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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 5, September/October 2020
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233
It has been reported that eosinophils and their granule-
associated molecules have been isolated from necrotic and
thrombotic lesions, and these structures were extracted from
small arterial walls, especially after acute ischaemic damage to
the endocardium. These findings suggest that eosinophils may
cause inflammation, thrombosis and embolus-induced vascular
damage.
32-34
It has been reported that eosinophils are related to arterial
tortuosity, thrombosis, cardiac syndrome X, dilatation and
aneurysm in patients with hypereosinophilic syndromes.
35,36
Cytotoxic secretions secreted from eosinophils have been
suggested to cause direct medial destruction leading to
aneurysmal formation or spontaneous intimal dissection and
sudden cardiac death.
37
This suggests that eosinophil secretion
may be one of the causes of vascular injury, therefore eosinophils
may affect the cardiovascular system via an inflammatory
mechanism.
Lymphocytes are related to the immune response and
systemic inflammation. Stress-induced low lymphocyte
levels (lymphopaenia) have been found to be associated with
inflammatory conditions and adverse cardiovascular events.
11,12
Low lymphocyte counts might result from increased cortisol
levels that induce apoptosis specifically in lymphocytes but
also increase the total WBC count.
38
Eosinophil elevation
and low lymphocyte levels reflect systemic inflammation and
physiological stress and contribute to the development of
cardiovascular disease.
13-15,20
A strong correlation was found between CAE and low
HDL-C levels, and this study suggests that low HDL-C levels
could lead to isolated CAE.
39
Several studies have previously
reported that HDL-C levels decrease in the presence of systemic
inflammation, and systemic and vascular inflammation impair
the structure of HDL-C and disrupt its function, reducing its
protective effect on the vascular endothelium.
40-43
In this study, we observed that HDL-C levels were lower
in the isolated CAE group than in the NCA group (Table 1).
This finding may be reflective of the systemic and vascular
inflammation consistent with previous studies. Moreover, the
low HDL-C levels observed in the isolated CAE group may be
considered one of the mechanisms responsible for endothelial
dysfunction and vascular destruction. Nevertheless, larger
studies that focus only on this issue are necessary to draw more
concrete conclusions.
IncreasedWBC count,WBC sub-type and sub-type ratios have
been accepted as important inflammatory markers in forecasting
cardiovascular outcomes.
11,44
Elevated eosinophil count and
ELR values and decreased lymphocyte levels are associated
with systemic inflammation and atherosclerosis.
13,16,17,45,46
In some
studies, the relationship between some haematological parameters
actively functioning in inflammation, such as neutrophils,
lymphocytes, monocytes and eosinophils, and parameters
such as the monocyte-to-HDL-C ratio (MHR), neutrophil-
to-lymphocyte ratio (NLR), and platelet-to-lymphocyte ratio
(PLR) and their relationship with coronary artery ectasia has
been revealed.
13,14,47-49
However, as far as we know, the relationship
between CAE and ELR has not previously been studied.
Based on the role of inflammation in the aetiopathogenesis of
isolated CAE and in light of the study results, we hypothesised
that ELR may be associated with isolated CAE. The present
study revealed an increased eosinophil count and a decreased
lymphocyte count in isolated CAE patients compared to subjects
with NCA (Table 1). However, we did not observe a significant
association between eosinophil count and Markis classification,
diffuse ectasia or vessel count (Tables 2–5). Likewise, we did
not observe a significant difference between lymphocyte count
and Markis classification or vessel count (Tables 2–5). However,
the study showed that ELR was significantly associated with
these parameters (Tables 2-5). In addition, correlation analyses
revealed a significant association between lymphocyte count and
Markis classification, diffuse ectasia and vessel count (Table 5).
This indicates that the eosinophil count was higher in isolated
CAE compared to NCA but was not correlated with the severity
of CAE. However, lymphocyte count and ELR value not only
increased in isolated CAE patients but also were significantly
correlated with the severity of isolated CAE. The data obtained
in this study suggest that an analysis of only lymphocyte and
eosinophil levels may not provide reliable results, whereas the
use of ELR as a systemic inflammatory marker may be more
reliable. Although the sensitivity and specificity of ELR for
predicting isolated CAE were low in the ROC analysis, all
correlation analyses in other areas found that ELR indicated the
presence and severity of isolated CAE.
Since the study was designed retrospectively, data on acute
or chronic diseases that may affect ELR were obtained in
accordance with patient statements. Some patients may not
have been aware of inflammatory diseases such as allergic
rhinitis, conjunctivitis or atopic dermatitis, or they may not
have declared these diseases. Because advanced equipment such
as intravascular ultrasound could not be used in this study,
the coronary arteries of the subjects examined could not be
confirmed to be completely normal. These factors may explain
the results of the ROC analysis.
Limitations
Although there may be an atherosclerotic plaque over large
segments, the related vessel can be observed as normal
angiographically.
50,51
In this study, it was not possible to confirm
that the coronary arteries were completely normal because
a device such as intravascular ultrasound could not be used.
Second, as the study was retrospective, inflammatory markers
such as CRP could not be investigated or compared to ELR.
Conclusions
The results of this study may contribute to the aetiopathogenesis
of isolated CAE. As a new, simple, effortless and cost-effective
inflammatory marker, ELR may be able to forecast isolated
CAE in daily clinical practice. Increased ELR may explain the
vascular destruction, endothelial dysfunction, thrombosis and
distal microvascular embolisation seen in isolated CAE patients.
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