ACR Meeting Abstracts

ACR Meeting Abstracts

Abstract Number: 1788

Lipoprotein Subfractions and Cardiovascular Disease in Systemic Lupus Erythematosus

Simantini Sakhardande1, Monica Purmalek1, Maureen Sampson2, Yenealem Temesgen-Oyelakim3, Alice Fike4, Taufiq Salahuddin5, Balaji Natarajan5, Zerai Manna6, Elizabeth Joyal6, Marcus Chen5, Sarfaraz Hasni6, Nehal N. Mehta5,7, Alan Remaley5 and Mariana J. Kaplan1, 1Systemic Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, 2CC/NIH, Bethesda, MD, 3Office of the Clinical Director,National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, 4Office of the Clinical Director, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, 5NHLBI, National Institutes of Health, Bethesda, MD, 6National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, 7National Heart Lung Blood Institute, Cardiovascular and Pulmonary Division, NHLBI, National Institutes of Health, Bethesda, MD

Meeting: 2015 ACR/ARHP Annual Meeting

Date of first publication: September 29, 2015

Keywords: , , ,

Session Information

Date: Monday, November 9, 2015

Title: Systemic Lupus Erythematosus - Clinical Aspects and Treatment Poster Session II

Session Type: ACR Poster Session B

Session Time: 9:00AM-11:00AM

Background/Purpose: Risk of atherosclerotic cardiovascular disease (CVD) is significantly enhanced in systemic lupus erythematosus (SLE) compared to age and gender matched controls. While this risk is not explained by the Framingham equation, lipoprotein abnormalities in phenotype and function have been detected in SLE. Recent studies in the general population suggest that CV risk may be more closely related to atherogenic lipoprotein particle numbers than LDL cholesterol. However, this association in SLE remains incompletely characterized. To this effect, associations between lipoprotein particle subfractions and disease activity, vascular dysfunction, and arterial inflammation in SLE and healthy controls were assessed.

Methods: SLE (n=20) and age and gender matched controls (n=15) underwent vascular function and anatomical assessments measuring peripheral arterial tonometry of the microvasculature (Endopat), arterial stiffness by cardio-ankle vascular index (CAVI), aortic inflammation by FDG-PET/CT, and quantification of plaque by coronary CT angiogram (CTA).  Particle concentrations of lipoprotein subfractions and particle sizes were measured by nuclear magnetic resonance spectroscopy (LipoScience).

Results: Lupus and control individuals did not differ in age, gender, tobacco use, standard lipid profile, BMI, or Framingham score. Total HDL, medium HDL, and intermediate–density lipoprotein (IDL) particle counts were significantly decreased in SLE (p=0.02, 0.015, 0.018, respectively) while VLDL and small VLDL particle counts were increased (p=0.048 and 0.035, respectively). In SLE, arterial stiffness assessed by CAVI correlated positively with total HDL particle count (r=0.489, p=0.03) and negatively with large VLDL particle count (r=-0.553, p=0.01). Arterial inflammation, assessed by target:background ratio in FDG-PET/CT, significantly correlated with medium VLDL particle count (r=0.51, p=0.05), while noncalcified burden of the right coronary artery negatively correlated with large+medium VLDL particle counts (r=-0.57, p=0.05). There was a significant difference (p=0.023) in small HDL particle count (p=0.023) between SLE patients on prednisone (median=11.4 [IQR:  7.3-15.1]) and not on prednisone (median=19.9 [IQR: 13.8-21.8]). Furthermore, there was a negative correlation between SLEDAI and total HDL particle count in SLE (r=-0.454, p=0.044).

Conclusion:  Individuals with SLE demonstrate significant differences in lipoprotein particle size and composition that associate with markers of vascular risk. The role medications play in these abnormalities remains to be determined. Longitudinal analysis will assess whether abnormalities in lipoprotein composition predict progression of CVD in SLE and determine the utility of following changes in lipoprotein subfractions as therapeutic targets.

Disclosure: S. Sakhardande, None; M. Purmalek, None; M. Sampson, None; Y. Temesgen-Oyelakim, None; A. Fike, None; T. Salahuddin, None; B. Natarajan, None; Z. Manna, None; E. Joyal, None; M. Chen, None; S. Hasni, None; N. N. Mehta, None; A. Remaley, None; M. J. Kaplan, None.

To cite this abstract in AMA style:

Sakhardande S, Purmalek M, Sampson M, Temesgen-Oyelakim Y, Fike A, Salahuddin T, Natarajan B, Manna Z, Joyal E, Chen M, Hasni S, Mehta NN, Remaley A, Kaplan MJ. Lipoprotein Subfractions and Cardiovascular Disease in Systemic Lupus Erythematosus [abstract]. Arthritis Rheumatol. 2015; 67 (suppl 10). https://acrabstracts.org/abstract/lipoprotein-subfractions-and-cardiovascular-disease-in-systemic-lupus-erythematosus/. Accessed .

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