Poster Number 2842 Non-Calcified Coronary Artery Plaque Associates with Adverse Lipoprotein Profiles in Systemic Lupus Erythematosus. L. Durcan1, A. Arbab-Zadeh2, M.A. Connelly3, J.D. Otvos3, L.S. Magder4, M. Petri5. 1. Division of Rheumatology, University of Washington, 2. Department of Cardiology, Johns Hopkins University Hospital, 3. LabCorp, Raleigh, 4. Department of Epidemiology and Public Health, University of Maryland , 5. Division of Rheumatology, Johns Hopkins University Hospital. BACKGROUND Biomarker Calcified Plaque Non-Calcified Plaque Spearmen Correlation Coefficient P-value VLDL & Chylomicron Particles (total) (nmol/L) 0.05 0.67 -0.06 0.62 Large VLDL & Chylomicrons Particles (nmol/L) 0.20 0.09 0.18 0.13 Medium VLDL Particles (nmol/L) 0.07 0.56 -0.00 0.97 Small VLDL Particles (nmol/L) 0.00 0.99 -0.05 0.68 LDL Particles (total) (nmol/L) 0.14 0.26 0.034 IDL Particles (nmol/L) 0.66 -0.02 0.89 Large LDL Particles (nmol/L) 0.44 0.15 0.22 Small LDL Particles (nmol/L) 0.02 HDL Particles (total) (µmol/L) 0.17 0.16 Large HDL Particles (µmol/L) -0.04 0.75 -0.03 0.83 0.10 0.42 -0.07 0.57 Small HDL Particles (µmol/L) 0.11 0.36 0.21 0.086 VLDL Size (nm) 0.082 0.25 0.038 LDL Size (nm) 0.49 0.70 HDL Size (nm) -0.08 0.50 -0.13 0.30 Triglyceride (total) (mg/dL) 0.24 0.043 Lipoprotein Insulin Resistance Score 0.080 0.044 RESULTS Systemic lupus erythematosus (SLE) associates with an excess of atherosclerotic cardiovascular (CV) disease and related mortality. This is contributed to, but cannot be fully explained, by traditional CV risk factors, treatments and SLE-specific factors. Coronary artery calcium scores, by computed tomography (CT) have been shown to predict atherosclerotic burden and CV events. Non-calcified plaque, common in SLE, can also be quantified and may be more metabolically active and unstable. Routine lipids are unhelpful in distinguishing SLE patients with or without either coronary artery calcification or non-calcified plaque. Nuclear magnetic resonance (NMR) spectroscopy allows determination of the size and concentration of lipoprotein classes and subclasses, and has been used to evaluate CV risk in many populations. Patients Sixty-nine SLE patients were evaluated: 64 (93%) female, 49 (71%) were African-American and 20 (29%) were Caucasian. Eight (13%) were 40-49, 29 (42%) were 50-59, and 16 (23%) were 60-69 years old, 16 (23%) were 70 or older. CT Findings Significant non-calcified plaque was present in 41 (59%). Coronary artery calcification was present in 14 (20%). Statistical Analysis Individuals with non calcified plaque had significantly larger very low-density lipoprotein particles (44.8 ±5.5 nm versus 47.7 ±6.1 nm, p= 0.042). (None of the other lipoprotein parameters were significantly different between those who had calcified or non-calcified plaque on comparison with those who did not). Considering the volume and extent of calcified and non-calcified plaque: (Table 1) higher triglycerides were observed with increasing levels of coronary artery calcification. Increasing volumes of non-calcified plaque were associated with higher low density lipoprotein particle number and larger very low density lipoprotein size. The lipoprotein insulin resistance scores were also positively associated with non-calcified plaque. OBJECTIVES To determine whether differences in lipoprotein particle numbers or size (by nuclear magnetic resonance spectroscopy) can distinguish between SLE patients with and without coronary artery calcification. To establish whether NMR parameters associate with quantified calcified and non-calcified plaque. METHODS CT Evaluation As part of the Hopkins Lupus Cohort, SLE patients, without known atherosclerotic disease, had coronary CT angiography performed. The burden of atherosclerosis was evaluated (calcified and non calcified plaque). Coronary artery calcium scores were calculated according to the Agatston system. Lipoprotein Parameters Lipoprotein particle numbers and size were evaluated by NMR. Statistical Analysis The initial statistical analysis compared those with and without calcified and NCP using t-tests. Further evaluation involved the calculation of correlation coefficients to evaluate the relationship between lipoprotein abnormalities and the burden of calcified and non-calcified plaque. CONCLUSION Much of the accelerated mortality in SLE is attributable to cardiovascular disease. Cardiovascular risk factors, medications and SLE specific factors are known to contribute, but do not fully explain the increased risk of death from cardiovascular causes in this population. Non-calcified plaque is highly prevalent in SLE, our study found differences in low density lipoprotein, very low density lipoproteins and insulin resistance measures. These parameters are not evaluated in routine lipid profiles. Further longitudinal analysis will determine whether these abnormalities associate with progression of atherosclerotic disease. Table 1. Analysis of quantified calcified and non-calcified coronary artery scores and NMR lipoproteins. VLDL= Very low density lipoprotein, LDL= Low density lipoprotein, IDL= Intermediate density lipoprotein, HDL= high density lipoprotein Acknowledgement: The Hopkins Lupus Cohort was funded by NIH AR 43727.