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Investigating Aortic Valve Calcification via Isolation and Culture of T Lymphocytes using Feeder Cells from Irradiated Buffy Coat
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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
PubMed

Insights

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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