RT Journal Article SR Electronic T1 Risk Factors for Clinical Coronary Heart Disease in Systemic Lupus Erythematosus: The Lupus and Atherosclerosis Evaluation of Risk (LASER) Study JF The Journal of Rheumatology JO J Rheumatol FD The Journal of Rheumatology SP 322 OP 329 DO 10.3899/jrheum.090306 VO 37 IS 2 A1 SAHENA HAQUE A1 CAROLINE GORDON A1 DAVID ISENBERG A1 ANISUR RAHMAN A1 PETER LANYON A1 AUBREY BELL A1 PAUL EMERY A1 NEIL McHUGH A1 LEE SUAN TEH A1 DAVID G.I. SCOTT A1 MOHAMED AKIL A1 SOPHIA NAZ A1 JACQUELINE ANDREWS A1 BRIDGET GRIFFITHS A1 HELEN HARRIS A1 HAZEM YOUSSEF A1 JOHN McLAREN A1 VERONICA TOESCU A1 VINODH DEVAKUMAR A1 JAMAL TEIR A1 IAN N. BRUCE YR 2010 UL http://www.jrheum.org/content/37/2/322.abstract AB Objective. Accelerated atherosclerosis and premature coronary heart disease (CHD) are recognized complications of systemic lupus erythematosus (SLE), but the exact etiology remains unclear and is likely to be multifactorial. We hypothesized that SLE patients with CHD have increased exposure to traditional risk factors as well as differing disease phenotype and therapy-related factors compared to SLE patients free of CHD. Our aim was to examine risk factors for development of clinical CHD in SLE in the clinical setting. Methods. In a UK-wide multicenter retrospective case-control study we recruited 53 SLE patients with verified clinical CHD (myocardial infarction or angina pectoris) and 96 SLE patients without clinical CHD. Controls were recruited from the same center as the case and matched by disease duration. Charts were reviewed up to time of event for cases, or the same “dummy-date” in controls. Results. SLE patients with clinical CHD were older at the time of event [mean (SD) 53 (10) vs 42 (10) yrs; p < 0.001], more likely to be male [11 (20%) vs 3 (7%); p < 0.001], and had more exposure to all classic CHD risk factors compared to SLE patients without clinical CHD. They were also more likely to have been treated with corticosteroids (OR 2.46; 95% CI 1.03, 5.88) and azathioprine (OR 2.33; 95% CI 1.16, 4.67) and to have evidence of damage on the pre-event SLICC damage index (SDI) (OR 2.20; 95% CI 1.09, 4.44). There was no difference between groups with regard to clinical organ involvement or autoantibody profile. Conclusion. Our study highlights the need for clinical vigilance to identify modifiable risk factors in the clinical setting and in particular with male patients. The pattern of organ involvement did not differ in SLE patients with CHD events. However, the higher pre-event SDI, azathioprine exposure, and pattern of damage items (disease-related rather than therapy-related) in cases suggests that a persistent active lupus phenotype contributes to CHD risk. In this regard, corticosteroids and azathioprine may not control disease well enough to prevent CHD. Clinical trials are needed to determine whether classic risk factor modification will have a role in primary prevention of CHD in SLE patients and whether new therapies that control disease activity can better reduce CHD risk.