Temporal changes of oxidative stress and ferroptosis-associated biomarkers in STEMI patients undergoing primary PCI and their correlation with myocardial reperfusion injury

Myocardial ischemia-reperfusion injury in ST-elevation myocardial infarction (STEMI) involves complex mechanisms, including oxidative stress and ferroptosis, but the timing and relationship of these processes with cardiac injury markers remain unclear. This study investigated how oxidative stress and ferroptosis-associated biomarkers change over time and their correlations with cardiac injury markers in STEMI patients undergoing primary percutaneous coronary intervention (PCI). A prospective cohort of 25 STEMI patients undergoing primary PCI was studied. Serum levels of cardiac injury biomarkers (Troponin I, CK-MB) and oxidative stress/ferroptosis markers (superoxide dismutase [SOD], total antioxidant capacity [TAC], glutathione peroxidase [GPx], lipid peroxidation products [LPO], serum iron, and ferritin) were measured at pre-PCI, and at 6, 12, 24, and 48 h post-PCI. Temporal trends and Pearson correlations between these biomarkers were analyzed. Markers of oxidative stress and ferroptosis-associated biomarkers demonstrated distinct time-dependent patterns post-reperfusion: SOD and TAC peaked early (6–12 h), while GPx initially decreased. LPO levels peaked at 6 h. Serum iron transiently declined, and ferritin showed a temporary increase at 6–12 h. Activities of antioxidant enzymes (SOD, GPx, TAC) showed inverse correlations with peak and cumulative cardiac injury markers in this pilot cohort, whereas higher LPO and iron showed positive correlations with greater myocardial damage observed here. CK-MB associations were stronger than those with Troponin I in this pilot cohort. In this pilot cohort, oxidative stress and ferroptosis-associated biomarkers showed rapid early changes after reperfusion in STEMI patients undergoing primary PCI, correlating with myocardial injury extent (stronger correlations with CK-MB than troponin I). These findings suggest early oxidative stress and iron dysregulation as potential therapeutic targets for reperfusion injury, warranting confirmation in larger studies. Why carry out this study? • Myocardial ischemia-reperfusion injury in ST-elevation myocardial infarction (STEMI) involves complex mechanisms, including oxidative stress and ferroptosis, but the timing and relationship of these processes with cardiac injury markers remain unclear. • Understanding the temporal changes of these biomarkers after PCI could reveal new therapeutic targets. • Clarifying how these biomarkers correlate with cardiac injury markers (Troponin I, CK-MB) may improve management of reperfusion injury. What was learned from the study? • Oxidative stress and ferroptosis-associated markers exhibited dynamic changes post-reperfusion: antioxidant enzymes (SOD, TAC) peaked at 6–12 hours, lipid peroxidation peaked at 6 hours, serum iron temporarily decreased, and ferritin increased transiently. • Higher antioxidant activity was associated with less myocardial injury, whereas higher lipid peroxidation and iron levels was associated to greater damage. • K-MB showed stronger associations than troponin I with these biomarkers. • Early oxidative and ferroptotic processes appear to contribute to reperfusion injury and warrant further investigation as potential therapeutic targets.