Oxidative Stress and Antioxidant Defense in Acute Myocardial Infarction: A Prospective Observational Study

Abstract

Background: Acute myocardial infarction (AMI) is associated with myocardial ischemia, cellular injury, inflammation and disturbances in redox homeostasis. Oxidative stress plays an important role in myocardial injury through excessive generation of reactive oxygen species and subsequent lipid peroxidation. Malondialdehyde (MDA) is a commonly used indicator of lipid peroxidation, whereas superoxide dismutase (SOD) represents an important enzymatic component of the endogenous antioxidant defense system. Assessment of these biomarkers at different time points may provide insight into the early oxidative and antioxidant responses following myocardial infarction.
Aim: To evaluate the early kinetic changes in oxidative stress and antioxidant defense biomarkers, namely malondialdehyde (MDA) and superoxide dismutase (SOD), in patients with acute myocardial infarction during the first 12 hours after hospital admission.
Materials and Methods: This prospective observational study was conducted in the Department of Biochemistry in collaboration with the Departments of Cardiology and Emergency Medicine at MGM Medical College and Hospital, Navi Mumbai, from August 2024 to April 2026. A total of 110 patients diagnosed with myocardial infarction were included after obtaining written informed consent. Blood samples were collected at admission (0 hour) and 12 hours after admission. Serum MDA was estimated using the Kei Satoh method, while SOD activity was determined using the Marklund and Marklund method. The results were expressed as mean ± standard deviation (SD). Paired t-test was used to compare the biomarker levels between the two time points and p < 0.05 was considered statistically significant.
Results: The mean serum MDA level significantly decreased from 9.6652 ± 0.9244 nmol/mL at admission to 6.4385 ± 1.5219 nmol/mL at 12 hours (p < 0.0001). In contrast, mean SOD activity significantly increased from 83.4033 ± 8.9211 U/mL at admission to 127.1918 ± 16.5676 U/mL at 12 hours (p < 0.0001). The simultaneous decrease in MDA and increase in SOD demonstrated a significant early shift in the oxidative-antioxidant profile following myocardial infarction.
Conclusion: Patients with acute myocardial infarction demonstrated significant early alterations in oxidative stress and antioxidant defense. The decrease in MDA together with an increase in SOD activity between admission and 12 hours suggests dynamic modulation of lipid peroxidation and endogenous antioxidant defense during the early phase following myocardial infarction. Serial assessment of MDA and SOD may provide useful biochemical information regarding early redox changes associated with myocardial infarction.