Accelerated atherogenesis in autoimmune rheumatic diseases

The observation that systemic inflammatory rheumatic diseases such as rheumatoid arthritis (RA) are associated with a significantly increased rate of cardiovascular disease, which often occurs at a younger age than in the normal population, is particularly important given the increasing interest in...

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Bibliographic Details
Published in:Autoimmunity reviews 2002-12, Vol.1 (6), p.338-347
Main Authors: Bacon, P.A, Stevens, R.J, Carruthers, D.M, Young, S.P, Kitas, G.D
Format: Article
Language:English
Subjects:
Arteriosclerosis - etiology
Arthritis, Rheumatoid - complications
Atherosclerosis
Autoimmune Diseases - complications
C-Reactive Protein - physiology
Cardiovascular disease
Endothelium, Vascular - physiopathology
Heart Diseases - etiology
Humans
Immunosuppression
Inflammation
Inflammation - etiology
Lupus Erythematosus, Systemic - complications
Models, Cardiovascular
Rheumatic Diseases - complications
Rheumatoid arthritis
Sphingolipids - physiology
Tumor Necrosis Factor-alpha - physiology
Vasculitis
Vasculitis - etiology
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Summary:The observation that systemic inflammatory rheumatic diseases such as rheumatoid arthritis (RA) are associated with a significantly increased rate of cardiovascular disease, which often occurs at a younger age than in the normal population, is particularly important given the increasing interest in the role of inflammation in atherogenesis in the general population. This review examines the accumulating evidence for accelerated atherogenesis of RA and updates the hypothesis that vasculitis plays a major role in this. Endothelial dysfunction (ECD), widely regarded as initial lesion in atherogenesis, has been shown to occur commonly in primary vasculitis. This ECD is a diffuse event, demonstrable in more than one vascular bed. It is not simply due to scarring in the vessel wall, related to the focal inflammation of the underlying vasculitis, since it may be reversed by suppression of the immune inflammation. However, the mechanisms for this ECD differ from that of the primary vasculitis. Preliminary evidence suggests that inflammatory mediators such as CRP, TNF, or sphingolipids may be involved. The diffuse ECD of vasculitis may have important consequences for both the progression of the primary disease and for cardiovascular events. A model for the role of vasculitis-induced ECD in the accelerated atherogenesis of rheumatic diseases is presented. These concepts are discussed together with the messages they suggest for ‘idiopathic’ atherosclerosis in the general population.
ISSN:1568-9972
1568-9972
DOI:10.1016/S1568-9972(02)00100-3