Kaplan Mariana J
Division of Rheumatology, Department of Internal Medicine, University of Michigan Medical School, University of Michigan Health System, Ann Arbor 48109-5680, USA.
Transl Res. 2009 Aug;154(2):61-9. doi: 10.1016/j.trsl.2009.05.005. Epub 2009 Jun 17.
Systemic lupus erythematosus (SLE) is associated with an increase in the risk of premature cardiovascular complications caused by accelerated atherosclerosis, which significantly contributes to morbidity and mortality. Standard Framingham risk factors seem to be less important predictors of cardiovascular events than the presence of active SLE, and the immune dysregulation characteristic of lupus seems to play a dominant role in atherogenesis. Although both SLE-specific and nonspecific mechanisms have been proposed to play a prominent role in the induction of premature vascular damage in this disease, the exact etiology remains unclear. This review summarizes some of the proposed mechanisms that may promote accelerated vascular damage in lupus and explores potential targets for cardiovascular risk prevention in this patient population.
系统性红斑狼疮（SLE）与因动脉粥样硬化加速导致的心血管并发症风险增加相关，这对发病率和死亡率有显著影响。与活动性SLE的存在相比，标准的弗明汉姆风险因素似乎不是心血管事件的重要预测指标，狼疮特有的免疫失调特征似乎在动脉粥样硬化形成中起主导作用。尽管有人提出SLE特异性和非特异性机制在该疾病过早血管损伤的诱导中都起重要作用，但确切病因仍不清楚。本综述总结了一些可能促进狼疮中血管损伤加速的机制，并探讨了该患者群体心血管风险预防的潜在靶点。
