The Correlation Between Cardiac Oxidative Stress and Inflammatory Cytokine Response Following Myocardial Infarction

Abstract

Our study was conducted to investigate the potential correlation between cardiac oxidative stress and inflammatory cytokine response following myocardial infarction. A total of 120 patients harboring acute myocardial infarction who underwent percutaneous coronary intervention (PCI) at our hospital were included. Their general clinical data were analyzed, and comparisons were made regarding the levels of inflammatory factors, oxidative stress markers, heart pump function, and cardiac function. The correlation between cardiac oxidative stress and inflammatory cytokine response was assessed using Pearson's linear correlation. Following treatment, significant reductions were seen in the serum levels of cortisol, thyroid-stimulating hormone (TSH), B-type natriuretic peptide (BNP), C-reactive protein (CRP), signal transducer and activator of transcription 3 (STAT3), interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor (TNF), and catalase (CAT) compared to pre-treatment levels. Conversely, the levels of growth hormone (GH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), total antioxidant capacity (T-AOC), cardiac output (CO), and cardiac index (CI) were significantly elevated. Serum cortisol (r = 0.481, P =.001), BNP (r = 0.437, P =.001), CRP (r = 0.542, P =.001), STAT3 (r = 0.835, P =.001), TSH (P =.001), IL-8 (r = 0.867, P =.001), TNF-α (r = 0.439, P =.001), and cardiac oxidative stress demonstrated significantly positive correlations (P