Characteristics of lipid metabolism, lipid peroxidation products (LPP), and antioxidative potential were determined in patients with acute myocardial infarction. Minor variations of serum total cholesterol, LDL, and triglycerids were detected in patients with small-focal MI. After completion of therapy cholesterol dropped only in patients with transmural infarction. LDL cholesterol was low prior to therapy in all patients and continued to decrease in transmural MI. All patients had high dienic congugate levels in plasma and erythrocytes that did not change under effect of baseline therapy. The level of secondary LPP (MDA) in erythrocytes was high and remained unaltered during treatment. Antioxidative potential measured as SOD activity was elevated in all patients. Glutathione reductase, glutathione peroxidase, and catalase activities decreased throughout the treatment period. Patients with acute IM developed oxidative stress during heart attack, it persisted for a long time and was responsible for suppression of pentosophosphate cycle in erythrocytes associated with low activity of glutathione reductase and catalase that needed reduced NADPH2 codehydrogenase to manifest itself. Patients with small-focal and transmural AMI experienced elevation of oxidative potential in erythrocytes and membranopathy. Baseline therapy failed to normalize production of primary and secondary LPP in patients with MI and eliminate oxidative stress that developed during heart attacks and persisted after the termination of therapy. It is concluded that correction of metabolic disturbances requires antioxidative therapy to neutralize LPP.