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Updated: Jul 17, 2026
04:30
Investigating Aortic Valve Calcification via Isolation and Culture of T Lymphocytes using Feeder Cells from Irradiated Buffy Coat
Published on: February 4, 2021
Aortic valve calcification in systemic lupus erythematosus
A N Kiani1, E K Fishman, M Petri
1Division of Rheumatology, Johns Hopkins University, School of Medicine, Baltimore, MD, USA.
Lupus
|January 11, 2007
Summary
Aortic valve calcification is rare in systemic lupus erythematosus (SLE) but linked to novel cardiovascular risks and hypercoagulability. Unlike the general population, it
Area of Science:
- Cardiology
- Rheumatology
- Vascular Biology
Background:
- Aortic valve calcification (AVC) commonly associates with atherosclerosis in the general population.
- Systemic lupus erythematosus (SLE) is an autoimmune disease with increased cardiovascular risk.
- The prevalence and associations of AVC in SLE patients are not well-established.
Purpose of the Study:
- To investigate the prevalence of AVC in patients with SLE.
- To identify factors associated with AVC in this cohort.
Main Methods:
- Helical CT scans were used to assess AVC in 199 SLE patients.
- Patient demographics, cardiovascular risk factors, medications, and antiphospholipid antibody status were analyzed.
- Statistical analysis identified significant associations with AVC.
Main Results:
- AVC was present in 1.5% of SLE patients, contrasting with 43% coronary calcium and 17% carotid plaque.
- Associations were found with high-sensitivity C-reactive protein (hs-CRP), fibrinogen, lipoprotein(a), prednisone, methotrexate, and antiphospholipid antibody positivity (lupus anticoagulant).
- AVC was not associated with coronary calcium or carotid plaque in SLE patients.
Conclusions:
- AVC is uncommon in SLE patients but linked to specific cardiovascular risk factors and hypercoagulability.
- Unlike the general population, AVC in SLE does not correlate with subclinical atherosclerosis markers like coronary calcium or carotid plaque.
- These findings suggest unique pathophysiological mechanisms for AVC in SLE.
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