![Show Menu](styles/mobile-menu.png)
![Page Background](./../common/page-substrates/page0043.png)
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.
References
1.
Swaye PS, Fisher LD, Litwin P, Vignola PA, Judkins MP, Kemp HG,
et
al.
Aneurysmal coronary artery disease.
Circulation
1983;
67
: 134–138.
2.
Falsetti HL, Carrol RJ. Coronary artery aneurysm. A review of the
literature with a report of 11 new cases.
Chest
1976;
69
: 630–636.
3.
Oliveros RA, Falsetti HL, Carroll RJ, Heinle RA, Ryan GF.
Atherosclerotic coronary artery aneurysm. Report of five cases and
review of literature.
Arch Intern Med
1974;
134
: 1072–1076.
4.
Newburger JW, Takahashi M, Gerber MA, Gewitz MH, Tani LY, Burns
JC,
et al
. Diagnosis, treatment, and long-term management of Kawasaki
disease: a statement for health professionals from the Committee on
Rheumatic Fever, Endocarditis and Kawasaki Disease, Council on
Cardiovascular Disease in the Young, American Heart Association.
Circulation
2004;
110
: 2747–2771.
5.
Ross R. Atherosclerosis – an inflammatory disease.
N Engl J Med
1999;
340
: 115–126.
6.
Demopoulos VP, Olympios CD, Fakiolas CN, Pissimissis EG,
Economides NM, Adamopoulou E,
et al
. The natural history of aneu-
rysmal coronary artery disease.
Heart
1997;
78
: 136–141.
7.
Markis JE, Joffe CD, Cohn PF, Feen DJ, Herman MV, Gorlin R.
Clinical significance of coronary arterial ectasia.
Am J Cardiol
1976;
37
: 217–222.
8.
Calvier L, Miana M, Reboul P, Cachofeiro V, Martinez-Martinez E,
de Boer RA,
et al
. Galectin-3 mediates aldosterone-induced vascular
fibrosis.
Arterioscler Thromb Vasc Biol
2013;
33
: 67–75.
9.
Joo HG, Goedegebuure PS, Sadanaga N, Nagoshi M, Bernstorff W,
Eberlein TJ. Expression and function of galectin-3, a b-galactoside-
binding protein activated T lymphocytes.
J Leukocyte Biol
2001;
69
:
555–564.
10. Dong S, Hughes RC. Macrophage surface glycoproteins binding to
galectin-3 (Mac-2-antigen).
Glycoconj J
1997;
14
(2): 267–274.
11. Nakahara S, Oka N, Raz A. On the role of
galectin-3
in cancer apopto-
sis.
Apoptosis
2005;
10
(2): 267–275.
12. Dumic J, Dabelic S, Flögel M. Galectin-3: an open-ended story.
Biochim
Biophys Acta
2006;
1760
(4): 616–635.
13. De Boer RA, Voors AA, Muntendam P, van Gilst WH, van Veldhuisen
DJ. Galectin-3: a novel mediator of heart failure development and
progression.
Eur J Heart Fail
2009;
11
: 811–817.
14. Sano H, Hsu DK, Apgar JR, Yu L, Sharma BB, Kuwabara I,
et al.
Critical role of galectin-3 in phagocytosis by macrophages.
J Clin Invest
2003;
112
: 389–397.
15. Arar C, Gaudin JC, Capron L, Legrand A. Galectin-3 gene (LGALS3)
expression in experimental atherosclerosis and cultured smooth muscle
cells.
FEBS Lett
1998;
430
: 307–311.
16. MacKinnon AC, Liu X, Hadoke PW, Miller MR, Newby DE, Sethi
T. Inhibition of galectin-3 reduces atherosclerosis in apolipoprotein
E-deficient mice.
Glycobiology
2013;
23
: 654–663.
17. Anand IS, Rector TS, Kuskowski M, Adourian A, Muntendam P, Cohn
JN. Baseline and serial measurements of galectin3 in patients with heart
failure: Relationship to prognosis and effect of treatment with valsartan
in the ValHeFT.
Eur J Heart Fail
2013;
15
: 511–518.
18. Aboeata AS, Sontineni SP, Alla VM, Esterbrooks DJ. Coronary artery
ectasia: current concepts and interventions.
Front Biosci
2012;
4
:
300–310.
19. Williams MJA, Stewart RAH. Coronary artery ectasia, local pathology
or diffuse disease.
Cathet Cardiovasc Diagn
1994;
33
: 116–119.
20. Isner JM, Donaldson RF, Fortin AH, Tischler A, Clarke RH.
Attenuation of the media of coronary arteries in advanced atherosclero-
sis.
Am J Cardiol
1986;
58
: 937–939.
21. Schoenhagen P, Ziada KM, Vince DG, Nissen SE, Tuzcu EM. Arterial
remodeling and coronary artery disease: the concept of “dilated” versus
“obstructive” coronary atherosclerosis.
J Am Coll Cardiol
2001;
38
:
297–306.
22. Bond MG, Adams MR, Bullock BC. Comlicating factors in evaluating
coronary artery atherosclerosis.
Artery
1981;
9
: 21–29.
23. Ylä-Herttuala S, Jaakkola O, Solakivi T, Kuivaniemi H, Nikkari T. The
effect of proteoglycans, collagen and lysyl oxidase on the metabolism
of low density lipoprotein by macrophages.
Atherosclerosis
1986;
62
(1):
73–80.
24. Schwartz CJ, Valente AJ, Sprague EA, Kelley JL, Nerem RM. The