(Hypertension. 1999;33:793-799.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Assessment of Arterial Compliance by Carotid Midwall Strain-Stress Relation in Hypertension
From the Department of Medicine and the Cardiovascular Center, The New York Hospital–Cornell Medical Center, New York, NY, and Institute of Gerontology and Geriatrics, University of Firenze, Firenze, Italy (R.P.).
Correspondence to Richard B. Devereux, MD, Division of Cardiology, Box 222, The New York Hospital–Cornell Medical Center, New York, NY 10021. E-mail rbdevere{at}mail.med.cornell.edu
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Abstract |
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Abstract—To elucidate the relations between arterial hypertrophy and compliance in hypertension, we studied 205 unmedicated hypertensive patients (129 men and 76 women) and 82 normotensive adults (56 men and 26 women) from an employed population by carotid ultrasound, noninvasive applanation tonometry, and echocardiography. Carotid midwall strain and circumferential stress were calculated at end diastole and peak systole. The relations of luminal and midwall strain to the increment in circumferential stress from end diastole to peak systole (
carotid stress in normal subjects) were used to
calculate ratios of observed/predicted carotid luminal and midwall
strain. Mean stress-corrected luminal strain (82±26%) and midwall
strain (78±23%) were lower (both P<0.001) in
hypertensive patients than in normal adults. Stress-corrected luminal
strain identified 14% of hypertensive patients with low
arterial compliance, while stress-corrected midwall strain
was low in 18% of patients. Patients with subnormal carotid midwall
strain were older (61±12 versus 54±12 years, P<0.01)
and had larger carotid diameters (6.6±0.8 versus 5.7±0.8 mm,
P=0.002) and higher brachial pulse pressures (71±25
versus 63±17 mm Hg, P<0.05) than other
patients. Patients with arterial hypertrophy
had lower stress-corrected midwall strain than those without
hypertrophy (70±24% versus 79±23%,
P=0.05), whereas no difference was observed in
stress-corrected luminal strain (P=0.40).
Stress-corrected midwall strain tended to be lower in patients with
discrete atherosclerotic plaques than in those without (74±20% versus
79±24%, P=0.15). Compared with patients with normal
left ventricular geometry, those with concentric
hypertrophy had larger carotid diameters (6.6±0.7 versus
5.8±0.9 mm, P<0.05) and lower stress-corrected
luminal strain (62±11% versus 85±25%, P<0.05) and
midwall strain (59±10% versus 81±22%, P<0.05).
Therefore, stress-corrected midwall strain identifies patients with
reduced arterial compliance, increased arterial
wall thickness, and abnormal left ventricular geometry
better than conventional measures based on arterial
lumen diameters.
Key Words: carotid arteries • hypertension, chronic • hypertrophy, arterial • hypertrophy, left ventricular • compliance, arterial
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Introduction |
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The chronic increase in blood pressure during sustained hypertension increases arteriolar wall thickness.1 2 In addition, decreased large-artery compliance is a major determinant of increased pulse pressure.3 4 Decreased arterial compliance in hypertensive patients has been attributed both to elevated distending pressure and to hypertension-induced wall thickening that keeps arterial wall stress mainly unchanged despite elevated blood pressure.5 6 However, despite numerous studies of the influence of risk factors on carotid artery intimal-medial thickness (IMT),7 8 9 the relation between arterial wall hypertrophy and compliance in hypertension has not been clearly elucidated. Recently, we evaluated the relation of carotid midwall strain to the increment in carotid stress during systole (
carotid stress) as a measure of arterial
compliance in normotensive adults.10 In this study we
examined carotid midwall mechanics in normotensive and hypertensive
individuals to identify the characteristics of hypertensive patients
with reduced arterial compliance by the carotid midwall
strain-stress relation. |
Methods |
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Subjects
The study group consisted of 205 asymptomatic unmedicated hypertensive patients (63% male; 34% nonwhite; age, 55±12 years; brachial arterial pressure, 158±21/93±11 mm Hg; body mass index, 26.6±4.0 kg/m2) and a reference group of 82 normotensive adults (68% male; 21% nonwhite; age, 50±17 years; brachial arterial pressure, 122±12/73±9 mm Hg; body mass index, 25.1±4.0 kg/m2) from an employed population in New York.11 12 Hypertensive patients had systolic blood pressure >140 mm Hg, diastolic blood pressure >90 mm Hg, or both. Segmental left ventricular (LV) wall motion abnormalities and valvular regurgitation or stenosis were excluded by 2-dimensional and Doppler echocardiograms. On the basis of the Second National Health and Nutrition Examination Survey (NHANES II), subjects were classified as overweight if body mass index was >27.8 kg/m2 for men and >27.3 kg/m2 for women.13 Subjects had no clinical evidence of coronary heart disease and gave informed consent under protocols approved in 1979 and regularly thereafter.
Echocardiographic Methods
M-mode and 2-dimensional echocardiograms were performed by a
skilled research technician and interpreted by a single investigator
(M.J.R.), as previously described.14 Penn convention
measurements were used for LV mass,15 16 and American
Society of Echocardiography
measurements17 were used for LV internal diameter and wall
thicknesses. When optimal orientation of the LV could not be obtained,
correctly oriented 2-dimensional linear dimensions were made by the
American Society of Echocardiography
recommendations.18 Brachial blood pressure was taken 3
times and averaged at the end of the echocardiogram. Gender-specific
partition values for LV mass/body surface area used to classify LV
geometric patterns were the same as those previously used for
comparison with ambulatory blood pressures.19 Patients
were classified as abnormal if the LV relative wall thickness was
>0.4120 or if the LV mass/body surface area was >108
g/m2 in women or >118 g/m2
in men.21
Carotid Ultrasound
A Biosound Genesis II system (OTE Biomedica) or Acuson
128 (Acuson, Inc) equipped with a 7.0- to 7.5-MHz transducer was used
to scan the common, internal, and external carotid arteries for
discrete carotid plaques.8 11 12 13 14 22 23 24 Two-dimensionally
guided M-mode recordings of the distal common carotid artery
1 cm proximal to the carotid bulb with simultaneous ECG
and carotid pressure waveforms were recorded on videotape and
digitized with the use of a frame grabber and customized software.
Electronic calipers were used to measure the internal diameter
(Dd) and far wall IMT
(IMTd) at end diastole, recognized
from the nadir of the simultaneous arterial
pressure waveform or the minimal arterial diameter, as well
as the diameter at peak systole (Ds). All
measurements were performed on several cycles by a single investigator
(M.J.R.) and averaged.
As previously described,24 a multiple regression equation predicting IMT from other potentially relevant variables was IMTd=0.00586(Age)+0.015267(Body Surface Area)+0.16569. The ratio observed/predicted IMTd was calculated for each subject, and arterial hypertrophy was identified if this ratio was >2 SD above the mean ratio of the reference population.
Arterial Function Assessment
Arterial pressure waveforms were recorded
noninvasively by placing a solid-state high-fidelity external pressure
transducer (model SPT-301; Millar Instruments, Inc) over the right
common carotid artery while recording M-mode images of the left
common carotid artery.25 Orientation and pressure applied
to the transducer were adjusted to achieve applanation of the artery
between the transducer and underlying tissue, as has been validated to
yield accurate estimates of intra-arterial pulse pressure
by comparison with simultaneous invasive pressure
recordings.26 27 The transducer is internally
calibrated (1 mV=10 mm Hg) and registers absolute changes in
applied pressure over a range of 300 mm Hg. Actual carotid
pressures were obtained by external calibration; on the basis of the
observation that mean arterial pressure is nearly identical
in all capacitance vessels,28 29 mean brachial artery
pressure was considered to equal the planimetrically computer-derived
mean blood pressure of the carotid waveform. Alternative
analyses in which carotid diastolic pressure was
also set equal to brachial diastolic pressure yielded
similar results and are not reported separately.
Arterial Compliance and Stiffness Indices
As previously described,10 carotid luminal strain,
the percent systolic expansion of the arterial
lumen,30 was calculated as
[(Ds-Dd)/Dd]x100.
Carotid pressures Dd, Ds,
and IMTd were used to calculate several measures
of regional arterial stiffness, including Peterson's
elastic modulus, Young's elastic modulus,31 and a
pressure-independent measure (ß).32 33 Systemic
arterial compliance was estimated by the ratio stroke
volume/brachial pulse pressure.34 In addition, the
arterial compliance index was calculated using a method
modified25 from that described by Randall et
al.35 This index was normalized for body surface area.
Cardiac output was calculated from echocardiographic
diastolic and systolic LV
volumes.36
Measures of Carotid Midwall Function
As previously described in detail,10 carotid
midwall strain was derived with the use of a cylindrical model, adapted
from Shimizu et al,37 which assumes that the volumes of
the total carotid wall and of its inner and outer halves during the
cardiac cycle are constant. If it is assumed that the
arterial long axis remains constant, inner shell
cross-sectional areas at end diastole and at end systole
are equal, allowing use of end-diastolic carotid lumen
diameter and wall thickness and peak systolic diameter to
calculate the systolic thickness of the inner
arterial wall shell as well as other midwall dimensions.
From these values, previously reported equations10 were
used to calculate carotid midwall strain (expressed as percentage), the
midwall Peterson's elastic modulus, the midwall Young's elastic
modulus, and the midwall ß.
Carotid end-systolic stress was estimated at the midwall from
M-mode tracings, with the adaption of a cylindrical
model37 previously used for cardiac
studies,38 39 and the same approach was used to calculate
carotid end-diastolic stress. These values were used to
calculate the increment in carotid stress during the cardiac cycle
(carotid stress).
Equations relating carotid luminal strain and carotid midwall strain to
carotid stress in the clinically normal subjects were used to
predict the expected carotid luminal and midwall strain, respectively,
for observed carotid stress. The ratios of observed/predicted
carotid strains were then derived to yield measures of carotid luminal
and midwall strain adjusted for the imposed stress, called
stress-corrected carotid strain.
Statistical Analysis
Data are presented as mean±SD. Continuous variables
were compared by 1-way ANOVA, followed by the Scheffé post hoc
test. Independent sample t tests and ANCOVAs that took into
account relevant covariates were used to compare mean values between
groups. Proportions were compared among groups by the
2 statistic. The independence of relations
between continuous variables was evaluated by linear regression.
The null hypothesis was rejected at 2-tailed P<0.05.
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Results |
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Relation of Carotid Luminal Strain and Midwall Strain to
Carotid StressFigure 1 shows the relation in hypertensive patients of carotid luminal strain to
carotid stress
(top; r=0.29, P<0.001) and of carotid midwall
strain to carotid stress (bottom; r=0.39,
P<0.001). Stress-corrected luminal strain (82±26%) and
midwall strain (78±23%) in hypertensive patients were on average
subnormal (both P<0.001 versus mean values of 100% and
99% in normal adults). Similarly, after adjustment for age,
conventional measures of arterial stiffness were higher in
hypertensive than in normotensive individuals (6.1±2.5 versus
5.0±2.5, P=0.002 for ß; 636±264 versus 502±204
dyne/cm2 per millimeter
x10-6, P<0.001 for Young's
modulus). The significance of these differences was greater for
stress-corrected luminal strain (t=5.36) and
stress-corrected midwall strain (t=6.89) than for ß
(t=-3.09) or Young's modulus (t=-4.17),
primarily because of lower within-group coefficients of variation for
stress-corrected strains (25%) than for traditional stiffness
measures (40%).
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Figure 2 compares the distribution of stress-corrected luminal strain in normal subjects and hypertensive patients. As seen in the bottom panel, the distribution of stress-corrected luminal strain was shifted to the left in hypertensive patients, with 14% below the 5th percentile of normal. Figure 3 compares the distributions of stress-corrected midwall strain in normal subjects and hypertensive patients. The distribution of stress-corrected midwall strain in the latter group was also shifted to the left, with 18% below the 5th percentile of normal.
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Characteristics of Hypertensive Patients With Reduced Arterial
Compliance
Those in the subgroup of hypertensive patients with low
stress-corrected midwall strain were older and had higher brachial and
carotid systolic and diastolic blood pressures and
higher brachial pulse pressures than the other patients (Table 1). There were no statistical
differences between patient groups in gender, race, or body size.
Although hypertensive patients with low stress-corrected midwall strain
had slightly larger LV wall thickness, mass, and relative wall
thickness than those with normal stress-corrected midwall strain, these
differences did not approach statistical significance. Hypertensive
patients with low stress-corrected luminal strain also had higher
brachial and carotid systolic and diastolic blood
pressures (Table 2). There were no
significant differences with regard to age, gender, race, or body size.
Patients with low stress-corrected luminal strain had slightly thicker
interventricular septa but similar LV mass compared with
the remaining patients.
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Carotid Luminal and Midwall Mechanics in Hypertensive
Patients
Hypertensive patients with low stress-corrected luminal strain had
larger carotid systolic and diastolic diameters
than those with normal stress-corrected luminal strain (6.9±0.9 versus
6.5±0.9, P=0.01; 6.5±0.9 versus 5.8±0.8,
P<0.001, respectively). There was no difference in
arterial cross-sectional area between subgroups of
patients. Patients with low stress-corrected midwall strain had larger
carotid systolic and diastolic diameters than the
other patients (7.0±0.9 versus 6.5±0.9, P<0.001; 6.5±0.8
versus 5.7±0.8, P=0.002, respectively). In contrast to the
lack of difference when patients were grouped by level of
stress-corrected luminal strain, those with low stress-corrected
midwall strain had larger cross-sectional areas than those with normal
stress-corrected midwall strain (20.7±6.6 versus 17.2±5.5,
P<0.001).
According to a previously derived regression equation,26 arterial hypertrophy was present in 15% of hypertensive patients. These patients had lower carotid midwall strain and stress-corrected midwall strain than those without arterial hypertrophy, whereas no difference was observed in luminal or stress-corrected luminal strain (Table 3). Discrete atherosclerotic plaques were detected in 27% of hypertensive patients. Both stress-corrected carotid luminal and midwall strain were lower in those with plaque compared with those without, but this did not approach statistical significance.
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After adjustment for age, hypertensive patients with low stress-corrected luminal strain had higher ß (9.8±3.1 versus 5.5±1.9) and Young's modulus (1032±378 versus 568±160 dyne/cm2 per millimeter x10-6) (both P<0.001) than the other hypertensive patients. Similarly, after adjustment for age, those with low stress-corrected midwall strain had higher ß (9.6±3.0 versus 5.4±1.8) and Young's modulus (1002±372 versus 565±161 dyne/cm2 per millimeter x10-6) (both P<0.001) than the other hypertensive patients. As expected, after adjustment for age, midwall measures of arterial stiffness were higher in hypertensive patients with low stress-corrected midwall strain than in the other hypertensive patients (9.3±3.4 versus 5.0±1.8 for midwall ß; 2921±1044 versus 1665±564 dyne/cm2 per millimeter x10-6 for midwall Young's modulus) (both P<0.001).
Carotid Midwall Mechanics and LV Hypertrophy
Compared with hypertensive patients with normal LV geometry and
concentric remodeling, those with concentric hypertrophy
had lower luminal strain and midwall strain as well as
stress-corrected luminal strain and midwall strain (Table 4). The patients with eccentric LV
hypertrophy had lower luminal and midwall strain as well as
stress-corrected luminal and midwall strain, but these differences did
not attain statistical significance. Carotid stress did not differ
among the LV geometric patterns.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Measurement of arterial compliance may provide evidence of vascular changes that precede the development of overt atherosclerotic disease.40 Therefore, noninvasive assessment of arterial compliance may aid in early detection and subsequent prevention of atherosclerotic disease. Risk factors for vascular disease, including older age, high blood pressure and cholesterol, diabetes, and LV hypertrophy, are known to be associated with decreased arterial compliance.24 41 42 43 44 45 46 47 48
Several methods of noninvasive assessment of arterial
compliance rely on the relation between systolic lengthening of
arterial lumen diameter in relation to the corresponding
change in blood pressure.32 33 34 However, conventional
methods do not examine the average strain of the arterial
wall, approximated by the behavior of the midwall of the artery, nor do
they take into account the average imposed stress. On the basis of
research on the left ventricle that demonstrated that shifting the
examination of LV mechanics to the midwall improves understanding of
ventricular function in individuals with abnormal cardiac
geometry,49 ,50 we recently used carotid ultrasound and the
highly skill-dependent technique of carotid applanation tonometry to
evaluate in apparently normal adults a measure of arterial
compliance based on carotid midwall strain and its relation to the
increment in carotid stress during systole (carotid
stress).10 In that study, carotid midwall strain was
unrelated to gender, positively related to carotid stress, and
negatively related to age, overweight, and standard measures of
arterial stiffness. In addition, stress correction
strengthened the negative relation of carotid midwall strain with age,
suggesting that assessment of carotid midwall mechanics may enhance
noninvasive assessment of the compliance of conduit arteries.
In this study of hypertensive patients, carotid midwall strain was
positively related to carotid stress, albeit slightly less closely
than in normotensive individuals.10 The likely explanation
for this is that hypertensive patients respond to elevated blood
pressure heterogeneously, with proportionate increases in
normally compliant connective tissue and muscular elements in some
patients but disproportionate increases in noncompliant connective
tissue in others.49
We have previously demonstrated that increased carotid wall thickness
is associated with decreased carotid distensibility in hypertensive
patients compared with age-matched normotensive subjects.8
In our initial report,25 when differences in wall
thickness were taken into account using Young's elastic modulus,
carotid artery stiffness was not statistically greater in hypertensive
patients than in normotensive subjects. In contrast, the present
study of substantially larger hypertensive and normotensive populations
reveals statistically higher arterial stiffness by
conventional indices in hypertensive patients, a difference that became
more striking when the new measures of arterial mechanics
were used. Moreover, the present study demonstrates that the
carotid arterial wall is stiffer in hypertensive patients
than in normotensive subjects when compared at a given circumferential
stress (assessed by stress-corrected strains), when
arterial wall thickness is taken into account (Young's
modulus and midwall Young's modulus), and when the curvilinear
arterial pressure-diameter relation is taken into account
(ß and midwall ß).
In our study, carotid stress was statistically indistinguishable in
normotensive adults and hypertensive patients. Because carotid luminal
strain was reduced (by 19% on average) in hypertensive patients, use
of stress-corrected luminal strain identified 14% of patients with low
arterial compliance. A slightly larger proportion of
hypertensive patients (18%) had low arterial compliance by
stress-corrected midwall strain. These patients were older and had
thicker arterial walls and higher blood pressures than the
hypertensive patients with normal stress-corrected midwall strain. In
addition, all conventional measures of arterial stiffness
were higher in hypertensive patients with low stress-corrected midwall
strain.
In a previous study,47 we demonstrated that hypertensive patients with concentric LV hypertrophy have a greater increase in arterial wall thickness, cross-sectional area, and conventional measures of arterial stiffness at the operating level of distending pressure than hypertensive patients with other LV geometric patterns. In the present study, those with concentric LV hypertrophy had reduced stress-corrected luminal and midwall strain. Stress-corrected luminal and midwall strain also tended to be more subnormal in those with eccentric LV hypertrophy than in those with normal LV geometry. An intriguing result is that LV hypertrophy is related to stress-corrected midwall strain but not to conventional measures of arterial stiffness, implying that the association between LV hypertrophy and arterial dysfunction is better assessed by use of carotid midwall mechanics.
Conclusion
Stress-corrected midwall strain may identify hypertensive patients
with reduced arterial compliance, increased
arterial wall thickness, and abnormal LV geometry better
than conventional arterial function measures based on
arterial lumen diameters.
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Acknowledgments |
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This study was supported in part by grants HL-18323, HL-30605, and HL-47540 from the National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md, and by a grant from the Michael Wolk Heart Foundation. We thank Mariane C. Spitzer, RDMS, for her expertise in the performance of the ultrasound studies.
Received March 13, 1998; first decision April 20, 1998; accepted December 4, 1998.
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