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Abstract Number: 2898

Atherosclerosis In Systemic Lupus Erythematosus (SLE) and Controls, -An Analysis Of SLE Subgroups

Johanna Gustafsson1, Kerstin Jensen-Urstad2, Marie Herlitz-Lindberg2, Sonia Möller1, Susanne Pettersson1, Iva Gunnarsson1, Anders Larsson3 and Elisabet Svenungsson4, 1Department of Medicine, Rheumatology Unit, Karolinska Institutet, Stockholm, Sweden, 2Department of Clinical Physiology, Södersjukhuset, Karolinska Institutet, Stockholm, Sweden, 3Department of Clinical Chemistry and Pharmacology, Akademiska Hospital, Uppsala, Sweden, 4Department of Medicine, Unit of Rheumatology, Karolinska Institutet, Stockholm, Sweden

Meeting: 2013 ACR/ARHP Annual Meeting

Keywords: Atherosclerosis, Cardiovascular disease, Nephritis and systemic lupus erythematosus (SLE)

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Session Information

Title: Systemic Lupus Erythematosus - Clinical Aspects: Cardiovascular and Other Complications of Lupus

Session Type: Abstract Submissions (ACR)

Background/Purpose: Atherosclerosis is often assumed to be the main underlying cause of premature vascular events (VE) among patients with systemic lupus erythematosus (SLE) and accelerated atherosclerosis is frequently considered to be a general feature of SLE, though not confirmed in all studies. Since SLE is a very heterogeneous disease we studied the occurrence of atherosclerosis in unselected and in predefined subgroups of SLE patients. Individually matched population controls were used as comparators.

Methods: 281 SLE patients and 281 population controls, individually matched for age, sex, and region of living were included. All were investigated clinically including CVD risk factors and inflammatory biomarkers. The same investigator performed B-mode ultrasonography of carotid arteries. Mean intima media thickness (mIMT) and plaque occurrence (local IMT>1mm) were tabulated. Paired analyses were performed.

Results: In both groups: mean age was 48±14 years, 93% were females.

Patients had slightly thicker mIMT than controls (0.59±0.01 vs 0.57±0.01, p=0.003), but plaque occurrence did not differ, 20% and 16% respectively.

Manifest CVD (ischemic heart, cerebro- and peripheral vascular disease) was more common in patients (12 % vs. 1 %, p<0.0001).

Patients had lower high (HDL), low density lipoprotein (LDL) and albumine, but higher triglycerides (TG), apoB/A, C-reactive protein, homocysteine, cystatin C, creatinine, tumor necrosis factor receptor (TNFR) 1 and 2, and vascular cell adhesion molecule-1 (p<0.005 for all). Patients were more often on antihypertensive-, lipid-lowering, aspirin and warfarin treatments (p<0.05 for all).

Among SLE patients, after age adjustment: Manifest CVD was associated with plaques (p<0.0001), but not with mIMT (p=0.3). 

mIMT was associated with smoking, sBP, HDL(negatively), LDL, TG, apoB/A, and glucose(p<0.05 for all).

Plaques were positively associated with smoking, sBP, TG, albumine, cystatin C, nephritis, TNFR 1 and 2, SLICC>1, and antihypertensive treatment, and negatively associated with leukopenia (p<0.05 for all).

Multivariable-adjusted models: In patients, age, sBP and apoB/A remained associated with mIMT (p<0.05 for all). Age, sBP and manifest CVD remained for plaques (p<0.05).

Stratified analyses: Analysis of SLE subgroups (nephritis(112+112), SSA/SSB(131+131) and anti phospholipid (aPL) (75+75)-positivity) compared to individually matched controls revealed that  patients diagnosed with nephritis selectively had more plaques than their respective controls (p=0.008) and mIMT was was also thicker in the nephritis group (p=0.006). Thicker mIMT was also present in the SSA/SSB and aPL subgroups (p<0.05). 

Conclusion: This is, to our knowledge, the largest study of atherosclerosis in SLE patients/matched population controls. Manifest CVD was more common among patients, but enhanced occurrence of atherosclerotic plaques was not a general feature of SLE as it was essentially confined to patients with a history of nephritis. mIMT was slightly thicker in patients, a more general SLE feature, but not associated with manifest CVD in this study. Our results imply that renal disease is an important driving factor behind accelerated atherosclerosis in SLE.


Disclosure:

J. Gustafsson,
None;

K. Jensen-Urstad,
None;

M. Herlitz-Lindberg,
None;

S. Möller,
None;

S. Pettersson,
None;

I. Gunnarsson,
None;

A. Larsson,
None;

E. Svenungsson, None.

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