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Predictors of progression in atherosclerosis over 2 years in systemic lupus erythematosus
Adnan N Kiani1, Wendy S Post, Laurence S Magder
1Department of Medicine, Division of Rheumatology, Johns Hopkins University School of Medicine Baltimore, 1830 East Monument Street Suite 7500, Baltimore, MD 21205, USA.
Insights
Cardiovascular risk factors like smoking and high cholesterol accelerate atherosclerosis in SLE patients. Disease activity did not significantly impact atherosclerosis progression over two years.
Area of Science:
- Rheumatology
- Cardiology
- Vascular Biology
Background:
- Cardiovascular disease is a leading cause of mortality in Systemic Lupus Erythematosus (SLE).
- Subclinical atherosclerosis progression is a key concern in SLE management.
- Understanding the drivers of atherosclerosis in SLE is crucial for risk stratification and prevention.
Purpose of the Study:
- To assess the association between cardiovascular risk factors (CVRFs) and SLE disease activity with 2-year changes in subclinical atherosclerosis.
- To identify predictors of coronary artery calcium (CAC) and carotid atherosclerosis progression in SLE patients.
Main Methods:
- 187 SLE patients underwent serial CT scans for CAC and carotid duplex ultrasound for intima-media thickness (IMT) and plaque over 2 years.
- Cardiovascular risk factors and disease activity markers were assessed regularly throughout the study.
- Statistical analyses examined correlations between clinical measures and atherosclerosis progression.
Main Results:
- CAC progression correlated with total serum cholesterol and smoking.
- Carotid IMT progression was associated with systolic blood pressure, hsCRP, and WBC count.
- Carotid plaque progression linked to systolic BP, WBC count, physician's global assessment, lymphocyte count, urine protein, and SLE duration.
Conclusions:
- SLE disease activity markers (SLEDAI, anti-dsDNA, etc.) were not associated with atherosclerosis progression.
- Age and hypertension predicted carotid IMT and plaque progression.
- Age, smoking, and cholesterol predicted CAC progression.
Objectives:
Cardiovascular disease remains the major cause of death in SLE. We assessed the degree to which cardiovascular risk factors (CVRFs) and disease activity were associated with 2-year changes in measures of subclinical atherosclerosis.
Methods:
One hundred and eighty-seven SLE patients participating in a placebo-controlled trial of atorvastatin underwent multi-detector CT [for coronary artery calcium (CAC)] and carotid duplex [for carotid intima-media thickness (IMT) and carotid plaque] twice, 2 years apart. During the 2 years, patients were assessed every 3 months for CVRF. Both groups were combined for analysis, as atorvastatin did not differ from placebo in preventing progression of coronary calcium. We examined the correlation between these clinical measures and progression of CAC, IMT and plaque during the follow-up period.
Results:
In an analysis adjusting for age, gender and ethnicity, CAC progression was positively associated with total serum cholesterol measured over the 2-year period (P = 0.04) and smoking (P = 0.003). Carotid IMT progression was associated with systolic BP (P = 0.003), high-sensitivity CRP (hsCRP) (P = 0.013) and white blood cell (WBC) count (P = 0.029). Carotid plaque progression, defined as patients without carotid plaque at baseline with subsequent development of plaque at follow-up, was associated with systolic BP (P = 0.003), WBC count (P = 0.02), physician's global assessment (P = 0.05), blood lymphocyte count (P = 0.048), urine protein (P = 0.017) and duration of SLE (P = 0.019).
Conclusion:
Our data did not provide evidence of an association between measures of SLE disease activity (SLEDAI, anti-dsDNA, anti-phospholipid and treatment) and progression of subclinical atherosclerosis. Age and hypertension were associated with the progression of carotid IMT and plaque. Age, smoking and cholesterol were associated with progression of CAC.
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