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Atherosclerosis and systemic lupus erythematosus
M Urowitz1, D Gladman, I Bruce
1University of Toronto, Director Centre of Prognosis Studies in The Rheumatic Diseases and The University of Toronto Lupus Clinic, The Toronto Hospital, Western Division, 399 Bathurst Street, 1-318, Toronto, Ontario, M5T 2S8, Canada. urowitz@utoronto.ca
Insights
Systemic lupus erythematosus (SLE) accelerates atherosclerosis, increasing cardiovascular risks like heart attack in young women. Understanding these mechanisms may enable earlier diagnosis and prevention strategies.
Area of Science:
- Rheumatology
- Cardiology
- Immunology
Background:
- Systemic lupus erythematosus (SLE) is associated with increased mortality and morbidity.
- Accelerated atherosclerosis is a significant clinical manifestation in SLE patients.
- Cardiovascular events like myocardial infarction are observed in young SLE patients.
Purpose of the Study:
- To investigate the mechanisms behind accelerated atherosclerosis in SLE.
- To identify risk factors contributing to cardiovascular disease in SLE.
- To explore potential preventive strategies for atherosclerosis in SLE.
Main Methods:
- Clinical observation of cardiovascular events in SLE patients.
- Postmortem examination findings related to atherosclerosis.
- Analysis of contributing factors including disease activity, anticardiolipin syndrome, and corticosteroid use.
Main Results:
- Accelerated atherosclerosis is a recognized complication in SLE, seen both clinically and pathologically.
- Disease activity, anticardiolipin syndrome, and corticosteroid-induced hyperlipidemia are implicated in its development.
- SLE may act as an independent risk factor for atherosclerosis.
Conclusions:
- The precise mechanisms of accelerated atherosclerosis in SLE require further elucidation.
- Antimalarials show potential in mitigating corticosteroid-induced hyperlipidemia.
- Accumulating evidence of subclinical atherosclerosis supports earlier diagnosis and intervention in SLE patients.
Abstract:
The description of late-stage mortality and morbidity has been an important contribution to the understanding of systemic lupus erythematosus (SLE) in the past decade. Among the major factors in this clinical spectrum of SLE is the development of accelerated atherosclerosis. This condition has been recognized clinically with the documentation of myocardial infarction and angina in young women with SLE. This accelerated atherosclerosis has also been recognized at postmortem examinations. The exact mechanism for accelerated atherosclerosis remains unclear. However, disease activity with its immunologic events, the anticardiolipin syndrome, and the effect of corticosteroids in promoting hyperlipidemia contribute to its development. It appears that SLE may be a risk factor, in addition to the usual risk factors for the development of atherosclerosis. It has recently been shown that antimalarials may prevent some of the hyperlipidemia caused by corticosteroids. As evidence for the presence of subclinical atherosclerosis in these patients is accumulating, earlier diagnosis and treatment of events may be possible, and preventive measures may be instituted earlier.