Department of Pathology, Microbiology and Immunology, Vanderbilt University.
Department of Medicine, Division of Rheumatology and Immunology, Vanderbilt Medical Center.
Curr Opin Rheumatol. 2021 Mar 1;33(2):211-218. doi: 10.1097/BOR.0000000000000773.
Accelerated atherosclerosis is a significant comorbidity and the leading cause of death for patients with systemic lupus erythematosus (SLE). It is now apparent that SLE-accelerated atherosclerosis is not driven solely by traditional cardiovascular risk factors, adding complexity to disease characterization and mechanistic understanding. In this review, we will summarize new insights into SLE-accelerated atherosclerosis evaluation, treatment, and mechanism.
Recent work highlights the need to incorporate inflammatory biomarkers into cardiovascular disease (CVD) risk assessments. This is especially true for SLE patients, in which mechanisms of immune dysfunction likely drive CVD progression. There is new evidence that commonly prescribed SLE therapeutics hinder atherosclerosis development. This effect is achieved both by reducing SLE-associated inflammation and by directly improving measures of atherosclerosis, emphasizing the interconnected mechanisms of the two conditions.
SLE-accelerated atherosclerosis is most likely the consequence of chronic autoimmune inflammation. Therefore, diligent management of atherosclerosis requires assessment of SLE disease activity as well as traditional cardiovascular risk factors. This supports why many of the therapeutics classically used to control SLE also modulate atherosclerosis development. Greater understanding of the mechanisms underlying this condition will allow for the development of more targeted therapeutics and improved outcomes for SLE patients.
加速的动脉粥样硬化是系统性红斑狼疮（SLE）患者的一种严重合并症，也是其主要死亡原因。现在很明显，SLE 加速的动脉粥样硬化不仅仅是由传统的心血管危险因素驱动的，这增加了疾病特征和机制理解的复杂性。在这篇综述中，我们将总结 SLE 加速的动脉粥样硬化评估、治疗和机制的新见解。
最近的研究强调需要将炎症生物标志物纳入心血管疾病（CVD）风险评估中。对于 SLE 患者来说尤其如此，因为免疫功能障碍的机制可能会导致 CVD 进展。有新的证据表明，常用的 SLE 治疗药物会阻碍动脉粥样硬化的发展。这种效果既可以通过减少与 SLE 相关的炎症来实现，也可以通过直接改善动脉粥样硬化的指标来实现，强调了这两种疾病的相互关联的机制。
SLE 加速的动脉粥样硬化很可能是慢性自身免疫炎症的结果。因此，对动脉粥样硬化的精心管理需要评估 SLE 疾病活动以及传统的心血管危险因素。这也解释了为什么许多经典的用于控制 SLE 的治疗药物也能调节动脉粥样硬化的发展。对这种情况的机制有更深入的了解将允许开发更有针对性的治疗方法，并改善 SLE 患者的预后。
