THE STATE OF THE IMMUNE SYSTEM IN PATIENTS WITH ISCHEMIC HEART DISEASE

Abstract

Background. Ischemic heart disease remains the leading cause of global mortality, conventionally viewed as a lipid-storage disease. However, contemporary cardiovascular medicine has fundamentally shifted to recognize atherosclerosis and its ischemic clinical manifestations as predominantly chronic inflammatory and immune-mediated processes. The objective of this study was to comprehensively evaluate the state of both cellular and humoral components of the immune system in patients suffering from varying degrees of ischemic heart disease, aiming to identify specific immunological markers associated with clinical instability. Methods. A prospective, observational clinical study was conducted at the clinical base of the Faculty Therapy Department of the Andijan State Medical Institute. The study enrolled a total of 71 patients diagnosed with ischemic heart disease, who were subsequently categorized into two clinical groups based on disease presentation, specifically stable angina pectoris and unstable angina. The functional state of the immune system was evaluated by measuring the serum concentrations of highly sensitive C-reactive protein, major pro-inflammatory cytokines including Interleukin-6 and Tumor Necrosis Factor-alpha, as well as analyzing the cellular immune profile through the quantification of T-lymphocyte subpopulations. Results. The clinical and laboratory evaluation revealed profound immunological disturbances in patients with ischemic heart disease compared to established physiological norms. Furthermore, a highly significant discrepancy was observed between the clinical subgroups. Patients presenting with unstable angina demonstrated a marked and statistically significant hyperactivation of the systemic inflammatory response, evidenced by drastically elevated levels of Interleukin-6, Tumor Necrosis Factor-alpha, and highly sensitive C-reactive protein, alongside a pronounced imbalance in cellular immunity characterized by an altered ratio of T-helper to T-cytotoxic cells. Conclusion. The progression and clinical destabilization of ischemic heart disease are inextricably linked to the profound dysregulation of the systemic immune response. The significant elevation of pro-inflammatory cytokines and the critical imbalance in cellular immunity markers directly contribute to atherosclerotic plaque vulnerability, underscoring the necessity of incorporating immunological assessments into routine cardiovascular risk stratification and opening novel avenues for targeted immunomodulatory therapeutic strategies.