Browsing by Author "Tengiz, I"

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    No association of interleukin-6 gene polymorphism (-174 G/C) with premature coronary artery disease in a Turkish cohort
    Sekuri, C; Cam, FS; Sagcan, A; Ercan, E; Tengiz, I; Alioglu, E; Berdeli, A
    Objectives Interleukin (IL-6) may contribute to the inflammatory response by activating endothelial cells and stimulating the synthesis of fibrinogen. It might thus be important in the pathogenesis of inflammation associated with coronary artery disease (CAD). Several studies suggested that the -174 C allele was associated with an increased prevalence of coronary heart disease. The aim of this study was to investigate further the association of the IL-6 -174 G/C allele status with premature CAD. Methods A total of 120 patients and 105 controls were included in the study. The IL-6 -174 G/C polymorphism was genotyped using PCR-restriction fragment length polymorphism. Results The genotype distribution of the -174 G/C polymorphism was not different in premature CAD patients (GG: 53%; GC: 42.6%; CC: 4.3%) and controls (GG: 54.3%; GC: 39%; CC: 6.7%) (P=0.72). The prevalence of the C allele was 25.6% in patients and 26.1% in controls. By multiple regression analysis, family history, smoking, diabetes, and hypertension were independent risk factors of premature CAD, but not IL-6 genotype. Conclusions We conclude that the IL-6 -174 G/C polymorphism is not associated with the risk of premature CAD, and does not contribute to cardiovascular risk stratification.
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    The G894T polymorphism on endothelial nitric oxide synthase gene is associated with premature coronary artery disease in a Turkish population
    Cam, SF; Sekuri, C; Tengiz, I; Ercan, E; Sagcan, A; Akin, M; Berdeli, A
    Introduction: The aim of the present study was to investigate the association between premature coronary artery disease and Glu298Asp polymorphism of the endothelial nitric oxide synthase gene. Materials and methods: The eNOS gene polymorphism was analysed in 115 (mean age, 48.1 +/- 7.9 years) Turkish patients with a diagnosis of premature coronary artery disease and 83 (mean age, 44.6 +/- 1.4 years) control subjects. The Glu298Asp polymorphism of the endothelial nitric oxide synthase gene was determined by polymerase chain reaction and restriction fragment length polymorphism. Results: The patients group showed an increase in the frequency of the T allele compared to controls (0.456 versus 0.169, p=0.0001). There was a significant association between the TT genotype and premature coronary artery disease [eNOS TT vs. TG and GG; OR=17.000 (CI 95% 3.952-73.125, p=0.0001)]. The eNOS T/G genotypes were not associated with the number of affected vessels (p > 0.05). In addition, the family history of premature coronary artery disease, smoking, diabetes, obesity, dyslipidemia and eNOS TT genotype were independent risk factors of coronary artery disease. The patients with eNOS TT genotype had 15 fold risk of coronary artery disease compared with the control group [OR= I 5,356(Cl 95%3.262-77.289, p=0.001)]. Conclusions: These results suggest that premature coronary artery disease is associated with the Glu298Asp polymorphism of the endothelial nitric oxide synthase gene in our population. (c) 2004 Elsevier Ltd. All rights reserved.
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    LACK OF ASSOCIATION BETWEEN MCP-1 GENE POLYMORPHISM (-2518G/A) AND PREMATURE CORONARY ARTERY DISEASE
    Cam, FS; Sekuri, C; Sagcan, A; Ercan, E; Tengiz, I; Alioglu, E; Berdeli, A
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    Decreased erythropoietin levels after cardiac ischemia
    Ercan, E; Duman, C; Sonmez, G; Tengiz, I; Alioglu, E; Turk, U; Sekuri, C; Cam, S
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    Polymorphisms of the methylenetetrahydrofolate reductase, vascular endothelial growth factor, endothelial nitric oxide synthase, monocyte chemoattractant protein-1 and apolipoprotein E genes are not associated with carotid intima-media thickness
    Alioglu, E; Turk, U; Cam, S; Abbasaliyev, A; Tengiz, I; Ercan, E
    BACKGROUND: Single nucleotide polymorphisms in the 5,10-methylenetetrahydrofolate reductase (MTHFR), vascular endothelial growth factor (VEGF), endothelial nitric oxide synthase (eNOS), monocyte chemoattractant protein-1 (MCP-1) and apolipoprotein E (ApoE) genes appear to be a genetic risk factor for atherosclerosis. Common carotid intima-media thickness (cIMT) provides information on the severity of atherosclerosis.OBJECTIVE: To investigate the relationship between cIMT and gene polymorphisms associated with atherosclerosis in Turkish patients with coronary artery disease (CAD).METHODS: Sixty-two patients with angiographically diagnosed stable CAD were divided into two groups according to their cIMT values (group 1: n=35, cIMT of 1 mm or greater; group 2: n=27, cIMT of less than 1 mm). MTHFR 677 C/T, VEGF-460 C/T, eNOS 894 G/T, MCP-1-2518 A/G and ApoE (E2, E3 and E4) gene polymorphisms (where A is adenine, C is cytosine, G is guanine and T is thymine) were analyzed by polymerase chain reaction and restriction fragment length polymorphism. Evaluations of cardiovascular risk factors and coronary atherosclerotic lesions were performed in all patients. Serum homocysteine and high-sensitivity C-reactive protein were measured and compared between the two groups.RESULTS: Serum high-sensitivity C-reactive protein (P=0.04) and homocysteine (P=0.006) levels were higher in group 1 than in group 2. The ratio of multivessel CAD and previous myocardial infarction was significantly higher in group 1 than in group 2 (P=0.014). In the study population, no significant difference in cIMT was observed according to the polymorphisms studied. Only hyperhomocysteinemia (OR 1.17 [95 % CI 1.01 to 1.35], P=0.033) and previous myocardial infarction (OR 3.76 [95 % CI 1.10 to 12.81], P=0.034) maintained a significant correlation with cIMT on multiple logistic regression analysis.CONCLUSION: cIMT is increased in patients with hyperhomocysteinemia, inflammation and extended CAD. MTHFR 677 C/T, VEGF-460 C/T, eNOS 894 G/T, MCP-1-2518 A/G and ApoE single nucleotide polymorphisms were not associated with increased cIMT.
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    Renin-angiotensin system gene polymorphisms and premature coronary heart disease
    Sekuri, C; Cam, FS; Ercan, E; Tengiz, I; Sagcan, A; Eser, E; Berdeli, F; Akin, M
    Introduction Experimental and clinical studies demonstrated that the renin-angiotensin system (RAS) affects the pathogenesis of atherosclerosis and prognosis of coronary heart disease (CHD). The aim of this study was to investigate the genotype distribution and the allele frequencies of three RAS genes polymorphisms and their effects on premature CHD in a Turkish population. Materials and methods One-hundred and fifteen Turkish patients with premature CHD and 128 controls were included into the study. Angiotensin-converting enzyme (ACE), angiotensin II type 1 (AT(1)) receptor and angiotensinogen (AGT) gene polymorphisms were analysed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). Results The patients group showed an increased frequency of the ACE D allele compared with controls (65% vs. 35%, p=0.0001). There was a significant association between the DD genotype and premature CHD (ACE DD vs. ID and II; odds ratio [OR]=2.82 [CI 95% 1.33-2.91, p=0.002]). Also, we observed increased premature CHD risk associated with higher frequencies of the AGT MM genotype in patients when compared with controls (AGT MM VS. TT and MT OR=1.92 [Cl 95% 1.11-3.33, p=0.018]). We found a significant association between AT(1)-receptor AA genotype and decreased risk of premature CHD (AT1R AA vs. AC and CC, OR= 0.57[CI 95% 0.34-0.95, p=0.03]). Conclusions We demonstrated that increased premature CHD risk is associated with higher frequencies of the ACE DD and AGT MM genotypes. These findings indicate a synergistic contribution of ACE DD and AGT MM polymorphisms to the development of premature CHD. Also, our results suggest that family history, smoking, diabetes, hypertension, obesity and ACE DD genotype were independent risk factors for premature CHD.
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    No association of IL-6 gene polymorphism (474 G/C) with premature coronary artery disease
    Sekuri, C; Cam, FS; Tengiz, I; Sagcan, A; Ercan, E; Akin, M; Berdeli, A
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    G protein β3 subunit gene polymorphism in Turkish hypertensives
    Alioglu, E; Ercan, E; Tengiz, I; Yildiz, A; Türk, UO; Saygi, S; Çam, FS; Berdeli, A
    Objective: G protein is one of the most important regulators of intracellular signaling pathways. C825T polymorphism of G protein (33 subunit is associated with increased intracellular signal transduction. The 825T allele has been found associated with a variety of cardiovascular risk factors, including hypertension. The aim of the present study was to investigate the association between the C825T polymorphism of the G protein beta 3 subunit and essential hypertension in Turkish population. Methods: This cross-sectional, case-controlled study included 209 patients with essential hypertension (Patient group) and 82 subjects with normal blood pressure (Control group). The G protein 133 subunit C825T gene polymorphism was determined by polymerase chain reaction. Hypertension was defined according to JNC VII criteria. Statistical analysis was performed using Chi square and unpaired t tests. Logistic regression analysis was used to study association between hypertension and genotypes. Results: We found that the frequencies of the G protein 133 subunit C825T polymorphism in hypertensive and control groups were 17.7%, 59.3%, 23.0% and 32.9%, 48.8%, 18.3%, (CC, CT, TT) respectively (chi(2)=7.963, p=0.019). In the multivariate logistic regression analysis CT genotype had 2.2 (OR=2.262, 95% CI 1.228-4.167, p=0.009), and TT genotype had 2.3 times (OR=2.335, 95% CI 1.089-5.008, p=0.029) greater risk of hypertension compared to CC genotype. Conclusion: It seems that the G protein (33 subunit C825T gene polymorphism is associated with systolic and diastolic blood pressure. Furthermore, the study indicates that the G protein 133 subunit may be a susceptible gene to essential hypertension. (Anadolu Kardiyol Derg 2008; 8: 337-5)
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    Association between the eNOS (Glu298Asp) and the RAS genes polymorphisms and premature coronary artery disease in a Turkish population
    Berdeli, A; Sekuri, C; Cam, FS; Ercan, E; Sagcan, A; Tengiz, I; Eser, E; Akin, M
    Background: The renin-angiotensin system (RAS) and endothelial nitric oxide (NO) affect the pathogenesis of atherosclerosis and prognosis of coronary artery disease (CAD). Previous epidemiologic data suggested that genetic factors are more likely to affect young rather than old people. Our objective was to investigate the association between the polymorphisms of eNOS (Glu298Asp) and the RAS genes and premature CAD in a Turkish population. Methods: A total of 115 Turkish patients with premature CAD and 83 controls were included in the study. ACE I/D, AT1R A/C, AGT T/M and eNOS Glu298Asp gene polymorphisms were analysed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). Results: It was found that increased premature CAD risk is associated with higher frequencies of the ACE DD [OR: 2.600 (CI 95% 1.395-4.847,p=0.002)], AGT MM [OR=2.407 (Cl 95% 1.267-4.573,p=0.007)] and eNOS 894TT [OR-17.000 (CI 95% 3.952-73.125,p<0.001)] genotypes. Carriers of ACE DD+eNOS 894TT (p=0.002), AGT MM+eNOS 894TT (p=0.001), ATIR AA+eNOS 894TT and ATIR non-AA+eNOS 894TT (p=0.002) genotypes were significantly associated with the risk of premature CAD.
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    The relationship between severity of coronary artery disease and endothelial dysfunction
    Tengiz, I; Ercan, E; Sekuri, C; Aliyev, E; Saygy, S; Guneri, S; Akin, M; Nalbantgil, I