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Atherosclerosis is a vascular disease characterized by the build up of lipid derived plaques, and an individual’s risk of acute coronary syndrome is related to plaque burden and composition. Multiple risk markers for atherosclerosis and CVD act in a synergistic way through inflammatory pathways. One such inflammatory marker is serum amyloid A (SAA), which associates with HDL, negating its antiatherogeinc properties, which may have a causal role in atherosclerosis development. This study examined if SAA was related to CVD burden, and if this influenced the antiatherogenic properties of HDL. Subjects (n=240) referred to the rapid chest pain clinic at the Ulster Hospital UK, had atherosclerotic burden assessed by cardiac computerised tomography (CCT) and were classified as no CVD; mild CVD stenosis <50% and moderate/severe CVD stenosis >50%. HDL 2 and HDL 3 were isolated from serum by rapid ultracentrifugation. SAA was measured by an ELISA procedure, lipids by a colorimetric method and CETP activity by a fluorimetric assay. Results: Although lipids were similar in HDL 2 across the groups, lipids decreased in HDL 3 with increasing CVD burden. In addition, the concentration of SAA and the activity of CETP increased with increasing CVD burden (see table). Additionally, ordinal regression analysis illustrated that HDL 3 -SAA and HDL 2 -CETP where independently related to CVD burden (p=0.001). Conclusions: This study has shown that SAA was associated with increased CVD burden and that HDL had altered lipid composition and increased CETP activity. Thus, SAA and CETP may be useful biomarkers for the detection and assessment of CVD. Funded by Heart-Research UK