Risk factors for clinical coronary heart disease in systemic lupus erythematosus: the lupus and atherosclerosis evaluation of risk (LASER) study.
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.


CONCLUSIONS
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.
Haque
Sahena
S
arc Epidemiology Unit, School of Translational Medicine, University of Manchester, Manchester, UK.
Gordon
Caroline
C
Isenberg
David
D
Rahman
Anisur
A
Lanyon
Peter
P
Bell
Aubrey
A
Emery
Paul
P
McHugh
Neil
N
Teh
Lee Suan
LS
Scott
David G I
DG
Akil
Mohamed
M
Naz
Sophia
S
Andrews
Jacqueline
J
Griffiths
Bridget
B
Harris
Helen
H
Youssef
Hazem
H
McLaren
John
J
Toescu
Veronica
V
Devakumar
Vinodh
V
Teir
Jamal
J
Bruce
Ian N
IN
D000328:Adult; D000367:Age Factors; D050197:Atherosclerosis / Q000209:etiology*; D001794:Blood Pressure; D016022:Case-Control Studies; D003327:Coronary Disease / Q000209:etiology*; D005260:Female; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000150:complications*; D008297:Male; D008875:Middle Aged; D018579:Patient Selection; D012189:Retrospective Studies; D018570:Risk Assessment; D012307:Risk Factors; D012720:Severity of Illness Index; D012737:Sex Factors