(Circulation. 1999;100:1387-1393.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
Association Between Local Pulse Pressure, Mean Blood Pressure, and Large-Artery Remodeling
From the Departments of Pharmacology (P.B., C.B., B.L., S.L.) and Internal Medicine (X.G.), Broussais Hospital, and INSERM U337 (P.B., C.B., P.L., X.G., B.L., S.L.), Paris, France.
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Abstract |
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Background—The aim of the present study was to determine the respective influences of local pulse pressure and mean blood pressure on arterial remodeling in humans at 2 arterial sites: a central, predominantly elastic artery (the common carotid artery) and a peripheral muscular artery (the radial artery).
Methods and Results—Forty-three healthy subjects and 124 never-treated hypertensive patients were included in the study. Intima-media thickness and internal diameter of the carotid and radial arteries were noninvasively determined with high-definition echo-tracking devices. Pulse pressure was measured locally with applanation tonometry. Multivariate regression models including mean blood pressure and local pulse pressure were established in the whole population. Carotid internal diameter and intima-media thickness were strongly influenced (P<0.0001) by carotid pulse pressure but not by mean blood pressure or brachial pulse pressure, independently of age and sex. Radial artery internal diameter was correlated with age but not with mean blood pressure or radial pulse pressure. Radial artery intima-media thickness was correlated with mean blood pressure (P<0.001) but not with radial pulse pressure.
Conclusions—Carotid pulse pressure was a strong independent determinant of carotid artery enlargement and wall thickening, whereas mean blood pressure and brachial pulse pressure were not, indicating the prominent influence of local pulsatile mechanical load on arterial remodeling. These relationships were observed at the site of an elastic artery but not at the site of a muscular artery, suggesting the contribution of cyclic stretching to the pulse pressure–induced arterial remodeling.
Key Words: blood pressure • arteries • remodeling • hypertrophy • hypertension • carotid arteries
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Introduction |
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Large-artery damage is a major factor in cardiovascular morbidity and mortality. Increased arterial stiffness with aging and hypertension contributes to a further rise in pulse pressure (PP) and systolic blood pressure (SBP) at any given value of mean arterial pressure.1 2 Independently of mean blood pressure (MBP), PP is a strong determinant of cardiovascular events, including coronary heart disease and stroke.3 4 5 Various mechanisms have been suggested, including reduced coronary perfusion and a remodeling of large arteries in response to the chronic increase in circumferential wall stress.1 2 3 4 5 During essential hypertension, large-artery remodeling is characterized mainly by an increase in intima-media thickness (IMT) aimed at maintaining circumferential wall stress, lumen enlargement of proximal elastic arteries, and no change in the lumen diameter of distal muscular arteries.1 6 Wall thickening may facilitate the development of atherosclerotic lesions.1 6 7 8 The association between carotid intima-media thickening and coronary heart disease7 8 might thus involve a common mechanical factor, such as PP. However, the precise links between local mechanical factors and large-artery remodeling remain to be determined.
Although a growing body of work led to the conclusion that cyclic strain is a major determinant of the phenotype and growth of vascular smooth muscle cells in vitro,9 10 11 the effect of pulsatile circumferential wall stress on large-artery remodeling has been little studied. In humans, brachial PP was associated with increased wall thickness at the site of the common carotid artery (CCA),7 8 12 but few studies showed that this relationship was independent of MBP and age.12 In addition, in these studies7 8 12 as well as in the above-mentioned epidemiological studies,3 4 5 PP was calculated from brachial SBP and diastolic BP (DBP) and was not measured at the precise site of the wall thickness measurement, preventing any definitive conclusion as to a causal association. Because of the physiological pulse-pressure amplification between central and peripheral arteries,1 13 brachial PP is a poor estimate of the local pressure regimen that acts on the arterial wall. To determine the relationship between cyclic stress and arterial remodeling, it is necessary to measure PP locally, at the site of the arterial segment whose geometry is studied.
Thus, the main objective of the present study was to determine the respective influences of pulsatile and steady mechanical loads on arterial geometry in humans. We also hypothesized that the effect of pulsatile mechanical load on arterial remodeling could be more easily detected at the site of an elastic artery (the CCA), which undergoes high stroke changes in diameter, than at the site of a muscular artery (the radial artery [RA]), in which stroke changes in diameter are much lower.
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Methods |
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Patients and Subjects
One hundred sixty-seven subjects were included in the study: 124 never-treated ambulatory hypertensive patients from 24 to 70 years of age, referred to the hypertension unit of Broussais Hospital, and 43 normal subjects from 23 to 76 years old. Essential hypertension was defined by the presence of a sustained increase in blood pressure (BP), ie, as casual sitting BP
140 mm Hg (SBP) or 90 mm Hg
(DBP) measured by sphygmomanometer and auscultatory methods (phase I
and V of Korotkoff sounds), and the absence of clinical or laboratory
evidence suggestive of secondary forms of hypertension. Only 9 patients
among the 124 referred for hypertension proved to have normal BP values
on assessment for the study. They were included in the
multivariate analysis because it took into
account BP as a continuous variable. None of the patients had
atherosclerotic plaque on the CCA, and only 5 had a plaque on the
carotid bifurcation or the internal carotid. Normotensive control
subjects were derived from medical personnel and their family members
with supine SBP <140 mm Hg and DBP <90 mm Hg. All
subjects were free of clinical evidence of coronary artery or
cerebrovascular disease. No patients with valvular heart
disease, arrhythmia, or renal disease were included. The study was approved by the institutional review committee of Broussais Hospital, and the subjects gave informed consent.
Arterial Measurements
The noninvasive investigation was performed in a controlled
environment kept at 22±1°C after subjects had reclined at rest for
15 minutes. A senior technician (B.L.) and physician (P.B.), trained
and certified in vascular echography, performed BP and
arterial measurements.
Brachial BP
Brachial BP was measured with a mercury sphygmomanometer at the
start of the investigation, with the subject in the sitting position.
Supine BP was then monitored every 3 minutes by an oscillometric method
(Dinamap model 845, Critikon) during the entire investigation. Brachial
artery pressure values (SBP, DBP, MBP, and PP) used in further
calculations were the averages of 5 measurements performed during 3
successive 15-minute periods, corresponding to baseline BP
measurements, then to carotid and radial measurements.
CCA and RA Pressures and Pressure Waveforms
CCA and RA pressure waveforms were recorded noninvasively
with a pencil-type probe incorporating a high-fidelity strain gauge
transducer (SPT-301, Millar Instruments), as previously described by
our group14 and others.15 The transducer has
a small pressure-sensitive area (0.5x1.0 mm) with a frequency
response >2 kHz that is coplanar with a larger area (7 mm
diameter) of flat surface that is in contact with the skin overlying
the pulse. The accuracy of the probe has been validated in
humans.14 15 Noninvasively measured carotid pulse contours
and invasively measured ascending aortic pulses have been shown to have
close similarities in both time and frequency
domains.15
We validated local PP measurement through 3 steps. First, we checked the internal calibration of the tonometer with a mercury manometer. The agreement of the 2 methods was excellent, with a mean absolute difference of 1.2 mm Hg. Second, we checked whether the geometric and mechanical patterns of the tube could influence the value of PP, measured through the applanation principle, using 2 silicon rubber tubes with opposite geometric and mechanical patterns. The distensible tube had a 2.5-fold larger diameter and a 14.5-fold lower elastic modulus than the stiff tube. The agreement between internal and external PPs was good, with a 10.4±0.5% underestimation with tonometer in the distensible tube and 7.3±0.2% overestimation in the stiff tube and with mean absolute differences of 0.20 mm Hg and 0.24 mm Hg, respectively. Finally, in 16 patients undergoing cardiac catheterization for suspected coronary artery disease, we14 previously reported good agreement between PP measured at the site of the carotid artery (PPcar) with applanation tonometry and PP measured invasively at the level of the aortic arch (PPao): PPcar=(0.98±0.11)xPPao+(0.13±8.14); r=0.96; mean difference=10 mm Hg.
Arterial Internal Diameter and Wall Thickness
Carotid internal diameter and wall thickness were measured on
the right CCA and 2 cm beneath the carotid bifurcation with a 7.5-MHz
pulsed ultrasound echo-tracking system (Wall Track System, Neurodata)
that analyzed the radiofrequency signal originating from an M
line perpendicular to the longitudinal and transversal axes of the
artery, selected on the 2D B-mode image (Sigma 44 Kontron). This system
has been validated and described in detail16 and used for
various clinical studies.14 17
Measurements of RA internal diameter and wall thickness were obtained on the right arm with a 10-MHz ultrasound system that analyzed the radiofrequency signal (NIUS 02; SMH), previously described and validated18 and used in clinical studies.17 The repeatability of carotid and radial measurements has been reported previously.17
Mean circumferential wall stress (
, in kPa) was calculated
according to Lamé's equation as =MBPxDi/2h, where
Di is mean internal diameter and h is wall thickness.
Statistics
Data are expressed as mean±SD. Quantitative variables were
compared by means of an unpaired Student t test and
categorical variables by means of a 
2
test. Correlation matrixes for CCA and RA parameters were
done by Spearman rank test. Multivariate regression
models19 were constructed for the entire population
and systematically included MBP. The other variables included in
the model were chosen by a multivariate variable
selection procedure among the following variables: age, sex, body
surface area, carotid or radial PP, brachial PP, and heart rate. The
algorithm allows the selection of a set of variables among all
possible pertinent ones on the basis of the maximization of
R2. Up to 5 variables were kept
until R2 reached a plateau. Once the
set of variables was determined for the parameter of
interest, a robust multiple stepwise regression analysis was
performed. This procedure has been shown to be more robust to the
marginal violation of normality assumption and to the presence of
outliers than classic parametric regression. The resulting
model depends more on the body of data than on the excessive weight of
some observations. A value of P<0.05 was considered
significant. The statistical analysis was performed with NCSS
6.0 software (J.L. Hintze, Kaysville, Utah).
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Results |
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Baseline Characteristics
Baseline characteristics of normotensives and hypertensives did not differ significantly (Table 1
). By definition, hypertensives
presented higher levels of SBP, MBP, DBP, and PP than
normotensives. However, age, sex ratio, tobacco use, fasting glucose
level, and lipid levels did not differ between the 2 populations.
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CCA Parameters
Hypertensives had larger and thicker carotid arteries than
normotensives (Table 2). Therefore,
carotid wall cross-sectional area was markedly increased. No difference
in wall-to-lumen ratio was observed. Thus, circumferential wall stress
was higher in hypertensives. Carotid PP was higher in hypertensives
than in normotensives (Table 2), like brachial and radial PP
(Tables 1
and 3). In
multivariate analysis of the entire population,
the brachial/carotid PP ratio, an index of the PP amplification
phenomenon, was attenuated by aging (P<0.001) and
potentiated by MBP (P<0.05).
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In univariate analysis of the entire population,
carotid internal diameter was significantly related to carotid PP
(r=0.33; P<0.0001) but not to brachial PP
(r=0.09; P=NS) (Table 4 and Figure 1); carotid IMT was significantly related
to carotid PP (r=0.42; P<0.0001) and to brachial
PP (r=0.27; P<0.001) (Table 4 and Figure 2). Despite significant interrelations
between variables of interest (Table 4),
multivariate models (Tables 5 and 6)
provided useful information. Indeed, 47% of the variance of carotid
diameter was explained by the model that included sex, carotid PP,
heart rate, and age in the population as a whole (Table 5).
Carotid PP was strongly and independently associated with internal
diameter (Table 5) and IMT (Table 6), whereas MBP was
not. After similar adjustments, a significant correlation was observed
between carotid PP and wall cross-sectional area (P<0.0001;
data not shown). Thus, in addition to age, carotid PP was the strongest
predictor of dilatation of the carotid artery and of wall
hypertrophy, explaining as much as 18% and 12% of the
variance (R2 increment) of internal
diameter and IMT, respectively (Tables 5 and 6). It is
noteworthy that none of the other factors classically associated with
IMT increase (eg, cholesterol level or smoking) influenced
the model in this sample of subjects and patients.
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When brachial PP, measured with a Dinamap monitor, was introduced
into the multivariate model instead of carotid PP, no
significant correlation was observed with internal diameter (Table 5), IMT (Table 6), or wall cross-sectional area.
Correla-tions between brachial PP measured with Dinamap and
carotid artery parameters (as well as RA
parameters; see below) were not significantly modified when
sphygmomanometer brachial PP was used instead of Dinamap brachial
PP.
RA Parameters
The RA of hypertensives was thicker than that of normotensives and
not dilated (Table 3). Subsequently, wall cross-sectional area
and wall-to-lumen ratio were markedly increased in hypertensives, which
normalized circumferential wall stress. Radial PP was increased in
hypertensives and was of the same magnitude as brachial PP.
In normotensives and hypertensives considered as a whole, RA PP was not
correlated with internal diameter (Table 5) or IMT (Table 6).
MBP significantly influenced RA IMT (Table 5)
independently of age and sex. Brachial PP did not influence RA diameter
(Table 5) or IMT (Table 6).
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Discussion |
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To the best of our knowledge, the present study is the first to determine the respective influences of local pulsatile and steady pressures on large-artery remodeling in normotensive subjects and never-treated hypertensive patients. The 2 new findings are as follows: (1) local PP is a strong independent determinant of CCA enlargement and wall thickening, whereas brachial PP and MBP are not; and (2) the predominant role of pulsatile mechanical load on arterial remodeling is observed at the site of a central elastic artery, the CCA, but not at the site of a distal muscular artery, the RA.
Enlargement of the large arteries with aging and MBP has been extensively described1 14 and is generally attributed to fracture of the load-bearing elastin fibers in response to the fatiguing effect of tensile stress. The present study, which shows that local PP is a strong independent determinant of carotid artery enlargement whereas MBP is not, suggests that pulsatile stress plays a more important role than steady stress. According to engineering principles,20 the fatiguing effect of cyclic stress is dependent on both the number of cycles (duration times frequency) and the amplitude of each cycle. Interestingly, in the present study, carotid diameter was significantly influenced by its clinical equivalents: age, heart rate, and carotid PP. Carotid artery diameter enlargement might explain why circumferential wall stress was not normalized in hypertensives despite wall thickening, in contrast to the RA.
Carotid wall thickening was related to brachial PP in some studies in essential hypertensive patients7 12 but not to carotid PP locally measured with applanation tonometry. To determine the relationship between cyclic stress and arterial remodeling, it is necessary to measure PP locally, at the site of the arterial segment whose geometry is studied, because of the physiological PP amplification between central and peripheral arteries.1 13 14 15 In older subjects, the augmentation of central PP can cancel out the normally present higher peripheral arterial PP seen in young subjects,1 13 14 15 and PP tends to be similar in both central and peripheral arteries. This is well illustrated by 2 findings of the present study: (1) the brachial/carotid PP ratio, an index of the PP amplification phenomenon, was significantly attenuated by aging and potentiated by MBP; and (2) carotid PP was a strong determinant of carotid artery internal diameter and IMT, whereas brachial PP was not.
Local PP was related to carotid IMT but not to radial IMT, suggesting that the amplitude of stroke change in diameter, 10-fold higher at the site of the CCA than at the site of the RA, could be a mechanism by which PP influences IMT. This finding is in accordance with numerous in vitro studies showing that cyclic stretching exerts a greater influence than static load on phenotype and growth of vascular smooth muscle cells (including synthesis of DNA, smooth muscle myosin, and collagen).9 10 11
The present study has some limitations. First, in addition to mechanical factors, neurohumoral and genetic factors should be considered, because they can directly influence the remodeling not only of conduit arteries but also of arterioles, leading to an earlier return of wave reflections and an increase in PP. Second, the time-dependent relation between increased PP and arterial remodeling could not be determined in the present study because of its cross-sectional design. Third, we cannot exclude that the strength of the correlation might depend more on the accuracy of the measurement than on the physiology involved (for instance, that carotid tonometric PP, measured by a trained investigator, could simply be more accurate than Dinamap MBP or PP). Fourth, ultrasound imaging cannot discriminate between the intimal and medial layers of the vessel wall to distinguish true arteriosclerosis (ie, the adaptive response of the medial layer to changes in tensile stress) from atherosclerosis (which is viewed as a disorder restricted to the intimal layer).6 7 8 However, the CCA is usually spared of atherosclerosis, in contrast to the carotid bifurcation and proximal internal carotid.
In conclusion, carotid PP was a strong independent determinant of carotid artery remodeling, whereas MBP and brachial PP were not. The predominant role of pulsatile mechanical load on arterial remodeling was observed at the site of an elastic artery but not at the site of a muscular artery. Pulsatile circumferential wall stress, which may exert a fatiguing effect on elastic fibers and a growth effect on smooth muscle cells, should be taken into account when large-artery remodeling is studied.
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Acknowledgments |
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This study was performed with grants from Institut National de la Santé et de la Recherche Médicale (INSERM grant 35 494014), as well as a grant (BIOMED) from the European Community.
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Footnotes |
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Reprint requests to Professeur Stéphane Laurent, Service de Pharmacologie, Assistance Publique-Hôpitaux de Paris, Hôpital Broussais, 96, rue Didot, 75674 Paris Cedex 14, France.
Received April 12, 1999; revision received June 14, 1999; accepted June 17, 1999.
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E. Agabiti-Rosei, G. Mancia, M. F. O'Rourke, M. J. Roman, M. E. Safar, H. Smulyan, J.-G. Wang, I. B. Wilkinson, B. Williams, and C. Vlachopoulos Central Blood Pressure Measurements and Antihypertensive Therapy: A Consensus Document Hypertension, July 1, 2007; 50(1): 154 - 160. [Full Text] [PDF]
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 A. Paini, P. Boutouyrie, D. Calvet, M. Zidi, E. Agabiti-Rosei, and S. Laurent Multiaxial Mechanical Characteristics of Carotid Plaque: Analysis by Multiarray Echotracking System Stroke, January 1, 2007; 38(1): 117 - 123. [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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P. Verdecchia, F. Angeli, and S. Taddei At the Beginning of Stiffening: Endothelial Dysfunction Meets "Pulsology" Hypertension, October 1, 2006; 48(4): 541 - 542. [Full Text] [PDF]
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B. Ariff, A. Zambanini, S. Vamadeva, D. Barratt, Y. Xu, P. Sever, A. Stanton, A. Hughes, and S. Thom Candesartan- and Atenolol-Based Treatments Induce Different Patterns of Carotid Artery and Left Ventricular Remodeling in Hypertension Stroke, September 1, 2006; 37(9): 2381 - 2384. [Abstract] [Full Text] [PDF]
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 M. F. O'Rourke and J. B. Seward Central Arterial Pressure and Arterial Pressure Pulse: New Views Entering the Second Century After Korotkov Mayo Clin. Proc., August 1, 2006; 81(8): 1057 - 1068. [Abstract] [Full Text] [PDF]
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J. E. Sharman, R. Lim, A. M. Qasem, J. S. Coombes, M. I. Burgess, J. Franco, P. Garrahy, I. B. Wilkinson, and T. H. Marwick Validation of a Generalized Transfer Function to Noninvasively Derive Central Blood Pressure During Exercise Hypertension, June 1, 2006; 47(6): 1203 - 1208. [Abstract] [Full Text] [PDF]
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 C. Vlachopoulos, F. Kosmopoulou, N. Alexopoulos, N. Ioakeimidis, G. Siasos, and C. Stefanadis Acute mental stress has a prolonged unfavorable effect on arterial stiffness and wave reflections. Psychosom Med, March 1, 2006; 68(2): 231 - 237. [Abstract] [Full Text] [PDF]
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A. Paini, P. Boutouyrie, D. Calvet, A.-I. Tropeano, B. Laloux, and S. Laurent Carotid and Aortic Stiffness: Determinants of Discrepancies Hypertension, March 1, 2006; 47(3): 371 - 376. [Abstract] [Full Text] [PDF]
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 L. F. Drager, L. A. Bortolotto, M. C. Lorenzi, A. C. Figueiredo, E. M. Krieger, and G. Lorenzi-Filho Early Signs of Atherosclerosis in Obstructive Sleep Apnea Am. J. Respir. Crit. Care Med., September 1, 2005; 172(5): 613 - 618. [Abstract] [Full Text] [PDF]
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 C. Vlachopoulos, D. Panagiotakos, N. Ioakeimidis, I. Dima, and C. Stefanadis Chronic coffee consumption has a detrimental effect on aortic stiffness and wave reflections Am. J. Clinical Nutrition, June 1, 2005; 81(6): 1307 - 1312. [Abstract] [Full Text] [PDF]
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S. Laurent, P. Boutouyrie, and P. Lacolley Structural and Genetic Bases of Arterial Stiffness Hypertension, June 1, 2005; 45(6): 1050 - 1055. [Abstract] [Full Text] [PDF]
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 R. S. Reneman, J. M. Meinders, and A. P.G. Hoeks Non-invasive ultrasound in arterial wall dynamics in humans: what have we learned and what remains to be solved Eur. Heart J., May 2, 2005; 26(10): 960 - 966. [Abstract] [Full Text] [PDF]
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 J. E. Sharman, Z. Y. Fang, B. Haluska, M. Stowasser, J. B. Prins, and T. H. Marwick Left Ventricular Mass in Patients With Type 2 Diabetes Is Independently Associated With Central but not Peripheral Pulse Pressure Diabetes Care, April 1, 2005; 28(4): 937 - 939. [Full Text] [PDF]
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 J.E. Sharman, J.R. Cockcroft, and J.S. Coombes Cardiovascular implications of exposure to traffic air pollution during exercise QJM, October 1, 2004; 97(10): 637 - 643. [Abstract] [Full Text] [PDF]
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D. Calvet, P. Boutouyrie, E. Touze, B. Laloux, J.-L. Mas, and S. Laurent Increased Stiffness of the Carotid Wall Material in Patients With Spontaneous Cervical Artery Dissection Stroke, September 1, 2004; 35(9): 2078 - 2082. [Abstract] [Full Text] [PDF]
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Yasmin, C. M. McEniery, S. Wallace, I. S. Mackenzie, J. R. Cockcroft, and I. B. Wilkinson C-Reactive Protein Is Associated With Arterial Stiffness in Apparently Healthy Individuals Arterioscler Thromb Vasc Biol, May 1, 2004; 24(5): 969 - 974. [Abstract] [Full Text]
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R. M.A. Henry, P. J. Kostense, J. M. Dekker, G. Nijpels, R. J. Heine, O. Kamp, L. M. Bouter, and C. D.A. Stehouwer Carotid Arterial Remodeling: A Maladaptive Phenomenon in Type 2 Diabetes but Not in Impaired Glucose Metabolism: The Hoorn Study Stroke, March 1, 2004; 35(3): 671 - 676. [Abstract] [Full Text] [PDF]
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T. J.L. Vuurmans, P. Boer, and H. A. Koomans Effects of Endothelin-1 and Endothelin-1 Receptor Blockade on Cardiac Output, Aortic Pressure, and Pulse Wave Velocity in Humans Hypertension, June 1, 2003; 41(6): 1253 - 1258. [Abstract] [Full Text] [PDF]
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 T. Simon, P. Boutouyrie, J.M. Simon, B. Laloux, C. Tournigand, A.I. Tropeano, S. Laurent, and P. Jaillon Influence of Tamoxifen on Carotid Intima-Media Thickness in Postmenopausal Women Circulation, December 3, 2002; 106(23): 2925 - 2929. [Abstract] [Full Text] [PDF]
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R. Pini, M. C. Cavallini, F. Bencini, G. Silvestrini, E. Tonon, W. De Alfieri, N. Marchionni, M. Di Bari, R. B. Devereux, G. Masotti, et al. Cardiovascular remodeling is greater in isolated systolic hypertension than in diastolic hypertension in older adults: the Insufficienza Cardiaca negli Anziani Residenti (ICARE) a Dicomano Study J. Am. Coll. Cardiol., October 2, 2002; 40(7): 1283 - 1289. [Abstract] [Full Text] [PDF]
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J.-M. Corpataux, E. Haesler, P. Silacci, H. B. Ris, and D. Hayoz Low-pressure environment and remodelling of the forearm vein in Brescia-Cimino haemodialysis access Nephrol. Dial. Transplant., June 1, 2002; 17(6): 1057 - 1062. [Abstract] [Full Text] [PDF]
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I. B. Wilkinson, K. Prasad, I. R. Hall, A. Thomas, H. MacCallum, D. J. Webb, M. P. Frenneaux, and J. R. Cockcroft Increased central pulse pressure and augmentation index in subjects with hypercholesterolemia J. Am. Coll. Cardiol., March 20, 2002; 39(6): 1005 - 1011. [Abstract] [Full Text] [PDF]
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I.S. Mackenzie, I.B. Wilkinson, and J.R. Cockcroft Assessment of arterial stiffness in clinical practice QJM, February 1, 2002; 95(2): 67 - 74. [Full Text] [PDF]
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C. Vlachopoulos, K. Hirata, and M. F. O'Rourke Pressure-Altering Agents Affect Central Aortic Pressures More Than Is Apparent From Upper Limb Measurements in Hypertensive Patients: The Role of Arterial Wave Reflections Hypertension, December 1, 2001; 38(6): 1456 - 1460. [Abstract] [Full Text] [PDF]
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I. B. Wilkinson, S. S. Franklin, I. R. Hall, S. Tyrrell, and J. R. Cockcroft Pressure Amplification Explains Why Pulse Pressure Is Unrelated to Risk in Young Subjects Hypertension, December 1, 2001; 38(6): 1461 - 1466. [Abstract] [Full Text] [PDF]
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P. Boutouyrie, D. P. Germain, A.-I. Tropeano, B. Laloux, F. Carenzi, M. Zidi, X. Jeunemaitre, and S. Laurent Compressibility of the Carotid Artery in Patients With Pseudoxanthoma Elasticum Hypertension, November 1, 2001; 38(5): 1181 - 1184. [Abstract] [Full Text] [PDF]
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 P. Boutouyrie, S. Laurent, B. Laloux, O. Lidove, J.-P. Grunfeld, and D. P Germain Non-invasive evaluation of arterial involvement in patients affected with Fabry disease J. Med. Genet., September 1, 2001; 38(9): 629 - 631. [Full Text] [PDF]
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C. Labat, P. Lacolley, M. Lajemi, M. de Gasparo, M. E. Safar, and A. Benetos Effects of Valsartan on Mechanical Properties of the Carotid Artery in Spontaneously Hypertensive Rats Under High-Salt Diet Hypertension, September 1, 2001; 38(3): 439 - 443. [Abstract] [Full Text] [PDF]
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S. Boumaza, S. M. Arribas, M. Osborne-Pellegrin, J. C. McGrath, S. Laurent, P. Lacolley, and P. Challande Fenestrations of the Carotid Internal Elastic Lamina and Structural Adaptation in Stroke-Prone Spontaneously Hypertensive Rats Hypertension, April 1, 2001; 37(4): 1101 - 1107. [Abstract] [Full Text] [PDF]
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A. M. Dart and B. A. Kingwell Pulse pressure--a review of mechanisms and clinical relevance J. Am. Coll. Cardiol., March 15, 2001; 37(4): 975 - 984. [Abstract] [Full Text] [PDF]
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 I. B Wilkinson, H. MacCallum, P. C Hupperetz, C. J van Thoor, J. R Cockcroft, and D. J Webb Changes in the derived central pressure waveform and pulse pressure in response to angiotensin II and noradrenaline in man J. Physiol., February 1, 2001; 530(3): 541 - 550. [Abstract] [Full Text] [PDF]
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P. Boutouyrie, R. Corvisier, M. Azizi, D. Lemoine, B. Laloux, M.-C. Hallouin, and S. Laurent Effects of acupuncture on radial artery hemodynamics: controlled trials in sensitized and naive subjects Am J Physiol Heart Circ Physiol, February 1, 2001; 280(2): H628 - H633. [Abstract] [Full Text] [PDF]
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 D. T. Nash Diabetes Mellitus and Cardiovascular Disease The Diabetes Educator, January 1, 2001; 27(1): 28 - 34. [PDF]
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H. Tanaka, F. A. Dinenno, K. D. Monahan, C. A. DeSouza, and D. R. Seals Carotid Artery Wall Hypertrophy With Age Is Related to Local Systolic Blood Pressure in Healthy Men Arterioscler Thromb Vasc Biol, January 1, 2001; 21(1): 82 - 87. [Abstract] [Full Text] [PDF]
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Y.-L. Liang, L. M. Shiel, H. Teede, D. Kotsopoulos, J. McNeil, J. D. Cameron, and B. P. McGrath Effects of Blood Pressure, Smoking, and Their Interaction on Carotid Artery Structure and Function Hypertension, January 1, 2001; 37(1): 6 - 11. [Abstract] [Full Text] [PDF]
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P. Boutouyrie, C. Bussy, D. Hayoz, J. Hengstler, N. Dartois, B. Laloux, H. Brunner, and S. Laurent Local Pulse Pressure and Regression of Arterial Wall Hypertrophy During Long-Term Antihypertensive Treatment Circulation, June 6, 2000; 101(22): 2601 - 2606. [Abstract] [Full Text] [PDF]
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