Author + information
- Habil Yücel1,
- Abdullah Doğan2,
- Yasin Türker3,
- Atilla İçli4,
- Salaheddin Akçay5,
- İbrahim Ersoy2,
- Fatih Aksoy2 and
- Recep Sütçü6
Slow coronary flow (SCF) is slow progression of contrast agent in the coronary arteries in the absence of stenosis in epicardial coronary vessels. Its pathophysiological mechanisms are uncertain. Several hypotheses have been suggested for SCF, including a form of early phase of atherosclerosis, microvascular dysfunction, inflammation, imbalance between vasoconstrictor and vasodilatory factors, and platelet function disorder. Endothelial nitric oxide synthase (eNOS) has important role in modulating smooth muscle tonus and vessel diameter. eNOS gene Glu298Asp polymorphism has been associated with altered function of this gene and its products. Experimental and clinical data suggesting that; in the absence of eNOS, endothelial functions and luminal remodeling is impaired, the vessel wall thickness is increased, atherosclerosis accelerated and got complicated.
The aim of this study was to investigate the association between SCF and eNOS gene Glu298Asp polymorphism.
Forty patients with SCF and otherwise normal coronary arteries (mean age 52±9 years), 35 patients with coronary artery disease (CAD) (mean age 55±9 years) and 30 patients with normal coronary angiograms (mean age 51±8 years) were included in the study. TIMI frame count ≥40 frames for the left anterior descending artery was considered as SCF. Glu298Asp polymorphisms of the eNOS gene were analysed by polymerase chain reaction. Demographic characteristics and major risk factors for atherosclerosis were evaluated in the study groups. The severity of SCF and CAD was assessed based on the number of involved vessel.
There was no significant difference with respect to age and gender between groups. The percentage of smoking was higher in the CAD group than in the SCF and control groups. There was no statistical difference in genotype distribution among the groups. The genotype distribution in SCF group was as follows: GG genotype frequency was 21 (52,5%), GT genotype frequency was 15 (37,5%) and TT genotype frequency was 4 (10%). The genotype distribution in CAD group was as follows: GG genotype frequency was 15(42,9%), GT genotype frequency was 14 (40%) and TT genotype frequency was 6 (17,1%). The genotype distribution in control group was as follows: GG genotype frequency was 16 (53,3%), GT genotype frequency was 13 (43,3%) and TT genotype frequency was 1 (3,3%). In the dominant and recessive models of statistical analysis, there was no statistically significant difference among groups.
Our findings show that there is no significant association between Glu298Asp polymorphism of eNOS gene and SCF in the present study.