Association of rs10757274 and rs2383206 Polymorphisms on 9p21 locus with Coronary Artery Disease in Turkish Population

BACKGROUND AND OBJECTIVES: Genetic predisposition is an important risk factor for coronary artery disease (CAD). In this study, we aimed to evaluate the impact of rs10757274 and rs2383206 polymorphisms in chromosome 9p21 on presence and severity of CAD in a Turkish population. SUBJECTS AND METHODS: A total of 646 patients who underwent coronary angiography were included in this study. Coronary vessel score and Gensini score were calculated to assess the angiographic severity of CAD. Alleles of AA, AG, and GG were determined for rs10757274 (polymorphism-1) and rs2383206 (polymorphism-2) polymorphisms located in chromosome 9p21 from the blood samples. RESULTS: There was a significant difference between the alleles in polymorphism-1 in the presence of coronary artery disease (38.9% in AA, 48.0% in GG and 56.4% in AG, p=0.017). However, there was no difference between the alleles in polymorphism-2. According to vessel scores, there was a significant difference between the alleles in polymorphism-1 (AA 0.71±1.04, GG 0.88±1.07, AG 1.06±1.12, p=0.018). In polymorphism-2, vessel scores did not show a difference between the alleles. In polymorphism-1, there was a significant difference in Gensini score (p=0.041). Gensini scores did not differ between the alleles in polymorphism-2 (p>0.05 for all). In multivariate analyses, none of the alleles was an independent factor for presence of CAD. CONCLUSION: The presence of rs10757274 polymorphism including AG allele in chromosome 9p21 was related to CAD. However, this relationship was not independent of other cardiovascular risk factors.

Corrected thrombolysis in myocardial infarction frame counts in diabetic patients with angiographically normal coronary arteries

To evaluate corrected thrombolysis in myocardial infarction [TIMI] frame count [CTFC] in patients with angiographically normal coronary arteries and diabetes mellitus, a condition known to be associated with microvascular dysfunction. Patients who underwent coronary angiography in Gazi University Hospital, Ankara, Turkey between January 2000 and January 2005 were studied. Corrected TIMI frame count was calculated over the left anterior descending [LAD], left circumflex [Cx] and right coronary arteries [RCA] in 118 diabetic and 122 non-diabetic patients with normal coronary angiogram. The mean CTFC values of the LAD, Cx, and the RCA were similar in diabetics and nondiabetics 21.0 +/= 7.5 versus 21.3 +/= 9.6, 23.3 +/= 9.7 versus 23.5 +/= 10.8, 17.9 +/= 6.7 versus 18.7 +/=7.4 respectively, p>0.05 for all comparisons. In stepwise multivariate linear regression analysis, body surface area had a significant correlation with CTFC of all the 3 coronary arteries. We conclude that CTFC in diabetics and non-diabetics with angiographically normal coronary arteries is similar. Since microvascular disease is an inherent component of diabetes, our finding may reflect the inadequacy of CTFC in predicting microvascular disease in diabetic patients with normal coronary angiograms

Plasma homocysteine level in cardiac syndrome X and its relation with duke treadmill score

To investigate the plasma homocysteine level and the relationship between plasma homocysteine level and duke treadmill score DTS in cardiac syndrome X CSX patients. Seventy-nine patients 36 male, 43 female, mean age: 50 +/- 8.8 years admitted to Gazi University Hospital, Ankara, Turkey with typical effort angina, positive stress test, and angiographically normal coronary arteries between January and September 2006 were included in this prospective and controlled study. Thirty asymptomatic patients 11 male, 19 female, mean age: 47.6 +/- 8.3 years with 2 cardiovascular risk factors were chosen as a control group. Plasma homocysteine level was measured in both groups and DTS was calculated in the CSX group. Plasma homocysteine was measured with the AxSYM homocysteine immunoassay method in both groups. Plasma homocysteine level was higher in the CSX group compared to the control group 16.5 +/- 4.9 ?mol/L, n=79, versus 12.4 +/- 4.1 ?mol/L, n=30, p<0.001. The DTS was -2.7 +/- 5.3 in the CSX group. There was a negative correlation between the DTS and homocysteine levels in the CSX group. r=-0.506, p<0.001. Plasma homocysteine level, which is known to cause endothelial dysfunction and microvascular ischemia were higher in CSX patients. Also, this increase in homocysteine level inversely correlated with the DTS, which represents the magnitude of ischemia