Observational cohort studies in SLE have led to the description of accelera
ted atherosclerosis as an important cause of mortality and morbidity in thi
s disease. The clinical observation of coronary artery disease occurring in
premenopausal females with SLE gave rise to the concept of the bimodal mor
tality pattern. This pattern was confirmed in autopsy and epidemiological s
tudies. These studies identified hypercholesterolemia and particularly its
persistence in the first three years of disease, hypertension, and lupus it
self as important risk factors for the development of accelerated atheroscl
erosis in these patients. It also became evident that corticosteroid therap
y plays an important role in the elevation of plasma lipids while antimalar
ials resulted in a reduction of plasma cholesterol, LDL, and VLDL, especial
ly in steroid-induced hyperlipidemia. Studies of clinical outcomes for athe
rosclerotic disease (angina, myocardial infarction) have shown a prevalence
of 6-12% in a number of SLE cohorts. However, more sensitive investigation
s including myocardial perfusion imaging and carotid ultrasound have demons
trated a prevalence of atherosclerotic disease in 40% of patients studied.
Further studies of SLE disease process, including immunological factors, ma
y more clearly define the pathogenesis of accelerated atherosclerosis in pa
tients with SLE, and may help elucidate mechanisms of atherosclerosis in th
e general population.