Reactive Oxygen Species After Myocardial Infarction: From Pathophysiological Mechanisms to Prognostic and Therapeutic Implications

Myocardial infarction (MI) remains a major cause of death and heart failure despite reperfusion. Reopening an occluded coronary artery salvages viable myocardium but creates an ischemia–reperfusion environment in which reactive oxygen species (ROS) and reactive nitrogen species (RNS) can contribute to injury. Postinfarction redox responses continue through inflammation, repair, and remodeling. Their effects depend on species, concentration, source, compartment, timing, molecular targets, and local antioxidant capacity; controlled redox signaling is essential for normal vascular, metabolic, and immune function. This narrative review focuses primarily on type 1 MI, particularly reperfused ST-segment elevation MI. It examines mitochondrial and enzymatic oxidant sources, including nicotinamide adenine dinucleotide phosphate (NADPH) oxidases, xanthine oxidoreductase, nitric oxide synthases, and myeloperoxidase, alongside secondary lipid- and nitrogen-derived products. It considers their roles in microvascular dysfunction, cardiomyocyte injury and death, inflammatory amplification, fibrosis, ventricular dysfunction, heart failure, and arrhythmic vulnerability. Circulating oxidative-stress biomarkers may be associated with infarct severity or later outcomes, but generally provide indirect information and have limited validation for clinical decision-making. Broad antioxidant strategies have not yielded consistent clinical benefit. More precise therapeutic approaches require source- and compartment-specific targeting, appropriate timing and patient selection, reliable measures of target engagement, and benefit beyond contemporary MI care.