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. The), 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 or-an 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 pi-c-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. (First Release Dec 1 2009: J Rheumatol 2010:37:322-9; doi: 10.3899/jrheum.090306)