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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 26, No 1, January/February 2015
AFRICA
9
patients was determined with specific IgE (sIgE) and skin-prick
tests to aero-allergens.
sIgE levels were determined with the CAP FEIA method
(Pharmacia, Uppsala, Sweden), which detects sensitisation in
the serum against inhaled allergens (wild grass, house dust
mite, animal dander, yeasts, grass pollen, trees). The result was
considered positive if the measured value was greater than 0.35
kU/l.
The skin-prick test (SPT) was done using Allergopharma
(Joachim Ganzer KG, Reinbeck, Germany) commercial allergen
solutions. A total of 44 different allergens consisting of house
dust mite, grass, wild grass, tree pollens, fungi, animal dander
and insects were tested and children with at least one positive test
were considered atopic. Asthma patients who had a positive sIgE
and sensitivity against at least one aero-allergen on the SPT were
included in the atopic asthma group.
Immunocompromised patients, patients with a history of
chronic inflammation/rheumatological disorders, diabetes,
hypertension, hypercholesterolaemia and those with autoimmune
diseases or a history of smoking exposure were excluded.
Asthma patients with an exacerbation of their asthma within the
previous month or with symptoms of respiratory tract infection
were also excluded.
The control group consisted of 57 gender- and age-matched
healthy children. They were chosen from children referred to
the paediatric cardiology out-patient clinics due to innocent
murmur. The control group was evaluated with regard to familial
and personal history of hyperlipidaemia and atopy, chronic
and/or severe infections, and rheumatological and autoimmune
diseases. Children were included in the control group if they had
no sign of atopic diseases and no personal familial history of
atopy. The control group was also selected from non-smoking
households.
The local ethics committee approved the study. Informed
consent was obtained from the parents of all subjects in the
study and control groups.
The patients in the study group and the healthy controls were
weighed with an electronic digital scale that was sensitive to 0.1
kg. Body height was measured and body mass index (BMI) was
calculated with the formula: weight (kg)/height
2
(m
2
).
A detailed medical history was obtained and a physical
examination was performed by the same paediatric cardiologist.
Blood pressure was recorded and all subjects were evaluated with
a respiratory function test.
Plasma lipid levels were measured after 12 hours of fasting.
Serum total cholesterol, high-density lipoprotein (HDL) and
low-density lipoprotein (LDL) cholesterol levels were measured
with Alcyon 300 (Abbott Laboratories, USA) equipment by
enzymatic methods. High-sensitivity C-reactive protein (hs-CRP)
levels in the study and control groups were measured on an
automatic analyser, based on the turbidimetry method.
Blood pressure measurements were done after 15 minutes
of rest; the right brachial artery pressure was measured by
sphygmomanometer with an appropriate cuff. Both systolic (Ps)
and diastolic blood pressure (Pd) were measured, and after three
measurements the mean value was obtained. Pulse pressure (PP)
was calculated as PP
=
Ps – Pd.
All the patients and control groupunderwent two-dimensional,
M-mode and Doppler studies using GE Vingmed Vivid 7-model
echocardiography (GE Vingmed, Ultrasound AS, Horten,
Norway) with a 3-MHz transducer. All the subjects were at rest
and lying in the left decubitus position during the examination.
End-diastolic left ventricular posterior wall thickness
(LVPWTed), left ventricular end-diastolic and systolic diameters
(LVED, LVES), left atrial diameter (LA) and aortic anulus
diametersweremeasured.Theejectionfraction(EF)andfractional
shortening (FS) were measured fromM-mode echocardiographic
tracings. The measurements were determined with standard
techniques in accordance with the recommendations of the
American Society of Echocardiography.
17
Mean pulmonary
artery pressure of all subjects was calculated from pulmonary
artery accelaration time.
A long-axis viewof the abdominal aorta of the subxiphoid area
was recorded and maximum systolic (Ds) and minimum diastolic
diameter (Dd) was measured by M-mode echocardiography.
All echocardiographic measurements were done by the same
experienced paediatric cardiologist and intra-observer variability
was evaluated with intraclass correlation coefficient (ICC); ICC
was 0.9 (excellent reliability).
All aortic measurements were made as previously described
by Lacombe
et al
.
10
Aortic strain (S) was calculated from the
changes in aortic diameter, and pressure strain elastic module
was also calculated from the aortic strain and the changes in
brachial artery systolic and diastolic pressure using the formulae:
S
=
(Ds – Dd)/Dd and Ep
=
(Ps – Pd)/S.
Pressure strain normalised (Ep*) by diastolic pressure was
calculated with the equation: Ep*
=
Ep/Pd. Aortic distensibility
(DIS) was calculated according to the previously proposed and
evaluated equations
10-15
as: DIS
=
[2(Ds – Dd)/Dd(Ps – Pd)]
×
10
-6
cm/dyne.
S and DIS represent the distensibility or elasticity of the
aortic wall; Ep and Ep* represent the stiffness of the aortic wall,
and Ep and Ep* are the mean stiffness of the aorta. S and Ep*
are dimensionless ratios, whereas Ep has a dimension and is
represented with the unit of N/m
2
(force/unit area).
Statistical analyses
All statistical analyses were performed using Systat statistical
software (version 15.0 for Windows; SPSS Inc, Chicago,
IL, USA). Data were tested for homogeneity of variance
with the Shapiro–Wilk test. The Student’s
t
-test (unpaired)
and chi-squared test were used for comparison of statistical
difference between the groups. Correlations with the aortic
elasticity parameters were evaluated with Pearson’s correlation
test. Statistical significance was taken as
p
<
0.05. All data were
presented as mean
±
SD.
Results
The study group consisted of 50 children (24 female, 26 male)
with asthma. According to the GINA guidlines, 26 of the
patients had mild intermittant asthma, six had mild persistent
and 18 had intermediate persistent asthma. None of the patients
had severe asthma. In 37 of the asthma patients, sIgE was
positive and these patients were accepted as the atopic asthma
group; 27 of these patients received immunotherapy.
The mean age of the asthma group was 11.7
±
2.7 years and of
the control group, 12.3
±
2.8 years (34 female, 23 male). There was
no difference between the groups in terms of age, gender and BMI