Background - Atrial fibrillation (AF) is the most common sustained arrhythmia in patients with chronic ischemic heart disease (CIHD). While structural remodeling is well-documented, the exact neurohumoral and inflammatory triggers require further clarification. Objective: To investigate the features of catecholamine metabolism and cellular immune status in patients with CIHD complicated by AF. Methods: A total of 82 patients with CIHD were examined, divided into two groups: Group 1 (n=44) with concomitant AF, and Group 2 (n=38) without AF. The control group consisted of 20 healthy volunteers. Plasma levels of epinephrine and norepinephrine were determined using high-performance liquid chromatography. Immune status was assessed by measuring tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), high-sensitivity C-reactive protein (hs-CRP), and T-lymphocyte subpopulations (CD3+, CD4+, CD8+). Results: Patients with CIHD and AF demonstrated a significant sympathetic overdrive, with norepinephrine levels reaching 485.2 ± 32.4 pg/mL compared to 342.6 ± 28.1 pg/mL in the non-AF group (p < 0.05). This was accompanied by profound immune dysregulation. TNF-α and IL-6 concentrations were 1.8 and 2.1 times higher, respectively, in the AF group compared to controls. Furthermore, a decreased CD4+/CD8+ immunoregulatory index was observed in the AF cohort. Conclusion: The presence of atrial fibrillation in CIHD is associated with combined sympathoadrenal hyperactivation and systemic immune-inflammatory response. These pathophysiological shifts likely create a vicious cycle that promotes both electrical and structural myocardial remodeling.

chronic ischemic heart disease, atrial fibrillation, catecholamines, immune status, inflammation, cytokines.

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