Prevalence and correlates of accelerated atherosclerosis in systemic lupus erythematosus.
BACKGROUND
Although systemic lupus erythematosus is associated with premature myocardial infarction, the prevalence of underlying atherosclerosis and its relation to traditional risk factors for cardiovascular disease and lupus-related factors have not been examined in a case-control study.


METHODS
In 197 patients with lupus and 197 matched controls, we performed carotid ultrasonography, echocardiography, and an assessment for risk factors for cardiovascular disease. The patients were also evaluated with respect to their clinical and serologic features, inflammatory mediators, and disease treatment.


RESULTS
The risk factors for cardiovascular disease were similar among patients and controls. Atherosclerosis (carotid plaque) was more prevalent among patients than the controls (37.1 percent vs. 15.2 percent, P<0.001). In multivariate analysis, only older age, the presence of systemic lupus erythematosus (odds ratio, 4.8; 95 percent confidence interval, 2.6 to 8.7), and a higher serum cholesterol level were independently related to the presence of plaque. As compared with patients without plaque, patients with plaque were older, had a longer duration of disease and more disease-related damage, and were less likely to have multiple autoantibodies or to have been treated with prednisone, cyclophosphamide, or hydroxychloroquine. In multivariate analyses including patients with lupus, independent predictors of plaque were a longer duration of disease, a higher damage-index score, a lower incidence of the use of cyclophosphamide, and the absence of anti-Smith antibodies.


CONCLUSIONS
Atherosclerosis occurs prematurely in patients with systemic lupus erythematosus and is independent of traditional risk factors for cardiovascular disease. The clinical profile of patients with lupus and atherosclerosis suggests a role for disease-related factors in atherogenesis and underscores the need for trials of more focused and effective antiinflammatory therapy.
Roman
Mary J
MJ
Division of Cardiology, Weill Medical College of Cornell University, the Hospital for Special Surgery, New York, NY 10021, USA. mroman@med.cornell.edu
Shanker
Beth-Ann
BA
Davis
Adrienne
A
Lockshin
Michael D
MD
Sammaritano
Lisa
L
Simantov
Ronit
R
Crow
Mary K
MK
Schwartz
Joseph E
JE
Paget
Stephen A
SA
Devereux
Richard B
RB
Salmon
Jane E
JE
D000305:Adrenal Cortex Hormones / Q000627:therapeutic use; D000328:Adult; D000367:Age Factors; D001161:Arteriosclerosis / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000209:etiology*; D001323:Autoantibodies / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis; D023201:CD40 Ligand / Q000097:blood; D002318:Cardiovascular Diseases; D002340:Carotid Artery Diseases / Q000000981:diagnostic imaging / Q000453:epidemiology / Q000209:etiology*; D016022:Case-Control Studies; D005260:Female; D006801:Humans; D016015:Logistic Models; D008180:Lupus Erythematosus, Systemic / Q000150:complications* / Q000188:drug therapy / Q000276:immunology; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D015995:Prevalence; D012307:Risk Factors; D014463:Ultrasonography
D000305:Adrenal Cortex Hormones; D001323:Autoantibodies; D023201:CD40 Ligand; D002097:C-Reactive Protein