This article analyzes the pathogenetic relationship between lipid peroxidation, malondialdehyde, and activation of the sympathoadrenal system in ischemic heart disease. Ischemic heart disease is currently considered not only as a consequence of coronary artery narrowing, but also as a complex pathological process associated with oxidative stress, endothelial dysfunction, microcirculatory disorders, neurohumoral activation, and metabolic imbalance. Myocardial ischemia activates the sympathoadrenal system and increases the secretion of adrenaline and noradrenaline. Catecholamines increase heart rate, myocardial contractility, and myocardial oxygen demand. At the same time, their excessive production contributes to mitochondrial dysfunction, generation of reactive oxygen species, and activation of lipid peroxidation. Malondialdehyde, one of the main end-products of lipid peroxidation, is an important biochemical marker associated with cell membrane damage, PZLP modification, endothelial dysfunction, and atherosclerotic plaque instability. The relationship between sympathoadrenal hyperactivity and increased MDA levels in ischemic heart disease is important for assessing myocardial injury, arrhythmogenicity, and cardiac remodeling risk.