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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.

Objective: The incidence of atrial fibrillation (AF) in patients with ST segment elevation myocardial infarction (STEMI) varies between 7% and 21%, and most of these studies were in the thrombolytic era. However, the frequency of new-onset AF during the primary percutaneous coronary intervention (PCI) period is still unclear. We aimed to investigate the frequency of new-onset AF and its effects on long-term clinical events in patients undergoing primary PCI. Methods: A total of 1,603 patients who were diagnosed with STEMI and underwent primary PCI were included in the study. All the patients were monitored for at least 48 hours after the procedure. The primary endpoint of the study was defined as new-onset AF during hospitalization. Results: The median follow-up period of our study was 44 months. New-onset AF developed in 85 (6.1%) patients. CHADs-VASc > 2, KILLIP > 2, and left atrial diameter were found to be independent predictors for the development of new-onset AF. In the AF (+) group, the all-cause and in-hospital mortality rates were found to be significantly higher. New-onset AF development in patients with STEMI was detected as an independent predictor of in-hospital mortality. Conclusion:In the era of primary percutaneous transluminal coronary angioplasty, new-onset AF rates were found to be lower than the literature data. In addition, new-onset AF was found to be a predictor of in-hospital mortality, and deaths occurred mostly in the early period. Therefore, close follow-up of these patients in the early period and re-evaluation in terms of AF burden when the patient becomes stable are important.

Background: Patients with acute coronary syndrome (ACS) have about a three-fold risk for developing contrast-induced acute kidney injury(CI-AKI). Investigating studies on routine hydration therapy have frequently included patients with stable coronary artery disease and high risk of CI-AKI [estimated glomerular filtration rate (eGFR) < 60 ml/min]. However, data on routine hydration treatment in non-ST segment elevation myocardial infarction (NSTEMI) patients with eGFR ≥60 ml/min are insufficient. We aimed to investigate the association between routine hydration therapy and CI-AKI development in NSTEMI patients at low risk for nephropathy. Methods and results: We randomly assigned a total of 401 NSTEMI patients to two groups: the routine hydration group (198 patients) and the nonhydration group (control group) (203 patients). Intravenous hydration with isotonic saline (1 ml/kg/h, 0.9% sodium chloride) was given for 3–12 h before and 24 h after contrast exposure to the hydration group. CI-AKI was defined as the increase in serum creatinine values 0.5 mg/dl or 25% between 48 and 72 h after the invasive procedures. In our study, the incidence of CI-AKI development in the routine hydration group (7.1%) was significantly lower than in the nonhydration group (14.1%) (P: 0.02). This study revealed that older age, amount of contrast media, and routine hydration were independent risk factors for developing CI-AKI (P < 0.01, P: 0.04, P < 0.01, respectively). Conclusion: We found that preprocedural and postprocedural intravenous hydration therapy reduces the development of CI-AKI in patients with NSTEMI at low risk for CI-AKI. We suggest administering routine hydration therapy in all ACS patients regardless of eGFR values.