From the Alfred and Baker Medical Unit, Alfred Hospital, and the Baker
Medical Research Institute, Melbourne, Australia.
Correspondence to Dr Christoph Gatzka, Alfred Heart Centre, Commercial Rd, Prahran, Vic 3181, Australia. E-mail cdg{at}ee.latrobe.edu.au
Abstract
Abstract—To elucidate the
relationship between coronary artery disease (CAD), aortic
stiffness, and left ventricular structure, we recruited 55
subjects (33 men; average age, 63±1 years) with previously unknown CAD
from a healthy general population sample, as well as 55 control
subjects matched for gender, age, and serum cholesterol
level. We measured arterial blood pressure and the
systolic expansion of the transverse aorta and left
ventricular structure by
echocardiography. Aortic stiffness was higher in
CAD patients than in controls, with a brachial pulse pressure of 59±3
versus 52±2 mm Hg and stiffness indices of
Ep=212±26 versus 123±13 kN/m2 and ß=16±2
versus 9±1 (all P<0.01). Mean arterial
pressure was similar in both groups during the measurements (95±2
versus 93±2 mm Hg, P=NS). Most CAD patients
(61%) were in the highest stiffness quartile defined by the normal
control values (P<0.05 versus control). Left
ventricular mass index was also higher in CAD patients than
in matched controls (139±5 versus 123±4 g/m2,
P<0.05). We conclude that aortic stiffness and left
ventricular mass are increased in subjects newly diagnosed
as having CAD. This might explain previously reported associations of
an increased mortality, particularly from CAD, found among subjects
with elevated pulse pressures.
It has been shown recently that pulse pressure, a measure
closely related to aortic stiffness, predicts future all-cause,
cardiovascular, and especially coronary
mortality in the general population.1 A number of
factors may be responsible for an increase in mortality in association
with an increase in aortic stiffness. It increases left
ventricular pulsatile work and hence leads to left
ventricular hypertrophy, with a higher demand
for coronary blood flow.2 In addition,
coronary perfusion is changed unfavorably, with a reduced
supply due to a decreased diastolic blood
pressure.3
However, if coronary artery disease (CAD) were associated at
baseline with an increase in aortic stiffness, then the relation
between pulse pressure and subsequent increased coronary
mortality might just reflect this association. This notion is supported
by previous work in younger patients and patients after myocardial
infarction.4 5 To address this issue in a more
general manner, we determined aortic stiffness and left
ventricular structure in a case-control study in subjects
with and without CAD. Subjects were drawn from a general population
sample and matched for age, gender, and total cholesterol,
since the latter has been found to be related to arterial
stiffness in patients with CAD.6 7 8
Methods
Subjects
Gender-, age-, and cholesterol level–matched control
subjects were recruited from among questionnaire respondents who
indicated that they had no past history of myocardial infarction or
angina and did not currently experience chest pain. Control subjects
did not undergo an ECG stress test because of the low specificity of
the test in this cohort with a low pretest probability of disease.
Criteria for matching were age ±2 years and total serum
cholesterol ±1 mmol/L.
Investigations
Afterward, echocardiography was performed with a
Hewlett-Packard 77020A phased-array echo-Doppler System. Transverse
aortic measurements were made from the suprasternal notch as previously
described.10 Systolic (SBP) and
diastolic (DBP) arterial pressures (mean of 3
readings) used in this analysis were recorded at the
brachial artery by sphygmomanometry immediately after completion of the
suprasternal view while the subjects were still recumbent. Mean
arterial pressure was calculated by adding 1/3 of the pulse
pressure to DBP. All echo-Doppler assessments were performed by a
single operator who was unaware of the categorization of subjects as
cases or controls. Subsequent measurements were made on screen with
electronic calipers, again without knowledge of the case/control status
of the subject. Interventricular (IVS) and left
ventricular posterior wall thickness (PW) were measured
from leading edge to leading edge at end diastole. Left
ventricular internal diameter (LVID) was measured at end
diastole. Left ventricular mass (LVM) was
determined as
LVM=0.6+0.832x[(LVID+PW+IVS)3-
LVID3] g. For subjects in whom only either
the IVS or PW could be accurately determined, the available measurement
was doubled and used in the formula. Minimum end-diastolic
(Dd) and maximum systolic
(Ds) diameters for the transverse aortic arch
were measured with the M-mode beam perpendicular to the aortic wall.
The aortic stiffness indices Ep and ß were
computed as
Ep=(SBP-DBP)xDd/(Ds-Dd)
N/m2 and ß=(ln SBP-ln
DBP)xDd/(Ds-Dd).
Five measurements of all variables were obtained for each subject,
and the mean was used in calculations. Coefficients of variation for
repeated measurements in the present study were 2.3% and 1.9% for
posterior and left ventricular septal wall thickness and
2.3% for diastolic LVID, respectively.
Adequate images were not obtained in all cases because of technical
difficulties in image acquisition, but these failure rates were similar
in both groups. Thus, LVM was obtained in 39 cases and 40 controls and
aortic measurements in 39 cases and 42 controls.
Statistical Analysis
Results
CAD patients and controls were matched for gender, age, and serum
cholesterol levels
(Table
At the time of the measurement of aortic stiffness (during
echocardiography in the recumbent position), mean
arterial pressure was almost identical between CAD patients
and control subjects (95±2 versus 93±2 mm Hg, P=NS),
thereby not confounding the stiffness measurements. Pulse pressure,
however, was significantly higher in the CAD patients than in the
controls. The average aortic diameter was slightly larger in controls
than in CAD patients (this difference was not significant). CAD
patients had markedly stiffer aortas than did asymptomatic
controls: both aortic stiffness indices, Ep and
ß, were significantly higher in CAD patients than in controls.
When CAD patients and control subjects were divided into quartiles
defined by aortic stiffness measured in the controls
(Figure
Discussion
The major finding of this case-control study was that the proximal
aorta is stiffer in patients with newly diagnosed CAD than in matched
control subjects. In keeping with this, we have shown that CAD patients
have a very high likelihood of being in the highest quartile of
stiffness when quartiles are defined by measurements in subjects
presumably free of CAD. Left ventricular wall thickness was
also higher in CAD patients than in controls.
Our finding of an increased aortic stiffness in patients with CAD is in
keeping with previous smaller studies.4 7 11 12
Another study has shown that proximal aortic stiffness is increased
progressively with the number of diseased coronary blood
vessels in patients investigated after myocardial
infarction.5 This finding might account for the
increased coronary mortality associated with an increased pulse
pressure found in male subjects drawn from a similar general population
sample. That study classified subjects according to quartiles of pulse
pressure, similar to our classification (Figure
The diagnosis of CAD in our study was based on clinical criteria, ie,
if subjects presented with typical exertional angina and had a
positive exercise test. Although not part of the study protocol, we
were subsequently able to determine that within 24 months of their
participation, 60% of the CAD subjects were known to have undergone
coronary angiography in the course of their routine clinical
management, which in turn demonstrated hemodynamically
significant stenoses in 78% of those investigated. A further
10% of those investigated had evidence of coronary disease of
lesser magnitude. Of all 55 CAD subjects, 39% had had a
revascularization procedure (coronary
artery bypass graft or angioplasty or both) performed within 24 months.
Hence, we conclude that the selection criteria used did indeed in the
main correctly identify subjects with previously undiagnosed CAD.
Notwithstanding this, as well as the possibility that
"angiographically negative" case subjects experienced myocardial
ischemia due to other causes (eg, coronary spasm,
microvascular disease), it is possible that the CAD group contained
some cases inappropriately so classified. However, this seems unlikely
to have seriously confounded our results.
The measures of aortic stiffness used in this study require
determination of minimal and maximal aortic diameters, together with
sphygmomanometrically measured brachial pressures as a surrogate for
intra-aortic pressure. Although the property of pulse pressure
amplification at more distal arterial sites is well
recognized, this generally has been demonstrated for comparison between
femoral and proximal aortic sites where it is evident for young but not
older subjects.13 The age of participants in the
present study, together with the use of brachial pressures, makes
it unlikely that the assumption of pressure equivalence will have
introduced significant error. Indeed, a recent study in which brachial
systolic and diastolic pressures were used to
calibrate subclavian arterial waveforms registered by
applanation tonometry found no significant difference between
calibrated subclavian waveforms and those recorded from the
proximal aorta.14 Another study compared invasive
with noninvasive measurements and found excellent correlation between
both measures independent of whether subjects had CAD or
not.12
The variability of echocardiographically determined
indices of aortic stiffness has been found previously to be <10% for
interobserver comparisons and also for measurements repeated at 4-week
intervals.7 15 In addition, pulse pressure
measurement is independent of echocardiographic
assessments. In our study, the pulse pressure data are
consistent with the aortic stiffness measurement. This argues
against the results observed here being an artifact introduced by
potential confounding factors in the measurement of aortic root
diameter by echocardiography.
Differences between the CAD patients and control subjects were evident
in regard to blood pressure and the number of subjects taking
antihypertensive medication. These factors may be expected to have
opposing effects in that hypertension is associated with increased
aortic stiffness, whereas the use of antihypertensive medication has
been shown to reduce arterial
stiffness.16 17 Although the various classes of
antihypertensive medication may not affect aortic properties similarly,
there were too few subjects to permit analysis by class of
medication. The difference in blood pressure between CAD patients and
controls was small, however, and unlikely to account for the marked
difference in Ep and ß between CAD patients and
control subjects.
Echocardiographic left ventricular
hypertrophy has been found to be predictive of future
cardiovascular events in hypertensive subjects, in
those with CAD, and in disease-free
subjects.18 19 20 21 The left ventricular
hypertrophy seen in the CAD patients compared with controls
might reflect the effect of a higher input impedance associated with
increased aortic stiffness, a different average cardiac load over 24
hours, or growth factors such as insulin, which were not assessed in
this study.22 23
In conclusion, we have shown in a case-control study that proximal
aortic stiffness as well as left ventricular mass is
increased in subjects with newly detected CAD in a general population
sample; patients with CAD are likely to be in the highest quartile of
aortic stiffness distribution. This might contribute to previously
reported associations between pulse pressure and an increased
subsequent mortality, particularly from CAD.
Acknowledgments
This study was made possible by a grant from the Victorian
Health Promotion Foundation. We are grateful to the Anti-Cancer Council
of Victoria for helpful collaboration.
Received January 24, 1998;
first decision February 11, 1998;
accepted April 14, 1998.
References
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© 1998 American Heart Association, Inc.
Third Workshop on Structure and Function of Large
Arteries: Part III
Relation Between Coronary Artery Disease, Aortic Stiffness, and Left Ventricular Structure in a Population Sample
Key Words: aorta • arterial compliance • coronary artery disease • ventricular function, left
Consecutive volunteer screenees attending the Health 2000 Diet
and Cancer Study of the Anti-Cancer Council of Victoria were invited to
self-complete a modified Rose chest-pain
questionnaire.9 The Health 2000 Study is a cohort
study whereby some 50 000 Melbourne inhabitants are to be followed up
to examine the relationship between diet and the incidence of various
forms of cancer. The aim of the screening process was to identify
subjects with chest pain due to ischemic heart disease that had
not been previously recognized. Initial questions in the survey
identified subjects who knew of a previous diagnosis of myocardial
infarction and/or angina. Subsequent questions identified the presence
of exertional chest pain (the site of which was also marked on a
cartoon figure). A total of 5160 questionnaires were returned. Those
subjects who were aware of a previous diagnosis of myocardial
infarction and/or angina were excluded from further participation. The
remaining 760 subjects, whose responses indicated that they experienced
exertional chest pain plausibly due to myocardial ischemia,
were invited to undergo a clinical interview and ECG stress test; only
50% of invited subjects attended. Subjects who had an ECG indicative
of a prior myocardial infarction or significant ST deviation at rest
were excluded from further participation. The ECG stress test was
performed according to a modified Bruce protocol on a treadmill. A
total of 57 subjects, who developed 
1.5 mm ST-segment
depression, were classified as positive cases. Of these subjects with a
positive stress test, 55 agreed to participate in this study.
On the day of the study, subjects arrived in the morning after
an overnight fast. Cases were investigated within days of the positive
ECG stress test. Height and weight were recorded, and a fasting
blood sample was drawn.
All data are expressed as mean±SEM except where indicated
otherwise. Statistical comparisons were made using Student's
t and 
2 tests as appropriate;
2-tailed probabilities for a separate variance estimate are given where
applicable. Because Ep and ß data are skewed,
nonparametric tests were used to compare groups. The
analysis by quartiles was restricted to subjects older than 55
years with a mean arterial pressure <107 mm Hg as
suggested by previous work.1 All other subgroups
(ie, those younger than 55 years or with a mean arterial
pressure >107 mm Hg) contained too few subjects for a meaningful
analysis. Data were complete for 28 CAD patients and 30
controls for the analysis by quartile. Values were considered
significant if P<0.05. All computations were done using
SPSS software for Windows, version 7.0. 
). No significant
differences were found for weight, height, or body mass index. Both CAD
patients and controls had similar values for triglycerides
and HDL and LDL cholesterol. Only a small proportion of CAD
patients and controls were current cigarette smokers (3 in each group).
More CAD patients than controls were taking antihypertensive medication
(36% versus 7%, P<0.01). Left ventricular
mass index and posterior wall thickness were higher in CAD patients
than in controls.
View this table:
[in a new window]
Table 1. Data for CAD Patients and Control Subjects Matched for Gender,
Age, and Serum
Cholesterol ), 61% of CAD patients were found
to be in the highest stiffness quartile (P<0.05).
View larger version (28K):
[in a new window]
Figure 1. Distribution of CAD patients along quartiles defined by
aortic stiffness Ep (N/m2) in control subjects.
Analysis was restricted to CAD patients and controls older than
55 years with a mean arterial pressure of <107
mm Hg. P value shows significance of 2 test
for CAD patients vs control subjects.
). When limited to
subjects older than 55 years with a mean arterial pressure
<107 mm Hg, subjects in the highest stiffness quartile had a
relative risk of 1.9 of dying from CAD compared with the rest of the
cohort.1 Interestingly, that study found that no
such association existed for cerebrovascular mortality. Hence, the
higher prevalence of CAD in subjects with a higher aortic stiffness as
demonstrated in our study might account for this additional CAD
mortality.
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 M. L. Hixon, C. Obejero-Paz, C. Muro-Cacho, M. W. Wagner, E. Millie, J. Nagy, T. J. Hassold, and A. Gualberto Cks1 Mediates Vascular Smooth Muscle Cell Polyploidization J. Biol. Chem., December 15, 2000; 275(51): 40434 - 40442. [Abstract] [Full Text] [PDF]
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T. L. Medley, T. J. Cole, C. D. Gatzka, W. Y.S. Wang, A. M. Dart, and B. A. Kingwell Fibrillin-1 Genotype Is Associated With Aortic Stiffness and Disease Severity in Patients With Coronary Artery Disease Circulation, February 19, 2002; 105(7): 810 - 815. [Abstract] [Full Text] [PDF]
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