Arthritis & Rheumatism, Volume 62,
November 2010 Abstract Supplement

Abstracts of the American College of
Rheumatology/Association of Rheumatology Health Professionals
Annual Scientific Meeting
Atlanta, Georgia November 6-11, 2010.


Subclinical Atherosclerosis Is Increased in Systemic SclerosisA Case-Control Study.

Au1,  Karen M., McMahon1,  Maureen A., Furst3,  Daniel E., Hahn4,  Bevra H., Ragavendra1,  Nagesh, Bechtel1,  Amber, Sahakian1,  Lori

UCLA School of Medicine, Los Angeles, CA
University of California Los Angeles, Los Angeles, CA
University of California Los Angeles Medical School, Los Angeles, CA
University of California Los Angeles School of Medicine, Los Angeles, CA

Objective:

Systemic sclerosis (SSc) is associated with vasculopathy and endothelial cell injury, which could potentially increase the risk of atherosclerosis. Carotid artery ultrasound can detect subclinical atherosclerosis by measuring carotid intima-media thickness (IMT) and presence of carotid plaque. Studies have suggested that IMT is elevated in SSc, but there is little evidence that plaque is more prevalent in SSc compared to healthy patients.

Normal high-density lipoprotein (HDL) is anti-inflammatory and prevents low-density lipoprotein (LDL) oxidation. While HDL is protective, an altered form known as pro-inflammatory high-density lipoprotein (piHDL) may increase atherosclerotic risk and may actually potentiate LDL oxidation. Serum piHDL is a novel marker of atherosclerotic risk in lupus and rheumatoid arthritis. The objective of the study was to determine 1) the prevalence of subclinical atherosclerosis (carotid plaque and IMT measurement) in SSc and 2) serum piHDL levels as a potential novel marker of atherosclerotic risk in SSc.

Methods:

A cross-sectional study of 32 patients with SSc and 32 age-, sex-, and race-matched healthy controls in a single center was conducted. All subjects received bilateral carotid ultrasounds measuring plaque and IMT and were read by a single reader (NR) who was blinded to the diagnosis. Cholesterol studies and a cell free assay to measure presence of piHDL were performed.

Results:

The average age of the patients was 48 (mean age SSc 48, controls 47) and included 15 limited SSc and 17 diffuse SSc subjects. Total cholesterol (P=0.20) and LDL (P=0.13) were similar between SSc and controls. SSc patients had lower HDL (SSc 54.2 vs. controls 63.4, P=0.01) and higher triglycerides compared to controls (142.3 vs. 110.1, P=0.02). Carotid plaque was significantly more prevalent in SSc patients compared to controls (14 SSc patients vs. 7 controls; P= 0.043). Presence of carotid plaque was equally distributed among limited and diffuse SSc patients (9 limited, 8 diffuse). Average IMT was higher in patients with SSc than controls (0.582 ± 0.11 vs. 0.557 ± 0.14; P=0.059). SSc patients had similar rates of piHDL compared to controls (SSc 21.4%, controls 25%). piHDL was not associated with plaque (P=0.65) nor with average IMT (P=0.10) in our SSc cohort.

Conclusion:

Prevalence of subclinical atherosclerosis is greater in patients with SSc compared with healthy controls. This preliminary data suggests that pro-inflammatory HDL is not a marker of atherosclerosis in SSc.

To cite this abstract, please use the following information:
Au, Karen M., McMahon, Maureen A., Furst, Daniel E., Hahn, Bevra H., Ragavendra, Nagesh, Bechtel, Amber, et al; Subclinical Atherosclerosis Is Increased in Systemic SclerosisA Case-Control Study. [abstract]. Arthritis Rheum 2010;62 Suppl 10 :594
DOI: 10.1002/art.28362

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