were similar in nonsurvivors
and survivors, in contrast to their aortic PWV changes
(Figure 3). These data suggest that the presence of an
intrinsic vasculopathy characterized by the loss of sensitivity to BP
and reversibility of aortic stiffness is a major factor contributing to
the mortality of ESRF patients.
The role of BP in predicting the prognosis of hemodialyzed
patients is quite controversial. Charra et
al17 reported more prolonged
survival of patients with an MBP <99 mm Hg than of patients with an
MBP 
99 mm Hg. However, those data were not adjusted for confounders
such as age, sex, or prior history of cardiovascular disease. To the
contrary, Zager et al18
showed that the impact of BP on cardiovascular mortality was modest,
and recent studies on ESRF patients showed that low DBP was associated
with higher
mortality.1 19 The
data in the literature indicate that the majority of hemodialyzed
patients have DBP within the normal range and exhibit systolic
hypertension with widely ranging pulse
pressures.20 Increased pulse
pressure is a cardiovascular risk factor in the general
population.21 22
The wide range of pulse pressures in ESRF patients is principally the
consequence of arterial
stiffening23 and, as such, is
a marker of underlying arterial abnormalities. After adjustment for
arterial stiffness, it was found not to be an independent risk factor
in the present population
In agreement with data published on ESRF patients, age was
the most significant prognostic factor for all-cause mortality but not
for cardiovascular mortality.1
The positive history of prior cardiovascular disease was the strongest
independent predictor of cardiovascular mortality. In agreement with
published data, the presence of LV hypertrophy was also an independent
predictor of all-cause mortality, but it was more significantly a
predictor of cardiovascular
mortality24 25
(Table 3).
In agreement with Salem and
Bower,26 the present results
suggest that antihypertensive treatment per se has a favorable effect.
As our results show, prolonged survival seems to more closely reflect
the use of an ACE inhibitor than the other drugs or the number of drugs
per se. The use of ß-blockers and/or dihydropyridine calcium blockers
had no direct relationship with the outcome. The relationship between
survival and perindopril seems to be one of the strongest statistically
(Table 3) but must be interpreted cautiously, inasmuch as
the present study was not designed to compare the effect of different
antihypertensive drugs on survival as such, and the regiment at target
BP was influenced by their tolerance and the optimal effect on BP.
Several studies on high-risk populations have shown that ACE inhibitors
have a favorable prognostic effect, reducing death rates and
cardiovascular
complications.27 28
The present findings suggest that a similar favorable effect of ACE
inhibitors could be observed in ESRF patients, but a specifically
designed, prospective, therapeutic trial is needed to confirm them. The
influence of the ACE inhibitor did not reflect a difference in BP
control or a direct and better effect on aortic stiffness. A blinded
and controlled study on ESRF patients showed that perindopril induced a
pressure-independent decrease of LV hypertrophy that was due to
reduction of the LV diameter and cavity volume, which are independent
predictors of survival in these
patients.29
In conclusion, the present data indicate that persistence of aortic stiffness reversibility (or sensitivity) in response to BP lowering had a beneficial and BP-independent impact on the survival of ESRF patients, suggesting that the presence of more advanced vascular lesions characterized by the loss of BP reversibility of aortic stiffness is a major factor contributing to the mortality of ESRF patients. This finding emphasizes the need to test other alternative therapies in ESRF patients in whom antihypertensive drugs are unable to alter aortic PWV. The second finding of the present study suggests that ACE inhibitors have a favorable effect on the patient’s outcome. However, this observation needs confirmation in a specifically designed, prospective, therapeutic trial. Finally, the extrapolation of the conclusions based on the present study may be limited because of the particular clinical characteristics of ESRF patients, who are at very high risk of cardiovascular complications; thus, further studies are needed to extend these findings to other populations.
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Acknowledgments |
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This work was supported by Groupe d’Etude de Pathophysiologie de l’Insuffisance Renale, the Société Française d’Hypertension Artérielle, and the Groupe de Pharmacologie Cardiovasculaire.
Received August 8, 2000; revision received October 13, 2000; accepted October 16, 2000.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
|---|
1. Blacher J, Guérin AP, Pannier B, et al. Impact of aortic stiffness on survival in end-stage renal disease. Circulation. 1999;99:2434–2439.
2.
Blacher J,
Asmar S, Djane S, et al. Aortic pulse wave velocity as a marker of
cardiovascular risk in hypertensive patients.
Hypertension. 1999;33:1111–1117.
3.
Avolio AP,
Chen S, Wang R, et al. Effects of aging on changing arterial compliance
and left ventricular load in a northern Chinese urban community.
Circulation. 1983;68:50–58.
4. Nichols WW, O’Rourke MF. Vascular impedance. In: McDonald’s Blood Flow in Arteries: Theoretical, Experimental and Clinical Principles. 4th ed. London, UK: Arnold; 1998:243–283.
5.
Asmar RG,
Pannier B, Santoni JP, et al. Reversion of cardiac hypertrophy and
reduced arterial compliance after converting enzyme inhibition in
essential hypertension.
Circulation. 1988;78:941–950.
6.
London GM,
Marchais SJ, Guérin AP, et al. Salt and water retention and calcium
blockade in uremia.
Circulation. 1990;82:105–113.
7.
Sahn DJ, De
Maria A, Kisslo J, et al. Recommendations regarding quantitation in
M-mode echocardiographic measurements.
Circulation. 1978;58:1072–1083.
8.
Devereux RB,
Reichek N. Echocardiographic determination of left ventricular mass in
man: anatomic validation of the method.
Circulation. 1977;55:613–618.
9. Simon AC, Levenson J, Bouthier JD, et al. Effects of chronic administration of enalapril and propranolol on the large arteries in essential hypertension. J Cardiovasc Pharmacol. 1985;7:856–871.[Medline] [Order article via Infotrieve]
10. DeLuca N, Rosiello G, Crispino M. Effects of chronic antihypertensive treatment with ketanserin versus metoprolol on blood pressure and large arteries compliance in humans: a cross-over double-blind study. J Clin Pharmacol. 1988;28:332–338.[Abstract]
11. Guérin A, Resplandy G, Marchais S, et al. The effect of haemodialysis on the pharmacokinetics of perindoprilat after long-term perindopril. Eur J Clin Pharmacol. 1993;44:183–187.[Medline] [Order article via Infotrieve]
12. Aronoff GR. Pharmacokinetics of nitrendipine in patients with renal failure: comparison to normal subjects. J Cardiovasc Pharmacol. 1984;6:974–976.
13. Wandel E, Weber M, Zschiedrich H, et al. Single-dose effect of nitrendipine on blood pressure of hemodialysis patients with hypertension. J Cardiovasc Pharmacol. 1987;9(suppl 9):295–299.
14.
Hanley JA,
McNeil BJ. The meaning and use of the area under a receiver operating
characteristic (ROC) curve.
Radiology. 1982;143:29–36.
15. British Standards Institution. Precision of Test Methods: Guide for the Determination of Reproducibility for a Standard Test Method. London, England: British Standards Institution; 1979. BS 5497, pt 1.
16.
Mourad JJ,
Girerd X, Boutouyrie P, et al. Increased stiffness of radial artery
wall material in end-stage renal disease.
Hypertension. 1997;30:1425–1430.
17. Charra B, Calemard E, Ruffet M, et al. Survival as an index of adequacy of dialysis. Kidney Int. 1992;41:1286–1291.[Medline] [Order article via Infotrieve]
18. Zager PH, Nikolic J, Brown RH, et al. "U"-curve association of blood pressure and mortality in hemodialysis patients. Kidney Int. 1998;54:561–569.[Medline] [Order article via Infotrieve]
19. Iseki K, Miyasato F, Tokuyama K, et al. Low diastolic blood pressure, hypoalbuminemia, and risk of death in a cohort of chronic hemodialysis patients. Kidney Int. 1997;51:1212–1217.[Medline] [Order article via Infotrieve]
20. London GM, Guérin AP, Marchais SJ. Pressure-overload cardiomyopathy in end-stage renal disease. Curr Opin Nephrol Hypertens. 1999;8:179–186.
21.
Darné B,
Girerd X, Safar M, et al. Pulsatile versus steady component of blood
pressure: a cross-sectional and prospective analysis on cardiovascular
mortality. Hypertension. 1989;13:392–400.
22.
Madhavan S,
Ooi WL, Cohen H, et al. Relation of pulse pressure and blood pressure
reduction to the incidence of myocardial infarction.
Hypertension. 1994;23:395–401.
23.
London
GM, Guérin AP, Pannier B, et al. Increased systolic pressure in
chronic uremia: role of arterial wave reflections.
Hypertension. 1992;20:10–19.
24. Silberberg JS, Barre PE, Prichard SS, et al. Impact of left ventricular hypertrophy on survival in end-stage renal disease. Kidney Int. 1989;36:286–290.[Medline] [Order article via Infotrieve]
25.
Parfrey PS,
Foley RN, Harnett JD, et al. Outcome and risk factors for left
ventricular disorders in chronic uremia.
Nephrol Dial Transplant. 1996;11:1277–1285.
26. Salem MM, Bower J. Hypertension in the hemodialysis population: any relation to one-year survival? Am J Kidney Dis. 1996;28:737–740.[Medline] [Order article via Infotrieve]
27. Konstam MA, Krononberg MW, Rousseau MF, et al. Effects of the angiotensin converting enzyme inhibitor enalapril on the long-term progression of left ventricular dilatation in patients with asymptomatic systolic dysfunction. Circulation. 1993;88(pt 1):2277–2283.
28.
The Heart
Outcome Prevention Evaluation Study Investigators. Effects of an
angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular
events in high-risk patients. N Engl
J Med. 2000;342:145–153.
29.
London GM,
Pannier B, Guérin AP, et al. Cardiac hypertrophy, aortic compliance,
peripheral resistance, and wave reflection in end-stage renal disease:
comparative effects of ACE inhibition and calcium channel blockade.
Circulation. 1994;90:2786–2796.
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 A. Protogerou, J. Blacher, G. S. Stergiou, A. Achimastos, and M. E. Safar Blood Pressure Response Under Chronic Antihypertensive Drug Therapy The Role of Aortic Stiffness in the REASON (Preterax in Regression of Arterial Stiffness in a Controlled Double-Blind) Study. J. Am. Coll. Cardiol., February 3, 2009; 53(5): 445 - 451. [Abstract] [Full Text] [PDF]
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|
 |
|
 J. B. Cannata-Andia and M. Naves-Diaz Phosphorus and Survival: Key Questions That Need Answers J. Am. Soc. Nephrol., February 1, 2009; 20(2): 234 - 236. [Full Text] [PDF]
|
|
|
|
 |
|
 D J BOWDEN, S R I AITKEN, I B WILKINSON, and A K DIXON Interobserver variability in the measurement of abdominal aortic calcification using unenhanced CT Br. J. Radiol., January 1, 2009; 82(973): 69 - 72. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K. Fox Benefits of perindopril all along the cardiovascular continuum: the level of evidence Eur. Heart J. Suppl., September 1, 2008; 10(suppl_G): G4 - G12. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. Ferrari Treatment with angiotensin-converting enzyme inhibitors: insight into perindopril cardiovascular protection Eur. Heart J. Suppl., September 1, 2008; 10(suppl_G): G13 - G20. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Danchin Which patients would benefit the most from the perindopril-amlodipine combination? Eur. Heart J. Suppl., September 1, 2008; 10(suppl_G): G29 - G35. [Abstract] [Full Text] [PDF]
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|
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 |
|
 N C Edwards, C J Ferro, J N Townend, and R P Steeds Aortic distensibility and arterial-ventricular coupling in early chronic kidney disease: a pattern resembling heart failure with preserved ejection fraction Heart, August 1, 2008; 94(8): 1038 - 1043. [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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|
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]
|
|
|
|
|
|
M. E. Safar Review: Pulse pressure, arterial stiffness and wave reflections (augmentation index) as cardiovascular risk factors in hypertension Therapeutic Advances in Cardiovascular Disease, February 1, 2008; 2(1): 13 - 24. [Abstract] [PDF]
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|
|
 |
|
 R. Agarwal and R. P. Light Arterial stiffness and interdialytic weight gain influence ambulatory blood pressure patterns in hemodialysis patients Am J Physiol Renal Physiol, February 1, 2008; 294(2): F303 - F308. [Abstract] [Full Text] [PDF]
|
|
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|
|
|
A. Qasem and A. Avolio Determination of Aortic Pulse Wave Velocity From Waveform Decomposition of the Central Aortic Pressure Pulse Hypertension, February 1, 2008; 51(2): 188 - 195. [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]
|
|
|
|
 |
|
 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]
|
|
|
|
|
|
D. L. Andress Bone and Mineral Guidelines for Patients with Chronic Kidney Disease: A Call for Revision Clin. J. Am. Soc. Nephrol., January 1, 2008; 3(1): 179 - 183. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. S. Borer Angiotensin-converting enzyme inhibition: a landmark advance in treatment for cardiovascular diseases Eur. Heart J. Suppl., September 1, 2007; 9(suppl_E): E2 - E9. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. Fox Contribution of perindopril to cardiology: 20 years of success Eur. Heart J. Suppl., September 1, 2007; 9(suppl_E): E10 - E19. [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]
|
|
|
|
|
|
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]
|
|
|
|
|
|
M. E. Safar Mechanism(s) of Systolic Blood Pressure Reduction and Drug Therapy in Hypertension Hypertension, July 1, 2007; 50(1): 167 - 171. [Full Text] [PDF]
|
|
|
|
|
|
M. M.H. Hermans, R. Henry, J. M. Dekker, J. P. Kooman, P. J. Kostense, G. Nijpels, R. J. Heine, and C. D.A. Stehouwer Estimated Glomerular Filtration Rate and Urinary Albumin Excretion Are Independently Associated with Greater Arterial Stiffness: The Hoorn Study J. Am. Soc. Nephrol., June 1, 2007; 18(6): 1942 - 1952. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. R. Khoshdel, S. L. Carney, B. R. Nair, and A. Gillies Better Management of Cardiovascular Diseases by Pulse Wave Velocity: Combining Clinical Practice with Clinical Research using Evidence-Based Medicine Clin. Med. Res., March 1, 2007; 5(1): 45 - 52. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Aronson, M. L. Fontes, Y. Miao, D. T. Mangano, and for the Investigators of the Multicenter Study of Risk Index for Perioperative Renal Dysfunction/Failure: Critical Dependence on Pulse Pressure Hypertension Circulation, February 13, 2007; 115(6): 733 - 742. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 F. Fantin, A. Mattocks, C. J. Bulpitt, W. Banya, and C. Rajkumar Is augmentation index a good measure of vascular stiffness in the elderly? Age Ageing, January 1, 2007; 36(1): 43 - 48. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. Laurent, J. Cockcroft, L. Van Bortel, P. Boutouyrie, C. Giannattasio, D. Hayoz, B. Pannier, C. Vlachopoulos, I. Wilkinson, H. Struijker-Boudier, et al. Expert consensus document on arterial stiffness: methodological issues and clinical applications Eur. Heart J., November 1, 2006; 27(21): 2588 - 2605. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 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]
|
|
|
|
|
|
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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N. Iwai, K. Kajimoto, Y. Kokubo, and H. Tomoike Extensive Genetic Analysis of 10 Candidate Genes for Hypertension in Japanese Hypertension, November 1, 2006; 48(5): 901 - 907. [Abstract] [Full Text] [PDF]
|
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|
S. Rajagopalan, S. Dellegrottaglie, A. L. Furniss, B. W. Gillespie, S. Satayathum, N. Lameire, A. Saito, T. Akiba, M. Jadoul, N. Ginsberg, et al. Peripheral Arterial Disease in Patients With End-Stage Renal Disease: Observations From the Dialysis Outcomes and Practice Patterns Study (DOPPS) Circulation, October 31, 2006; 114(18): 1914 - 1922. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. Banerjee, S. Brincat, H. Gregson, G. Contreras, C. Streather, D. Oliveira, and S. Nelson Pulse pressure and inhibition of renin-angiotensin system in chronic kidney disease Nephrol. Dial. Transplant., April 1, 2006; 21(4): 975 - 978. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Dhaun, J. Goddard, and DavidJ. Webb The Endothelin System and Its Antagonism in Chronic Kidney Disease J. Am. Soc. Nephrol., April 1, 2006; 17(4): 943 - 955. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Benetos and P. Lacolley From 24-Hour Blood Pressure Measurements to Arterial Stiffness: A Valid Short Cut? Hypertension, March 1, 2006; 47(3): 327 - 328. [Full Text] [PDF]
|
|
|
|
|
|
A P Patrianakos, D N Karakitsos, E de Groot, F I Parthenakis, E K Daphnis, and P E Vardas Alteration of proximal aorta biophysical properties in patients with end stage renal disease Heart, February 1, 2006; 92(2): 228 - 232. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Weber, J. Auer, M. F. O'Rourke, E. Kvas, E. Lassnig, G. Lamm, N. Stark, M. Rammer, and B. Eber Increased arterial wave reflections predict severe cardiovascular events in patients undergoing percutaneous coronary interventions Eur. Heart J., December 2, 2005; 26(24): 2657 - 2663. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. M. Mitsnefes, T. R. Kimball, J. Kartal, S. A. Witt, B. J. Glascock, P. R. Khoury, and S. R. Daniels Cardiac and Vascular Adaptation in Pediatric Patients with Chronic Kidney Disease: Role of Calcium-Phosphorus Metabolism J. Am. Soc. Nephrol., September 1, 2005; 16(9): 2796 - 2803. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. F. O'Rourke and M. E. Safar Relationship Between Aortic Stiffening and Microvascular Disease in Brain and Kidney: Cause and Logic of Therapy Hypertension, July 1, 2005; 46(1): 200 - 204. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. A. Ahimastos, A. K. Natoli, A. Lawler, P. A. Blombery, and B. A. Kingwell Ramipril Reduces Large-Artery Stiffness in Peripheral Arterial Disease and Promotes Elastogenic Remodeling in Cell Culture Hypertension, June 1, 2005; 45(6): 1194 - 1199. [Abstract] [Full Text] [PDF]
|
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|
|
|
T. Takenaka and H. Suzuki New strategy to attenuate pulse wave velocity in haemodialysis patients Nephrol. Dial. Transplant., April 1, 2005; 20(4): 811 - 816. [Abstract] [Full Text] [PDF]
|
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|
|
|
|
B. Pannier, A. P. Guerin, S. J. Marchais, M. E. Safar, and G. M. London Stiffness of Capacitive and Conduit Arteries: Prognostic Significance for End-Stage Renal Disease Patients Hypertension, April 1, 2005; 45(4): 592 - 596. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Mustata, C. Chan, V. Lai, and J. A. Miller Impact of an Exercise Program on Arterial Stiffness and Insulin Resistance in Hemodialysis Patients J. Am. Soc. Nephrol., October 1, 2004; 15(10): 2713 - 2718. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. Mahmud and J. Feely Review: Arterial stiffness and the renin-angiotensin-aldosterone system Journal of Renin-Angiotensin-Aldosterone System, September 1, 2004; 5(3): 102 - 108. [Abstract] [PDF]
|
|
|
|
|
|
C. M. McEniery, M. Schmitt, A. Qasem, D. J. Webb, A. P. Avolio, I. B. Wilkinson, and J. R. Cockcroft Nebivolol Increases Arterial Distensibility In Vivo Hypertension, September 1, 2004; 44(3): 305 - 310. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
I. B. Wilkinson, S. S. Franklin, and J. R. Cockcroft Nitric Oxide and the Regulation of Large Artery Stiffness: From Physiology to Pharmacology Hypertension, August 1, 2004; 44(2): 112 - 116. [Full Text] [PDF]
|
|
|
|
|
|
M. M. Mitsnefes, T. R. Kimball, S. A. Witt, B. J. Glascock, P. R. Khoury, and S. R. Daniels Abnormal Carotid Artery Structure and Function in Children and Adolescents With Successful Renal Transplantation Circulation, July 6, 2004; 110(1): 97 - 101. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Locatelli, A. Covic, C. Chazot, K. Leunissen, J. Luno, and M. Yaqoob Hypertension and cardiovascular risk assessment in dialysis patients Nephrol. Dial. Transplant., May 1, 2004; 19(5): 1058 - 1068. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
L. A. Stevens, O. Djurdjev, S. Cardew, E. C. Cameron, and A. Levin Calcium, Phosphate, and Parathyroid Hormone Levels in Combination and as a Function of Dialysis Duration Predict Mortality: Evidence for the Complexity of the Association between Mineral Metabolism and Outcomes J. Am. Soc. Nephrol., March 1, 2004; 15(3): 770 - 779. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. E. Safar, G. M London, and G. E. Plante Arterial Stiffness and Kidney Function Hypertension, February 1, 2004; 43(2): 163 - 168. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. M. London, R. G. Asmar, M. F. O'Rourke, M. E. Safar, and REASON Project Investigators Mechanism(s) of selective systolic blood pressure reduction after a low-dose combination of perindopril/Indapamide in hypertensive subjects: comparison with atenolol J. Am. Coll. Cardiol., January 7, 2004; 43(1): 92 - 99. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. J. Sarnak, A. S. Levey, A. C. Schoolwerth, J. Coresh, B. Culleton, L. L. Hamm, P. A. McCullough, B. L. Kasiske, E. Kelepouris, M. J. Klag, et al. Kidney Disease as a Risk Factor for Development of Cardiovascular Disease: A Statement From the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention Hypertension, November 1, 2003; 42(5): 1050 - 1065. [Full Text] [PDF]
|
|
|
|
|
|
M. J. Sarnak, A. S. Levey, A. C. Schoolwerth, J. Coresh, B. Culleton, L. L. Hamm, P. A. McCullough, B. L. Kasiske, E. Kelepouris, M. J. Klag, et al. Kidney Disease as a Risk Factor for Development of Cardiovascular Disease: A Statement From the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention Circulation, October 28, 2003; 108(17): 2154 - 2169. [Full Text] [PDF]
|
|
|
|
|
|
C. M. Giachelli Vascular Calcification: In Vitro Evidence for the Role of Inorganic Phosphate J. Am. Soc. Nephrol., September 1, 2003; 14(90004): S300 - 304. [Abstract] [Full Text]
|
|
|
|
|
|
B. Pannier, A.P. Guerin, S.J. Marchias, and G.M. London Benefits from angiotensin-converting enzyme inhibition in patients with renal failure: latest results Eur. Heart J. Suppl., July 1, 2003; 5(suppl_E): E18 - E22. [Abstract] [PDF]
|
|
|
|
 |
|
 E. Suzuki, K. Egawa, Y. Nishio, H. Maegawa, M. Tsuchiya, M. Haneda, H. Yasuda, S. Morikawa, T. Inubushi, and A. Kashiwagi Prevalence and Major Risk Factors of Reduced Flow Volume in Lower Extremities With Normal Ankle-Brachial Index in Japanese Patients With Type 2 Diabetes Diabetes Care, June 1, 2003; 26(6): 1764 - 1769. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. J. Oliver and D. J. Webb Noninvasive Assessment of Arterial Stiffness and Risk of Atherosclerotic Events Arterioscler Thromb Vasc Biol, April 1, 2003; 23(4): 554 - 566. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Bonapace, A. Rossi, M. Cicoira, L. Franceschini, G. Golia, L. Zanolla, P. Marino, and P. Zardini Aortic Distensibility Independently Affects Exercise Tolerance in Patients With Dilated Cardiomyopathy Circulation, April 1, 2003; 107(12): 1603 - 1608. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
E. Lurbe, M. I. Torro, E. Carvajal, V. Alvarez, and J. Redon Birth Weight Impacts on Wave Reflections in Children and Adolescents Hypertension, March 1, 2003; 41(3): 646 - 650. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
D. A Sica and T. W. Gehr Review: The pharmacokinetics and pharmacodynamics of angiotensin-receptor blockers in end-stage renal disease Journal of Renin-Angiotensin-Aldosterone System, December 1, 2002; 3(4): 247 - 254. [Abstract] [PDF]
|
|
|
|
|
|
J. W Groothoff, M. P Gruppen, M. Offringa, E. de Groot, W. Stok, W. J. Bos, J. C. Davin, M. R Lilien, N. C. van de Kar, E. D Wolff, et al. Increased Arterial Stiffness in Young Adults with End-Stage Renal Disease since Childhood J. Am. Soc. Nephrol., December 1, 2002; 13(12): 2953 - 2961. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. S. Hayward, A. P. Avolio, M. F. O'Rourke, P. Lantelme, C. Mestre, M. Lievre, A. Gressard, and H. Milon Arterial Pulse Wave Velocity and Heart Rate * Response: Heart Rate and Pulse Wave Velocity Hypertension, December 1, 2002; e9(6): . [Full Text] [PDF]
|
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|
|
|
G. M. London, S. J. Marchais, A. P. Guerin, F. Metivier, and H. Adda Arterial structure and function in end-stage renal disease Nephrol. Dial. Transplant., October 1, 2002; 17(10): 1713 - 1724. [Full Text] [PDF]
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|
|
|
A. Ichihara, M. Hayashi, M. Ryuzaki, M. Handa, T. Furukawa, and T. Saruta Fluvastatin prevents development of arterial stiffness in haemodialysis patients with type 2 diabetes mellitus Nephrol. Dial. Transplant., August 1, 2002; 17(8): 1513 - 1517. [Abstract] [Full Text] [PDF]
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|
Y. T. van der Schouw, A. Pijpe, C. E.I. Lebrun, M. L. Bots, P. H.M. Peeters, W. A. van Staveren, S. W.J. Lamberts, and D. E. Grobbee Higher Usual Dietary Intake of Phytoestrogens Is Associated With Lower Aortic Stiffness in Postmenopausal Women Arterioscler Thromb Vasc Biol, August 1, 2002; 22(8): 1316 - 1322. [Abstract] [Full Text] [PDF]
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|
|
|
G. F. Mitchell, J. L. Izzo Jr, Y. Lacourciere, J.-P. Ouellet, J. Neutel, C. Qian, L. J. Kerwin, A. J. Block, and M. A. Pfeffer Omapatrilat Reduces Pulse Pressure and Proximal Aortic Stiffness in Patients With Systolic Hypertension: Results of the Conduit Hemodynamics of Omapatrilat International Research Study Circulation, June 25, 2002; 105(25): 2955 - 2961. [Abstract] [Full Text] [PDF]
|
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|
|
|
D. Goldsmith, R. MacGinley, A. Smith, and A. Covic How important and how treatable is vascular stiffness as a cardiovascular risk factor in renal failure? Nephrol. Dial. Transplant., June 1, 2002; 17(6): 965 - 969. [Full Text] [PDF]
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|
|
P. Lantelme, C. Mestre, M. Lievre, A. Gressard, and H. Milon Heart Rate: An Important Confounder of Pulse Wave Velocity Assessment Hypertension, June 1, 2002; 39(6): 1083 - 1087. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Giannattasio, F. Achilli, M. Failla, A. Capra, A. Vincenzi, F. Valagussa, and G. Mancia Radial, carotid and aortic distensibility in congestive heart failure: effects of high-dose angiotensin-converting enzyme inhibitor or low-dose association with angiotensin type 1 receptor blockade J. Am. Coll. Cardiol., April 17, 2002; 39(8): 1275 - 1282. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. J. G. De Lima, M. L. C. Vieira, L. F. Viviani, C. J. Medeiros, L. E. Ianhez, L. Kopel, J. L. de Andrade, E. M. Krieger, and S. G. Lage Long-term impact of renal transplantation on carotid artery properties and on ventricular hypertrophy in end-stage renal failure patients Nephrol. Dial. Transplant., April 1, 2002; 17(4): 645 - 651. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. Blacher and M. Safar Specific aspects of high blood pressure in the elderly Journal of Renin-Angiotensin-Aldosterone System, March 1, 2002; 3(1_suppl): S10 - S15. [PDF]
|
|
|
|
|
|
S.E. Greenwald Pulse pressure and arterial elasticity QJM, February 1, 2002; 95(2): 107 - 112. [Full Text] [PDF]
|
|
|
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|
|
S. Meaume, A. Benetos, O.F. Henry, A. Rudnichi, and M.E. Safar Aortic Pulse Wave Velocity Predicts Cardiovascular Mortality in Subjects >70 Years of Age Arterioscler Thromb Vasc Biol, December 1, 2001; 21(12): 2046 - 2050. [Abstract] [Full Text] [PDF]
|
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|
|
G. M. London, B. Pannier, A. P. Guerin, J. Blacher, S. J. Marchais, B. Darne, F. Metivier, H. Adda, and M. E. Safar Alterations of Left Ventricular Hypertrophy in and Survival of Patients Receiving Hemodialysis: Follow-up of an Interventional Study J. Am. Soc. Nephrol., December 1, 2001; 12(12): 2759 - 2767. [Abstract] [Full Text] [PDF]
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T. SHOJI, M. EMOTO, K. SHINOHARA, R. KAKIYA, Y. TSUJIMOTO, H. KISHIMOTO, E. ISHIMURA, T. TABATA, and Y. NISHIZAWA Diabetes Mellitus, Aortic Stiffness, and Cardiovascular Mortality in End-Stage Renal Disease J. Am. Soc. Nephrol., October 1, 2001; 12(10): 2117 - 2124. [Abstract] [Full Text] [PDF]
|
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|
|
R. G. Asmar, G. M. London, M. E. O'Rourke, and M. E. Safar Improvement in Blood Pressure, Arterial Stiffness and Wave Reflections With a Very-Low-Dose Perindopril/Indapamide Combination in Hypertensive Patient: A Comparison With Atenolol Hypertension, October 1, 2001; 38(4): 922 - 926. [Abstract] [Full Text] [PDF]
|
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|
J. Blacher, A. P. Guerin, B. Pannier, S. J. Marchais, and G. M. London Arterial Calcifications, Arterial Stiffness, and Cardiovascular Risk in End-Stage Renal Disease Hypertension, October 1, 2001; 38(4): 938 - 942. [Abstract] [Full Text] [PDF]
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