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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 5, September/October 2020
228
AFRICA
normal coronary artery.
1-5
CAE aetiology has been attributed
to atherosclerosis (50% of cases), congenital malformations
(20–30% of cases) and inflammatory or connective tissue
disease (10–20% of cases).
6
CAE is considered a unique form
of atherosclerotic cardiovascular disease. Various studies have
indicated that CAE is characterised by a denser vascular
inflammation than occlusive coronary artery disease.
7,8
Some publications have reported that CAE causes coronary
slow flow in the coronary arteries, resulting in thrombosis. CAE
has also been suggested to cause clinical symptoms of ischaemic
heart disease and myocardial infarction without occlusive
coronary artery disease.
9
The ischaemic mechanism in patients
with CAE has not been fully clarified, as the basic cause of
ischaemia and angina is considered to be microvascular perfusion
impairment. The slow or turbulent flow during vasodilation is
believed to cause thrombosis in the ectatic segment or embolus
formation in the distal coronary artery, resulting in ischaemia.
3
Güleç
et al
. indicated that epicardial and microvascular perfusion
is destroyed in ectasia patients. The same study noted that the
thrombolysis in myocardial infarction square number could be
used to predict microvascular perfusion impairment when ectatic
and non-ectatic arteries were compared.
10
Eosinophil and lymphocyte cells are associated with
an immune response and inflammation. A low number of
lymphocyte cells is considered one of the main reasons for
progression of cardiovascular disease.
11,12
Eosinophil elevation
and low lymphocyte levels reflect systemic inflammation and
physiological stress.
13-15
Therefore the eosinophil-to-lymphocyte
ratio (ELR) is an indicator of systemic inflammation.
16,17
Eosinophils have a significant status inendothelial dysfunction,
inflammation, vasoconstriction and thrombosis.
18,19
Eosinophils
stimulate platelet activation and aggregation and contribute
to thrombus formation by inhibiting thrombomodulin.
20
Some publications have revealed that vascular anomalies,
such as aneurysms, may be associated with hypereosinophilic
syndrome.
21,22
Can eosinophils (with their strong vasoactive and
procoagulant effects) and the ELR (which is a good indicator
of systemic inflammation) be associated with isolated CAE and
its microvascular perfusion impairment? Although there is a
small study examining the relationship between blood eosinophil
concentration and CAE, no large studies that could indicate
a correlation between blood eosinophil level and ELR, and
CAE severity were found in the literature.
13
This study aimed
to determine whether there was an association between plasma
eosinophil level, ELR and the existence and severity of CAE.
Methods
Angiographic records of 16 240 Turkish patients who had
coronary angiography between January 2009 and June 2018 in
the Elazı
ğ
Education and Research Hospital were retrospectively
investigated for the presence of isolated CAE. The study
included 232 subjects with isolated CAE and 247 age- and
gender-matched subjects who had normal coronary anatomy
(NCA). The routine clinical and laboratory tests (complete
blood count, total biochemistry values and demographic data)
of the subjects were obtained from their files (Fig. 1).
The study was conducted according to the Helsinki principles,
and ethical approval was obtained from the TC Firat University
ethics committee. The ethics committee did not require informed
written consent forms as the data are anonymous.
Coronary angiographies were performed with Siemens Axiom
Artis FC diagnostic equipment using the Judkins technique
(Siemens Healthcare GmbH, Forchheim, Germany).
23
Nitro-
glycerin was not used during the coronary angiographies.
Coronary angiography records were gained from the left and
right anterior oblique cranial, anterior–posterior (AP) cranial,
right anterior oblique, caudal and horizontal positions. Isohexol
350 mg/ml (Amersham Health Co, Cork, Ireland) was used
for opacifity when performing the coronary angiogram; 6 ml
was administered into the coronary arteries at each position.
The angiography was recorded digitally with a frame rate of
25 frames/ms. The coronary artery diameters were determined
by computerised quantitative angiography. These evaluations
were gained by analysing the digital inputs obtained from the
coronary angiographies.
Scientific quantification coronary analysis software (Siemens
Healthcare Gmbh, Forcheim, Germany) was used for these
procedures. The computations were obtained at the proximal,
mid and distal segments of the coronary arteries to define the
artery segment as ectatic. The largest diameter of the segments
was taken into account.
CAE was defined as 1.5 times or more enlargement of the
coronary artery compared to the adjacent coronary artery.
Isolated CAE was defined as regional or widespread expansion
without significant coronary artery stenosis. Angiographic
stenosis of more than 50% of the coronary artery was considered
as significant occlusion. Patients without significant coronary
artery stenosis who had ectatic segments were included in
the isolated CAE group. The characteristics of CAE were
categorised as diffuse or discrete ectasia to classify the severity of
CAE. Fusiform dilatations of the coronary arteries were defined
as diffuse ectasia, and localised/focal vesicular or spheroidal
dilatation of the coronary arteries was defined as discrete ectasia
6
(Figs 2–5).
Classification by Markis
et al
. was used to determine
the distribution of CAE. This classification depends on the
diffuseness of ectasia. Accordingly, patients who have isolated
CAE were classified into four groups. Diffuse ectasia in two or
three vessels was defined as type I, diffuse ectasia in one vessel
and focal ectasia in another vessel was defined as type II, diffuse
ectasia in only one vessel was defined as type III and focal ectasia
was defined as type IV.
4
The coronary angiographies were evaluated by two
angiography experts who specialise in coronary angiography and
had no knowledge about the history of the patients.
Study exclusion criteria: subjects with acute coronary
syndrome at study entrance, significant coronary artery stenosis
(angiographic stenosis > 50%) or isolated coronary slow flow,
anaemia (Htc
<
30%), cardiac failure, thyroid dysfunction,
malignancy, chronic renal deficiency [glomerular filtration rate
(GFR)
<
60 ml/min/1.73 m
2
], chronic liver failure, chronic
obstructive pulmonary disease and/or bronchial asthma, or were
found to have used immunosuppressive therapy or steroids, or
subjects who had a body mass index of > 30 kg/m
2
were excluded.
Subjects who had a recent past of an acute infection and/or
high body temperature > 37.2°C or an inflammatory or allergic
disease were also excluded from the analysis.
Subjects who had taken antihypertensive medication and