(Hypertension. 2001;37:6.)
© 2001 American Heart Association, Inc.
Scientific Contributions |
Effects of Blood Pressure, Smoking, and Their Interaction on Carotid Artery Structure and Function
From the Vascular Research Group (Y.-L.L., L.M.S., H.T., D.K., B.P.M.), Department of Medicine, and Department of Epidemiology and Preventive Medicine (J.M.), Monash University, Melbourne, Australia; and Department of Electronic Engineering (J.D.C.), La Trobe University, Melbourne, Australia.
Correspondence to Prof Barry McGrath, Monash University Department of Vascular Sciences and Medicine, Dandenong Hospital, David Street, Dandenong 3175, Victoria, Australia.
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Abstract |
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Abstract—In the present study, we examined the relationships among carotid blood pressure, arterial geometry, and wall stress and determined the impact of hypertension, smoking status, and their interaction on these relationships. The study involved 679 subjects aged 49 to 82 years: 372 smokers (190 men and 182 women) and 307 nonsmokers (110 men and 197 women). Blood samples were taken to determine total cholesterol levels. Central pulse pressure was derived from measured brachial artery pressure with a linear regression equation from data obtained in a subgroup of 276 subjects that related brachial and carotid pulse pressures; the latter was measured with applanation tonometry. Carotid intima-media thickness (IMT), lumen diameter (D), and stiffness index (SI) were determined with high-resolution B-mode ultrasound. Mean and pulsatile circumferential stress (
C) was calculated according to the Laplace
relationship. Indexes of arterial geometry and function
were adjusted for age, height, and heart rate. Hypertension (treated
and/or screening blood pressure of >140/90 mm Hg) was
present in 71 nonsmokers and 186 smokers. Nonsmokers and smokers
did not differ in blood pressure and cholesterol levels.
Hypertension and smoking individually and interactively significantly
increased adjusted IMT, D, and SI. The radius-to–wall thickness ratio
(R/IMT) (where R=D/2) and C were increased in
hypertensives. SI was correlated with IMT (r=0.56,
P<0.001); radius-to–wall thickness ratio was inversely
correlated with central pulse pressure (r=-0.38,
P<0.001). Smoking did not influence these
relationships. In conclusion, carotid artery wall remodeling appears to
follow Laplace’s law but is insufficient to prevent an increase in
circumferential stress in hypertensive subjects. Unlike hypertension,
smoking does not influence the lumen-to-wall ratio but has a
significant effect on wall stiffness.
Key Words: aging • carotid arteries • pulse • blood pressure • smoking
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Introduction |
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It is well known from experimental and clinical studies that hypertension causes left ventricular and resistance arterial remodeling consistent with Laplace’s law for cylindrical structures with finite wall thickness.1 2 3 The common carotid artery is an elastic artery, of which the wall thickness increases with cardiovascular risk factors such as age and hypertension.4 5 6 Whether the Laplace relationship, which generally holds for cardiac wall and resistance artery wall remodeling, can describe changes in large conduit arteries like the carotid artery remains unclear.
Few studies have examined, in the same subjects, the structure-function relationships in large arteries. In a 4-year longitudinal study, Zureik et al7 showed that elevated brachial artery pulse pressure (PPbrachial) was associated with increasing common carotid artery intimal-medial wall thickness (IMT). Smoking increases age-related arterial wall thickness and arterial stiffness.8 9 10 The extent to which an increase in IMT in hypertension is due to vascular remodeling of the common carotid artery in response to high central blood pressure or is a marker of atherosclerosis or a combination of the 2 has not been defined. Moreover, the potential interactions between key cardiovascular risk factors such as smoking and hypertension in structure-function relationships have not been evaluated.
The aim of the present study, which included a large group of older subjects, was to examine the relationships among central blood pressure, carotid arterial geometry, and wall stress and to determine the impact of hypertension, smoking, and their interaction on these relationships.
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Methods |
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Subjects
Six hundred seventy-nine subjects were studied. Subjects were aged 49 to 82 years (mean 62.6 years) and were recruited through advertisement from an urban population in Melbourne, Australia. Exclusion criteria were serious illness such as cancer or organ failure, stenosis of >80% of either carotid artery, myocardial infarction, or stroke within the previous 6 months. All women were postmenopausal, and none were taking hormone replacement therapy. The study procedure was undertaken in a quiet, air-conditioned room. Subjects were advised not to consume coffee in the 8 hours before the study. Nonfasting blood samples were taken for analysis of total cholesterol.
Carotid IMT, Lumen Diameter, and Stiffness Index
An imaging study of the right common carotid artery was
performed with a high-resolution ultrasound machine (Diasonics DRF-400)
and a hand-held transducer with 7.5-MHz central frequency mechanical
sector transducer as previously reported.5 6 Three B-mode
and M-mode images in different directions (anterior, lateral, and
medial) were recorded. The images were digitized and saved on
computer via a customized computer program. The right common carotid
artery IMT and lumen diameter (D) measurements were analyzed
using methods previously described.5 6 Lumen radius (R)
was calculated as carotid lumen diameter divided by 2. Carotid
stiffness was determined in terms of the stiffness index (SI); this
index is given as
SI=Ln(Ps/Pd)/[(Ds-Dd)/Dd].11
Ps and Pd indicate systolic and diastolic
pressures, and Ds and Dd indicate systolic and
diastolic diameters.
Definition of Arterial Circumferential Stress
Circumferential stress (C) is generated
in the artery wall in response to transmural pressure and can be
calculated from the law of Laplace (in units of force per unit area) as
C=P · r/w, where P is central
transmural pressure, r is the lumen radius of the carotid artery (R),
and w is the carotid wall thickness (here taken as IMT). If the thin
wall approximation is accepted, the transmural pressure is
theoretically equal to the difference between instantaneous contained
blood pressure and local interstitial pressure (usually
approximated to zero). Also relevant is the concept of critical opening
pressure, the blood pressure at which the artery is patent but where
C=0. Inability to obtain a valid estimate at
either true transmural pressure or critical opening pressure
necessitates further assumptions concerning the calculation of
C. In the present study, we calculated
mean circumferential stress C(MAP) as P*r/w
and pulsatile wall stress (assuming 
R<<R) as
C(PP)=P*r/w.12
Determination of Central Pulse Pressure
A Dinamap device (CRITIKON 1846 SX) was used for brachial blood
pressure measurements recorded at 5-minute intervals throughout the
study (30 to 40 minutes) in all 679 subjects. The first Dinamap blood
pressure recording was excluded, and all subsequent blood
pressure measurements were averaged. Central blood pressure was
measured through applanation tonometry of the right common carotid
artery with a noninvasive pressure transducer (Millar Mikro-tip; Millar
Instruments) in 276 subjects. In this subgroup, carotid artery pressure
waveforms, obtained simultaneously with the brachial artery
Dinamap pressure recordings, were analyzed to obtain
central PP (PPcen) measurements through linear
interpolation with the oscillometrically obtained brachial mean and
diastolic blood pressures (MAP and DBP, respectively).
There was a close relationship between PPcen and
measured PPbrachial
(PPcen=0.86xPPbrachial-3.82;
r=0.81, P<0.001). The 95% CIs for slope and
intercept were 0.78 to 0.94 and -1.3 to 8.0, respectively. Multiple
regression analysis showed that this relationship was not
significantly influenced by gender, age, or heart rate (HR). This
expression was then applied to the entire study population to derive
PPcen from PPbrachial.
Data Analysis
Statistical analysis was performed using Microsoft Excel
97 and SPSS version 8. Data are reported as mean±SD. All main
parameters and indices were adjusted by age, height, and HR
with the formula
Yo=yi+b(xi-x), where
xi and yi are a part of the data points in a
linear regression with slope b; x is the mean value for variable
x; and Yo is the adjusted value for variable
y.13 This was done because age, height, and HR
are major factors known to affect arterial structure and
function.4 5 14 15 Hypertension was defined as
systolic blood pressure (SBP) of 
140 mm Hg and/or DBP
of 90 mm Hg or the current use of antihypertensive medications.
Student’s unpaired t test was used to determine the
significance of differences between subgroups (normotensive nonsmokers
[NTNS], hypertensive nonsmokers
[HTNS], normotensive smokers
[NTS], and hypertensive smokers
[HTS]). Differences were considered significant
at P<0.05. Univariate, bivariate, and linear
regression analyses were used to determine the relationships
between various indexes.
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Results |
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Table 1 summarizes the characteristics of the study population. There were 372 smokers (190 men and 182 women) and 307 nonsmokers (110 men and 197 women). Smokers had being smoking for
8 years (range 8 to 70.7 years), and average
use was 21.3 cigarettes/d (range 5 to 82). The mean±SD pack/y of
smoking was 42.2±20.6. Hypertension was present in 257 subjects
(38%). For the entire population, PPbrachial was
significantly higher than PPcen (58±13 versus
46±11 mm Hg, P<0.001).
Hypercholesterolemia (total
cholesterol >5.5 mmol/L) and/or the use of
cholesterol-lowering drug therapy was present in 174
subject (25.6%). Physical activity score was similar in both genders
and in all 4 subgroups. Eighty-five percent of subjects drank <2 and
none drank >4.5 standard drinks/d.
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Bivariate correlation analysis showed that for the whole group,
age was a key determinant of all indexes except for DBP. IMT
(r=0.37, P<0.001), LD (r=0.25,
P<0.001), SI (r=0.33, P<0.001),
PPcen (r=0.22, P<0.001),
SBPcen (r=0.18, P<0.001),
MAP (r=0.09, P<0.05), and both
C(MAP) and C(PP)
(r=0.09, P<0.05; r=0.10,
P<0.05) were all related to age. In the age group of 49 to
59 years, DBP correlated positively with age (r=0.13,
P<0.05), whereas in those >60 years old, DBP correlated
negatively with age (r=-0.10, P<0.05).
Indexes of carotid arterial geometry and function, adjusted
by age, height, and HR, are shown in Table 2. As expected, all blood pressure
measurements (SBP, DBP, MAP, and PP) differed significantly between
normotensive and hypertensive groups. PPcen was
greater in normotensive smokers than in nonsmokers but similar in the 2
hypertensive groups. IMT, D, and SI were increased in hypertensives and
in smokers compared with corresponding normotensive and nonsmoker
groups. The radius-to-wall thickness (R/IMT) ratio differed
significantly between normotensive and hypertensive groups
(NTNS versus HTNS
P<0.05, NTS versus
HTS P=0.05) but not between smoker and
nonsmoker groups. ANOVA revealed significant interactions between
smoking and blood pressure for IMT (F=31.2,
P<0.001), LD (F=46.3, P<0.001), and
SI (F=34.6, P<0.001), but not for R/IMT
(F=2.6, P=NS). Carotid
C(PP) differed significantly between the
normotensive and hypertensive groups and between normotensive smokers
and nonsmokers. For C(MAP), only the
difference between normotensive and hypertensive smokers reached
significance (Table 2).
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Multiple regression analysis showed strong interrelationships between indexes of arterial geometry and function adjusted for age, height, and HR and PPcen. Adjusted IMT and D were positively correlated with PPcen (r=0.59, P<0.001; r=0.34, P<0.001), and R/IMT was negatively correlated with PPcen (r=-0.38, P<0.001). The relationship between R/IMT and PPcen was not affected by smoking status (Figure 1). These relationships persisted when data from smokers and users of antihypertensive medication were excluded (IMT versus PPcen r=0.65, P<0.001; D versus PPcen r=0.34, P<0.005; R/IMT versus PPcen r=-0.42, P<0.001). Although IMT and LD both correlated with MAP (r=0.28 and 0.36, both P<0.001), there was no significant relationship between R/IMT and MAP (Figure 1). SI correlated with IMT in the whole group (r=0.56, P<0.001) and in both nonsmoking (r=0.60, P<0.001) and smoking (r=0.46, P<0.001) subgroups. SI was strongly related to PPcen (r=0.71, P<0.001).
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, thin trend line).
Adjusted IMT (r=0.19, P<0.001), SI
(r=0.20, P<0.001), D (r=0.16
P<0.05), and MAP (r=0.17, P<0.05)
were significantly correlated with pack-years of smoking, but
C(MAP), C(PP), and
PPcen did not relate to smoking status. As shown
in Figure 2, there was a dose-dependent
effect of smoking on both adjusted IMT and SI. Figure 3 shows modeled pressure-versus-strain
characteristics, using the values from the smoking and nonsmoking
groups. Arterial stiffness is represented by
the slope of the line at any point. Hypertension tended to move the
operating point up the curve, whereas the relationship in smokers had a
steeper gradient than the curve for nonsmokers.
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There was no significant difference in mean total cholesterol in the 4 groups (NTNS 5.86±0.96, HTNS 5.98±0.90, NTS 5.94±1.36, HTS 5.95±1.33). None of the measurements of arterial blood pressure nor any of the indexes of arterial structure or function were correlated with total cholesterol levels.
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Discussion |
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The present study in older subjects has confirmed the importance of age as a determinant of arterial structure and function as shown by the significant relationships between age and PPcen, IMT, LD, and SI. With advancing age, there is an increase in large artery stiffness caused by intrinsic structural abnormalities.1 The pathological processes of increased collagen and calcium deposition and thinning, fragmentation, and eventual fracturing of elastin in the large arteries are likely explanations. Moreover, as shown in Figure 4, it is likely that an increase in PPcen with advancing age is a key factor that contributes to an increase in IMT and a fall in R/IMT in accordance with Laplace’s law.
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PPcen, Carotid Arterial Geometry, and
Laplace’s Law
Circumferential stress, defined in accordance with Laplace’s law,
is likely to be the major contributing factor in the remodeling effects
of hypertension on the left ventricular wall and small
resistance arterioles.1 2 3 In accordance with Laplace’s
law, to resist changes in C the relationship
between blood pressure and R/IMT would have to be maintained. Wall
structural components and/or their relative proportions in larger
arteries are quite different from those of resistance vessels; the more
proximal the large artery, the less smooth muscle and more elastin
fibers are found. Thus, central arterial remodeling is
likely to be less obvious than that demonstrated in smaller resistance
arterioles. Even small change in smooth muscle content, however, may
cause a significant change in collagen/elastin interaction and in
stress carriage within elastic arteries. A number of studies have shown
an important influence of raised blood pressure on IMT and/or carotid
arterial diameter.2 7 16 In particular, PP has
been identified as a key factor that determines
cardiovascular geometry.7 12 17 The
strength of the relationships of carotid IMT and R/IMT to
PPcen shown in the present study provides
compelling evidence for operation of Laplace’s law in vivo in the
carotid artery in response to change in contained pressure. Our results
are consistent with those of Boutouyrie et al,18
who examined carotid and radial artery characteristics in 43
normotensive and 124 hypertensive subjects. They reported the local PP
was an independent determinant of diameter and wall thickness in the
carotid but not the radial artery. Moreover, in both their study and
the current one, MAP was not a determinant of carotid
arterial wall remodeling, suggesting that it is the
cyclical stretching that is important.
Carotid IMT is generally recognized to be a composite measure of intima and medial wall thickness, although it may well be a measure of total wall thickness.19 During recent years, IMT has emerged as a strong risk factor of cardiovascular disease and is generally regarded as a marker of atherosclerosis, yet the importance of the contribution of the smooth muscle layer in the arterial media to this measurement has been largely overlooked. The carotid arterial pressure-structure-function relationships described in the present study suggest that changes in this layer contribute significantly to changes in IMT in response to hypertension. Smoking and hypercholesterolemia are important risk factors that have been associated with an increased IMT. However, after correction for age, smoking status, and cholesterol level, PPcen remained an important determinant of IMT.
Smoking Status, Arterial Geometry, and
Function
Smoking is a key risk factor for cardiovascular
disease and leads to increased arterial stiffness and wall
thickness.8 9 10 In the present study, adjusted IMT was
9.2% thicker, D was 8.1% larger, and SI was 25.3% greater in
normotensive smokers than in nonsmokers. Moreover, as shown in Figure 3, these appear to be dose-dependent effects of smoking on IMT
and SI. Smoking status had no apparent effect on the negative
relationship between R/IMT and PPcen. It has been
suggested that atherosclerosis, a major complication of
smoking, may not result in increase stiffness of the
arterial wall until there in significant plaque
development.20 The results of the present study, with
a more direct method of assessing arterial wall stiffness
than the method used by the Atherosclerosis Risk in
Communities (ARIC) investigators, are not consistent with that
hypothesis, because SI was increased in the smokers, most of whom did
not have any significant plaque in the common carotid artery as defined
by an IMT of >1 mm. On the other hand, as shown in a recent
review by Safar et al,21 arterial wall
stiffness is not dependent on structural changes alone but is
significantly influenced by endothelium-dependent
vasomotor changes.
As shown in Figure 3, our results suggest that smoking increases
carotid stiffness independent of PP. This finding is consistent
with smokers operating on a steeper pressure-strain characteristic. In
this model, hypertension would move the operating point up the curve
(point A
B in the case of nonsmokers; point CD in the case of
smokers), whereas smoking causes additional functional/structural
changes that move the entire operating characteristic to the left. Our
data also showed that smoking and hypertension were interacting risk
factors that influenced IMT, LD, and SI but not R/IMT. Results similar
to those described with SI were found when the mechanical
characteristics of the carotid artery were described with a different
index of stiffness, namely, the distensibility coefficient, as
described by Gamble et al.19 Results that show
dissociation of the effect of HT and smoking were also recently
reported from the ARIC Study.22 In these noninvasive
studies, actual structure cannot be determined, and we can only
hypothesize as to what the underlying changes may be. Our results,
however, are consistent with smoking initially causing a
decreased ability of the carotid artery to contain pressure with a
corresponding increase in diameter, accompanied by wall changes that
cause increased stiffness. Endothelium-dependent
functional changes are also likely to contribute to the increased
stiffness, given the adverse effects smoking on
endothelial function.21
Circumferential stress was significantly greater in hypertensive subjects. This is consistent with the results reported by Ferrara et al23 and Boutouyrie et al.18 In hypertension, although remodeling occurs, the circumferential stress remains at a high level. It appears, therefore, that an increased transmural pressure in the carotid artery in hypertension is not adequately compensated for by increased IMT and that lumen diameter actually increases.
Figure 4 is a representation of the ways in which different risk factors may affect the carotid arterial wall. It is suggested that compensatory changes in the medial smooth muscle layer in response to increased PP are the major factor that causes increased IMT and arterial stiffness. The impact of smoking and probably other risk factors is likely to be due to wall damage secondary to intimal damage, with a breakdown in pressure opposing elements in the arterial wall leading to dilatation and increased stiffness because of rearrangement and loss of elastic fibers and sclerosis.
In the present study of older subjects, carotid
arterial wall remodeling in response to pressure was
consistent with Laplace’s law. Hypertension, most likely
working through PPcen, was associated with
increases in carotid IMT and LD, with wall remodeling, and with a
reduction in R/IMT, but this adaptation was insufficient to prevent an
increase in C. Smoking was associated with
similar proportional increases in carotid IMT and LD, with no change in
R/IMT. Both hypertension and smoking were interactive in their effects
on IMT, LD, and arterial wall stiffness. Thus, different
cardiovascular risk factors appeared to influence the
relationship among arterial geometry, wall stress, and
stiffness in different ways.
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Acknowledgments |
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This study was supported by grants-in aid from the National Health and Medical Research Council of Australia (904862), the National Heart Foundation of Australia (G95 M4418), and Monash University Postgraduate Publications Award. We thank Prof Anthony Dart for help with the statistical analysis.
Received May 12, 2000; first decision May 26, 2000; accepted July 24, 2000.
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A. Mahmud and J. Feely Effect of Smoking on Arterial Stiffness and Pulse Pressure Amplification Hypertension, January 1, 2003; 41(1): 183 - 187. [Abstract] [Full Text] [PDF]
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