Atherosclerosis in ANCA‐Associated Vasculitides

 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‐α 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 .