NEUROIMMUNE PATHOGENETIC RELATIONSHIP BETWEEN THE SYMPATHOADRENAL SYSTEM AND INFLAMMATORY MEDIATORS IN ISCHEMIC HEART DISEASE

This article analyzes the pathogenetic relationship between sympathoadrenal system activation and inflammatory mediators in ischemic heart disease. According to modern concepts, ischemic heart disease is not explained only by mechanical narrowing of the coronary arteries, but is considered a complex pathological process involving atherosclerotic plaque, endothelial dysfunction, impaired coronary microcirculation, oxidative stress, autonomic imbalance, and low-grade chronic inflammation. Myocardial ischemia activates the sympathoadrenal system and increases catecholamine secretion. As a result, heart rate, myocardial contractility, arterial blood pressure, and myocardial oxygen demand increase. At the same time, catecholamines may affect immune cells, the endothelium, and platelets, thereby enhancing the activity of inflammatory mediators such as IL-6, TNF-α, MCP-1, and CRP. Conversely, inflammatory mediators may impair autonomic regulation and contribute to prolonged sympathetic hyperactivity. Thus, a “neuroimmune vicious circle” is formed: ischemia activates the sympathoadrenal system, while sympathetic hyperactivity intensifies inflammation, oxidative stress, and endothelial dysfunction. These mechanisms play an important role in the progression of ischemic heart disease, atherosclerotic plaque instability, microvascular dysfunction, and adverse cardiovascular outcomes.