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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 26, No 1, January/February 2015
22
AFRICA
aortic wall. Aortic systolic (AoS) diameter was measured at the
time of full opening of the aortic valve, and diastolic (AoD)
diameter was measured at the peak of QRS. Three consecutive
beats were measured routinely and averaged.
Systolic and diastolic blood pressures were measured
simultaneously at the brachial artery by sphygmomanometry.
Pulse pressure was calculated as systolic minus diastolic blood
pressure.
The percentage change of the aortic root Ao (%) was
calculated to obtain the aortic strain:
Ao (%) =
100
×
(AoS − AoD)
________________
AoD
Other indices of the aortic elastic properties were measured.
Aortic distensibility index (cm
-2
dyn
-1
10
-6
)
=
2
×
(systolic diameter – diastolic diameter)
_________________________________
(diastolic diameter)
×
(pulse pressure)
The aortic stiffness index
β
=
ln(SBP/DBP)
_______________
(AoS−AoD)/AoD
All venous samples were collected in the morning after a 12-hour
overnight fast, for biochemical analyses. The blood samples were
centrifuged at 4 000 rpm at room temperature for 5 min, and
the plasma was frozen at –20°C until measurement of adhesion
molecules. Serum concentrations of ICAM-1, and VCAM-1
were measured using commercial enzyme immunoassay kits
(E-BIOSCIENCE, San Diego, USA), as instructed by the
manufacturer.
Statistical analysis
All data analyses were performed with the SPSS (Statistical
Package for Social Sciences) for Windows 17.0 computer
program (SPSS Inc. Chicago, IL, USA). Data were expressed
as mean
±
standard deviation. After testing for normality with
the Shapiro–Wilk test, continuous parameters were analysed
with non-parametric tests. The relationship between levels of
circulating adhesion molecules and aortic stiffness was assessed
by Spearman’s test. Since preliminary analysis did not reveal
significant interactions with cellular adhesion molecules, we did
not run models stratified by risk factors for aortic stiffness. A
p
-value of
<
0.05 was accepted as significant.
Results
Data from a total of 63 participants (mean age 55.6
±
10.58 years,
31 male) were included in the study. The baseline characteristics
of the study population are summarised in Table 1. Circulating
levels of adhesion molecules were VCAM-1: 12.604
±
3.904 ng/
ml and ICAM-1: 45.417
±
31.429 ng/ml. Aortic strain was 6.210
±
2.253%, stiffness index was calculated as 10.423
±
5.350 and
distensibility as 2.354
±
0.993
×
10
-3
/KPa (Table 2). We were
unable to demonstrate any correlation between the indices of
aortic stiffness and CAM-1 and ICAM-1 levels (Table 3).
Discussion
The potential role of soluble adhesionmolecules as biomarkers of
diagnosis, severity and prognosis of cardiovascular disease have
been investigated in a number of clinical studies. However, these
studies have found heterogeneous results. Ridker
et al
. reported
a significant association between increasing concentrations of
sICAM-1 and the risk of future myocardial infarction, especially
among participants with baseline sICAM-1 concentrations in
the highest quartile.
12
Blankenberg
et al
. found that VCAM-1, ICAM-1 and
E-selectin were significantly related to future cardiovascular
death in 2.7 years’ mean follow up of a prospective cohort of
1 245 patients.
3
Moreover, of all the inflammatory markers
evaluated, VCAM-1 levels revealed the strongest association
with future death, and added predictive value to the classic
risk factors and high-sensitivity C-reactive protein (CRP) in
determining the risk for future cardiovascular death.
In a prospective, nested, case–control study, median levels
of sICAM-1 but not sVCAM-1 were significantly higher at
baseline among men who developed peripheral arterial disease
(PAD) during a nine-year follow-up period.
13
In the study by
Hwang
et al
., E-selectin and ICAM-1 levels were significantly
increased in patients with coronary heart disease (CHD) and
carotid artery atherosclerosis compared with the control subjects.
However, levels of VCAM-1 were not significantly different
among patients in these groups.
14
In contrast to these findings, in a long-term, community-
based study, Malik
et al
. assessed the predictive ability of
baseline serum concentrations of soluble adhesion molecules
for fatal and non-fatal CHD. They found no strong association
of these adhesion molecules with CHD risk. Furthermore, they
reinforced their findings with a meta-analysis of previously
published prospective studies.
15
Table 1. Baseline characteristics of the patients
Characteristics
Number (%)
Age (years)
55.6
±
10.5
Males
31 (49.2)
Smoking
6 (9.5)
Hypertension
31 (49.2)
Diabetes mellitus
14 (22.2)
Hyperlipidaemia
11(17.5)
Coronary artery disease
18 (25.6)
Table 2. SerumVCAM and ICAM levels and
indices of aortic stiffness
Variables
Mean
±
SD (
n
=
63)
VCAM (ng/ml)
12.604
±
3.904
ICAM (ng/ml)
45.417
±
31.429
Aortic strain (%)
6.210
±
2.253
Stiffness index (
β
)
10.423
±
5.350
Distensibility (
×
10
-3
/KPa)
2.354
±
0.993
Table 3. Correlation between aortic strain, stiffness index,
distensibility and adhesion molecules
Variables
VCAM (ng/ml) ICAM (ng/ml)
r
p
r
p
Aortic strain (%)
–0.030 0.813 0.061 0.634
Stiffness index (
β
)
0.038 0.768 –0.095 0.458
Distensibility (
×
10
-3
/KPa)
–0.026 0.839 0.097 0.449