Reactive Oxygen and Nitrogen Species in Myocardial Infarction: Mechanistic Insights and Clinical Correlations.

Abstract

Background/objectives: Myocardial infarction (MI) remains a leading cause of morbidity and mortality worldwide, driven largely by underlying coronary artery disease (CAD). Reactive oxygen species (ROS) and reactive nitrogen species (RNS) play pivotal mechanistic roles in endothelial dysfunction, atherosclerotic plaque progression, and subsequent cardiac injury. Excessive production of these reactive species disrupts cellular redox balance, promotes mitochondrial dysfunction, and accelerates vascular inflammation, ultimately contributing to plaque rupture and MI. This study aimed to investigate the mechanistic associations and clinical correlations of individual ROS and RNS markers in patients with MI.

Methods: We conducted a case-control study including 86 patients with MI and 60 age- and sex-matched controls without cardiovascular disease, recruited from the Medina Cardiac Center in Saudi Arabia. The MI cohort was subdivided into ST-elevation MI (STEMI, n = 62) and non-ST-elevation MI (NSTEMI, n = 24) to explore potential differences in oxidative and nitrosative stress profiles. Serum levels of multiple ROS (including hydrogen peroxide, hydroxyl radical, and superoxide anion) and RNS (including nitric oxide and peroxynitrite) were quantified using validated fluorescence-based assays. Clinical and biochemical parameters, including lipid profiles, troponin, and left ventricular ejection fraction, were also assessed.

Results: Most ROS and RNS markers were significantly elevated in MI patients compared to controls (p < 0.05), except for nitrogen dioxide. Moderate to strong positive correlations were observed between ROS/RNS levels and serum total cholesterol and LDL-cholesterol (p < 0.001). In contrast, weak or non-significant correlations were found between ROS/RNS markers and serum troponin or left ventricular ejection fraction. Both STEMI and NSTEMI subgroups demonstrated significantly higher oxidative and nitrosative stress levels compared to controls, with distinct patterns between the subtypes.

Conclusions: This study underscores a mechanistic link between elevated ROS/RNS levels and myocardial infarction, supporting the importance of targeting oxidative and nitrosative pathways as potential therapeutic strategies.