Rate and determinants of progression of atherosclerosis in systemic lupus erythematosus.
OBJECTIVE
To determine the rate of atherosclerosis progression as well as the relationship of traditional risk factors, systemic lupus erythematosus (SLE)-related factors, and treatment to atherosis progression in SLE patients.


METHODS
Outpatients in the Hospital for Special Surgery SLE Registry underwent serial carotid ultrasound and clinical assessment in a longitudinal study.


RESULTS
Among 158 patients, 77 (49%) had persistent absence of atherosclerosis (carotid plaque), 36 (23%) had unchanged atherosclerosis, and 45 (28%) had progressive atherosclerosis, defined as a higher plaque score (new plaque in 25 patients and more extensive plaque in 20 patients) after a mean +/- SD interval of 34 +/- 9 months. Multivariate determinants of atherosclerosis progression were age at diagnosis (odds ratio [OR] 2.75, 95% confidence interval [95% CI] 1.67-4.54 per 10 years, P < 0.001), duration of SLE (OR 3.16, 95% CI 1.64-6.07 per 10 years, P < 0.001), and baseline homocysteine concentration (OR 1.24, 95% CI 1.06-1.44 per mumoles/liter, P = 0.006). SLE patients with stable plaque and progressive plaque differed only in baseline homocysteine concentration. Atherosclerosis progression was increased across tertiles of homocysteine concentration (16.2%, 36.4%, and 56.1%; P = 0.001), and homocysteine tertile was independently related to progression of atherosclerosis (OR 3.14, 95% CI 1.65-5.95 per tertile, P < 0.001). Less aggressive immunosuppressive therapy and lower average prednisone dose were associated with progression of atherosclerosis in univariate, but not multivariate, analyses. Inflammatory markers and lipids were not related to atherosclerosis progression.


CONCLUSIONS
Atherosclerosis develops or progresses in a substantial minority of SLE patients during short-term followup (10% per year on average). Older age at diagnosis, longer duration of SLE, and higher homocysteine concentration are independently related to progression of atherosclerosis. These findings show that aggressive control of SLE and lowering of homocysteine concentrations are potential means to retard the development and progression of atherosclerosis in SLE.
Roman
Mary J
MJ
Weill Medical College of Cornell University, and the Hospital for Special Surgery, New York, New York 10021, USA. mroman@med.cornell.edu
Crow
Mary K
MK
Lockshin
Michael D
MD
Devereux
Richard B
RB
Paget
Stephen A
SA
Sammaritano
Lisa
L
Levine
Daniel M
DM
Davis
Adrienne
A
Salmon
Jane E
JE
D000328:Adult; D050197:Atherosclerosis / Q000097:blood / Q000150:complications / Q000175:diagnosis*; D015415:Biomarkers; D002340:Carotid Artery Diseases / Q000000981:diagnostic imaging*; D018450:Disease Progression; D005260:Female; D005500:Follow-Up Studies; D006710:Homocysteine / Q000097:blood*; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000097:blood* / Q000150:complications; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D014463:Ultrasonography
D015415:Biomarkers; D006710:Homocysteine