It is currently accepted that
atherosclerosis is rather, or also, an inflammatory disease and, indeed,
vasculitis is defined by inflammatory infiltrates in blood vessel walls, albeit initially by different predominant cell populations and in arteries of different calibers. As for other chronic systemic inflammatory diseases, premature and accelerated
atherosclerosis has emerged during the last 5-10 years as an important facet of
vasculitides, independently of the other risk factors of
cardiovascular disease and also, apparently,
corticosteroids. Chronic systemic
inflammation, like persistently active
vasculitis, might play a role in early
atherosclerosis, through the actions of
C-reactive protein (CRP), some adhesion molecules, and/or
cytokines, as well as local
inflammation, perhaps through locally secreted
TNF-alpha and/or upregulation of
matrix metalloproteinases and oxidative stress. Endothelial cell dysfunction and increased arterial stiffness have also been found in
vasculitis patients. Notably, some
vasculitis treatments were able to reverse some of these endothelial cell anomalies. Unlike antineutrophil cytoplasm
autoantibodies (
ANCA), which were not shown to correlate with a higher risk of
atherosclerosis or cardiovascular events,
autoantibodies to endothelial cells,
heat-shock proteins, or
oxidized-LDL may also be implicated, although these latter are now thought to protect against
atherosclerosis. It is likely that other, as yet unidentified, factors facilitating
atherosclerosis may play more important roles in
vasculitides. Until their precise identification, it remains important to take into consideration and treat, every time it is necessary and possible, the other well-known cardiovascular risk factors.