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THU0339 Non-Calcified Coronary Artery Plaque Associates with Adverse Lipoprotein Profiles in Systemic Lupus Erythematosus
  1. L. Durcan1,2,
  2. A. Arbab-Zadeh3,
  3. M. Connelly4,
  4. J. Otvos4,
  5. L.S. Magder5,
  6. M. Petri2
  1. 1Rheumatology, University of Washington, Seattle
  2. 2Rheumatology
  3. 3Cardiology, Johns Hopkins, Baltimore
  4. 4Labcorp, Raleigh
  5. 5Epidemiology and Public Health, University of Maryland, Baltimore, United States

Abstract

Background Systemic lupus erythematosus (SLE) associates with excess 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 (CAC), by computed tomography (CT) have been shown to predict atherosclerotic burden and CV events. Non-calcified plaque (NCP), 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 CAC or NCP. Nuclear magnetic resonance (NMR) spectroscopy allows determination of the size and concentration of lipoprotein classes and subclasses.

Objectives To determine whether differences in NMR lipoprotein parameters can distinguish SLE patients with and without CAC. An additional aim was to establish whether NMR parameters associate with quantified NCP or calcified plaque.

Methods As part of a longitudinal lupus cohort, SLE patients had coronary CT angiography performed. The burden of atherosclerosis was evaluated (CAC, NCP). CAC scores were calculated according to the Agatston system. NCP was also categorized and scored for each patient. Lipoprotein particle numbers and size were evaluated by NMR. 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 NCP.

Results 69 SLE patients were evaluated, 49 (71%) African-American and 20 (29%) Caucasian. Significant NCP was present in 41 (59%) and CAC in 14 (20%). Individuals with NCP had significantly larger VLDL particles (44.8 ±5.5 nm versus 47.7 ±6.1 nm, p=0.042). Considering the volume and extent of CAC and NCP; (Table 1) higher triglycerides were observed with increasing levels of CAC. Increasing volumes of NCP were associated with higher LDL particle number and larger VLDL size. The lipoprotein insulin resistance scores were also positively associated with NCP. Table 1:Spearman Correlation for lipoprotein parameters and quantified coronary artery plaque.

Conclusions The mechanisms underlying atherosclerosis in SLE are poorly understood. NCP is highly prevalent in SLE and may be contributed to by differences in LDL, VLDL and insulin resistance measures, not evaluated in routine lipid profiles. Further longitudinal analysis will determine whether these abnormalities associate with progression of disease and can be considered prognostic markers.

Disclosure of Interest None declared

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