Adipokines and perivascular adipose tissues in coronary artery disease: depot-specific adipokine expression, adipocyte morphology, and links to metabolic dysfunction

Background Perivascular adipose tissue (PVAT) modulates vascular function through paracrine adipokine secretion and undergoes proinflammatory remodeling in coronary artery disease (CAD) and metabolic dysfunction. Depot-specific differences in adipokine expression and adipocyte morphology remain incompletely characterized. Methods Sixty CAD patients undergoing elective coronary artery bypass grafting were enrolled. Body composition was assessed by bioelectrical impedance analysis. Subcutaneous fat tissue (SFT), aortic PVAT, left internal mammary artery PVAT, and saphenous vein PVAT were analyzed by histology and qPCR for adipokines and inflammatory markers. Serum chemerin was measured by ELISA. Patients were stratified by BMI (≥ 30 vs. <30 kg/m 2 ). Results Adipocyte size differed significantly across depots (p<0.001), with larger adipocytes in SFT than in all PVAT depots (all p<0.001). The visceral fat indicator was independently associated with lower SFT adipocyte density after adjustment for age, sex, and SGLT2 inhibitor use (β = −0.639, p = 0.006), consistent with larger adipocytes. Aortic PVAT showed the highest expression of IL-1β, IL-6, MCP-1, and ICAM. Serum chemerin was associated with body fat percentage but did not differ significantly between BMI groups. Conclusion In CAD patients undergoing surgical revascularization, aortic PVAT exhibits a distinct proinflammatory profile, whereas SFT adipocyte hypertrophy is associated with visceral adiposity. Serum chemerin was associated with overall adiposity, although it did not differ significantly between BMI groups. These findings highlight depot-specific adipose tissue remodeling and visceral adiposity as potential contributors to cardiovascular risk in metabolically compromised CAD patients.