CVD, Atherosclerosis Risk in Systemic Lupus Erythematosus

Patients with systemic lupus erythematosus had a net progression of mean carotid intima-media thickness, with or without depression.

Women with systemic lupus erythematosus (SLE) and depression may be at an increased risk for subclinical cardiovascular disease (CVD), suggesting depression is an important modifiable risk factor for the condition, according to research published in Arthritis Care and Research.

Rosalind Ramsey-Goldman, MD, DrPH, from the Rheumatology Division at the Northwestern University Feinberg School of Medicine in Chicago, and colleagues conducted a prospective, case-control study of women with SLE to examine any relationship between depression and increased inflammation linked to CVD.

Participants (n=149) and control patients (n=126) were followed for 5 years. Baseline measurements of lupus disease activity and damage were determined via the validated SLE Disease Activity Index 2000 and the Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index. Depression screening was conducted using the Center for Epidemiologic Studies Depression Scale, and CVD risk factors were determined using a combination of a self-administered questionnaire and objective measurements.

Patients in the SLE group had higher rates of depression at baseline than those in the control group, at 29% vs 11% (mean Center for Epidemiologic Studies Depression Scale score, 11.5 vs 7.7; P =.001). Within the SLE group, those with depression had higher mean body mass index (30.98 ± 9.09 kg/m2) vs those without depression (27.38 ± 7.47 kg/m2; P =.014). No other significant differences in traditional CVD risk factors were noted, and no differences were found in mean SLE Disease Activity Index 2000 or Systemic Lupus International Collaborating Clinics/American College of Rheumatology Damage Index scores.

Over the course of 5 years, researchers saw a net progression of mean carotid intima-media thickness (CMIT) in all groups (control, SLE with depression, and SLE without depression). A mean increase of 0.026 mm (95% CI, 0.012-0.041) was noted in the SLE group without depression, and a mean increase of 0.064 mm (95% CI, 0.41-0.87) was noted in the SLE group with depression (P =.0096). No similar correlation was noted in the control group.

Carotid plaque was detected via B mode ultrasound in 36.9% of SLE cases; at 5 years, 45.0% of SLE cases and 37.3% of control cases had carotid plaque. No difference between plaque levels in the depressed vs nondepressed SLE group was noted at baseline or 5 years (P =1.0 and .10, respectively).

Summary & Clinical Applicability

The investigators noted that “several factors, including coping with chronic illness, pain, reduced physical functionality, and the use of corticosteroids, may all contribute to the increased risk of depression in women with SLE,” adding that depression negatively affects comorbidities, including “traditional CVD risk factors.”

“[W]omen with SLE and depression have increased progression of CMIT, but not carotid plaque, when compared with women with SLE who are non-depressed,” wrote Dr Ramsey-Goldman and colleagues. “[O]ur findings demonstrating a significant change in CMIT but not in carotid plaque may represent a subtle association between depression and the progression of subclinical atherosclerosis in women with SLE.”

Study Limitations

  • The cohort studied was small and did not include a sufficient number of patients with reported tobacco use to control for that particular CVD risk factor.
  • Follow-up time was restricted to 5 years, which may not have been a long enough time to predict carotid plaque progression.
  • There may be bias associated with a loss of follow-up within the study.
  • Generalizability may be limited by the older cohort with less active lupus that was studied during follow-up.


Jorge A, Lerttratanakul A, Lee J, et al. Depression and progression of subclinical cardiovascular disease in systemic lupus erythematosus. Arthrit Care Res. 2017;69:5-11. doi:101.1002/acr.22992 

This article originally appeared on Rheumatology Advisor