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FRI0127 Atherosclerosis and arterial disease in systemic lupus erythematosus
  1. J Frostegard1,
  2. E Svenungsson1,
  3. K Jensen-Urstad2,
  4. M Heimburger3,
  5. L Klareskog1,
  6. A Hamsten4,
  7. U De Faire5,
  8. J Witztum6
  1. 1Department of Rheumatology
  2. 2Department of Clinical Physiology
  3. 3Department of Rheumatology, Huddinge University Hospital, Stockholm, Sweden
  4. 4Department of Medicine
  5. 5Division of Cardiovascular-Epidemiology, Karolinska Hospital
  6. 6Department of Medicine, University of California San Diego, San Diego, USA

Abstract

Background Systemic lupus erythematosus (SLE) patients have increased morbidity and mortality in cardiovascular diseases. Whether this is caused by aggravated atherosclerosis has not been totally clarified. Since atherosclerosis recently has been shown to be an inflammatory disease it is important to study the inflammatory nature of SLE in this context. Furthermore the role of phospholipid antibodies and enhanced trombogenesis as well as the importance of other cardiovascular risk factors like LDL oxidation need to be studied in SLE patients.

Objectives To determine the cause of the enhanced risk of cardiovascular disease present in systemic lupus erythematosus.

Methods Twenty-six women (mean age 52 yrs) with SLE and a history of arterial disease (SLE cases) were compared with 26 age matched women with SLE but without manifest arterial disease (SLE controls) and 26 age matched population control women (population controls). Common carotid intima-media thickness (IMT) was measured by B-mode ultrasound as a surrogate measure of atherosclerosis. All were subject to clinical and laboratory evaluations with respect to known cardiovascular risk factors. A monoclonal antibody to oxLDL, EO6, was used to determine oxidation epitopes in LDL.

Results SLE cases had increased IMT as compared to population controls (IMT 0.66 mm ± 0.15 vs 0.59 ± 0.12, p = 0.037) while the IMT of SLE controls (0.60 mm ± 0.14) did not differ from that of population controls. Raised plasma concentrations of oxLDL- (p = 0.033); dyslipidemia with raised triglycerides (p < 0.001) and lipoprotein (a) (p = 0.002), and decreased HDL-cholesterol concentrations (p = 0.03); raised alfa-1-antitrypsin- (p = 0.002), antibodies to oxLDL (p < 0.001), lupus anticoagulant (p = 0.007) and homocysteine-levels (p = 0.03) discriminated between SLE cases and SLE controls. SLE cases had been subject to significantly higher cumulative prednisone dose than SLE controls (p = 0.04). Disease duration, smoking, blood pressure, BMI or diabetes mellitus did not differ significantly between the groups.

Conclusion We found that arterial disease in SLE is linked to aggravated atherosclerosis. However, unlike the situation in diabetes and hypertension, aggravated atherosclerosis was not present in SLE patients without signs of arterial disease. Dyslipidemia, systemic inflammation and raised concentrations of OxLDL, anti OxLDL antibodies, lupus anticoagulant and homocysteine distinguished women with SLE and arterial disease from both SLE controls and population controls.

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