Inflammation-associated HDL dysfunction in acute coronary syndrome: role of serum amyloid A

Background Lipid profile plays a central role in cardiovascular risk assessment. Elevated low-density lipoprotein (LDL) and reduced high-density lipoprotein (HDL) are well-established markers of atherosclerosis, while higher HDL levels are traditionally considered protective. However, systemic inflammation may alter HDL composition and impair its anti-atherogenic functions. Serum amyloid A (SAA), a major acute-phase protein, can associate with HDL particles and potentially modify their biological properties. Aim To evaluate the association between circulating SAA levels and lipid profile characteristics in patients with acute and chronic coronary artery disease (CAD). Methods Fifty-five patients with clinically confirmed CAD were recruited from a tertiary cardiology center and classified into acute coronary syndrome (ACS) and stable chronic CAD groups, together with healthy controls. Serum SAA concentrations were measured using enzyme-linked immunosorbent assay (ELISA). Levels HDL and LDL were determined using routine biochemical laboratory methods. Statistical analysis was conducted using the Mann–Whitney U test. Continuous variables are reported as medians (Mdn) with interquartile ranges (IQR). Results Serum amyloid A levels were significantly higher in patients with CAD compared with controls and peaked in ACS group (Mdn = 1.24 ng/mL, IQR 0.50–2.21) compared with chronic CAD (Mdn = 0.97 ng/mL, IQR 0.60–1.33), p = 0.004. High-density lipoprotein concentrations did not differ between ACS and chronic CAD, p = 0.673. In contrast, LDL levels were significantly elevated in ACS (Mdn = 2480 ng/mL, IQR 1640–3020) compared with chronic CAD (Mdn = 1200 ng/mL, IQR 1050–1545), p < 0.001. These findings suggest inflammation-driven alterations in lipoprotein composition during acute disease. Conclusion Acute coronary syndrome is characterized by a potent inflammatory response evidenced by markedly elevated SAA. Our findings demonstrate that systemic inflammation drives HDL remodeling, compromising its atheroprotective capacity despite stable quantitative levels. The serum amyloid A protein acts as a critical biomarker linking inflammatory burden to qualitative lipid metabolism alterations in coronary artery disease.