The role of inflammation and oxidative stress markers in the occurrence and severity of coronary artery disease in young patients with ST-segment elevation myocardial infarction

Background: Atherosclerosis is modulated by inflammation and oxidative stress, which play pivotal roles in the pathogenesis of coronary artery disease (CAD), especially in young patients without traditional risk factors for atherosclerosis. In this study, we aimed to study the role of some inflammatory and oxidative stress markers in triggering ST segment elevation myocardial infarction in Egyptian young patients and the potential correlation to the severity of coronary artery lesions in the Egyptian population. Methods: This case-control study recruited 115 premature STEMI patients (aged <45 years) and 55 age-matched healthy controls. Serum CRP, TNF-a, IL-10, and oxidative stress biomarkers [reduced glutathione, total antioxidants, L-ascorbic acid, nitric oxide (NO), and lipid peroxides] were assayed using commercially available kits and correlated with the coronary artery lesion severity, assessed by the SYNTAX score (SS). The ROC curve assessed the biomarker potential of CRP, TNF-a, IL-10, and the TNF-a/IL-10 ratio to discriminate patients from healthy controls. Results: In our study, we found that serum CRP (38.7 ± 1.9 versus 0.8 ± 0.04 mg/L; P < 0.001), TNF-a (68.4 ± 4.7 pg/mL versus 10.8 ± 0.7 pg/mL; P < 0.001), IL-10 (11.9 ± 0.8 pg/mL versus 8.7 ± 0.4 pg/mL; P = 0.001), and TNF-a/IL-10 ratio (6.8 ± 0.5 versus 1.7 ± 0.2; P < 0.001) were significantly higher in patients compared to healthy controls. Regarding oxidative stress markers, serum T-AOC levels (25.5 ± 0.9 versus 14.9 ± 0.4 U/mL; P < 0.001), NO (10.5 ± 0.3 versus 8.1 ± 0.3 nmol/mL; P < 0.001), serum LPO levels (15.8 ± 0.4 versus 4.1 ±0.2 mmol/L; P < 0.001) and lower GSH levels (3.8 ± 0.1 mg/mL versus 5.2 ± 0.2; P < 0.001) were significantly different in patients versus controls. CRP, TNF-a, and NO levels have been significantly correlated with the severity of CAD as assessed by the SYNTAX score. Conclusion: Inflammation and oxidative stress are pathogenically implicated in premature STEMI and correlated with the severity of CAD lesions. The investigated biomarkers can be utilized in risk stratification and are theranostically targetable.