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(Hypertension. 1995;26:48-54.)
© 1995 American Heart Association, Inc.
Articles |
Effects of Hypertension on Viscoelasticity of Carotid and Femoral Arteries in Humans
From Fundacion Favaloro, Buenos Aires, Argentina (R.A., J.B.), and the Centre de Médecine Préventive Cardiovasculaire, INSERM U28, Hôpital Broussais, Paris, France (J.L.M., A.S., F.B., J.L.).
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Abstract |
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Abstract We compared the properties of common carotid and femoral arteries of 16 normotensive and 14 hypertensive men. Arterial pressure and diameter were recorded noninvasively in each vessel by tonometric and echotracking devices. The x-y composition of pressure and diameter waves provided the diameter-pressure hysteresis loop. The elastic diameter-pressure curve and wall viscosity index were deduced after hysteresis elimination. The compliance-pressure and distensibility-pressure curves were derived from the diameter-pressure curve, allowing the calculation of effective compliance and distensibility at the prevailing pressure of each subject and isobaric compliance and distensibility at the same standard pressure in all subjects. Systolic, diastolic, mean, and pulse pressures and diameters in each vessel were higher in the hypertensive than the normotensive group, except carotid pulse diameter, which did not differ. The carotid diameter-pressure, compliance-pressure, and distensibility-pressure curves did not differ between groups. In the carotid artery hypertensive patients had isobaric compliance and distensibility values similar to those of normotensive subjects, despite lower effective compliance (P<.05) and distensibility (P<.01). The femoral diameter-pressure curve was higher (P<.05) and the femoral compliance-pressure and distensibility-pressure curves were lower (P<.01) in the hypertensive than the normotensive group. Hypertensive patients had effective and isobaric femoral compliance and distensibility values lower than to those of normotensive subjects (P<.001). In both arteries, viscosity index was higher in the hypertensive than the normotensive group (P<.001). In hypertension, the pressure-independent alterations of geometric and elastic properties were distributed preferentially to the femoral artery, and the alteration of wall viscosity affected carotid and femoral sites in a uniform manner.
Key Words: compliance • viscosity • ultrasonography • tonometry • hypertension, essential
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Introduction |
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It has been widely demonstrated that human hypertension is associated with two main modifications of the physical properties of large arteries: an increased diameter and a decreased compliance.1 Nevertheless, several important questions on this topic remain unresolved. First, it is not clear how arterial geometric and elastic changes are interrelated in hypertension, and it is unlikely that these changes sum up all the mechanical alterations, especially those related to the viscous properties of arterial walls.2 Second, the mechanisms of arterial dilation and stiffening are difficult to analyze because of the confounding effect of the pressure dependence of vascular elasticity.3 Indeed, pressure elevation per se dilates and stiffens arteries by stretching their walls independent of the contribution of other physiopathologic factors. This mechanical influence of pressure on arteries has been analyzed by several approaches.4 5 6 Finally, the topographic distribution of alterations of the mechanical properties of arteries remains to be established in hypertension. In particular, it is not well known whether the stiffening process is localized within certain sites of the arterial tree or is uniformly generalized.5 7 8 9 We carried out the present work to address these different points. A complete characterization of geometric, elastic, and viscous properties of arteries has been developed on the basis of noninvasive recordings of pressure and diameter pulses with tonometric10 and echotracking11 devices, allowing the determination of the pressure-diameter hysteresis loop.12 We applied this original methodology to carotid and femoral arteries, which have quite different topography in the circulation. We compared the physical properties of vessels between two groups of hypertensive and normotensive men of similar age.
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Methods |
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Study Subjects
Sixteen normotensive male control subjects and 14 ambulatory male patients with mild to moderate hypertension (defined as a supine diastolic pressure [Korotkoff phase V] of 95 to 114 mm Hg on an average of three outpatient visits) entered into the hemodynamic study (Table 1). All patients had not been treated for at least 1 month and had essential hypertension documented by classic laboratory tests.4 Hypertension was uncomplicated in all patients, and none had cardiac, neurological, or renal disease or arteriopathy of the legs. While the patients underwent echographic examination of peripheral arteries for routine clinical management, they were also submitted, after giving informed consent in accordance with the institutional ethics policy, to echotracking and tonometric measurements of arterial diameter and pressure in the carotid and femoral arteries.
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Pressure and Diameter Measurements
Subjects were examined in a quiet room at a controlled
temperature of 20±1°C while in the recumbent position. After 10
minutes of rest, brachial artery blood pressure was measured by a
sphygmomanometric procedure as the average of three consecutive
measurements. All echographic and tonometric measurements were
performed by the same physician, who was especially trained in these
vascular investigations. Echographic studies were performed with a
real-time B-mode ultrasound imager (Ultramark 4, Advanced Technology
Laboratories). The right common carotid and femoral arteries 2 to
3x10-2 m proximal to the bifurcation were examined with a
7.5-MHz probe. Scanning of the carotid artery was performed in the
anteroposterior projection, with the patient lying on his back with
the head in axis.13 Scanning of the femoral artery was
also performed in the anteroposterior position, with the patient lying
on his back with the lower limb in slight external
rotation.13 Subjects with the presence of echogenic
atherosclerotic plaque encroaching into the vessel lumen14
at the sites of echographic measurement were excluded from the study.
Such plaques were always absent in the carotid segment of echographic
measurement but were found in the femoral segment of echographic
measurement in about 10% of the subjects examined. Vessel wall
displacements were measured with an original echotracking device (AMA)
previously described in detail.11 15 Briefly, the
two-dimensional B-mode image allowed us to select an M-line
perpendicular to the artery. Vessel wall displacements then were
measured with a pulsed ultrasound echotracking system based on
Doppler shift. An electrocardiogram trigger allowed
the detection of the peak distension of the artery relative to its
initial diameter. The radio frequency signal of four successive cardiac
cycles was recorded, digitized, and stored in the memory module of
a computer. Two sample volumes, selected under cursor control, were
positioned on the far and near walls of arteries. The displacement of
the near and far arterial walls was measured by processing
the Doppler signals originating from the two selected sample
volumes. The instantaneous arterial diameter waveform was
obtained as the difference between the far and near wall displacements
every 3 milliseconds, and an ASCII file was generated and stored on
floppy disks. Systolic, diastolic, mean (integration of the
instantaneous curve), and pulse (difference between systolic and
diastolic values) diameters were determined.
The arterial pressure wave was recorded at the same site as the diameter but consecutively to diameter recordings, once the pulse of the subject had been regular and the wave shape similar for several consecutive cardiac beats (condition of steady-state oscillation of the arterial system). The noninvasive method of pressure wave measurement was based on the principle of applanation tonometry; its details have been described elsewhere.10 16 17 Briefly, we used a pencil-shaped probe held on the skin over the maximal arterial pulsation. The probe incorporated a micromanometer in its tip that had the same high-fidelity response as a conventional catheter (Millar Instruments Inc). Once the point of maximal arterial pulsation was located, the probe was placed over the vessel and pressed down on the artery against underlying rigid structures. When the curved surface of the artery was flattened (or applanated) by the probe, the circumferential stress in the wall of the vessel was balanced, and the pressure registered by the sensor was identical to the intra-arterial pressure.16 In practice we considered that the applanation of the vessel was achieved when a reproducible pulsatile pressure with a large pulse pressure amplitude could be obtained. Indeed, when the hold-down force needed to achieve applanation was excessive, the pressure wave showed a gradual increase in late diastole, with minimal change in the systolic pressure; this phenomenon tended to reduce the pulse pressure amplitude. Subjects who exhibited a distorted pressure principally caused by large amounts of overlying tissue were excluded from the study. Such a situation was extremely rare at the femoral site as we had eliminated obese subjects with a body mass index above 29 kg/m2. At the carotid site, however, the distortion of tonometric pressure was found in about 5% of the subjects examined. The instantaneous pressure waveforms of four cardiac cycles and the signal average given by the tonometer preamplifier were digitized every 1.25x10-3 seconds, equivalent to 800 samples per second. This sampling rate, higher than that required by the sampling theorem, was imposed by the pressure wave recorder (Windograph, Gould Inc). The pressure signal obtained by tonometry was calibrated in assigning the diastolic pressure measured by brachial sphygmomanometry to its minimum value, and the mean pressure (calculated as one third of pulse pressure plus diastolic pressure) assessed by brachial sphygmomanometry to its average value (Fig 1). This calibration procedure of the tonometric signal was based on the assumption that mean pressure did not change in large conduit arteries and that the diastolic pressure (as opposed to the systolic pressure) was not substantially different among brachial, carotid, and femoral arteries.18 During both diameter and pressure measurements the spikes corresponding to the QRS complex of the electrocardiogram were acquired and stored together with the diameter and pressure signals. To explore whether the compression of the carotid artery during tonometric measurement could stimulate the baroreceptors and therefore introduce confounding effects in the analysis of the carotid pulse waves, we measured by tonometry and compared pulse rates of the carotid and femoral pulse waves (Table 2). As we did not find significant differences in tonometric pulse rates between carotid and femoral arteries, we could discard a significant stimulation caused by the tonometric compression of the carotid artery.
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Pressure Dependence Analysis of Diameter, Compliance, and
Distensibility
We used a computerized procedure to determine the
pressure-diameter hysteresis loop12 19 and the purely
elastic pressure-diameter relationship (Asyst Software Technologies
Inc). ASYST is an advanced set of scientific software tools
for data acquisition, analysis, and presentation.
Briefly, in the present study it allowed us to develop a complex
program that converts external files provided by the echotracking
system and the Gould windograph recorder, analyzes pressure
and diameter, and constructs the pressure-diameter loop. The pressure
and diameter waveforms were identified according to the QRS complex of
the electrocardiogram. Each cardiac cycle, from both
pressure and diameter, was interpolated in time to obtain the same
number of data points. To this end each cardiac cycle from the pressure
and diameter signals (four to six beats) was resampled to 256 samples
per beat, and then the average pressure and diameter beat was
calculated. The procedure of resampling was performed by interpolation,
using as input the time array with the original number of samples
corresponding to pressure or diameter. The output was a new time array
containing 256 samples with the same time period. The choice of 256
points per beat allowed us to obtain about 85 points in the systolic
part of the cycle, which was sufficient to carry out the assessment of
the viscosity index. Then the pressure-diameter hysteresis loop was
obtained by x-y composition of diameter and
pressure waveforms. Such a loop involved elastic and viscous components
in its area (Fig 2). To obtain the purely elastic
pressure-diameter relationship, we transformed real pressure (P) into
elastic pressure (Pelastic) by using a first-order
differential equation20 that characterizes the
viscoelastic behavior of the arterial wall as a function of
a viscous coefficient (
) and the first derivative of diameter with
respect to time (dD/dt):
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 | (1) |
The value of was increased by iteration to obtain the
reduction of the hysteresis loop area until it reached a minimum value
that maintained the clockwise course of the loop (Fig 2).
The purely elastic relationship obtained by a hysteresis elimination
procedure was fitted by a logarithmic model previously applied to the
description of the elastic properties of large
arteries4 21 and transformed into a diameter-pressure
curve (Fig 2) according to the following formula expressing the
diameter (D) as a function of P with two constants, 
and ß,
determined by the fitting procedure:
 | (2) |
The compliance-pressure curve was calculated by deriving Equation 2 with respect to pressure (dD/dP). The distensibility-pressure curve was calculated by deriving Equation 2 normalized at each level of arterial diameter (1/D · dD/dP). The diameter-pressure, compliance-pressure, and distensibility-pressure curves were represented over the same range of blood pressure, from 50 to 150 mm Hg.
Elastic Parameters and Viscosity Index
The compliance-pressure and distensibility-pressure curves
allowed us to calculate effective values of compliance and
distensibility corresponding to the prevailing mean blood pressure of
each subject. The curves allowed us also to calculate isobaric values
of compliance and distensibility corresponding to the same standard
pressure in all subjects. This standard pressure was chosen arbitrarily
as the arithmetic average of mean blood pressure of the normotensive
and hypertensive groups, ie, (94.9±121.6)/2=108.2 mm Hg. This value
was the closest value from the prevailing mean blood pressure of each
group. Therefore, this standard pressure is likely to be
physiologically meaningful for comparing the two
groups of subjects, although it probably does not have any particular
meaning for an individual subject.
The wall viscosity index was computed according to Equation 1 by
increasing incrementally the coefficient until the minimum area of
the hysteresis loop (Fig 2) was obtained. The viscosity index was the
value at which the hysteresis loop area was minimal.
Statistical Analysis
Group data are expressed as mean±SD. Unpaired t test
was used to compare parameters between the normotensive and
hypertensive groups, and paired t test was used to compare
carotid and femoral parameters within groups. Differences
were considered significant at a value of P<.05.
Correlation was performed by least-squares regression.
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Results |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Pressure and Diameter Measurements
Table 3 summarizes pressure and diameter values of both arteries in the study groups. Systolic and pulse pressures were higher in the femoral artery than in the carotid artery in both the normotensive (P<.001) and hypertensive (P<.01) groups. Systolic, diastolic, and mean diameters were higher in the femoral artery than in the carotid artery in both groups (P<.001). Pulse diameter was higher in the femoral artery than in the carotid artery in the normotensive group (P<.01) but lower in the femoral artery than in the carotid artery in the hypertensive group (P<.05). A positive correlation existed between pulse diameter and pulse pressure when carotid and femoral data were pooled in the normotensive group (P<.001, Fig 3). Such a correlation did not exist in the hypertensive group. All pressure and diameter values were increased in the hypertensive group, except carotid pulse diameter, which was not different between the hypertensive and normotensive groups.
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) and carotid (
) data of
the normotensive group are pooled.
Pressure Dependence Analysis of Arterial
Diameter, Compliance, and Distensibility
The diameter-pressure, compliance-pressure, and
distensibility-pressure curves in the carotid artery were not
significantly different between the hypertensive and normotensive
groups (Fig 4). In the femoral artery, the
diameter-pressure curve was shifted toward higher values of diameter
(not significant for pressure above 130 mm Hg), and the
compliance-pressure and distensibility-pressure curves were shifted
toward lower values of compliance and distensibiliy in the hypertensive
group with respect to the normotensive group (Fig 5).
|
) and hypertensive
patients (
|
) and hypertensive
patients (
P<.01, 
P<.001, normotensive subjects vs
hypertensive patients, unpaired t test.
Elastic Parameters and Viscosity Index
Table 4 shows elastic parameters and
viscosity indexes in both groups. In the normotensive group, effective
and isobaric values of compliance were higher in the femoral artery
than in the carotid artery (P<.01), but effective and
isobaric values of distensibility were not different between both
arteries. In the hypertensive group, effective and isobaric values of
compliance and distensibility were lower in the femoral artery than in
the carotid artery (P<.05). Carotid artery isobaric values
of compliance and distensibility were similar in the two groups, but
effective values were lower (P<.05, P<.01) in
the hypertensive group than in the normotensive group. The femoral
artery had lower effective and isobaric values of compliance and
distensibility in the hypertensive group than in the normotensive group
(P<.001). Femoral and carotid wall viscosity indexes showed
no differences in each group, whereas the viscosity index was higher in
both arteries in the hypertensive than the normotensive group
(P<.001).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study provides a complete in vivo description of geometric, elastic, and viscous properties of carotid and femoral arteries in human hypertension. Two recent noninvasive vascular techniques, applanation tonometry and echotracking, previously used and validated in the literature,10 11 were applied for measuring pressure and diameter pulses in both arteries. The common segment proximal to the bifurcation of each artery was chosen for investigation because of its particular suitability for tonometric and echotracking procedures.15 Furthermore, both arteries are highly sensitive to the effects of cardiovascular risk factors,9 14 22 23 and therefore they are preferential targets for exploring the vascular changes of hypertension. The applanation tonometric procedure has shown good accuracy and reproducibility for recording pulse pressure contour in a peripheral vessel on the condition that the artery dilates symmetrically and that the elastic properties of surrounding tissues are high compared with those of the artery under investigation.10 17 We paid particular attention to such conditions being fulfilled in all individuals of the study. The echotracking device has also shown a high degree of reproducibility for measuring pulse diameter waves in both the common carotid and common femoral arteries.8 15 To optimize the accuracy of diameter and pressure measurements, the same physician especially trained in tonometric and echotracking techniques investigated all the subjects throughout the study. The autocorrelation of diameter and pressure pulses during four consecutive cardiac cycles allowed us to obtain a diameter-pressure hysteresis loop in the two arteries investigated.12 19 An original procedure of hysteresis elimination, based on the characterization of the viscoelastic behavior of the arterial wall,20 was used to determine the wall viscosity and purely elastic diameter-pressure curve. By deriving the latter curve with respect to pressure, we obtained the compliance-pressure curve. We also determined the distensibility-pressure curve after having normalized compliance to the arterial diameter because compliance mixes diameter with distensibility1 2 and therefore is a nonspecific descriptor of arterial wall elastic properties. These three curves were used for comparing arterial parameters between hypertensive and normotensive groups at the same level of pressure (isobaric conditions). This allowed us to eliminate the mechanical stretching effect of arteries by the elevated distending pressure of hypertensive patients.
A first objective of our work was to assess the effects of hypertension on the geometric properties of arteries. Mean, systolic, and diastolic values of diameters of the two arteries were increased in hypertensive patients with respect to control subjects. This finding is in accordance with previous studies showing that hypertension was associated with a dilation of large arteries.1 2 4 8 To explore whether this dilation was due to the mechanical stretching of arteries by the elevation of distending pressure, we compared the diameter-pressure curves of each artery in hypertensive and normotensive individuals. We found that the carotid dilation was primarily due to the increased distending pressure because carotid diameter-pressure curves were not different between the groups. This lack of difference indicates that at the same level of pressure hypertensive patients had the same carotid diameter as normotensive subjects. In contrast, dilation of the femoral artery persisted when hypertensive patients were compared at the same level of pressure with normotensive subjects, since the femoral diameter-pressure curve was reset toward higher values of diameter in the hypertensive group with respect to the normotensive group. This finding suggests that the femoral dilation of hypertensive patients was an intrinsic (pressure-independent) geometric change. We completed investigation of the geometric properties by analyzing pulse diameter in both arteries and in both groups. We found that carotid pulse diameter was not different in hypertensive and normotensive groups, whereas femoral pulse diameter was reduced in hypertensive patients. This suggests that the pulsatile distension of the femoral artery was impaired in hypertension, whereas that of the carotid artery was unaffected. These results appear to conflict with those reported in a previous study24 that investigated carotid and femoral arteries with the echotracking procedure in two hypertensive and normotensive groups. This previous study showed that carotid pulse diameter was reduced, and femoral pulse diameter was unchanged in hypertensive patients. The main reason for the discrepancy with the present work is that in the control group of the previous study, pulse diameter was lower in the femoral artery than in the carotid artery. This observation is in contrast to our data and inconsistent with the positive correlation found in our control group between pulse diameter and pulse pressure of the two arteries pooled together. Our correlation suggests that the higher pulse diameter in the femoral artery than in the carotid artery was in part a mechanical consequence of the higher femoral pulse pressure. This latter phenomenon corresponds to the well-known physiological amplification of the pressure pulse between the distal femoral site and the proximal carotid site.18 Finally, our findings on mean and pulse values of carotid and femoral diameters demonstrate that hypertension altered preferentially the geometric properties of the femoral artery by inducing an intrinsic dilation and a loss of pulsatile distension, alterations that were not observed in the carotid artery.
Another major point of investigation of our work was to analyze the elastic properties of arteries and to provide information on the intrinsic pressure-independent elastic change of the arterial walls in hypertension. In the carotid artery, we found that the compliance-pressure and distensibility-pressure curves were not different between hypertensive patients and control subjects. This means that at the same level of pressure hypertensive patients had carotid compliance and distensibility values similar to those of normotensive control subjects and suggests that the intrinsic elastic properties of the carotid artery were not modified by hypertension. This analysis was confirmed by the comparison of effective and isobaric values of compliance and distensibility between the hypertensive and normotensive groups. We found that effective values of compliance and distensibility of the carotid artery were reduced 21% and 27%, respectively, in hypertensive patients with respect to control subjects, whereas isobaric values were unchanged. These findings demonstrate that the carotid stiffening observed at the prevailing blood pressure of hypertensive patients was primarily due to the mechanical wall stretching of the increased distending pressure, as previously reported.6 In the femoral artery, the results were different because the femoral compliance-pressure and distensibility-pressure curves were shifted toward lower values in hypertensive patients with respect to control subjects. Thus, at the same pressure level as normotensive subjects, hypertensive patients had lower values of femoral compliance and distensibility. These findings were confirmed by the comparison of effective and isobaric values of femoral compliance and distensibility between groups. Effective values of femoral compliance and distensibility were reduced 48% and 53%, respectively, in hypertensive patients with respect to control subjects. Isobaric values of femoral compliance and distensibility were also reduced 33% and 37%, respectively, in hypertensive patients. Therefore, the femoral stiffening of hypertensive patients was not solely a mechanical response of the arterial walls to the pressure elevation but also an intrinsic pressure-independent change of the elastic properties. Furthermore, the fact that femoral distensibility was reduced demonstrated directly an alteration of elastic properties of femoral walls since distensibility is a specific descriptor of arterial wall elasticity. On the other hand, the observation that femoral compliance was reduced despite the larger femoral diameter of hypertensive patients suggested that the femoral dilation was not sufficient to compensate for the loss of femoral distensibility. Finally, the comparison of elastic parameters between the two arteries in the control group showed that effective and isobaric values of compliance were higher in the femoral artery than in the carotid artery, whereas distensibility did not differ between the vessels. This suggested that the larger femoral diameter contributed to the greater femoral compliance in the control group. On the other hand, in the hypertensive group effective and isobaric values of compliance and distensibility were lower in the femoral artery than in the carotid artery. This confirmed the preferential stiffening effect of hypertension on the femoral artery. The reasons for the disparity between the stiffening processes of both vessels could not be determined in the present work. Several mechanisms might play a role, such as the higher hydrostatic pressure in the femoral artery, the particular shearing conditions caused by the curvature of the femoral artery, or the higher susceptibility of the femoral artery to cardiovascular risk factors.9 14 Whatever the precise mechanisms, the fact that the femoral artery was more stiffened than the carotid artery in hypertension could focus vascular investigation on the femoral site with respect to the early detection of hypertensive arterial changes as well as to their progression or regression.
A last point of investigation was the assessment of the wall viscosity of arteries. Wall viscosity has been estimated as the area of the diameter-pressure hysteresis loop during the procedure of loop elimination. It must be considered as an index of wall viscosity because the calculation of the true wall viscosity would have required us to determine the stress-strain hysteresis relationship. Unfortunately, because wall thickness was not measured in this work, wall stress could not be calculated. We found that compared with control subjects, hypertensive patients had an increased wall viscosity index in the carotid artery and in the femoral artery. Thus, contrary to the geometric and elastic alterations that predominated in the femoral artery, the change in wall viscosity affected proportionally the carotid and femoral vessels. This increased wall viscosity might be the consequence of hypertensive vascular hypertrophy and particularly of the participation of the smooth muscle in that hypertrophy. Indeed, the smooth muscle component among the arterial wall constituents has been demonstrated to be responsible for the viscous behavior of the diameter-pressure relationship.25 26 Furthermore, the increased wall viscosity found in the present study is compatible with our previous observations of increased intima-media thickness in the carotid and femoral arteries.13
In conclusion, the present study demonstrated that the physical properties of large arteries were markedly modified in the presence of hypertension. Such modifications concerned the geometry, wall elasticity, and wall viscosity of the vessel, but the distribution of the geometric and elastic changes was preferential in the femoral artery and that of viscous alterations was uniform in carotid and femoral arteries. The topographic dissociation between elastic and viscous responses of the arterial wall to hypertension suggested that the elastic alterations might be related to local phenomena dependent on the singularities of the arterial system. In contrast, the viscosity abnormalities could reflect more general influences of hypertension on large artery smooth muscle. Overall, these findings indicated that geometry, elasticity, and viscosity of the arterial walls should be considered independently when assessing the development of hypertensive vascular change and its response to antihypertensive treatment.
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Footnotes |
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Reprint requests to Professeur Alain Simon, Centre de Médecine Préventive Cardiovasculaire, Hôpital Broussais, 96 rue Didot, 75674 Paris Cedex 14, France.
Received February 9, 1994; first decision April 13, 1994; accepted March 9, 1995.
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 L. Lim, N. Cheung, G. Gazzard, Y.-H. Chan, T.-Y. Wong, and S.-M. Saw Corneal Biomechanical Properties and Retinal Vascular Caliber in Children Invest. Ophthalmol. Vis. Sci., January 1, 2009; 50(1): 121 - 125. [Abstract] [Full Text] [PDF]
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C. Giannattasio, P. Salvi, F. Valbusa, A. Kearney-Schwartz, A. Capra, M. Amigoni, M. Failla, L. Boffi, F. Madotto, A. Benetos, et al. Simultaneous Measurement of Beat-to-Beat Carotid Diameter and Pressure Changes to Assess Arterial Mechanical Properties Hypertension, November 1, 2008; 52(5): 896 - 902. [Abstract] [Full Text] [PDF]
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A. D. Stewart, B. Jiang, S. C. Millasseau, J. M. Ritter, and P. J. Chowienczyk Acute Reduction of Blood Pressure by Nitroglycerin Does Not Normalize Large Artery Stiffness in Essential Hypertension Hypertension, September 1, 2006; 48(3): 404 - 410. [Abstract] [Full Text] [PDF]
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D. G. Edwards, A. L. Gauthier, M. A. Hayman, J. T. Lang, and R. W. Kenefick Acute effects of cold exposure on central aortic wave reflection J Appl Physiol, April 1, 2006; 100(4): 1210 - 1214. [Abstract] [Full Text] [PDF]
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R. L. Armentano, J. G. Barra, D. B. Santana, F. M. Pessana, S. Graf, D. Craiem, L. M. Brandani, H. P. Baglivo, and R. A. Sanchez Smart Damping Modulation of Carotid Wall Energetics in Human Hypertension: Effects of Angiotensin-Converting Enzyme Inhibition Hypertension, March 1, 2006; 47(3): 384 - 390. [Abstract] [Full Text] [PDF]
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A. E. DeVan, M. M. Anton, J. N. Cook, D. B. Neidre, M. Y. Cortez-Cooper, and H. Tanaka Acute effects of resistance exercise on arterial compliance J Appl Physiol, June 1, 2005; 98(6): 2287 - 2291. [Abstract] [Full Text] [PDF]
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K. L. Moreau, K. M. Gavin, A. E. Plum, and D. R. Seals Ascorbic Acid Selectively Improves Large Elastic Artery Compliance in Postmenopausal Women Hypertension, June 1, 2005; 45(6): 1107 - 1112. [Abstract] [Full Text] [PDF]
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 R.L. Armentano, E.I. C. Fischer, D. B. Santana, D. Craiem, H. Vernhet, B. Jean, S. Lust, J. P. Laroche, A. Bonafe, I. Quere, et al. Wall Viscosity of the Stented Arteries * Response Stroke, September 1, 2004; 35(9): 2013 - 2013. [Full Text] [PDF]
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K. L Moreau, A. J Donato, D. R Seals, C. A DeSouza, and H. Tanaka Regular exercise, hormone replacement therapy and the age-related decline in carotid arterial compliance in healthy women Cardiovasc Res, March 1, 2003; 57(3): 861 - 868. [Abstract] [Full Text] [PDF]
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M. A. Zulliger, N. T. M. R. Kwak, T. Tsapikouni, and N. Stergiopulos Effects of longitudinal stretch on VSM tone and distensibility of muscular conduit arteries Am J Physiol Heart Circ Physiol, December 1, 2002; 283(6): H2599 - H2605. [Abstract] [Full Text] [PDF]
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E. J. Balkestein, J. A. Staessen, J.-G. Wang, J. J. van der Heijden-Spek, L. M. Van Bortel, C. Barlassina, G. Bianchi, E. Brand, S.-M. Herrmann, and H. A. Struijker-Boudier Carotid and Femoral Artery Stiffness in Relation to Three Candidate Genes in a White Population Hypertension, November 1, 2001; 38(5): 1190 - 1197. [Abstract] [Full Text] [PDF]
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 K. D. Monahan, H. Tanaka, F. A. Dinenno, and D. R. Seals Central Arterial Compliance Is Associated With Age- and Habitual Exercise-Related Differences in Cardiovagal Baroreflex Sensitivity Circulation, October 2, 2001; 104(14): 1627 - 1632. [Abstract] [Full Text] [PDF]
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L. M.A.B. Van Bortel, H. A.J. Struijker-Boudier, and M. E. Safar Pulse Pressure, Arterial Stiffness, and Drug Treatment of Hypertension Hypertension, October 1, 2001; 38(4): 914 - 921. [Abstract] [Full Text] [PDF]
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K. D. Monahan, F. A. Dinenno, D. R. Seals, C. M. Clevenger, C. A. Desouza, and H. Tanaka Age-associated changes in cardiovagal baroreflex sensitivity are related to central arterial compliance Am J Physiol Heart Circ Physiol, July 1, 2001; 281(1): H284 - H289. [Abstract] [Full Text] [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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 R. Din-Dzietham, D. Liao, A. Diez-Roux, F. J. Nieto, C. Paton, G. Howard, A. Brown, M. Carnethon, and H. A. Tyroler Association of Educational Achievement with Pulsatile Arterial Diameter Change of the Common Crotid Artery The Atherosclerosis Risk in Communities (ARIC) Study, 1987-1992 Am. J. Epidemiol., October 1, 2000; 152(7): 617 - 627. [Abstract] [Full Text] [PDF]
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H. Tanaka, F. A. Dinenno, K. D. Monahan, C. M. Clevenger, C. A. DeSouza, and D. R. Seals Aging, Habitual Exercise, and Dynamic Arterial Compliance Circulation, September 12, 2000; 102(11): 1270 - 1275. [Abstract] [Full Text] [PDF]
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H. D. Intengan and E. L. Schiffrin Structure and Mechanical Properties of Resistance Arteries in Hypertension : Role of Adhesion Molecules and Extracellular Matrix Determinants Hypertension, September 1, 2000; 36(3): 312 - 318. [Abstract] [Full Text] [PDF]
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H. D. Intengan, L. Y. Deng, J. S. Li, and E. L. Schiffrin Mechanics and Composition of Human Subcutaneous Resistance Arteries in Essential Hypertension Hypertension, January 1, 1999; 33(1): 569 - 574. [Abstract] [Full Text] [PDF]
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R. L. Armentano, S. Graf, J. G. Barra, G. Velikovsky, H. Baglivo, R. Sanchez, A. Simon, R. H. Pichel, and J. Levenson Carotid Wall Viscosity Increase Is Related to Intima-Media Thickening in Hypertensive Patients Hypertension, January 1, 1998; 31(1): 534 - 539. [Abstract] [Full Text] [PDF]
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A. J. Bank, H. Wang, J. E. Holte, K. Mullen, R. Shammas, and S. H. Kubo Contribution of Collagen, Elastin, and Smooth Muscle to In Vivo Human Brachial Artery Wall Stress and Elastic Modulus Circulation, December 15, 1996; 94(12): 3263 - 3270. [Abstract] [Full Text]
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R. Weber, N. Stergiopulos, H. R. Brunner, and D. Hayoz Contributions of Vascular Tone and Structure to Elastic Properties of a Medium-Sized Artery Hypertension, March 1, 1996; 27(3): 816 - 822. [Abstract] [Full Text]
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H. Tanaka, D. R. Seals, K. D. Monahan, C. M. Clevenger, C. A. DeSouza, and F. A. Dinenno Regular aerobic exercise and the age-related increase in carotid artery intima-media thickness in healthy men J Appl Physiol, April 1, 2002; 92(4): 1458 - 1464. [Abstract] [Full Text] [PDF]
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