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Abstract Number: 2637

Assessment of Plaque Thickness and Area in Patients with SLE As Measures of Atherosclerosis – Associations with Disease Activity

Sara Croca1, Maura Griffin2, David Isenberg3, Andrew Nicolaides4 and Anisur Rahman5, 15 University Street, University College London, London, United Kingdom, 2Vascular Screening and Diagnostic Centre, London, United Kingdom, 3Centre for Rheumatology Research, Arthritis Research UK Centre for Adolescent Rheumatology, University College London, London, United Kingdom, 4St Georges London/Nicosia Medical School, University of Nicosia, Cyprus, Nicosia, Cyprus, 5Centre for Rheumatology Research, University College London, London, United Kingdom

Meeting: 2014 ACR/ARHP Annual Meeting

Keywords: Atherosclerosis, systemic lupus erythematosus (SLE) and ultrasound

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Session Information

Title: Systemic Lupus Erythematosus - Clinical Aspects and Treatment: Epidemiology, Women's Health, Cardiovascular and CNS

Session Type: Abstract Submissions (ACR)

Background/Purpose

SLE is an independent risk factor for cardiovascular disease (CVD). Traditional risk stratification tools underestimate CVD risk in patients with SLE. Previous vascular ultrasound (US) studies have reported intima-media thickness (IMT) and presence of plaques in the carotid arteries of patients with SLE. However, some patients have femoral but not carotid plaques and alternative measures such as plaque thickness (pT) and plaque area (pA) may be more sensitive and informative than IMT.

Methods

We carried out carotid and femoral US of 100 patients fulfilling ACR classification criteria for SLE with no history of CVD. Mean IMT of the common carotid artery (CCA) was measured using automated software. Plaque was defined as a focal structure of thickness >1.2 mm from media-adventitia interface to intima-lumen interface. Where plaque was present, pT was measured using manual callipers and pA measured using image analysis software.

Statistical analysis using Spearman’s correlation was carried out to investigate association between IMT, pA, pT and auto-antibody profile, lipids and homocysteine levels, blood pressure (BP), treatment and smoking status. Anti-apolipoprotein A1 (anti-ApoA1) IgG and IgM and anti-HDL antibodies were measured using direct ELISA protocols. Other clinical/serological data were obtained from medical records/patient interview.

Results

No patients had thickened CCA IMT (>0.1cm) but 37 had plaque in at least one site and 15 had plaque in ≥3 sites. The factors associated with  pT, pA and CCA IMT are summarized in Tables 1 and 2. Whereas CCA IMT was primarily influenced by traditional risk factors such as BP, total cholesterol and LDL, pT and pA correlated with a wider range of variables including higher disease activity, elevated homocysteine, cholesterol:HDL ratio and IgG anti-HDL level.

Table 1 – Factors associated with CCA IMT
Variable Spearman Correlation (r2) p-value
Age at scan (yrs) 0.55 <0.0001
Disease duration (yrs) 0.39 0.02
Systolic BP 0.4 <0.0001
Diastolic BP 0.22 0.03
Mean BP 0.32 0.001
Number of sites with plaque 0.39 <0.0001
Total plaque  area (sq mm) 0.40 <0.0001
Total plaque thickness (mm) 0.40 <0.0001
Total cholesterol (mmol/l) 0.36 0.0002
LDL (mmol/l) 0.31 0.002
Anti-apoA1 IgG in early disease 0.24 0.02
Table 2- Factors associated with plaque area and thickness
Variable Correlation with plaque area (Spearman r 2) p-value Correlation with plaque thickness (Spearman r 2) p-value
Age at scan (yrs) 0.56 <0.0001 0.58 <0.0001
Disease duration (yrs) 0.29 0.004 0.32 0.0001
Systolic BP 0.27 0.007 0.29 0.004
No of sites with plaque 0.99 <0.0001 0.99 <0.0001
Mean CCA IMT 0.39 <0.0001 0.39 <0.0001
Anti-La positivity -0.33 0.001 -0.33 0.001
Persistent moderate/high disease activity 0.21 0.035 0.18 0.07
Persistent low disease activity -0.21 0.035 -0.18 0.07
Serum homocysteine 0.31 0.04 0.31 0.05
Serum triglyceride 0.27 0.007 0.28 0.005
Total cholesterol/HDL ratio 0.25 0.013 0.23 0.02
IgG anti-HDL 0.21 0.03 0.21 0.039
No of BILAG A flares of disease activity 0.23 0.023 0.21 0.03

Conclusion

Although some authors have hypothesised a link between disease activity and atherosclerosis in SLE, this has not been shown convincingly in studies of IMT. More sensitive measurements such as pA and pT may help in linking disease activity and serology with atherosclerosis in SLE. This could help us target CVD risk reduction therapies to appropriate patients.


Disclosure:

S. Croca,
None;

M. Griffin,
None;

D. Isenberg,
None;

A. Nicolaides,
None;

A. Rahman,
None.

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