Cardiovascular Journal of Africa: Vol 31 No 3 (May/June 2020)

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CARDIOVASCULAR JOURNAL OF AFRICA • Volume 31, No 3, May/June 2020 AFRICA 151
sectional study also demonstrated higher plasma Gal-3 levels
in patients with carotid atherosclerosis than in those without.33
These findings indicate the role of Gal-3 in atherosclerotic plaque
instability, macrophage activation and increased monocyte
recruitment. Furthermore, studies involving long-term follow up
have suggested that Gal-3 levels may represent an independent
predictor of cardiovascular events and mortality in patients with
CAD.40 Finally Gal-3 plays a key role in vascular inflammation
and fibrosis induced by aldosterone.8
In light of these data, it appears reasonable to assume a
cause-and-effect relationship between elevated serum Gal-3
levels in isolated CAE patients and the development of ectasia
through weakening of the arterial wall as a result of a number
of mechanisms including atherosclerosis, vascular inflammation
and oxidative stress.
Furthermore, in our study, patients with isolated CAE
were further classified into four groups based on the extent of
ectasia. Serum Gal-3 levels did not differ significantly among
these four groups, suggesting that Gal-3 may be associated with
the atherosclerotic process rather than the severity of ectasia.
However, the number of patients in each subgroup was too
low to draw a firm conclusion. Considering several studies
examining the physiopathology of CAE and showing a more
intense inflammatory process compared to those with CAD,
similar fibrinogen and hs-CRP levels in our study as biomarkers
of inflammation may be explained on the basis of a subtler
inflammatory process.
There are some limitations to this study. Its small sample
size and single-centre design are the main limitations. Another
limitation involves the fact that normal coronary arteries were
defined on the basis of contrast angiography of the lumen
without using IVUS. Therefore, the presence of underlying
atherosclerotic plaques might have been overlooked. In addition,
normal epicardial arteries in the control group were not able
to be evaluated for vasospasm or microvascular dysfunction
with an independent method, which can be deemed another
limitation.
Conclusion
This study is the first to show a significant increase in serum
Gal-3 levels in patients with isolated CAE, indicating that Gal-3
may play a role in the pathogenesis of CAE, similar to CAD.
Based on our study results, we suggest that increased Gal-3
levels may affect coronary remodelling in a way that favours the
development of ectasia. However, further studies at a cellular
level in larger series are warranted to gain a better understanding
of the role of Gal-3 in patients with isolated CAE.
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