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    Association between Platelet-to-Lymphocyte Ratio and Contrast-Induced Nephropathy in Patients Undergoing Percutaneous Coronary Intervention for Acute Coronary Syndrome
    (Karger, 2015) Demircelik, Muhammed Bora; Kurtul, Alparslan; Ocek, Hakan; Cakmak, Muzaffer; Ureyen, Cagin; Eryonucu, Beyhan
    Objective: Contrast-induced nephropathy (CIN) is associated with significantly increased morbidity and mortality after percutaneous coronary intervention (PCI). Patients with acute coronary syndrome (ACS) are at higher risk of CIN. The platelet-to-lymphocyte ratio (PLR) is closely linked to inflammatory conditions. We hypothesized that PLR levels on admission can predict the development of CIN after PCI for ACS. Subjects and Methods: A total of 426 patients (mean age 63.17 +/- 13.01 years, 61.2% males) with ACS undergoing PCI were enrolled in this study. Admission PLR levels were measured before PCI. Serum creatinine values were measured before and within 72 h after the administration of contrast agents. Patients were divided into 2 groups: the CIN group and the no-CIN group. CIN was defined as an increase in serum creatinine level of >= 0.5 mg/dl or 25% above baseline within 72 h after contrast administration. Results: CIN developed in 53 patients (15.9%). Baseline PLR was significantly higher in patients who developed CIN compared to those who did not (160.8 +/- 29.7 and 135.1 +/- 26.1, respectively; p < 0.001). Multivariate analyses found that PLR [odds ratio (OR) 3.453 +/-, 95% confidence interval (CI) 1.453-8.543; p = 0.004] and admission creatinine (OR 6.511, 95% CI 1.759-11.095; p = 0.002) were independent predictors of CIN. Conclusions: The admission PLR level is an independent predictor of the development of CIN after PCI in ACS. (C) 2015 S. Karger AG, Basel
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    The Relationship Between Adropin Levels and the Slow Coronary Flow Phenomenon
    (Springer India, 2015) Demircelik, Bora; Kurtul, Alparslan; Ocek, Hakan; Cakmak, Muzaffer; Cetin, Mustafa; Ureyen, Cagin; Eryonucu, Beyhan
    There is accumulating evidence that inflammation plays a major role in the development of the slow coronary flow (CSF) phenomenon. In this study, we aimed to study the new biomarker adroin levels as it relates to CSF. Patients who underwent coronary angiography before and had no significant epicardial coronary disease were included in the study. Patients who had thrombolysis in myocardial infarction frame counts (TFCs) above the normal cutoffs were considered to have CSF and those within normal limits were considered to have normal coronary flow (NCF). NCF group over the age of 30 were selected from patients with normal coronary arteries. The adropin levels and biochemical profiles of all patients were studied and analyzed with coronary flow parameters. There were 58 patients in the CSF group and 50 patients in the NCF group. The mean adropin level was significantly lower in CSF group than in NCF group (3.2 +/- 0.71 vs. 4.9 +/- 1.51 ng/mL, p < 0.001). There was a significant correlation between the adropin levels and TFC (r = -0.676, p < 0.001). Multivariable regression analysis showed that the adropin levels were an independent predictor of the CSF phenomenon (odds ratio = 1.041, 95 % confidence interval: 1.004-1.114, p = 0.014). In this study, we show that patients with CSF have decreased levels of adropin. We further show a strong correlation between the adropin levels and coronary blood flow. We conclude that decreased adropin levels might be a useful tool in predicting CSF in patients who undergo coronary angiography.