title: Predictors of progression in atherosclerosis over 2 years in systemic lupus erythematosus.
abstract: OBJECTIVE
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Medicine, Division of Rheumatology, Johns Hopkins University School of Medicine Baltimore, 1830 East Monument Street Suite 7500, Baltimore, MD 21205, USA.
authors.forename: Adnan N
authors.initials: AN
authors.lastname: Kiani
authors.forename: Wendy S
authors.initials: WS
authors.lastname: Post
authors.forename: Laurence S
authors.initials: LS
authors.lastname: Magder
authors.forename: Michelle
authors.initials: M
authors.lastname: Petri
mesh_terms: D000328:Adult; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D050197:Atherosclerosis / Q000175:diagnosis* / Q000188:drug therapy / Q000453:epidemiology; D000069059:Atorvastatin; D002118:Calcium / Q000378:metabolism; D002340:Carotid Artery Diseases / Q000175:diagnosis / Q000453:epidemiology; D059168:Carotid Intima-Media Thickness; D015897:Comorbidity; D003331:Coronary Vessels / Q000378:metabolism / Q000473:pathology; D018450:Disease Progression; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000175:diagnosis* / Q000188:drug therapy / Q000453:epidemiology; D008297:Male; D008396:Maryland / Q000453:epidemiology; D011758:Pyrroles / Q000627:therapeutic use
chemical_list: D000924:Anticholesteremic Agents; D006538:Heptanoic Acids; D011758:Pyrroles; D000069059:Atorvastatin; D002118:Calcium