Browsing by Author "Tengiz I."

Now showing 1 - 9 of 9
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    Atorvastatin treatment decreases inflammatory and proteolytic activity in patients with hypercholesterolemia
    (Klinika Kardiologii CMKP, 2004) Ercan E.; Tengiz I.; Altuglu I.; Sekuri C.; Aliyev E.; Ercan H.E.; Akin M.
    Background. Statins have anti-inflammatory and anti-platelet effects, which are known as non-lipid effects. Statin treatment can decrease endogenous inflammatory response. Aim. To study the effects of atorvastatin on matrix metalloproteinase-9 (MMP-9) and high sensitive C-reactive protein (hs-CRP) - markers of the proteinolytic and inflammatory activity. Methods. In this prospective study 44 patients with hypercholesterolemia were randomly assigned into 2 groups; Group 1 (n=22) treated with atorvastatin and diet for 2 months, and Group 2 (n=22) - diet alone. MMP-9 and hs-CRP were measured at baseline and two months later. Results. Groups were matched for age, sex and baseline characteristics. Lipid levels decreased by 32% (LDL from 153.9±26.6 to 94.5±20.8 mg/dl, p<0.005) in the atorvastatin group and by 9% in the diet alone group. Atorvastatin lowered plasma CRP from 5.16±1.9 to 2.88±1.06 mg/L (p<0.001) and MMP-9 activity from 64.3±28.1 to 35.4±20.0 ng/ml (p<0.0001). Atorvastatin-induced reductions in CRP and MMP-9 were greater than in the diet alone group. MMP-9 levels did not show significant changes in Group 2 after two months of diet. Conclusions. Atorvastatin treatment decreases inflammatory and proteolytic activity in patients with hypercholesterolemia.
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    Renin-angiotensin system gene polymorphisms and premature coronary heart disease
    (JRAAS Limited, 2005) Sekuri C.; Cam F.S.; Ercan E.; Tengiz I.; Sagcan A.; Eser E.; Berdeli A.; 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 (AT1) 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 [CI 95% 1.11-3-33, p=0.018]). We found a significant association between AT1-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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    Association between the eNOS (Glu298Asp) and the RAS genes polymorphisms and premature coronary artery disease in a Turkish population
    (2005) Berdeli A.; Sekuri C.; Sirri Cam F.; Ercan E.; Sagcan A.; Tengiz I.; Eser E.; Akin M.
    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. 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). 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 (CI 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), AT1R AA+eNOS 894TT and AT1R non-AA+eNOS 894TT (p=0.002) genotypes were significantly associated with the risk of premature CAD. This study indicates a synergistic contribution of RAS genes (ACE I/D, AGT T/M, AT1R T/C) and eNOS Glu298Asp polymorphisms to the development of the premature CAD. © 2004 Elsevier B.V. All rights reserved.
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    The G894T polymorphism on endothelial nitric oxide synthase gene is associated with premature coronary artery disease in a Turkish population
    (2005) Cam S.F.; 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=15.356(CI 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. © 2004 Elsevier Ltd. All rights reserved.
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    Association of platelet-activating factor acetylhydrolase gene polymorphism with premature coronary artery disease in Turkish patients
    (2006) Şekuri C.; Çam F.S.; Tengiz I.; Ercan E.; Bayturan Ö.; Berdeli A.
    Objective: Platelet-activating factor (PAF) is a phospholipid with multiple actions that is involved in inflammatory diseases as well as in atherogenesis. It is inactivated by a plasma enzyme, PAF-acetylhydrolase (PAF-AH). Deficiency of this enzyme in plasma is caused by a missense mutation in the gene (G994T). The aim of this study was to investigate association of this mutation with premature coronary artery disease (CAD). Methods: One hundred and fifteen unrelated Turkish patients with a diagnosis of premature CAD and 128 unrelated healthy subjects were enrolled in this study. Genotyping was performed by polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP). Results: The prevalence of the G994T mutation in the patients was 2.60 % (heterozygote), and 0 % in the controls. There was no significant difference in allele frequency and genotype distribution among the study groups. Conclusion: The G9943T mutation in the plasma PAF acetylhydrola se gene is not associated with premature CAD in Turkish subjects.
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    No association of interleukin-6 gene polymorphism (-174 G/C) with premature coronary artery disease in a Turkish cohort
    (2007) Sekuri C.; Cam F.S.; Sagcan A.; Ercan E.; Tengiz I.; Alioglu E.; Berdeli A.
    OBJECTIVES: Interleukin-6 (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. © 2007 Lippincott Williams & Wilkins, Inc.
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    G protein β3 subunit gene polymorphism in Turkish hypertensives
    (2008) Alioǧlu E.; Ercan E.; Tengiz I.; Yildiz A.; Saygi U.ö.T.S.; Çam F.S.; Berdeli A.
    Objective: G protein is one of the most important regulators of intracellular signaling pathways. C825T polymorphism of G protein β3 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 β3 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 β3 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 β3 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 (χ2=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 β3 subunit C825T gene polymorphism is associated with systolic a diastolic blood pressure. Furthermore, the study indicates that the G protein β3 subunit may be a susceptible gene to essential hypertension.
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    Effect of monocyte chemoattractant protein-1 (MCP-1) gene polymorphism in Turkish patients with premature coronary artery disease
    (2008) Cam S.F.; Sekuri C.; Sagcan A.; Ercan E.; Tengiz I.; Alioglu E.; Berdeli A.
    Objectives. It has been suggested that monocyte chemoattractant protein-1 (MCP-1) is important in the initiation of atherosclerosis and crucial in monocyte recruitment into the subendothelial lesions. Recent studies have demonstrated that MCP-1 -2518 A>G polymorphism is associated with susceptibility to coronary artery disease (CAD). Since there are conflicting reports on the possible association of MCP-1 -2518 A>G polymorphism with CAD, we investigated the role of this polymorphism in Turkish patients with premature CAD. Material and methods. Genomic DNA was collected from 171 premature CAD patients and 151 healthy individuals. MCP-1 -2518 A>G polymorphism was genotyped using the PCR-RFLP method. Results. There were no differences between genotype distribution and allele frequencies in the premature CAD and control groups (AA: 49.7 %; AG: 40.3 %; GG: 10.0 % in premature CAD groups and AA: 53.7 %; AG: 34.4 %; GG: 11.9 % in controls; p = 0.53). The prevalence of the G allele was 0.302 in patients and 0.291 in controls. Conclusions. Our data demonstrate that MCP-1 -2518 A>G polymorphism is not associated with premature CAD in Turkish patients. Further studies are needed to elucidate the role of this polymorphism in the pathogenesis of CAD in various populations. © 2008 Informa UK Ltd (Informa Healthcare, Taylor & Francis AS).
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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
    (Pulsus Group Inc., 2009) Alioglu E.; Turk U.; Cam S.; Abbasaliyev A.; Tengiz I.; Ercan E.
    Background: Single nucleotide polymorphisms in the 5,10-methyl-enetetrahydrofolate 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. © 2009 Pulsus Group Inc. All rights reserved.