We assessed the relation between platelet-to-lymphocyte ratio (PLR) on admission and contrast-induced nephropathy (CIN) in patients with non-ST-segment elevation acute coronary syndrome (NSTE-ACS). A total of 488 patients with NSTE-ACS who underwent urgent coronary angiography were enrolled. Levels of PLR and creatinine were measured before angiography and at 72 hours after angiography. Patients were divided into 2 groups, namely, the CIN group, 80 patients (16.3%; age 65.3 ± 12.5years; 66.7% men) and the non-CIN group, 408 patients (83.7%; age 61.2 ± 12.3 years; 72.5% men). Patients in the CIN group had significantly higher PLR than those in the non-CIN group (152.9 ± 99.6 vs 120.4 ± 66.1, P < .001). In logistic regression analysis, PLR (odds ratio [OR] 1.004, 95% confidence interval [CI] 1.001-1.007, P = .02), diabetes mellitus (OR 1.75, 95% CI 1.02-2.98, P = .03), and ST-segment depression on admission electrocardiogram (OR 1.68, 95% CI 1.00-2.81, P = .04) were independent predictors of CIN. The PLR was an independent predictor of CIN after angiography in patients with NSTE-ACS.

Contrast-induced acute kidney injury (CI-AKI) is associated with increased mortality, morbidity, and prolonged hospitalization. Patients with acute coronary syndrome (ACS) have a 3-fold higher risk of developing CI-AKI. The aim of our study was to evaluate the predictors of CI-AKI and long-term prognosis in patients with ACS who developed CI-AKI (1083 patients were enrolled). Contrast-induced acute kidney injury was defined as an increase of ≥0.5 mg/dL and/or an increase of ≥25% of pre-percutaneous coronary intervention (PCI) to post-PCI serum creatinine levels within 48 to 72 hours after the procedure. Primary end point was defined as all-cause mortality, myocardial infarction, and cerebrovascular event at long-term follow-up (36 ± 12 months). Contrast-induced acute kidney injury occurred in 178 (16.4%) of the 1083 patients. The primary end points were significantly high in patients with ACS who developed CI-AKI ( P < .001). The occurrence of CI-AKI was identified as an independent predictor of primary end point. Risk of CI-AKI development was more frequently seen in patients with ACS. Also, patients who developed CI-AKI have worse prognosis at long-term follow-up. Additional preventive treatment strategies need to be developed in this group of patients.

Background Cardiovascular disease is one of the leading causes of death worldwide. According to the results of various studies, protein convertase subtilisin kexin type-9 (PCSK9) was determined as a novel risk factor for stable coronary artery disease. Few studies have investigated the relationship between PCSK9 levels and the severity of coronary artery disease in patients with acute coronary syndrome; thus, we herein aimed to investigate this relationship in patients with non-ST-elevation myocardial infarction (NSTEMI) who underwent coronary angiography. Patients and methods Herein, 168 patients with NSTEMI were prospectively enrolled, and severity of atherosclerotic lesions was determined using SYNergy between percutaneous coronary intervention with TAXus and cardiac surgery (SYNTAX), Gensini and Jeopardy scores. Plasma PCSK9 levels, lipid parameters and C-reactive protein levels were measured after a 12-h fasting period. The relationship of PCSK9 levels and clinical and laboratory parameters of patients with their SYNTAX, Gensini and Jeopardy scores was investigated. Results Pearson correlation analysis showed a strong positive correlation between PCSK9 and the three scores (P < 0.001, r > 0.5 for all). In ROC analysis, a mid-high SYNTAX score of at least 25 was predicted with a sensitivity of 81% and a specificity of 63% when the PCSK9 level was higher than 52.8 ng/ml (area under a curve 0.76, P < 0.001). Multivariate linear regression analysis revealed that PCSK9, low-density lipoprotein cholesterol and creatinine levels were independent predictors of a high SYNTAX score. Conclusion Taken together, high PCSK9 levels may be a risk factor for adverse events in patients with NSTEMI. Aggressive lipid-lowering therapies may benefit this group of patients.

Background Coronary artery ectasia (CAE) is described as the enlargement of a coronary artery segment by 1.5 times or more, which is generally associated with the atherosclerotic process. Atherosclerotic changes lead to arterial remodeling result in CAE. In our study, we measured serum transforming growth factor (TGF)-β1 levels, which have a protective role against atherosclerosis. Further, we aimed to assess the TGF-β1 gene variants rs1800469 (–509C>T, c.−1347C>T) and rs1800470 (c.+29T>C, p.Pro10Leu, rs1982073), which might have an effect on TGF production. Overall, 2877 patients were screened including 56 patients with CAE and 44 patients with normal coronary arteries who were included in the study. Serum TGF-β1 levels were measured using ELISA and compared between two groups. Additionally, TGF-β1 rs1800469 and rs1800470 gene variations were determined using TaqMan® SNP Genotyping Assays. Results Serum TGF-β1 levels were significantly lower in patients with CAE than in controls (p=0.012). However, there was no difference in terms of the genotype and allele distributions of TGF-β1 rs1800469 and rs1800470 polymorphisms. Serum TGF-β1 levels were higher in individuals carrying the TGF-β1 rs1800470 G allele (GG+AG) than in individuals with normal homozygous AA genotype in the CAE group (p=0.012). Conclusion Our findings suggest that lower serum TGF-β1 levels are associated with an increased risk for CAE development and that TGF-β1 polymorphisms exert a protective effect. Furthermore, TGF-β1 rs1800470 G allele carriers were shown to have higher TGF-β1 levels in the CAE group. This suggests that having the G allele in the TGF-β1 rs1800470 polymorphism could prevent CAE development.

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