Pagnoux Christian, Chironi Gilles, Simon Alain, Guillevin Loïc
Department of Internal Medicine, French National Referral Center for Necrotizing Vasculitides and Systemic Sclerodermas, Hôpital Cochin, Université Paris 5-René Descartes, Paris, France.
Ann N Y Acad Sci. 2007 Jun;1107:11-21. doi: 10.1196/annals.1381.002.
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.
目前人们普遍认为，动脉粥样硬化相当程度上或者也可以说是一种炎症性疾病，事实上，血管炎的定义是血管壁存在炎症浸润，尽管最初炎症浸润的主要细胞群不同，且发生在不同管径的动脉中。与其他慢性全身性炎症性疾病一样，在过去5至10年中，过早和加速的动脉粥样硬化已成为血管炎的一个重要方面，与心血管疾病的其他危险因素无关，显然也与皮质类固醇无关。慢性全身性炎症，就像持续活跃的血管炎一样，可能通过C反应蛋白（CRP）、一些黏附分子和/或细胞因子的作用，以及局部炎症，可能通过局部分泌的肿瘤坏死因子-α和/或基质金属蛋白酶的上调以及氧化应激，在早期动脉粥样硬化中发挥作用。血管炎患者还存在内皮细胞功能障碍和动脉僵硬度增加的情况。值得注意的是，一些血管炎治疗能够逆转其中一些内皮细胞异常。与抗中性粒细胞胞浆抗体（ANCA）不同，ANCA未显示与动脉粥样硬化或心血管事件的较高风险相关，针对内皮细胞、热休克蛋白或氧化型低密度脂蛋白的自身抗体也可能与之有关，尽管现在认为后者具有抗动脉粥样硬化作用。可能还有其他尚未确定的促进动脉粥样硬化的因素在血管炎中发挥更重要的作用。在其确切身份被确定之前，每次有必要且有可能时，考虑并治疗其他众所周知的心血管危险因素仍然很重要。
