Heart failure and its progression is associated with changed lymphocyte profile in epicardial adipose tissue

Introduction Chronic inflammation is increasingly recognized as a key contributor to the development and progression of heart failure (HF), with epicardial adipose tissue (EAT) emerging as an important local immunomodulatory organ. This study examined lymphocyte populations in EAT and subcutaneous adipose tissue (SAT) across different stages of HF and compared them with individuals without HF to clarify their potential role in HF progression. Methods Lymphocyte subsets in EAT, SAT, and peripheral blood were analyzed by flow cytometry in subjects with HF stage D, HF stage C, and subjects without HF. Circulating hormones and inflammatory proteins were quantified using ELISA and Luminex assays. Results Subjects with HF stage D exhibited a reduction in T helper (Th), cytotoxic T (Tc), natural killer T (NKT), and B cells in EAT compared with both HF stage C subjects and subjects without HF, alongside changes observed in the circulation. In contrast, HF stage C was characterized by a significantly increased presence of Th2 and Th17 lymphocytes in EAT, indicating active immune remodeling during intermediate stages of HF. This stage was also associated with elevated circulating levels of Intracellular Adhesion Molecule-1, suggesting enhanced lymphocyte trafficking into adipose tissue. Across all study groups, EAT consistently contained a higher proportion of pro-inflammatory lymphocytes compared with SAT. Conclusion Together, these findings demonstrate that HF progression is accompanied by dynamic and stage-dependent changes in lymphocyte composition within adipose tissue, supporting the concept that a progressively pro-inflammatory EAT microenvironment may contribute to myocardial inflammation dysfunction-associated HF progression.