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Abstract Number: 2238

Alpha-Chlorofatty Acid Does Not Correlate with Baseline Subclinical Cardiovascular Disease in Systemic Lupus Erythematosus

Mary A. Mahieu1, Camelia Guild2, Carolyn J. Albert3, George Kondos4, James Carr5, Daniel Edmundowicz6, David A. Ford7 and Rosalind Ramsey-Goldman8, 1Internal Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, 2Pediatrics and Center for Outcomes Research, Saint Louis University, Saint Louis, MO, 3Saint Louis University, Saint Louis, MO, 4University of Illinois at Chicago, Chicago, IL, 5Northwestern University Feinberg School of Medicine, Chicago, IL, 6Temple University School of Medicine, Philadelphia, PA, 7Department of Biochemistry and Molecular Biology, Saint Louis University, Saint Louis, MO, 8Medicine/Rheumatology, Northwestern University Feinberg School of Medicine, Chicago, IL

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: cardiovascular disease and systemic lupus erythematosus (SLE)

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Session Information

Title: Systemic Lupus Erythematosus: Clinical Aspects

Session Type: Abstract Submissions (ACR)

Background/Purpose: Serum alpha-chlorofatty acid (α-ClFA) directly reflects in vivo myeloperoxidase activity, an important regulator of atherogenesis. The objective of our study was to investigate whether α-ClFA may be a biomarker for detection of subclinical cardiovascular disease (CVD) in patients with systemic lupus erythematosus (SLE).

Methods: One hundred eighty-five women with SLE and 186 controls participated in this ancillary study of the Study of Lupus Vascular and Bone Long-term Endpoints (SOLVABLE). Information on demographics, CVD risk factors, SLE risk factors, and baseline laboratory assessments were obtained at the first study visit. Using stored serum, α-ClFA was measured by liquid chromatography-electrospray ionization mass spectrometry with selected reaction monitoring detections. Each sample was run in triplicate. Coronary artery calcium (CAC) and aorta calcium (AC) were measured by either electron beam computed tomography (EBCT) or multi-detector computed tomography (MDCT), and calcium scores were calculated with a densitometric program using the Agatston method. Outcome measures were the presence of higher risk CAC or AC scores (CAC >10 or AC >100) versus lower risk scores (CAC ≤10 or AC ≤100). Descriptive characteristics and univariate analyses were used to identify significant associations. Multivariate analyses controlled for established traditional CVD risk factors and variables found to be significant in the univariate analysis by p<0.05 between cases and controls.

Results: SLE patients had higher baseline levels of α-ClFA than controls (42.2 fmol/μl ± 19.2 vs 34.5 fmol/μl ± 10.9, p=0.014). Cases with lower risk CAC and AC scores had statistically higher levels of α-ClFA compared to controls (42.0 fmol/μl ± 17.6 vs 33.7 fmol/μl ± 10.5, p=0.010 for CAC; 40.4 fmol/μl ± 12.3 vs 33.9 fmol/μl ± 10.5, p=0.023 for AC). In contrast, cases and controls with higher risk CAC and AC scores had similar α-ClFA levels (43.3 fmol/μl ± 21.5 vs 44.0 fmol/μl ± 14.8, p=0.951 for CAC; 39.3 fmol/μl ± 7.8 vs 37.6 fmol/μl ± 13.1, p=0.743 for AC). In multivariate analyses, SLE had the strongest independent association with higher risk CAC scores (odds ratio (OR) 5.81; 95% confidence interval (CI) 2.28 to 14.83), followed by dyslipidemia (OR 5.67; 95% CI 1.50 to 21.36), and older age (OR 1.11; 95% CI 1.05 to 1.17). Dysplipidemia was defined as fasting total cholesterol >200, low-density lipoprotein >100, high-density lipoprotein <40, triglyceride >150, or use of lipid-lowering medication. SLE also had the strongest independent association with higher risk AC scores (OR 3.73; 95% CI 1.59 to 8.78), followed by history of tobacco use (OR 2.31; 95% CI 1.13 to 4.74), older age (OR 1.17; 95% CI 1.10 to 1.25), and c-reactive protein level (OR 1.05; 95% CI 1.01 to 1.11). α-ClFA was not independently associated with higher risk CAC scores (OR 1.00; 95% CI 0.99 to 1.01) or higher risk AC scores (OR 1.01; 95% CI 0.99 to 1.02).

Conclusion: SLE had the strongest association with the presence of higher risk subclinical CVD as measured by CAC and AC scores.  Baseline serum α-ClFA levels were not independently associated with higher risk CAC or AC scores.


Disclosure:

M. A. Mahieu,
None;

C. Guild,
None;

C. J. Albert,
None;

G. Kondos,
None;

J. Carr,
None;

D. Edmundowicz,
None;

D. A. Ford,
None;

R. Ramsey-Goldman,
None.

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