Cardiac oxidative stress following myocardial infarction demonstrated significantly positive correlations with inflammatory cytokines including STAT3 (r=0.835) and IL-8 (r=0.867) (P=0.001).
Observational (n=120)
No
Is there a correlation between cardiac oxidative stress and inflammatory cytokine response in patients following acute myocardial infarction treated with PCI?
Cardiac oxidative stress strongly correlates with inflammatory cytokine responses following myocardial infarction, suggesting these biomarkers may serve as predictors of MI severity.
valor p: p=<.05
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 < .05). Additionally, a significant negative correlation was found between GH ( r = −0.654, P = .001) and immune balance ( P < .05). This study evaluated the severity of myocardial infarction using indicators such as CO and CI. This study found a significant correlation between cardiac oxidative stress and inflammatory cytokines after myocardial infarction, suggesting their potential as predictors of myocardial infarction severity.
Duan et al. (Sun,) conducted a observational in Acute myocardial infarction (n=120). Percutaneous coronary intervention (PCI) vs. Pre-treatment baseline was evaluated on Correlation between cardiac oxidative stress and inflammatory cytokine response (p=<.05). Cardiac oxidative stress following myocardial infarction demonstrated significantly positive correlations with inflammatory cytokines including STAT3 (r=0.835) and IL-8 (r=0.867) (P=0.001).