ABSTRACT
ABSTRACT Introduction: We investigated the relationship between the newly-defined systemic immune-inflammation index and the new-onset atrial fibrillation in patients undergoing coronary artery bypass grafting. Method: This study included 392 patients who underwent coronary artery bypass grafting. We divided the participants into two groups as those with and without new-onset atrial fibrillation. Prior to coronary artery bypass grafting, we evaluated blood samples, including systemic immune-inflammation index, and other laboratory parameters of the patients. We formulized the systemic immune-inflammation index score as platelet × neutrophil/lymphocyte counts. Results: The findings revealed that new-onset atrial fibrillation occurred in 80 (20.4%) of 392 patients during follow-ups. Such patients had higher systemic immune-inflammation index, neutrophil/lymphocyte ratio, and C-reactive protein levels than those who did not develop new-onset atrial fibrillation (P<0.001, P<0.001, P=0.010, respectively). In receiver operating characteristic curve analysis, systemic immune-inflammation index levels > 712.8 predicted new-onset atrial fibrillation with a sensitivity of 85% and a specificity of 61.2% (area under the curve: 0.781, 95% confidence interval: 0.727-0.835; P<0.001). Conclusion: Overall, systemic immune-inflammation index, a novel inflammatory marker, may be used as a decisive marker to predict the development of atrial fibrillation following coronary artery bypass grafting.
ABSTRACT
Abstract Introduction: Endothelial progenitor cells (EPCs) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase enzyme activity may affect the vessel wall and have a role in development of aortic aneurysms. EPCs originate from hematopoietic stem cells and can be enumerated from peripheral blood samples by flow cytometry. In this study, we aimed to evaluate the relation of EPC number and NADPH oxidase enzyme activity in the development of thoracic aortic aneurysm (TAA). Methods: Patients with TAA (n=30) and healthy individuals without TAA (control, n=10) were included in our study. Characterization and enumeration of EPC from peripheral blood samples were performed by flow cytometry with panels including markers of EPCs (CD34/CD133/CD309/CD146/CD144). Additionally, NADPH oxidase enzyme activity (capacity) was also measured by the dihydrorhodamine 123 (DHR 123) test. Results: The enumeration of EPC with CD34+/CD146+ marker showed that the number of mean EPC/106 cells was increased in the patient group (41.5/106 cells), but not in the control group (20.50/105 cells) (P<0.01). Additionally, patients with TAA presented significantly lower NADPH oxidase activity by DHR assay than healthy controls (mean stimulation index: 60.40± 7.86 and 75.10±5.21, respectively) (P<0.01). Conclusion: Our results showed that the number of EPCs is significantly higher in aortic aneurysm patients and may have a role in disease progression. The crosstalk between NADPH oxidase enzyme capacity and EPC number may be useful as a parameter to explain the clinical progression of TAA.