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    Serum cystatin C and neutrophil gelatinase-associated lipocalin in predicting the severity of coronary artery disease in diabetic patients
    (2016) Okyay, Kaan; Yildirir, Aylin; Cicek, Mutlu; Aydinalp, Alp; Muderrisoglu, Haldun; 0000-0002-9635-6313; 0000-0001-8750-5287; 0000-0002-3761-8782; 0000-0001-6134-8826; 27182610; AAG-8233-2020; A-4947-2018; AAD-5841-2021; AAK-7355-2020
    Objective: Cystatin C and neutrophil gelatinase-associated lipocalin (NGAL) are biomarkers of renal functions. We evaluated their roles in predicting the severity of coronary artery disease (CAD). Methods: Fifty-two consecutive type 2 diabetic patients (32 males, 65.7 +/- 8.6 years) who underwent coronary angiography (CAG) for stable CAD were included in this single-center, prospective, cross-sectional study. Patients with an estimated glomerular filtration rate <60mL/min/1.73m(2) and with a history of by-pass surgery and/or coronary stent implantation were excluded. The vessel score and Gensini score were calculated to assess the presence and severity of CAD. Mann-Whitney U test, Spearman test, and multiple linear regression analysis were used for the main statistical analyses. Results: Serum cystatin C levels were higher in patients with multivessel disease than in those with single vessel disease [1260 ng/mL (953-1640) vs. 977 ng/mL (599-1114), p=0.017]. According to the median Gensini score, the higher score group also had higher cystatin C levels than the lower score group [1114 ng/mL (948-1567) vs. 929 ng/mL (569-1156), p=0.009]. However, serum NGAL levels were similar between these subgroups. There was a positive correlation between cystatin C and Gensini score (r=0.334, p=0.016). Multiple linear regression analysis revealed serum cystatin C as an independent predictor of the Gensini score (beta=0.360, t=2.311, p=0.026). These results may aid in defining cystatin C as a surrogate marker of the extent of CAD in further clinical trials. Conclusion: Serum Cystatin C, but not NGAL levels, could predict the severity of CAD in diabetic patients.
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    The role of oxidative DNA damage and GSTM1, GSTT1, and hOGG1 gene polymorphisms in coronary artery disease risk
    (2016) Okyay, Kaan; Kadioglu, Ela; Tacoy, Gulten; Ozcagli, Eren; Akboga, Mehmet K.; Cengel, Atiye; Sardas, Semra; 0000-0001-6134-8826; 27182613; AAK-7355-2020
    Objective: Atherosclerotic coronary artery disease (CAD) appears to be a multifactorial process caused by the interaction of environmental risk factors with multiple predisposing genes. Therefore, in this study we aimed to determine the role of oxidative DNA damage and some variations in glutathione S-transferase (GSTM1 and GSTT1) and DNA repair (hOGG1) genes in CAD risk. Methods: A case-control study was conducted on 59 individuals who had undergone coronary angiographic evaluation. Of these, 29 were patients diagnosed with CAD (mean age = 61.5 +/- 10.3) and 30 were controls examined for reasons other than suspected CAD and who had angiographically documented normal coronary arteries (mean age = 60.4 +/- 11.6). Basal DNA damage as well as pyrimidine and purine base damage were evaluated in peripheral blood lymphocytes using the modified comet assay. Polymerase chain reaction-restriction length polymorphism (PCR-RFLP)-based assay was used for genotyping. Results: Basal DNA damage levels in patients [9.16 (3.26)] were significantly higher than those in controls [7.59 (3.23); p=0.017], and basal DNA and pyrimidine base damage levels were significantly correlated with disease severity based on Gensini scoring (r=0.352, p= 0.006; r= 0.318, p=0.014, respectively). However, no significant differences were observed in terms of oxidized DNA bases between patients and controls. The frequencies of studied genotypes (GSTM1, GSTT1, and hOGG1) were similar between groups. Conclusion: The results of this study pointed out the role of DNA damage in CAD and its severity. However, GSTM1, GSTT1, and hOGG1 gene polymorphisms seemed to have no effect on individual susceptibility for disease progression.
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    Is there a relationship between resistin levels and left ventricular end-diastolic pressure?
    (2018) Yildirir, Aylin; Yildirim, Ozge Turgay; Sade, Leyla Elif; Hasirci, Senem Has; Kozan, Hatice; Ozcalik, Emre; Okyay, Kaan; Bal, Ugur Abbas; Aydinalp, Alp; Muderrisoglu, Haldun; 0000-0002-9635-6313; 0000-0002-6731-4958; 29615544; AAK-7355-2020; AAG-8233-2020
    Objective: Resistin, a cysteine-rich peptide, is associated with atherosclerosis and diabetes. Resistin levels increase corresponding to coronary artery disease (CAD) and heart failure severity. Since resistin level tends to elevate with symptomatic heart failure, it is expected to be associated with left ventricular end-diastolic pressure (LVEDP). However, there is no relevant literature on the relationship between resistin levels and LVEDP. We aimed to evaluate the association between resistin levels and LVEDP, severity of CAD, carotid intima-media thickness (CIMT), and echocardiographic diastolic dysfunction parameters. Methods: For this study, 128 euvolemic patients with creatinine clearance >50 mg/dL and without acute coronary syndrome, who had typical chest pain or were stress test positive, were enrolled. Resistin level was measured by Enzyme-linked immunosorbent assays (ELISA) method. Severe CAD is defined as >= 50% stenosis in one of the major coronary arteries. LVEDP was measured during left heart catheterization. Results: After coronary angiography, 60 patients (46.9%) had severe CAD. The mean LVEDPs were similar for patients with and without severe CAD (p=0.480). The resistin levels did not differ between the groups (p=0.154). The resistin levels did not correlate with LVEDP (r=-0.045, p=0.627), ejection fraction (EF; r=0.110, p=0.228), the Gensini score (r=-0.091, p=0.328), and CIMT (r=0.082, p=0.457). No significant correlation was found between the echocardiographic diastolic dysfunction parameters and resistin levels. Conclusion: There was no significant correlation between resistin level and LVEDP, CAD severity, echocardiographic diastolic dysfunction parameters, and CIMT. Further studies are warranted to determine the efficacy of resistin in clinical use.