CARDIOVASCULAR JOURNAL OF AFRICA • Volume 25, No 1, January/February 2014
AFRICA
13
and a negative correlation between TIMI frame count and FMD.
6
In
our study, FMD was impaired in patients with CSF, and negatively
correlated with TIMI frame count. We found no correlation
between genotyping and FMD in this study. These results suggest
that endothelial dysfunction is an important process in CSF.
The most significant limitations of the present study include
the small sample size; the control group was not a normal
population of subjects, for ethical reasons; we could not measure
inflammatory markers such as C-reactive protein, interleukins,
NO and PAI-1 levels; and we could not perform intravascular
ultrasonography on the patients for the determination of intimal
thickening and calcification.
Conclusion
This study shows that brachial artery FMD was impaired and the
4G allele of the
PAI-1
4G/5G polymorphism was less prevalent
among CSF patients. However, large-scale genetic studies need
to be undertaken in CSF populations in order to understand the
underlying mechanisms of aetiopathogenesis.
References
1.
Tambe AA, Demany MA, Zimmerman HA, Mascarenhas E. Angina
pectoris and slow flow velocity of dye in coronary arteries, a new
angiographic finding.
Am Heart J
1972;
84
: 66–71.
2.
Beltrame JF, Limaye SB, Horowitz JD. The coronary slow flow
phenomenon – a new coronary microvascular disorder.
Cardiology
2002;
97
: 197–202.
3.
Sezgin AT, Sigirci A, Barutcu I,
et al
. Vascular endothelial function in
patients with slow coronary flow.
Coron Artery Dis
2003;
14
: 155–161.
4.
Pekdemir H, Cin VG, Cicek D,
et al
. Slow coronary flow may be a sign
of diffuse atherosclerosis. Contribution of FFR and IVUS.
Acta Cardiol
2004;
59
: 127–133.
5.
Gullu H, Erdo
ğ
an D, Cali
ş
kan M,
et al
. Interrelationship between
noninvasive predictors of atherosclerosis: transthoracic coronary flow
reserve, flow mediated dilation, carotid intima-media thickness, aortic
stiffness, aortic distensibility, elastic modulus, and brachial artery diam-
eter.
Echocardiography
2006;
23
: 835–842.
6.
Ari H, Ari S, Erdogan E, Tiryakioglu KH, Koca V, Bozat T. The effects
of endothelial dysfunction and inflammation on slow coronary flow.
Arch Turk Soc Cardiol
2010;
38
: 327–333.
7.
Daemen MJ, Lombardi DM, Bosman FT, Schwartz SM. Angiotensin II
induces smooth muscle cell proliferation in the normal and injured rat
arterial wall.
Circ Res
1991;
68
: 450–456.
8.
Rigat B, Hubert C, Alhenc-Gelas F, Cambien F, Corvol P, Soubrier F.
An insertion/deletion polymorphism in the angiotensin I-converting
enzyme gene accounting for half the variance of serum enzyme levels.
J Clin Invest
1990;
86
: 1343–1346.
9.
Danser AH, Schalekamp MA, Bax WA,
et al
. Angiotensin converting
enzyme in the human heart: effect of the deletion/insertion polymor-
phism.
Circulation
1995;
92
: 1387–1388.
10. Yalcın AA, Kalay N, Caglayan AO,
et al
. The relationship between slow
coronary flow and angiotensin converting enzyme and ATIIR1 gene
polymorphisms.
J Natl Med Assoc
2009;
101
: 40–45.
11. Tanriverdi H, Evrengul H, Mergen H,
et al
. Early sign of atherosclerosis
in slow coronary flow and relationship with angiotensin-converting
enzyme I/D polymorphism.
Heart Vessels
2007;
22
: 1–8.
12. Moncada S, Higgs A. The L-arginine–nitric oxide pathway.
N Engl J
Med
1993;
329
: 2002–2012.
13. Kugiyama K, Yasue H, Okumura K,
et al
. Nitric oxide activity is
deficient in spasm arteries of patients with coronary spastic angina.
Circulation
1996;
94
: 266–271.
14. Nakayama M, Yasue H, Yoshimura M,
et al
. T-786C mutation in the
5
′
-flanking region of the endothelial nitric oxide synthase gene is asso-
ciated with coronary spasm.
Circulation
1999;
99
: 2864–2870.
15. Hibi K, Ishigami T, Tamura K, et al. Endothelial nitric oxide synthase
gene polymorphism and acute myocardial infarction.
Hypertension
1998;
32
: 521–526.
16. Hingorani AD, Liang CF, Fatibene J,
et al
. A common variant of the
endothelial nitric oxide synthase (Glu298Asp) is a major risk factor for
coronary artery disease in the UK.
Circulation
1999;
100
: 1515–1520.
17. Colombo MG, Paradossi U, Andreassi MG,
et al
. Endothelial nitric
oxide synthase gene polymorphisms and risk of coronary artery
0.431
0.331
0.231
0.131
0.031
60 65 70 75 80 85 90 95
Temperature (°C)
Fluorescence
Melting peaks
I/I
0.411
0.311
0.211
0.111
0.011
60 65 70 75 80 85 90 95
Temperature (°C)
Fluorescence
Melting peaks
D/D
0.214
0.164
0.114
0.064
0.014
60 65 70 75 80 85 90 95
Temperature (°C)
Fluorescence
Melting peaks
I/D
Fig. 1.
Melting peak profiles of real-time PCR for wild (A) and
mutated genotype (B: heterozygous and C: homozy-
gous) profiles for the
ACE
gene in the controls and
cases with coronary slow flow.
A
B
C
