Mary A Mahieu1, Camelia P Guild2, Carolyn J Albert2, George T Kondos2, James J Carr2, Daniel Edmundowicz2, David A Ford2, Rosalind Ramsey-Goldman2. 1. From the Department of Medicine, Division of Rheumatology, and Department of Radiology, Northwestern University Feinberg School of Medicine, Chicago, Illinois; Departments of Pediatrics and Center for Outcomes Research and of Biochemistry and Molecular Biology, and Center for Cardiovascular Research, Saint Louis University, Saint Louis, Missouri; Department of Medicine, Section of Cardiology, University of Illinois at Chicago College of Medicine, Chicago, Illinois; and Department of Medicine, Section of Cardiology, Temple University School of Medicine, Philadelphia, Pennsylvania, USA.M.A. Mahieu, MD, Department of Medicine, Division of Rheumatology, Northwestern University Feinberg School of Medicine; C.P. Guild, MPH, Department of Pediatrics and Center for Outcomes Research, Saint Louis University School of Medicine; C.J. Albert, BA, Department of Biochemistry and Molecular Biology, and Center for Cardiovascular Research, Saint Louis University School of Medicine; G.T. Kondos, MD, Department of Medicine, Section of Cardiology, University of Illinois Chicago College of Medicine; J.J. Carr, MD, Department of Radiology, Northwestern University Feinberg School of Medicine; D. Edmundowicz, MD, Department of Medicine, Section of Cardiology, Temple University School of Medicine; D.A. Ford, PhD, Department of Biochemistry and Molecular Biology, and Center for Cardiovascular Research, Saint Louis University School of Medicine; R. Ramsey-Goldman, MD, DrPH, Department of Medicine, Division of Rheumatology, Northwestern University Feinberg School of Medicine. mary-mahieu@northwestern.edu. 2. From the Department of Medicine, Division of Rheumatology, and Department of Radiology, Northwestern University Feinberg School of Medicine, Chicago, Illinois; Departments of Pediatrics and Center for Outcomes Research and of Biochemistry and Molecular Biology, and Center for Cardiovascular Research, Saint Louis University, Saint Louis, Missouri; Department of Medicine, Section of Cardiology, University of Illinois at Chicago College of Medicine, Chicago, Illinois; and Department of Medicine, Section of Cardiology, Temple University School of Medicine, Philadelphia, Pennsylvania, USA.M.A. Mahieu, MD, Department of Medicine, Division of Rheumatology, Northwestern University Feinberg School of Medicine; C.P. Guild, MPH, Department of Pediatrics and Center for Outcomes Research, Saint Louis University School of Medicine; C.J. Albert, BA, Department of Biochemistry and Molecular Biology, and Center for Cardiovascular Research, Saint Louis University School of Medicine; G.T. Kondos, MD, Department of Medicine, Section of Cardiology, University of Illinois Chicago College of Medicine; J.J. Carr, MD, Department of Radiology, Northwestern University Feinberg School of Medicine; D. Edmundowicz, MD, Department of Medicine, Section of Cardiology, Temple University School of Medicine; D.A. Ford, PhD, Department of Biochemistry and Molecular Biology, and Center for Cardiovascular Research, Saint Louis University School of Medicine; R. Ramsey-Goldman, MD, DrPH, Department of Medicine, Division of Rheumatology, Northwestern University Feinberg School of Medicine.
Abstract
OBJECTIVE: Alpha-chlorofatty acid (α-ClFA) is one product of myeloperoxidase activity in vivo during atherogenesis and may be a biomarker for cardiovascular disease (CVD). We investigated if serum α-ClFA is associated with subclinical CVD as measured by coronary artery and aorta calcium scores (CAC and AC, respectively) in women with and without systemic lupus erythematosus (SLE). METHODS: This pilot project analyzed baseline data from 173 women with SLE and 186 women without SLE participating in a 5-year longitudinal investigation of the Study of Lupus Vascular and Bone Long-term Endpoints (SOLVABLE). Data collection included demographic information, CVD and SLE risk factors, and laboratory assessments. Alpha-ClFA was measured in stored serum by liquid chromatography-mass spectrometry. CAC and AC were measured by computed tomography. Outcome measures were CAC and AC present (CAC > 0 or AC > 0) versus absent (CAC = 0 or AC = 0). Associations between risk factors and CAC or AC were tested with descriptive statistics and multivariate analyses. RESULTS: Women with SLE had higher α-ClFA levels than women without SLE (42.0 fmol/25 µl ± 37.3 vs 34.5 fmol/25 µl ± 21.9; p = 0.020). In analyses including individual CVD risk factors, having SLE was independently associated with the presence of CAC (OR 3.42, 95% CI 1.72 to 6.78) but not AC. Alpha-ClFA was not associated with the presence of CAC or AC in patients with SLE. CONCLUSION: SLE, but not serum α-ClFA, was associated with the presence of CAC in this pilot project.
OBJECTIVE:Alpha-chlorofatty acid (α-ClFA) is one product of myeloperoxidase activity in vivo during atherogenesis and may be a biomarker for cardiovascular disease (CVD). We investigated if serum α-ClFA is associated with subclinical CVD as measured by coronary artery and aorta calcium scores (CAC and AC, respectively) in women with and without systemic lupus erythematosus (SLE). METHODS: This pilot project analyzed baseline data from 173 women with SLE and 186 women without SLE participating in a 5-year longitudinal investigation of the Study of Lupus Vascular and Bone Long-term Endpoints (SOLVABLE). Data collection included demographic information, CVD and SLE risk factors, and laboratory assessments. Alpha-ClFA was measured in stored serum by liquid chromatography-mass spectrometry. CAC and AC were measured by computed tomography. Outcome measures were CAC and AC present (CAC > 0 or AC > 0) versus absent (CAC = 0 or AC = 0). Associations between risk factors and CAC or AC were tested with descriptive statistics and multivariate analyses. RESULTS:Women with SLE had higher α-ClFA levels than women without SLE (42.0 fmol/25 µl ± 37.3 vs 34.5 fmol/25 µl ± 21.9; p = 0.020). In analyses including individual CVD risk factors, having SLE was independently associated with the presence of CAC (OR 3.42, 95% CI 1.72 to 6.78) but not AC. Alpha-ClFA was not associated with the presence of CAC or AC in patients with SLE. CONCLUSION:SLE, but not serum α-ClFA, was associated with the presence of CAC in this pilot project.
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