Cardiovascular Journal of Africa: Vol 26 No 1 (January/February 2015)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 26, No 1, January/February 2015 AFRICA 11
aorta in children with asthma and in a control group. Our
hypothesis was that since asthma is a chronic inflammatory
disease, it could lead to the early development of atherosclerosis
in childhood-onset asthma.
To detect the effect of inflammation, we included patients
with a diagnosis of asthma of at least three years’ duration.
As a marker of atherosclerosis, we evaluated abdominal aortic
stiffness parameters with transthoracic echocardiography.
Stiffness and distensibility assessments of the abdominal aorta
play an important role in evaluation of the elasticity of the
arterial system. If there is atherosclerosis, aortic stiffness, Ep and
Ep* will increase, whereas DIS and S will decrease. S and DIS
represent the elasticity of the abdominal aortic wall.
In the literature, aortic distensibility has been shown to
be useful in adults as a non-invasive method to detect early
atherosclerosis. The increased stiffness causes an increase in
pulse pressure and a decrease in diastolic blood pressure,
thereby causing increased left ventricular afterload and increased
fatigue in arterial wall tissues. Previous studies have shown that
measurement of aortic stiffness helps in the early detection of
atherosclerosis, and the abdominal aorta becomes stiffer with
age, hypertension, atherosclerosis, tobacco-smoking, obesity, and
in β-thalassaemia patients and patients with Marfan syndrome
and Kawasaki disease.11,13,14
Lacombe et al. demonstrated that in subjects older than
20 years of age, S, Ep and Ep* were related to age due to
atherosclerosis.10 We calculated S, Ep, Ep* and distensibility
using the formula proposed by Lacombe and Lage et al.10,15
Okubo found that aortic distensibility varies with age; it was low
in infants, increased gradually to a peak from 10–15 years, and
then decreased with age.11
Atherosclerosis and asthma are both chronic inflammatory
diseases. Inflammation leads to impairment of endothelial
function. When the inflammation is chronic, this causes
acceleration of atherosclerosis.18 In the literature, some studies
have stated that asthma itself could be a risk factor for heart
disase and stroke.19,20
Related to increased oxidative stress, asthma is a chronic
inflammatory disease.21 The association between chronic
inflammation and oxidative stress is well documented. In asthma
patients with inflammatory conditions, elevated levels of reactive
oxygen species, such as hydroxyl radicals, superoxides and
peroxides have been reported.22 Chronic inflammation has
also been increasingly associated with endothelial dysfunction,
atherosclerosis and arterial stiffness, and these in turn with
adverse cardiovascular events and common inflammatory
pathways.23,24
Some studies have evaluated the relationship between adult-
onset asthma and atherosclerosis but the results are contradictory.
Onufrak et al. showed that in adult-onset asthma patients, the
risk of atherosclerosis was increased.25 However, in another
study by Otsuki et al., carotid atherosclerosis was reduced in
asthmatic adult patients treated with inhaled corticosteroids
compared with matched controls, and they found that inhaled
corticosteroids had protective effects against atherosclerosis.26
Weiler et al. found significant correlations between
measurements of periferal arterial stiffness and FEV1 in
adult asthmatics, and suggested the presence of a common
systemic, most likely inflammatory pathway involving both
the cardiovascular and respiratory systems.27 In another study
of adult asthmatics, Sun et al. found that that patients with
severe asthma had increased brachial–ankle pulse-wave velocity
(baPWV) compared with those with stable asthma and control
subjects. Furthermore, baPWV was elevated in patients with
stable asthma compared with the control subjects.28
However, there are only a few studies evaluating the
relationship between childhood-onset asthma and atherosclerosis.
In the study of Cakmak et al., 29 carotid intima–media thickness
(CIMT) in asthmatic children was found to be higher compared
to the control group and there was a positive correlation between
CIMT and total oxidant status. They studied only children
with mild asthma who were not using prophylactic inhaled
corticosteroids.
In all these studies, CIMT was evaluated as a marker of
atherosclerosis. However, in our study, we evaluated abdominal
aortic stiffness as a sign of atherosclerosis in childhood asthma.
In our investigation, the study population consisted of
children with stable asthma. We did not evaluate aortic stiffness
parameters in children with severe asthma. Further studies
including larger population size and children with severe asthma
may reveal different results regarding abdominal aortic stiffness.
In our study, we used only hs-CRP as an inflammatory
marker. An inflammatory marker showing oxidant status could
not be studied.
Table 4. Aortic stiffness parameters in patients with
intermediate severity asthma and the control group
Intermediate-
severity asthma
patients ( n = 18)
Control group
(n = 57) p-value
Peak aortic velocity, cm/s 125.6 ± 16.7 123.5 ± 17.9 > 0.05
Ds, mm 11.4 ± 2.0 11.1 ± 1.9 > 0.05
Dd, mm 8.2 ± 1.5 8.2 ± 1.8 > 0.05
DIS, 10-6 cm2/dyne 1.31 ± 0.51 1.41 ± 0.66 > 0.05
S 0.39 ± 0.10 0.37 ± 0.14 > 0.05
Ep, N/m2 105.9 ± 42.4 116.5 ± 55.9 > 0.05
Ep* 1.71 ± 0.74 1.83 ± 0.90 > 0.05
Data are presented as mean ± standard deviation.
Dd: abdominal aorta diastolic diameter, DIS: aortic distensibility, Ds:
abdominal aorta systolic diameter, Ep: pressure strain elastic modulus,
Ep*: pressure strain normalised by diastolic pressure, S: aortic strain.
Table 5. Aortic stiffness parameters in asthma patients
with atopy and the control group
Asthma patients
with atopy
(n = 37)
Control group
(n = 57) p -value
Peak aortic velocity, cm/s 128.0 ± 16.5 123.5 ± 17.9 > 0.05
Ds, mm 11.5 ± 1.9 11.1 ± 1.9 > 0.05
Dd, mm 8.3 ± 1.3 8.2 ± 1.8 > 0.05
DIS, 10-6 cm2/dyne 1.31 ± 0.51 1.41 ± 0.66 > 0.05
S 0.38 ± 0.12 0.37 ± 0.14 > 0.05
Ep, N/m2 105.4 ± 35.6 116.5 ± 55.9 > 0.05
Ep* 1.69 ± 0.66 1.83 ± 0.90 > 0.05
Data are presented as mean ± standard deviation.
Dd: abdominal aorta diastolic diameter, DIS: aortic distensibility, Ds:
abdominal aorta systolic diameter, Ep: pressure strain elastic modulus,
Ep*: pressure strain normalised by diastolic pressure, S: aortic strain.