Key result
Cardiac oxidative stress strongly correlates with inflammatory cytokines like IL-8 and STAT3 post-MI.
Why the study?
The study was conducted to investigate the potential correlation between cardiac oxidative stress and inflammatory cytokine response following myocardial infarction.
Observational (n=120)
No
p-value: p=<.05
Cardiac oxidative stress and inflammatory cytokines are significantly correlated following acute myocardial infarction, suggesting they may serve as interconnected predictors of disease severity and cardiac remodeling.
Post-MI oxidative stress-cytokine correlations should not change practice; leaves open their value as remodeling biomarkers.
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.
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Duan et al. (2023) conducted an observational in Acute myocardial infarction (n=120). Cardiac oxidative stress was evaluated on Correlation between cardiac oxidative stress and inflammatory cytokine response (p=<.05). Cardiac oxidative stress demonstrated significantly positive correlations with inflammatory cytokines, including STAT3 (r = 0.835) and IL-8 (r = 0.867), following myocardial infarction.
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