(Hypertension. 1996;27:816-822.)
© 1996 American Heart Association, Inc.
Articles |
Contributions of Vascular Tone and Structure to Elastic Properties of a Medium-Sized Artery
From Division d'Hypertension (CHUV), and the Biomedical Engineering Laboratory, Swiss Federal Institute of Technology (N.S.), Lausanne, Switzerland.
Correspondence to Daniel Hayoz, Division d'Hypertension, Centre Hospitalier Universitaire Vaudois, 1011 Lausanne, Switzerland.
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Abstract |
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Abstract Isobaric compliance and distensibility of the radial artery were recently reported to be normal or slightly increased in untreated hypertensive patients. However, these findings provide no information on the intrinsic mechanical properties of the wall material. To address this question, we determined intima-media wall thickness, wall-to-lumen ratio, and incremental elastic modulus in the radial artery of 25 untreated hypertensive patients with blood pressure of 150±14/103±6 mm Hg (mean±SD) and 25 matched control subjects with blood pressure of 118±9/79±6 mm Hg. High-resolution echo-tracking for assessment of internal diameter and intima-media wall thickness was combined with measurements of blood flow velocity by Doppler and blood pressure by photoplethysmography. In addition, isobaric compliance and distensibility and incremental elastic modulus were measured at peak diameter during reactive hyperemia after a 5-minute brachial occlusion. No significant difference was found between the two groups for isobaric compliance or distensibility at baseline or during hyperemia. However, incremental elastic modulus at 100 mm Hg tended to be lower in hypertensive patients than control subjects (1.9±1.1 versus 2.5±1.2 mm Hg·104, P=.1) in resting conditions. Hypertensive patients and control subjects had similar internal diameters (2.47±0.32 versus 2.41±0.35 µm), but intima-media wall thickness and wall-to-lumen ratio were significantly increased in hypertensive patients compared with control subjects (0.268±0.032 versus 0.236±0.025 mm [P
.01] and
0.220±0.038 versus
0.195±0.028 [P.05], respectively). Peak
hyperemic blood flow response (hypertensive patients versus
control subjects: 349% versus 360% increase from baseline) and
reactive hyperemic dilation (7.2% versus 7.9%) were similar
in amplitude and duration in the two groups. These results suggest that
wall thickening is an adaptive process that reduces wall tension in
hypertensive patients while preserving a normal mechanical behavior of
the radial artery. This is most likely accomplished by modification of
the incremental elastic modulus of wall components rather than by a
change in vascular tone.
Key Words: compliance • vasomotion • hypertrophy
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Introduction |
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TopAbstractIntroductionMethods Results Discussion References |
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Hypertension is a well-established cardiovascular risk factor for stroke and ischemic heart disease.1 Although lesions in medium-sized arteries of specific vascular territories are a major cause of complications in hypertension, relatively little is known of the in vivo geometry and function of conduit arteries. Recently, new noninvasive methods have been developed to assess preclinical alterations of the cardiovascular system.2 3 4 Structural changes of the arterial wall and altered vascular smooth muscle activity have been observed in hypertension, with an increased wall-to-lumen ratio in the microcirculation and macrocirculation.5 6 7 Left ventricular hypertrophy and more recently increased carotid artery wall thickness have been reported to better predict the subsequent risk of cardiovascular events in hypertensive patients.2 3 4
Controversial reports on the elastic properties of arteries in response to hypertension have revealed the complexity and inhomogeneity of the adaptive changes as well as conceptual and methodological difficulties. Decreased elasticity has been documented in large elastic arteries (ie, aorta and carotid) and in muscular conduit arteries of the upper extremities (ie, brachial artery).8 9 10 11 However, recent studies from our laboratory and subsequently from others reported normal or even slightly increased radial artery isobaric compliance and distensibility.12 13 The two parameters reflect the combined effect of geometry (diameter, wall thickness) and intrinsic wall material properties (elastic modulus). Recent findings based on echo-tracking methods demonstrated wall thickening in the radial artery of hypertensive patients.14 Thus, as suggested by Mulvany,15 in the face of an increased wall-to-lumen ratio and an internal diameter similar to that of normotensive subjects, a preserved compliance and distensibility of the radial artery in hypertensive patients can be achieved only when the elastic modulus is reduced.
Little is known of the relative contribution of vascular tone and changes in arterial structure to the viscoelastic properties in chronic hypertension. In this study, we focused on the contributions of geometric parameters and vascular tone to the elastic behavior of the radial artery of patients with essential hypertension. We determined pulsatile changes of internal diameter, IMT, BP, and regional blood flow at baseline conditions and peak vasodilation during reactive hyperemia after a 5-minute arterial occlusion. The endothelium-dependent flow-mediated dilation of conduit arteries may be used as a noninvasive estimate of endothelial function after an ischemic stimulus.16 However, conflicting results have been reported regarding flow-mediated and muscarinic receptor–mediated dilation in several studies addressing functional alteration of conduit vessels in populations presenting with different cardiovascular risk factors.17 18 19 20 21 The diversity of the methods used and heterogeneity of the different vascular regions probably account for a great deal of the inconsistency reported in the literature.
The major findings of the present study are that (1) with a similar internal radius, hypertensive patients exhibit a significantly greater wall-to-lumen ratio compared with normotensive control subjects; (2) BP and wall-to-lumen ratio are positively correlated; (3) the preserved elastic response of the radial artery in hypertensive patients does not seem to be related to adaptive changes of vascular tone but results from modifications of intrinsic properties of the wall material; and (4) reactive hyperemic dilation is not impaired in mild essential hypertensive patients compared with matched control subjects.
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Methods |
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Twenty-five newly diagnosed and never-treated patients with mild or moderate hypertension (19 men, 6 women; aged 32 to 70 years; mean±SD, 48±11 years) and 25 normotensive subjects (17 men, 8 women; aged 25 to 71 years; mean±SD, 49±12 years) were enrolled in this study. At each visit, BP was measured with subjects in the seated position three times at 5-minute intervals after a 20-minute rest with the use of a standard mercury sphygmomanometer. Normotension was defined by BP values less than or equal to 140/90 mm Hg at repeated visits. Hypertension was defined by seated diastolic BP greater than 95 mm Hg (mean of three measures) on two consecutive visits at a 1-month interval. Patients with diabetes mellitus, valvular heart disease, cardiovascular events (stroke, myocardial infarction, angina pectoris, coronary artery bypass graft, or arrhythmia), or secondary forms of hypertension were excluded. No patient had undergone medical treatment before entering the study. All patients were informed about the nature of the study and gave their oral consent. The protocol of the study had been previously accepted by the Hospital Ethics Committee. The clinical characteristics of the patients and control subjects are summarized in Table 1
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Radial artery diameter and IMT were continuously recorded with a recently developed noninvasive, high-precision A-mode echo-tracking device. The description of the device (NIUS 02, Asulab SA), which is an upgraded version of a previous apparatus that used hardware tracking, as well as validation for diameter and IMT measurements and reproducibility data have been previously reported.22 23 24 Briefly, the right forearm of each subject was extended and secured in an immobilizing splint to avoid involuntary movements. A 10-MHz strongly focused piezoelectric transducer (operated in PW mode) was then positioned perpendicular to the radial arterial axis, 5 to 8 cm proximal to the wrist, without any skin contact. Stereo Doppler guidance was used to ensure a correct vertical position of the probe over the artery and then was turned on A-mode (radio-frequency echo line). The ultrasonic echoes reflected by the interfaces between blood and both anterior and posterior walls were sampled at 100 MHz and stored at a 500-Hz repetition frequency. The vascular and media-adventitia interfaces were subsequently selected by the operator on the radio-frequency echo line and automatically tracked to obtain diameter and IMT as well as their variations over time. The exact position of each selected interface was obtained by calculating in real time the position of the maximum of the corresponding peak in the radio-frequency line. The initial resolution given by the 100-MHz sampling frequency (corresponding to a spatial depth of 7.5 µm) was improved to close to 1 µm. The signal was finally stored at 50 Hz. The reduction from repetition frequency to this final sampling frequency was performed by averaging 10 samples, allowing the reduction of both noise and memory requirement. BP was measured at the right middle finger by a photoplethysmographic instrument (Finapres Ohmeda 2003, BOC Group Inc) linked to the ultrasonic echo-tracking device. This apparatus provides noninvasive continuous recordings of finger BP with a resolution of 2 mm Hg. This technique has been studied extensively and described in detail elsewhere.25
Simultaneous and continuous acquisitions of internal
arterial diameter and BP were processed to compute a cross
section–pressure relationship that was subsequently converted into
compliance-pressure and distensibility-pressure curves,
characterized over the entire range of pulse pressure.
Cross-sectional compliance (C) in the case of a cylindrical vessel
is given by C=
S/P, where S represents the change in
cross section of the lumen and P the change in BP.
Arterial cross-sectional distensibility (D) is the
compliance value normalized for the cross section and is defined by
D=1/Sx(S/P). Circumferential wall stress was calculated
as
MAPxd/2h, where MAP is mean arterial pressure, d is mean
internal diameter, and h is intima-media thickness.
Einc is defined as the slope of the stress-strain curve
by Einc=s/e, where s represents change in
stress and e change in strain. Strain is defined by
e=(d-d0/d0) where d0
is the diameter at zero transmural pressure. To avoid a procedure
requiring the measurement in the unloaded state (d0),
difficult to obtain in vivo, we applied Hooke's law for
thick-walled tubes, which defines
Einc=3x(1+LS/WS)/D,
where LS is lumen cross section, WS is wall cross section, and D is
distensibility.26 WS was defined by
WS=
Re2-Ri2,
where Re is external radius, and Ri is internal
radius derived from the mean internal diameter and mean IMT.
Einc was then expressed as a function of pressure and
circumferential wall stress (Einc-pressure and
Einc-stress curves).
All subjects were examined in the supine position after 30 minutes of rest in a room with a constant temperature of 22°C. The same observer made all the measurements during the study. Radial artery parameters were recorded during 10 minutes in the resting condition. Compliance, distensibility, and Einc were determined over several cardiac cycles as described above. In addition, radial blood flow velocity was measured by continuous-wave Doppler using a commercially available device (Doptek 2003, Deltex SA) with an 8-MHz transducer at an angle of 60°. This transducer is positioned distal to the 10-MHz probe, aimed at the site of the diameter measurement. No interferences between the two waves were noted throughout the duration of the experiment. Blood flow is the product of time-averaged mean velocity and arterial cross-sectional area obtained simultaneously from arterial diameter.
Ischemia was induced for 5 minutes by occluding the upper arm
with a cuff inflated at 30 mm Hg above systolic BP and ended
by sudden cuff deflation (reactive hyperemia). Because of
repeated loss of tracked echo signals due to involuntary movements of
the subjects during the procedure, recordings of 8 control
subjects and 9 hypertensive patients were not suitable for
analysis. Good-quality recordings were obtained in
17 control subjects and 16 hypertensive patients, preserving two
well-matched groups for all clinical parameters that
did not significantly deviate from the values presented in
Table 1
. Arterial parameters described above
were recorded during the entire procedure and until return to
preocclusion baseline diameter (total duration, approximately 15
minutes). Compliance, distensibility, and Einc were
calculated over a few (5 to 10) cardiac cycles at peak diameter
(between 40 and 60 seconds after upper-arm cuff release) during
hyperemia. Because of the detracking risk during the functional
maneuvers, only internal diameter recordings were performed
during reactive hyperemia. IMT at peak diameter
(IMTpd) was therefore extrapolated from the measured
preocclusion baseline WCSA and the internal diameter measured at peak
dilation (dipd). This is possible because WCSA is constant
in a given subject because of the incompressibility of the
arterial tissue.27 Therefore,
IMTpd was calculated as
(depd-dipd)/2, where
depd is external diameter at
peak dilation defined by
depd=
+(d2/4)].
Radial artery blood flow was determined from
simultaneous recording of blood velocity and
diameter the same way as under resting conditions.
Repeatability Coefficient
The repeatability coefficient of
internal radial artery diameter
and IMT was investigated in 10 subjects according to the British
Standard Institution definition.28 Mean values for
internal diameter and IMT were 2596±328 and 285±41 µm
(mean±SD),
respectively. The repeatability coefficient for short-term (20
minutes) intraobserver repeatability was 31 µm for IMT and 70 µm
for internal diameter.
Statistical Analysis
All values are expressed as
mean±SD, except in Figs 3 through
6, for which
mean±SEM was used. The different parameters
were compared between hypertensive patients and normotensive subject
using unpaired Student's t test data. For comparison of the
different curves between the two groups, areas under the curves were
compared for overlapping sections. Differences were considered
significant at a value of P<.05. Correlation coefficients
were calculated by standard methods. Independence of association was
assessed by stepwise multiple regression.
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) and control subjects (
). Values
are mean±SEM. Right, Intrinsic elastic properties of the wall material
of radial artery assessed by Einc-pressure curves and
Einc–circumferential stress curves in hypertensive
patients (
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Results |
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TopAbstractIntroductionMethods Results Discussion References |
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The radial artery parameters of the normotensive control subjects and hypertensive patients recorded at baseline conditions are listed in Table 2
. Isobaric internal
radial artery diameters were similar in both groups. IMT, WCSA, and
wall-to-lumen ratio were significantly increased in
hypertensive patients compared with control subjects. Nevertheless, the
distribution of individual values of WCSA and wall-to-lumen
ratio showed substantial overlap between hypertensive patients and
control subjects (Fig 1). Circumferential wall stress at
mean BP was not significantly different between the two groups.
Univariate analysis showed that WCSA was correlated
with systolic and diastolic BPs (r=.34,
P<.05 and r=.41, P<.01,
respectively) and the wall-to-lumen ratio with
systolic, diastolic, and pulse pressures
(r=.44, P<.01; r=.29,
P<.05; and r=.48, P=.0005,
respectively; Fig 2). In multivariate
analysis, the wall-to-lumen ratio and WCSA were
independently predicted by sex but not by age and body mass index. At
baseline conditions, compliance, distensibility, and Einc
did not differ significantly between hypertensive patients and control
subjects (Fig 3). However, there was a trend toward
lower values of the Einc-pressure curve in hypertensive
patients (P=.1) (Fig 3, right). When
Einc was
estimated for a given circumferential wall stress, the
Einc-stress curves of hypertensive patients and control
subjects were superimposed (Fig 3, right).
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The radial artery parameters of the subgroup of subjects
who underwent reactive hyperemia are listed in Table 3. The
forearm blood flow rise during reactive
hyperemia was not different in the two groups (349±71% versus
360±79%, hypertensive patients versus control subjects;
mean±SEM).
The reactive hyperemic dilation also was not different between
hypertensive patients and control subjects (7.2±1% and 7.9±1%
increase in diameter compared with resting values), despite a slight
delay in the time to peak response of diameter, a lower value in
maximal diameter, and a slower return to baseline in hypertensive
patients (Fig 4). The curves were generated by averaging
the individual mean diameter and radial artery flow data measured
continuously during the period of reactive hyperemia. When
compared with baseline conditions, compliance, distensibility, and
Einc were not significantly changed at peak diameter during
hyperemia in hypertensive patients or control subjects,
although compliance and distensibility tended to be slightly reduced
and Einc augmented in both groups during reactive
hyperemia (Table 3 and Fig 5). A subgroup of six
hypertensive patients showed a definite increase of Einc at
peak diameter during reactive hyperemia that exceeded the 95th
percentile compared with baseline conditions. No such change in
Einc was observed in the control group (Fig 6). No
significant correlation was found between this
increase of Einc and IMT, WCSA, wall-to-lumen
ratio, or BP parameters.
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Discussion |
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TopAbstractIntroductionMethods Results Discussion References |
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The present study demonstrates that for similar internal radial artery diameters, wall thickness, WCSA, and wall-to-lumen ratio were significantly increased in hypertensive patients compared with control subjects. Our data on radial artery wall thickness show a rather large overlap between control subjects and hypertensive patients very similar to data observed in several studies on cardiac hypertrophy and carotid and femoral artery wall thicknesses.29 30 By analogy to left ventricular adaptation to increased vascular load, these data suggest that the radial artery undergoes "eccentric hypertrophy" (no change in lumen with increased wall mass) rather than remodeling (reduced diameter with no change in wall mass) or "concentric hypertrophy" (reduced diameter with increased wall mass). Interestingly, we found the strongest correlation between wall-to-lumen ratio and pulse pressure. Evidence from previous reports has shown that pulse pressure independently predicts the risk for left ventricular hypertrophy and structural alteration of small vessels and cardiovascular events.31 32 33 Thus, pulse pressure may be regarded as a more potent stimulus of vessel growth than other BP parameters. Whether pulse pressure contributes to specific alterations of vessel geometry, as shown in the present study, needs further investigation. Furthermore, one cannot exclude the possibility that growth and remodeling coexist to a certain extent, as postulated for resistance vessels.7 Whether this process depends on BP level and/or the duration of hypertension also remains to be determined.
Vascular tone plays an important role in the resistive vessels in hypertension, whereas its role remains obscure in the conduit vessels.34 35 Reactive hyperemia after a 5-minute brachial occlusion was used to assess the contribution of vascular tone in conduit arteries in hypertension. This noninvasive maneuver induces a reasonable reduction of vascular tone in the distal arteries and did not significantly alter baseline compliance, distensibility, or Einc. Furthermore, it did not distinctly separate the hypertensive patients from control subjects. This corroborates preliminary data reported by other investigators showing equivalent responses of radial artery diameter and compliance under increasing intra-arterial infusion of sodium nitroprusside (Weihprecht et al, unpublished data, 1995) or the absence of changes in isobaric Einc after intra-arterial nitroglycerin infusion.36 Nevertheless, these results do not preclude the possibility that vascular tone may play a role in the elastic behavior of the radial artery. Indeed, a subgroup of hypertensive patients (6 of 16) showed a marked increase of Einc during vascular relaxation compared with resting values, suggesting that under certain circumstances, vascular tone may significantly contribute to maintaining normal biomechanical properties of the artery in hypertension.
Arterial distensibility reflects the combined effect of geometric parameters (diameter, wall thickness) and intrinsic wall properties (Einc). The formula used here to calculate Einc is derived for thick wall artery with homogeneous and isotropic materials. We thus recognize that anisotropy of the wall material may to some extent influence the calculated values presented here. A second limitation of the technique resides in the fact that the echo-tracking technique cannot accurately measure the adventitia. Thus, Einc truly refers to the modulus of the intima-media portion of the vessel. Given the fact that similar internal radial diameters were observed in both study groups, only a modification of the intrinsic mechanical properties of the wall material can explain preserved or slightly enhanced distensibility of the vessel wall.15 This is supported by recent work from Laurent et al37 showing a reduced isobaric elastic modulus of the radial artery wall material in essential hypertensive patients. Our observations show a slightly reduced Einc in the hypertensive patients that did not reach statistical significance compared with control subjects. The discrepancy between the two studies may be related to differences in the clinical parameters of the studied populations (ie, degree and duration of hypertension). Since intraluminal pressure is perceived by wall material as a pressure-induced stress, Einc is best determined for a given circumferential wall stress.38 In this respect, our results show no differences between normotensive subjects and hypertensive patients, suggesting an optimized adaptive response of the artery wall to the increased arterial pressure in newly diagnosed hypertensive patients. However, these conclusions are drawn only for this particular muscular artery and for this selected population. Recent data suggest that lower extremity conduit arteries may present earlier elastic alterations than carotid artery, but in the absence of wall thickness measurements, no information on the intrinsic properties of the wall material can be gained.39 The respective effects of high BP, local specific constraints on the vessel wall, and inhomogeneity of vascular responses to mechanical influences remain to be determined.
Flow-mediated arterial dilation in hypertensive patients remains a controversial issue. The importance of a preserved endothelial function is well demonstrated, and the dependence on nitric oxide or closely related compounds has been recently reported.16 Therefore, flow-mediated dilation during reactive hyperemia can be regarded as a noninvasive estimate for testing of the endothelial release of nitric oxide in conduit arteries. We demonstrate that in mild essential hypertension, reactive hyperemic dilation after upper occlusion is not significantly affected, suggesting a roughly preserved L-arginine–nitric oxide pathway. This result is in accordance with previous data demonstrating a normal responsiveness of the forearm vasculature to muscarinic agonists in hypertensive patients,18 but it contrasts with a number of animal experiments and clinical studies showing impaired dilation.17 40 41 42 43 Differences in the methods used and inhomogeneity of the arterial territories partly account for these discrepancies. Indeed, the technique used here does not allow one to separate the effect of increased blood flow from that of ischemia-related vasodilator metabolites that have been widely used to assess flow-mediated dilation. Moreover, transduction mechanisms and sensitivity differences between mechanical (shear stress) and biochemical (carbachol, acetylcholine) stimuli may further contribute to the differential responses. This is supported by studies on the coronary circulation showing that in the natural history of atherosclerosis, impairment of receptor-mediated activation of the endothelium precedes alteration of flow-mediated dilation.44 Shear stress may therefore be less sensitive than direct muscarinic receptor activation for detection of early L-arginine pathway dysfunction but does not necessitate intra-arterial infusion with all the risks associated with arterial puncture.
In conclusion, our results suggest that the radial artery develops an "eccentric hypertrophy" as an adaptive process to maintain wall tension in a normal range. To limit the consequences of hypertrophy on arterial impedance, the vessel corrects its intrinsic properties to normalize the distensibility. A modification of the composition and arrangement of the different wall components rather than a change in smooth muscle tone as shown here is most likely responsible for preserving the elastic and functional behaviors of this specific conduit artery. Histomorphometric studies will be necessary to determine the structural modifications of this adaptive process.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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This study was supported by grants from the Swiss National Research Foundation (FS: 32-42515.95) and UNIL-EPFL.
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References |
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