(Hypertension. 1999;33:787-792.)
© 1999 American Heart Association, Inc.
Scientific Contributions |
Assessment of Arterial Compliance by Carotid Midwall Strain-Stress Relation in Normotensive Adults
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—Examining left ventricular midwall as opposed to endocardial mechanics enhances understanding of left ventricular function in individuals with abnormal cardiac geometry. Accordingly, we used carotid ultrasound and applanation tonometry of arterial pressure to derive carotid midwall strain and its relation to carotid peak-systolic and end-diastolic stresses in 82 apparently normal, employed subjects (56 men, 26 women; median age, 47 years; 70% white; 21% overweight) with no evidence of coronary or valvular heart disease. Regression equations relating carotid luminal and midwall strain to the increment in carotid stress during systole (
carotid stress) were used to
predict strain for the observed stress. Observed/predicted carotid
luminal or midwall strain was calculated as a measure of carotid
luminal or midwall strain for imposed stress, termed stress-corrected
strain. Midwall carotid strain was similar in women and men but was
negatively related to older age (r=-0.35,
P=0.001) and higher body mass index
(r=-0.31, P=0.005) and brachial and
carotid blood pressure (r=-0.30 to -0.45, all
P<0.01). The pulsatile change in arterial
load, measured by carotid stress, was positively related to midwall
strain (r=0.44, P<0.001) more closely
than was carotid luminal strain. Regression analyses revealed
that carotid midwall strain was positively related to stress, with
additional negative relations to age and carotid diastolic
diameter (all P<0.001). Stress-corrected carotid
midwall strain was strongly and negatively correlated with midwall
elastic modulus and Young's modulus (both r=-0.77,
P<0.001), followed by elastic modulus
(r=-0.74, P<0.001), midwall Young's
modulus (r=-0.73, P<0.001), midwall
stiffness index (r=-0.70, P<0.001), and
stiffness index (r=-0.66, P<0.001).
Thus, in normal adults, carotid midwall strain is unrelated to gender,
is positively related to pulsatile carotid load as measured by
carotid stress, and is negatively related to age, overweight, and
standard measures of arterial stiffness.
Key Words: carotid arteries • compliance, arterial • ultrasonography
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Measurement of arterial compliance may provide indices of early vascular changes that antedate the development of major atherosclerotic disease.1 2 It is well known that risk factors for vascular disease, including older age, high blood pressure and cholesterol, diabetes, and the presence of left ventricular (LV) hypertrophy, are associated with decreased arterial compliance.3 4 5 6 7 8 9 10 11 12 13 14 15 Thus, noninvasive assessment of arterial compliance may be important for early detection and subsequent prevention of atherosclerotic disease. Several methods to assess arterial compliance noninvasively rely on the relation between systolic strain (lengthening) of the arterial lumen diameter in relation to the pulsatile blood pressure increase.2 16 17 However, conventional approaches do not examine the average strain of the arterial wall, approximated by lengthening at the arterial midwall, nor do they directly take into account the average stress on the arterial wall. Recent research on the left ventricle reveals that a change of approach to examination of LV midwall mechanics improves understanding of ventricular function in individuals with abnormal cardiac geometry.18 19 20 21 22 Therefore, the present study was undertaken to assess the level and correlates of the carotid midwall strain-stress relation in apparently normal adults.
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Methods |
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Subjects
The study group consisted of 82 apparently normal men and women drawn from a large employed population in New York.13 23 All subjects had normal blood pressure (<140/90 mm Hg) on no antihypertensive medication. Segmental wall motion abnormalities and valvular regurgitation or stenosis were excluded by 2-dimensional and Doppler echocardiography. On the basis of the Second National Health and Nutrition Examination Survey (NHANES II), subjects were classified as overweight if they had a body mass index >27.8 kg/m2 for men and >27.3 kg/m2 for women.24 Subjects had no clinical evidence of coronary heart disease and gave informed consent under protocols approved in 1979 and regularly thereafter.
Carotid Ultrasound
A Biosound Genesis II system (OTE Biomedica) equipped
with a 7.5-MHz transducer was used to scan the common, internal, and
external carotid arteries for discrete carotid
plaques.13 25 26 Two-dimensionally guided M-mode
recordings of the common carotid artery 
1 cm proximal to the
carotid bulb, with simultaneous ECG and carotid pressure
waveforms, were recorded on videotape and subsequently digitized.
Electronic calipers were used to measure the internal diameter
(Dd) and far wall intimal-medial thickness
(IMTd)27 at end
diastole, at the nadir of the simultaneous
arterial pressure waveform, or at minimal
arterial diameter, as well as the diameter at peak systole
(Ds). All measurements used in this study were
performed by a single experienced investigator (M.J.R.) on several
cycles and averaged. High interobserver and intraobserver
reproducibility for both carotid wall thickness and lumen diameter
measurements have been documented.25 28 29
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.30 Orientation and pressure applied
to the transducer were adjusted to applanate 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.31 32 Actual carotid blood pressures
were obtained by external calibration with the use of the mean brachial
artery pressure.25 33 34 An alternative method of
calibration that sets both the mean and diastolic carotid
pressures equal to those from the brachial artery did not alter the
results of the study (data not presented).
Arterial Compliance and Stiffness Indices
Carotid luminal strain, the percent systolic expansion
of the arterial lumen,12 was calculated
as
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Measures of Carotid Midwall Function
Carotid midwall strain was derived with the use of a cylindrical
model, adapted from Shimizu et al,18 which assumes that
the ratio of volumes of the inner and outer halves of the carotid wall
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 peak systole
are equal, as follows:
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Carotid peak-systolic stress (cPSS) was estimated at the
midwall from M-mode tracings, adapting a cylindrical
model39 previously used for cardiac
studies,40 in which
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Equations relating carotid luminal strain and carotid midwall strain to
carotid stress were then used to predict the expected carotid
luminal and midwall strain, respectively, for observed carotid
stress. The ratios of observed to predicted strains are termed
stress-corrected carotid luminal and midwall strain, respectively.
Statistical Analysis
Data management and analysis were performed with the use
of a computer equipped with SPSS 7 (SPSS) software. Data are
presented as mean±SD. Independent sample t tests
and ANCOVAs that took into account relevant covariates were used to
compare mean values between groups. Pearson correlation coefficients
and linear regression analyses were used to determine the
closeness and independence of association of variables to midwall
strain. The null hypothesis was rejected at P<0.05.
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Results |
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Subject Characteristics
The study population included 56 men and 26 women, with a median age of 50 years. Brachial and carotid artery blood pressures and pulse pressures were virtually identical in the 2 genders. When the population was divided at its median, mean brachial pulse pressure was lower in younger individuals (47±7 versus 54±11 mm Hg, P=0.001) and even more so in the carotid artery (41±11 versus 53±19 mm Hg, P<0.001), as a result of which pulse pressure augmentation from the central to peripheral circulation was greater in younger individuals (6±12 versus 1±17 mm Hg, P=0.01). A total of 17 individuals (11 men) were overweight. Brachial and carotid systolic blood pressures did not differ between weight strata, but both brachial and carotid diastolic blood pressures were higher in overweight individuals (78±6 versus 71±10 mm Hg, P=0.004 and 77±8 versus 68±11 mm Hg, P=0.001, respectively). Most study subjects (79%) were white. No racial differences were observed in any clinical variable.
Relations of Carotid Luminal and Midwall Measures to Clinical
Variables
Carotid luminal and midwall systolic and
diastolic diameters were larger in men than in women (Table 1), but carotid strain did not
differ between genders. Men had higher carotid end-systolic and
end-diastolic stress than women, but the gender-related
difference in carotid stress was not significant. No gender-related
differences were observed for other measures of arterial
compliance and stiffness (data not shown).
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In ANCOVAs, adjusted for gender, neither carotid luminal nor midwall
diastolic or systolic diameters or strains differed
statistically between overweight and normal-weight individuals (data
not presented). However, diastolic and
systolic arterial wall thicknesses were higher in
overweight individuals (mean, 0.81 versus 0.69 mm,
P=0.01 and 0.79 versus 0.65 mm, P=0.003).
Carotid peak-systolic stress tended to be lower in overweight
individuals (mean, 559 versus 631x103
dyne/cm2, P=0.06), but there was no
difference in carotid end-diastolic stress between the
groups (mean, 281 versus 289x103
dyne/cm2, P=0.71). As a consequence,
the carotid stress was lower in overweight individuals (mean, 278
versus 342x103 dyne/cm2,
P=0.01).
Luminal and midwall diameters, arterial wall thicknesses,
and luminal and midwall strain were statistically indistinguishable
between white and nonwhite individuals. Carotid peak-systolic
stress was slightly higher in whites (mean, 631 versus
555x103 dyne/cm2,
P=0.05), but carotid end-diastolic stress was
similar in the 2 groups. Therefore, carotid stress was higher in
whites (mean, 339 versus 285x103
dyne/cm2, P=0.04). Both carotid
luminal and midwall strain were higher in younger individuals (aged
<50 years) than in older individuals (15.4±3.6% versus 13.6±4.1%,
P=0.04 and 12.7±2.9% versus 10.6±3.0%,
P=0.002, respectively).
Univariate analyses (Table 2) revealed that both carotid midwall strain and luminal strain were negatively related to age and body size and that, in general, clinical variables were slightly more closely correlated with carotid midwall strain. In both genders, carotid midwall and luminal strain were negatively related to carotid systolic and diastolic blood pressures but not pulse pressures. In both genders, carotid luminal and midwall strains were negatively related to carotid diastolic diameter (r=-0.49 and -0.39, respectively, both P<0.001). Carotid systolic diameter was not related to either carotid luminal or midwall strain.
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Relations of Carotid Luminal Strain and Midwall Strain to
Carotid Stress
In men, carotid midwall strain was positively related to
carotid stress (r=0.56, P<0.001), while in
the smaller group of women this relation (r=0.29) did not
attain statistical significance. The overall positive relation between
carotid midwall strain and stress (r=0.44,
P<0.001) is displayed in the top panel of the Figure
, with the regression line relating
midwall strain to stress and its 95% CI. Carotid luminal strain was
also positively related to carotid stress in men (r=0.50,
P<0.001) but not in women (r=0.15,
P=0.45), with a moderate positive relation when men and
women were pooled (bottom panel, Figure).
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Regression equations relating carotid luminal and midwall strain to
carotid stress derived from data in the Figure were
used to predict values of the former variables for observed
carotid stress. Observed/predicted carotid strain was expressed as a
percentage in each individual to yield stress-corrected carotid luminal
and midwall strain.
The mean stress-corrected carotid luminal strain tended to be greater for individuals below the median age (104±23%) than for older individuals (94±27%, P=0.08). Stress-corrected luminal strain was lower in men (96±26%) than in women (108±23%, P=0.05). Mean stress-corrected luminal strain was 101±24% in whites and 94±31% in nonwhites (P=0.29). Stress-corrected luminal strain was nearly identical in normal-weight and overweight individuals.
Mean stress-corrected carotid midwall strain was lower in individuals above as opposed to below the median age of the population (91±25% versus 106±22%, P=0.007). Stress-corrected carotid midwall strain tended to be lower in men (96±25%) than in women (105±22%, P=0.14). There was no significant difference in stress-corrected carotid midwall strain between races or between overweight and normal-weight individuals. Stress correction of midwall strain slightly strengthened its negative relations with age and carotid diastolic blood pressure.
Regression Analyses
In a model with carotid luminal strain as the dependent
variable and age, carotid diastolic diameter, carotid
diastolic blood pressure, and carotid stress as
independent variables, carotid luminal strain was related
positively to carotid stress (ß=0.345, P=0.001) and
negatively to carotid diastolic diameter (ß=-0.461,
P<0.001) and age (ß=-0.195, P=0.035)
(multiple R=0.62). In a similar model, carotid midwall
strain was strongly related to carotid stress (ß=0.440,
P<0.001), age (ß=-0.403, P=0.001), and
carotid diastolic diameter (ß=-0.328,
P<0.001) (multiple R=0.67).
Relations of Carotid Luminal Strain and Midwall Strain to Other
Arterial Compliance Indices
Among the different measures of arterial compliance
and stiffness, carotid luminal strain was most closely and negatively
related to Peterson's elastic modulus, followed by Young's modulus
and ß, with a weaker positive relationship with carotid stress
(Table 3). Stress-corrected
carotid luminal strain was strongly and negatively correlated with
Young's modulus, followed by Peterson's elastic modulus and ß.
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Carotid midwall strain (Table 4) was
related to Peterson's elastic modulus, followed by midwall Peterson's
modulus, midwall ß, ß, Young's modulus, midwall Young's modulus,
and carotid stress. Stress-corrected midwall strain was strongly and
negatively related to midwall Peterson's modulus, followed by Young's
modulus, Peterson's modulus, midwall Young's modulus, midwall ß,
and ß. Of note, stress correction of both carotid luminal and midwall
strain strengthened their negative relations with all measures of
carotid arterial stiffness; the strongest negative relation
with each index of arterial stiffness was obtained with
stress-corrected midwall strain. Neither the arterial
compliance index nor pulse pressure/stroke volume was related to either
carotid midwall or luminal strain or stress-corrected strain.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Measures of arterial compliance estimate the ability of an artery to expand and contract with cyclic variation in arterial pressures caused by cardiac contraction and relaxation. The most robust noninvasive method to measure in vivo arterial thickness and strain is ultrasound imaging.4 41 42 The introduction of carotid artery applanation by high-fidelity tonometer has provided a method that, in the hands of highly skilled operators, can provide the central arterial pressure measurements needed for noninvasive calculation of measures of arterial compliance.31 32 The most commonly used compliance measurement is Peterson's elastic modulus, defined as the ratio of stress (pulse pressure) to strain (lengthening).16 Under usual loading conditions, a higher stress-strain elastic modulus represents greater arterial stiffness.16 Young's modulus was derived to adjust for the effect of arterial wall thickening on arterial stiffness.2 To reduce the impact of the curvilinear pressure-stiffness relationship on arterial stiffness, the stiffness index (ß) was developed.17 35 In one study, ß correlated well with the presence of atherosclerosis in pathological findings.43
However, conventional approaches do not examine the average strain of the arterial wall, approximated by systolic lengthening at the arterial midwall, nor do they directly take into account the average imposed stress.44 Thus, examining the average systolic strain of the arterial wall, approximated by measurements at the midwall, and relating it to the average imposed stress may enhance detection of reduced arterial compliance compared with conventional methods.
Although we found no gender-related difference in either carotid luminal or midwall strain, apparently normal men had higher carotid wall stresses than women. The greater stress on the arterial wall in men may be a hitherto unrecognized but pathophysiologically important mechanism contributing to the well-known gender-related difference in risk of arterial disease. In our study, carotid pulse pressure showed a greater increase with age than brachial blood pressure. The loss with age of pulse pressure amplification from central to peripheral arteries has been attributed to age-related degeneration of arterial elastic fibers.45
Our study demonstrates that midwall strain had a stronger negative
relation to age than did carotid luminal strain. As expected from
physiological considerations, adjustment of carotid
luminal and midwall strain for the imposed cyclic load strengthened the
negative relations with age. The reason for decreased carotid strain
with age may be an age-related progressive shift in load bearing during
systole from flexible elastic fibers to rigid collagen fibers that
accompanies age-associated arterial
dilatation.45 Our study showed that stress-corrected
carotid midwall strain was significantly lower in older individuals,
with a parallel trend for stress-corrected luminal strain. Thus, the
present findings suggest that the average mechanics of the several
components of the carotid artery wall may be better approximated by
calculating arterial strain and adjusting it for the
pulsatile increase in arterial load (carotid stress) at
the level of the arterial midwall. Further study will be
needed to determine whether similar negative relations between age and
midwall mechanics are also observed in peripheral
arteries.
The present study confirmed the expected negative relations between conventional measures of arterial stiffness and parameters of carotid luminal and midwall mechanics. A new and notable result of the present study is that the coefficient of determination (r2) between standard arterial stiffness measures and measures of arterial mechanics increased stepwise from those observed with carotid luminal strain (r2=0.26 to 0.37) to those with stress-corrected midwall strain (r2=0.44 to 0.59).
Conclusion
In normal adults, carotid midwall strain is unrelated to gender,
positively related to pulsatile carotid load, as measured by carotid
stress, and negatively related to age, overweight, and standard
measures of arterial stiffness. Stress correction of
carotid midwall strain strengthens its negative relations with age and
indices of arterial stiffness, suggesting that assessment
of carotid midwall mechanics may enhance noninvasive assessment of
conduit artery compliance.
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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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