Determinants of Accelerated Progression of Arterial Stiffness in Normotensive Subjects
and in Treated Hypertensive Subjects Over a 6-Year Period
Athanase Benetos, Chris Adamopoulos, Jeanne-Marie Bureau, Mohamed Temmar, Carlos Labat,
Kathryn Bean, Frédérique Thomas, Bruno Pannier, Roland Asmar, Mahmoud Zureik, Michel
Safar and Louis Guize
Circulation. 2002;105:1202-1207; originally published online February 18, 2002;
doi: 10.1161/hc1002.105135
Circulation is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
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Determinants of Accelerated Progression of Arterial
Stiffness in Normotensive Subjects and in Treated
Hypertensive Subjects Over a 6-Year Period
Athanase Benetos, MD, PhD; Chris Adamopoulos, MD; Jeanne-Marie Bureau, MD;
Mohamed Temmar, MD; Carlos Labat, BSc; Kathryn Bean, MA, MPH; Frédérique Thomas, PhD;
Bruno Pannier, MD; Roland Asmar, MD; Mahmoud Zureik, MD, PhD;
Michel Safar, MD; Louis Guize, MD
Background—Elastic artery stiffness, a result of arterial aging, is an independent indicator of cardiovascular risk. The aim
of the present longitudinal study was to compare the progression of aortic stiffness over a 6-year period in treated
hypertensive subjects and normotensive subjects, and to evaluate the determinants of this progression.
Methods and Results—Data for the present analysis were gathered from 483 subjects who had 2 health checkups at the
Centre d’Investigations Préventives et Cliniques, the first one in 1992–1993 and the second one in 1998 –1999.
Carotid-femoral pulse wave velocity (PWV) was used to evaluate aortic stiffness in 187 hypertensive subjects who were
under treatment at the time of the first visit and throughout the follow-up period, and in 296 subjects who were classified
as normotensive during the first visit and who remained treatment-free throughout the follow-up period. In both
populations, PWV progression was higher in older subjects. Annual rates of progression in PWV in treated
hypertensives were significantly higher than in normotensives. Only treated hypertensives with well-controlled blood
pressure levels at the time of both visits had a PWV progression similar to that of normotensives. In treated
hypertensives, high heart rate and high creatinine during the first visit were associated with an accelerated progression
in PWV.
Conclusions—The presence of high blood pressure, high heart rate, and high serum creatinine were the major determinants
of accelerated progression of aortic stiffness in treated hypertensives. This is the first longitudinal study to evaluate the
determinants of arterial aging over an extended period of time. (Circulation. 2002;105:1202-1207.)
Key Words: aging 䡲 heart rate 䡲 elasticity 䡲 hypertension
E
lastic artery stiffness, resulting in high pulse pressure
(PP) and accelerated pulse wave velocity (PWV), greatly
increases with age and could be an independent cardiovascular risk factor.1– 4 The effects of aging are different on
proximal, predominantly elastic arteries compared with distal, predominantly muscular arteries.5–7 Central arteries
stiffen progressively with age, whereas stiffness of muscular
arteries changes little with age.
Several cross-sectional studies have shown that in addition
to age, several other environmental and genetic factors can
influence arterial stiffness.5,7–9 Avolio et al7 showed that high
salt intake could have an independent effect on elastic artery
properties contributing to increased aortic stiffness with age.
Among cardiovascular risk factors, increase in blood pressure
is associated with increased stiffness, and because of this
hypertensives are thought to have accelerated arterial aging.10
Among the other cardiovascular risk factors, the presence of
dyslipidemia,11 diabetes,12 high heart rate (HR),13 and tobacco smoking14 are often associated with increased stiffness,
but the impact of these risk factors in the development of
arterial stiffness remains unclear. These observations are
based on short-term pharmacological studies and on crosssectional observational studies. The role of risk factors,
especially hypertension, on the long-term progression of
arterial stiffness has not yet been evaluated.
The aim of the present longitudinal study was to evaluate
the determinants of PWV progression over a 6-year period in
treated hypertensive subjects and in normotensive subjects.
Methods
Population
Subjects were examined at the Center d’Investigations Préventives et
Cliniques (the IPC Center). This medical center, which is subsidized
Received November 6, 2001; revision received December 28, 2001; accepted January 2, 2002.
From the Centre d’Investigations Préventives et Cliniques (A.B., C.A., J.-M.B., M.T., K.B., F.T., L.G.), Paris; Institut National de la Santé et de la
Recherche Médicale U258 (A.B., C.L., M.Z.), Villejuif; Hôpital Manhès (B.P.), Fleury Merogis; Institut Cardiovasculaire (R.A.), Paris; and Hôpital
Broussais (M.S.), Paris, France.
Correspondence to Athanase Benetos MD, PhD, Centre d’Investigations Préventives et Cliniques (IPC), 6-14, rue la Pérouse, 75116 Paris, France.
E-mail benetos@ipc.asso.fr
© 2002 American Heart Association, Inc.
Circulation is available at http://www.circulationaha.org
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DOI: 10.1161/hc1002.105135
Benetos et al
by the French national health care system (Sécurité Sociale–Caisse
Nationale d’Assurance Maladie), provides all working and retired
persons and their families with a free medical examination every 5
years. From June 1992 through April 1993, subjects aged 18 years or
more who came to the IPC Center for a medical examination were
invited to participate in a study for an evaluation of carotid-femoral
PWV. Four subjects were recruited on a daily basis and included the
following: the first 2 normotensive subjects of the day (systolic blood
pressure [SBP] ⬍140 and diastolic blood pressure [DBP]
⬍90 mm Hg), the first subject with high blood pressure (ⱖ140/
90 mm Hg) and without any antihypertensive drug treatment, and the
first subject with antihypertensive treatment. Six years later, we
invited subjects still living in the Paris area (n⫽1080) to undergo the
same clinical, biological, and arterial examinations. In response to
this invitation, 675 subjects (63% of the invited subjects) had their
second visit during the period of November 1998 through October
1999. According to the classification used in 1992–1993, 325 of the
patients who had the second examination were initially normotensives, 153 were initially untreated hypertensives, and 197 were
treated hypertensives. At the time of the first examination, there were
no significant differences in cardiovascular risk factors between
subjects who participated in the second survey and those who did
not. Because the aim of this study was to evaluate the progression in
arterial stiffness in treated hypertensives in comparison with normotensive subjects, data concerning untreated hypertensive subjects at
the time of the first visit were not included in the present analyses.
The ethics committee of Cochin Hospital approved the study
protocol, and written informed consent was obtained from all study
participants.
Clinical Investigations
PWV measurements were taken under the same conditions during
both examinations, including a constant room temperature of 19°C to
21°C. Two pressure waves were recorded transcutaneously at the
base of the neck for the right common carotid artery and over the
right femoral artery. PWV was determined as the foot-to-foot
velocity. Pulse transit time was determined as the average of 10
consecutive beats. The distance traveled by the pulse wave was
measured over the body surface as the distance between the 2
recording sites. Aortic PWV was calculated as the ratio of distance
to transit time. During the 1992–1993 examination, PWV was
calculated manually, whereas during the 1998 –1999 examination, an
automatic device was used (Complior, Colson). The validation of
this automatic method and its reproducibility have been previously
published.15
Supine blood pressure was measured using a manual sphygmomanometer. After a 10-minute rest period, blood pressure was
measured 3 times, and the average of the last 2 measurements was
used for statistical analyses.
All participants were administered a standardized questionnaire
that provided information related to occupation, medical history, past
and current medications, and personal habits such as cigarette
consumption. Subjects were classified as “nonsmokers,” “former
smokers,” or “current smokers.” Total serum cholesterol, highdensity lipoprotein (HDL) cholesterol, triglycerides, and fasting
plasma glucose were also measured.
Data Analysis
Values presented in this paper are mean⫾SEM. Mean initial values
of the main variables were compared using a Student t test. A
Student t-paired test was used to compare differences between the
first and second visits.
The association of each variable with baseline PWV and progression in PWV (evaluated in this analysis as the residual value after
adjustment for initial PWV) was assessed with Pearson correlation
coefficients for continuous variables and Student t tests for categorical variables. The contribution of each variable was also evaluated
in a multiple regression analysis by including the variables associated with PWV that had a P value ⬍0.10 in the univariate analysis.
To assess the progression of PWV independently of the progression of mean arterial pressure (MAP), we also evaluated the
Progression of Arterial Stiffness
1203
determinants of the ⌬PWV/⌬MAP ratio. We chose MAP rather than
SBP because MAP is not directly dependent on arterial stiffness.
The roles of age, HR, and creatinine in PWV progression were
also evaluated when these variables were considered as categorical
variables. For the purpose of these analyses, subjects were divided
into 2 age groups (ⱕ50 and ⬎50 years), into 3 HR categories (⬍60,
60 to 75, and ⬎75 beats/min), and into creatinine tertiles. Two-way
ANOVAs were carried out to evaluate the impact of each one of
these 3 parameters (age, HR, and creatinine) in the progression of
PWV after adjustment for covariates in normotensive and treated
hypertensive subjects.
Finally, to assess the role of blood pressure control on PWV
progression, treated hypertensives were classified into 4 groups
according to the control of MAP at the time of the first and/or second
visit. A MAP ⬍107 mm Hg was considered as “controlled” MAP,
because it corresponds to the value of the normal limits of SBP/DBP
(140/90 mm Hg).
Statistical analyses were carried out using the NCSS 2000 statistical software package. A P value ⬍0.05 was considered as statistically significant.
Results
Among normotensives, 296 (91.1%) remained treatment-free
during the 6-year period, whereas an antihypertensive medication had been prescribed for the other 29. Among treated
hypertensives, 187 (95%) continued their treatment and only
10 interrupted it. These 39 subjects who changed treatment
status were not included in the analysis.
Table 1 shows mean values for the clinical and biological
parameters assessed during the first and second visits in
normotensive and hypertensive patients. At visit 1, treated
hypertensive subjects, as compared with normotensive subjects, had higher body mass index (BMI), blood pressure
levels, PWV, triglycerides, and serum creatinine, and they
smoked less. In normotensive subjects, BMI, MAP, DBP,
PWV, HDL cholesterol, and serum creatinine significantly
increased between the first and the second visits, whereas
SBP and total cholesterol remained unchanged, and HR and
PP slightly decreased. In treated hypertensive subjects during
the same period, there was an increase in BMI, SBP, PP,
PWV, HDL cholesterol, and serum creatinine, whereas DBP,
MAP, HR, and total cholesterol remained unchanged.
Determinants of baseline (visit 1) PWV were assessed with
a multivariate analysis; age (P⬍0.0001), BMI (P⬍0.05), and
MAP (P⬍0.001) in normotensives, and age (P⬍0.0001), PP
(P⬍0.02), and HR (P⬍0.02) in hypertensives were independent determinants of baseline PWV. MAP was a significant
determinant of PWV when PP was not included in the model
(P⬍0.05). Total cholesterol, HDL cholesterol, glycemia, and
smoking were not correlated with baseline PWV.
Unadjusted annual progression of PWV in treated hypertensives was significantly higher than in normotensives
(147⫾22 versus 81⫾18 mm/s per year, P⫽0.02), and this
difference remained significant after adjustment for age, sex, and
initial PWV values (171⫾20 versus 66⫾16 mm/s per year,
P⫽0.0003, Figure 1).
The role of baseline clinical and biological parameters on
the progression in PWV over the 6-year period was assessed
in univariate and multivariate analyses (Table 2). The univariate analysis showed that in both normotensives and treated
hypertensives, PWV progression was more pronounced in
men than in women, but the contribution of sex was not
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TABLE 1. Demographic and Clinical Characteristics of Normotensive
and Hypertensive Subjects During the First (1992–1993) and Second
(1998 –1999) Visits
Normotensive Subjects
(n⫽296; 64.5% male)
Treated Hypertensive Subjects
(n⫽187; 63.1% male)
1st Visit
2nd Visit
1st Visit
2nd Visit
Age, y
47.6⫾0.6
54.1⫾0.6†
56.9⫾0.7‡
63.6⫾0.7†
BMI, kg/m2
24.5⫾0.2
25.3⫾0.2†
26.6⫾0.3‡
27.9⫾0.4†
SBP, mm Hg
128.0⫾0.7
144.5⫾1.0‡
149.7⫾1.3†
DBP, mm Hg
78.4⫾0.5
82.4⫾0.6†
88.3⫾0.7‡
87.2⫾0.7
MAP, mm Hg
94.9⫾0.5
98.1⫾0.6†
107.1⫾0.7‡
108.0⫾0.8
PP, mm Hg
49.6⫾0.4
47.1⫾0.7*
56.2⫾0.7‡
HR, bpm
67.8⫾0.7
65.5⫾0.5†
67.8⫾0.9
65.8⫾0.7*
PWV, m/s
9.84⫾0.13
10.35⫾0.10†
11.40⫾0.19‡
12.23⫾0.18†
129.5⫾0.9
62.5⫾1.2†
Cholesterol, mg/dL
228⫾3
231⫾3*
226⫾3
229⫾3
HDL, mg/dL
59.1⫾1.0
64.8⫾1.1†
58.4⫾1.2
60.3⫾1.6
102.0⫾1.7
Glucose, mg/dL
101.9⫾1.1
97.3⫾0.8
106.2⫾1.4
Triglycerides, mg/dL
89.2⫾4.2
100.2⫾4.6†
113.7⫾9.3‡
Creatinine, mg/L
9.37⫾0.09
9.95⫾0.08†
9.90⫾0.13‡
10.53⫾0.14†
Current smokers
20%
22%
12%‡
10%
118.1⫾4.7†
*P⬍0.01 and †P⬍0.001, second vs first visit; ‡P⬍0.001 normotensive vs treated hypertensive
subjects.
significant after adjustment for blood pressure and creatinine.
Age was a significant determinant of PWV progression in
both groups, and its contribution remained significant in the
multivariate analysis (Table 2). Age was also a significant
determinant of the progression of PWV/MAP ratio in normotensives (P⬍0.02) and in treated hypertensives (P⬍0.05).
In normotensives, PWV progression was positively correlated with SBP, DBP, and cholesterol, and negatively correlated with HDL. However, in the multivariate analysis, none
of these variables was significantly related to PWV
progression.
In treated hypertensives, visit 1 values of HR and creatinine were positively correlated with PWV progression, and
the contribution of these 2 variables remained significant in
the multivariate model (Table 2). These 2 variables were also
significant independent determinants of the progression in
PWV/MAP ratio, explaining respectively 7.2% (P⫽0.0001)
and 5.2% (P⫽0.0002) of its variability. By contrast, we did
not find any association between initial HR and creatinine,
and the progression of SBP or DBP levels.
Figure 1. Annual PWV progression in normotensive and treated
hypertensive subjects (adjusted for initial PWV, age, and sex);
†P⫽0.0003.
Figures 2 through 4 show the role of baseline values of age,
HR, and serum creatinine in PWV progression when these
parameters were considered as categorical variables (see Patients
and Methods). After multivariate adjustments including sex and
initial PWV, the annual PWV progression was higher in subjects
⬎50 years of age, in both normotensives (0.8⫾20 mm/s per year
in younger subjects versus 114⫾27 mm/s per year in older
subjects, P⬍0.0001) and treated hypertensives (102⫾41 mm/s
per year in younger subjects versus 244⫾23 mm/s per year in
older subjects, P⬍0.001) (Figure 2). Complementary adjustments for initial HR and creatinine did not change this result.
Figure 3 shows that annual PWV progression was more
pronounced in hypertensives with higher initial HR (49⫾37,
167⫾32, and 290⫾47 mm/s per year in the 3 HR groups
[P⬍0.001]). No such association was observed in normotensives. The 2-way ANOVA showed a significant difference in
the association between HR and PWV progression in normotensive and hypertensive subjects (interaction term, P⬍0.05).
An additional adjustment for the type of medication at the
time of the first and second visits did not modify the results.
Classifying subjects into tertiles for serum creatinine showed
significantly higher PWV progression in treated hypertensives
with higher serum creatinine (Figure 4). The annual PWV
increase was 34⫾48, 142⫾39, and 248⫾31 mm/s per year in the
first, second, and third tertiles, respectively (P⬍0.001). The
2-way ANOVA showed that the association between creatinine
and PWV progression was observed in hypertensives but not in
normotensives (interaction term, P⬍0.001).
Figure 5 shows that in well-controlled hypertensives, at both
visits (group 1; see Subjects and Methods for classification), the
annual progression in PWV was significantly lower than in the
other treated patients (49⫾40 mm/s per year in group 1 versus
213⫾47 and 223⫾44 mm/s per year in groups 3 and 4,
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Benetos et al
Progression of Arterial Stiffness
1205
TABLE 2. R2 Regression Coefficients of Univariate and Multivariate Analyses
Between Baseline (1st Visit) Clinical and Biological Parameters and Progression
in PWV*
Univariate Analysis
Multivariate Analysis
Normotensive
Subjects
Hypertensive
Subjects
Sex (M⬎F)
0.015‡
0.037‡
0.025 (P⫽0.13)
NS
Age (⫹)
0.041§
0.020‡
0.041‡
0.025‡
BMI
0.014
0.017
SBP (⫹)
0.032‡
0.003
DBP (⫹)
0.028‡
0.000
HR (⫹)
0.000
0.068§
Cholesterol (⫹)
0.017‡
0.001
HDL (⫺)
0.032‡
0.009
Creatinine
0.008
0.110§
Plasma glucose
0.003
0.013
Triglycerides (⫹)
0.035‡
0.002
Smoking status†
0.009
0.003
Normotensive
Subjects
Hypertensive
Subjects
0.013 (P⫽0.10)
0.084§
0.015 (P⫽0.06)
0.097§
Model R2
10%
22%
䡠䡠䡠
䡠䡠䡠
All variables were considered as continuous variables except for sex and smoking status.
Significant correlations are in bold. (M⬎F) indicates that the progression in PWV is more important
in men than women; (⫹), positive correlation; and (⫺), negative correlation.
*Residual value after adjustment for initial PWV.
†Current smokers vs others.
‡P⬍0.05; §P⬍0.001.
respectively, P⬍0.01). Patients in group 2 presented intermediate values of PWV progression (145⫾57 mm/s per year).
Progression in PWV in controlled, treated hypertensives was
similar to that of normotensives (49⫾40 versus 81⫾18 mm/s per
year, respectively).
The type of treatment and the number of antihypertensive
drugs at the time of the first and second visits were not
significantly associated with the progression of PWV (data
not shown). However, because we did not know the PWV
values before treatment, this study was not designed to
evaluate the effects of the different drugs on PWV.
Discussion
To our knowledge, this is the first longitudinal study to
evaluate the determinants of the progression of arterial
Figure 2. Annual PWV progression in younger (ⱕ50 years) and
older (⬎50 years) normotensive (left) and treated hypertensive
(right) subjects (adjusted for initial PWV and sex); †P⬍0.001 vs
younger subjects.
stiffness over an extended period of time. Results of the
present study show that the increase in stiffness over a period
of 6 years is more marked in treated hypertensives than in
normotensives, indicating accelerated arterial aging among
treated hypertensives. Three factors were identified as being
responsible for accelerated progression in PWV in treated
hypertensive patients, as follows: uncontrolled blood pressure
values, increased HR, and increased serum creatinine. By
contrast, no association between other major cardiovascular
risk factors and progression in aortic stiffness was found.
Accelerated Aging in Treated,
Uncontrolled Hypertensives
The annual increase in PWV with age that we observed in the
normotensives (81 mm/s per year) was very similar to that
Figure 3. Annual PWV progression according to HR levels in
normotensive (left) and treated hypertensive (right) subjects
(adjusted for initial PWV, age, MAP, and sex); *P⬍0.05;
†P⬍0.001 vs HR ⱕ60 bpm.
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Figure 4. Annual PWV progression according to creatinine levels in normotensive (left) and treated hypertensive (right) subjects (adjusted for initial PWV, age, MAP, and sex); †P⬍0.001 vs
serum creatinine ⬍8 mg/L.
reported in a large cross-sectional study in an urban Chinese
population (92 mm/s per year) composed essentially of
normotensive subjects.7 As was the case for the Chinese
urban population, this Parisian population presents a higher
progression in PWV than the Chinese rural population.
In the present study, treatment over the 6-year period was
conducted by the patients’ general practitioners without any
study-specific recommendations. It is important to note that
the general practitioners were not aware of PWV levels and
therefore did not take into account this parameter in the
management of patients at any time during the 6 years.
Therefore, the observed results reflect a “realistic” situation
in treated hypertensives in whom the main goal is to control
DBP (followed by SBP), but not PP or PWV, which better
reflect arterial aging. The absence of any association between
baseline blood pressure levels and PWV progression in
treated hypertensives (Table 2) does not negate the impact of
blood pressure levels in PWV progression. Actually, when
blood pressure levels remain elevated over an extended
period of time despite treatment, arterial aging is accelerated.
One might suggest that accelerated progression of PWV in
uncontrolled subjects does not reflect accelerated aging but
rather only increased distension pressure (leading to higher
PWV). However, a counter-argument is the fact that in
patients with uncontrolled blood pressure levels at both visits,
MAP did not significantly increase throughout the follow-up,
but PWV progression was more than 3 times higher than in
well-controlled hypertensives. Therefore, permanent blood
pressure elevation in treated subjects appears to promote
accelerated aging, at least partly independently from the
evolution of MAP itself. The present study cannot, however,
answer the question whether the relation between MAP and
PWV progression is linear or whether there is a threshold
value for MAP versus change in PWV. These results reinforce recent data from the Framingham cohort showing that
people with high blood pressure are more likely to present an
excessive increase in SBP and a decrease in DBP later in life,
which suggests accelerated arterial aging in subjects with
high blood pressure levels.16
HR and Acceleration of Arterial Stiffness
In treated hypertensives, the presence of increased HR during
the first visit was an additional factor for accelerated PWV
progression. Increased HR is associated with high cardiovascular disease mortality, independently of other risk factors.17,18 In cross-sectional studies, it has been shown that HR
was a significant determinant of arterial stiffness in hypertensives.13,19 The results of the present longitudinal study are
complementary to results showing that chronic increase in
HR contributes to arterial fatigue and to atherosclerotic
lesions.20 Previous studies have suggested that people with
increased HR have an increased risk of developing hypertension later in life.21 In the present study, this particular result
was not found. This may be explained by the fact that, as we
mentioned in the previous paragraph, the evolution of blood
pressure was directly influenced by physician intervention.
However, our results pertaining to the influence of high HR in
the progression of PWV (which was not taken into account in
the therapeutic strategies in this study) are in concordance
with the concept that increased HR may be a determinant of
accelerated arterial aging and may have deleterious effects on
patient outcome.
Serum Creatinine and Arterial Stiffness
Figure 5. Annual PWV progression (adjusted for initial PWV,
age, HR, and sex) in treated hypertensive subjects as a function
of MAP control (controlled⫽MAP⬍107 mm Hg) at the time of
the initial visit (V1) and the last visit (V2); *P⬍0.01 vs controlled
in both visits.
Our study shows that serum creatinine levels were a strong
independent determinant of the progression of aortic stiffness.
Previous studies have clearly shown that subjects with endstage renal failure present a marked increase in aortic stiffness
independently of mean blood pressure values and other
cardiovascular disease risk factors. In a cross-sectional analysis in a large population, we recently showed that increased
stiffness was significantly associated with creatinine clearance.22 A new finding from the present study is that serum
creatinine levels during the first visit were a strong predictor
for the long-term progression of PWV, indicating that kidney
alterations may accelerate elastic artery aging. It is interesting
to note that, as for HR, serum creatinine was a determinant of
PWV progression in hypertensive but not in normotensive
subjects. This result suggests that hypertensives are more
vulnerable than normotensive subjects to the deleterious
effects of certain risk factors.
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Benetos et al
Age and Progression in PWV
In a previous cross-sectional study,9 we reported the same
observation, suggesting a more pronounced increase in PWV
with age, after the age of 50 years. The present longitudinal
results confirm that in both normotensive and treated hypertensive subjects, the progression in arterial stiffness is more
pronounced in older subjects. This result corroborates the
epidemiological observation of a more pronounced increase
in SBP and PP, the main clinical manifestations of elastic
artery stiffness, after the age of 55 years.16
However, some previous cross-sectional studies have reported a linear age/PWV relationship.7,23 A possible explanation for this is that in cross-sectional studies, the older
patients with the higher aortic stiffness may be “absent” as a
result of a higher mortality rate in this subgroup of subjects.
Limitations of the Study
A limitation of the present study is that the determinants of
blood pressure evolution could not be assessed because of
treatment modifications— oriented by blood pressure levels—made by patients’ general practitioners. This limitation,
however, does not concern PWV, because practitioners were
not aware of PWV.
Another limitation of this study could be the small number
of subjects with diabetes and severe dyslipidemia, possibly
leading to a type II error, ie, the inability to detect a possible
contribution of these metabolic parameters on PWV progression because of the weak number of affected patients.
Finally, it is important to point out that in the present study
the direct distance between the common carotid and femoral
arteries was measured to determine PWV. However, there
was no consensus on which distance should be chosen for
carotid-femoral PWV measurements. Although this is of
limited importance for the present study, given that all
measurements were taken the same way, this is important
when comparisons with other studies are made.
In conclusion, the present longitudinal study shows that
accelerated arterial aging in treated hypertensive subjects is in
large measure explained by uncontrolled blood pressure
levels, high HR, and altered renal function. Controlling blood
pressure and lowering HR could reduce age-related progression of arterial stiffness.
Acknowledgments
This study was supported by Institut National de la Santé et de la
Recherche Médicale (INSERM) and the Caisse Nationale
d’Assurance Maladie. We also thank the Sanofi-Synthelabo pharmaceutical company for supporting this study.
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