Challenges in understanding the role of pregnancy morbidity in cardiovascular risk in SLE.
Challenges in understanding the role of pregnancy morbidity in cardiovascular risk in SLE.
复制标题
了解妊娠发病率在 SLE 心血管风险中的作用面临的挑战。
DOI：
10.1136/lupus-2014-000035
复制
发表时间：
2014
影响因子：
3.9
通讯作者：
Yazdany,Jinoos
中科院分区：
文献类型：
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作者：
Simard,JuliaF;Yazdany,Jinoos
心血管疾病（CVD）是系统性红斑狼疮（SLE）发病和死亡的主要原因。尽管在这一领域进行了广泛和持续的研究，但很少有风险因素，包括吸烟和高血压等传统风险因素，能解释很大比例的风险。有大量的科学文献表明，子痫前期后心血管危险因素如内皮功能障碍、高血压和动脉僵硬增加的患病率增加，代谢综合征和心血管疾病的未来风险也增加。2考虑到大多数SLE患者为育龄女性，且SLE患者有早期CVD发病率的报道，研究先兆子痫（及其他妊娠并发症）与随后CVD风险之间的关系对SLE具有重要意义。为此，研究人员利用129名患有系统性狼疮的妇女的横断面数据，探讨了妊娠并发症与随后的心血管疾病之间的联系。尽管他们提出了明确的问题和临床意义，但研究设计和现有数据只是暗示了一个答案。虽然与一般人群相比，狼疮妊娠的并发症如先兆子痫更为常见，但这些并发症仍然相对罕见。再加上一种相对罕见的疾病（SLE），该研究缺乏得出明确结论的统计能力，也不能完全解释潜在的混杂因素。然而，作者应该为他们所做的患者数量的积累而受到赞扬。这项工作应该被视为探索性的，为更明确的研究奠定了科学基础，可以揭示SLE、妊娠发病率和随后的心血管疾病风险之间的关系。妊娠是否作为一种血管应激测试，揭示了内皮细胞对损伤的易感性，表现为子痫前期，或者子痫前期本身是否会导致损伤，导致未来的心血管疾病，这些都是未知的。妊娠并发症是否应该提醒照顾SLE女性的临床医生注意随后的心血管疾病风险，是否需要更积极的危险因素修改？先兆子痫应该被视为“心脏压力测试失败”吗？最后，SLE和先兆子痫是否会显著增加CVD的风险，比单独存在任何一个风险因素都要高？Lin和Ramsey-Goldman等人的讨论很自然地回避了这些问题。为了在这项工作的基础上建立和评估这些问题，在未来的研究中将需要考虑到一些设计、数据收集和分析方面的考虑。单独检查不同的妊娠并发症是有意义的，因为先兆子痫可能会带来不同的风险，而不是像婴儿出生体重低这样的结果。此外，更充分地探索与SLE诊断相关的先兆子痫时间将是有趣的，因为在怀孕期间出现这两种情况可能会带来更高的风险。值得注意的是，在Lin和Ramsey-Goldman的研究中，大多数患者（三分之二）在诊断为SLE之前经历过先兆子痫。目前尚不清楚从怀孕到心血管疾病评估和危险因素修改之间需要多长时间，以及是否存在其他可修改的危险因素应该改变目前的筛查和治疗方法。此外，了解多胎妊娠和多胎妊娠如何影响这些关系将是很有趣的。
Cardiovascular disease (CVD) is a leading cause of morbidity and mortality in systemic lupus erythematosus (SLE). 1 Despite extensive and ongoing research in this area, few risk factors, including traditional ones such as smoking and hypertension, explain a significant proportion of the risk. There is a robust scientific literature showing that the prevalence of cardiovascular risk factors such as endothelial dysfunction, hypertension and increased arterial stiffness increase after preeclampsia, as do future risks of metabolic syndrome and CVD. 2 Given that a majority of patients with SLE are women of reproductive age and the reported early CVD morbidity in women with SLE, investigating the relationship between pre-eclampsia (and other pregnancy complications) and subsequent CVD risk is of great interest in SLE. To that end, investigators explored the link between pregnancy complications and subsequent CVD using cross-sectional data from 129 women with systemic lupus in this issue. 3 Despite their clear question and the clinical significance, the study design and available data only hint at an answer. Although complications such as pre-eclampsia have been shown to be more common in SLE pregnancies compared with the general population, these are still relatively rare complications. Coupled together with a relatively uncommon disease (SLE), the study lacks the statistical power to make definitive conclusions and cannot fully account for potential confounders. However, the authors should be commended for accumulating the number of patients they did. This work should be viewed as exploratory, building a scientific foundation for more definitive studies that can unravel the relationship between SLE, pregnancy morbidity and subsequent CVD risk. Whether pregnancy acts as a vascular stress test that unmasks endothelial vulnerability to injury that manifests as pre-eclampsia, or whether pre-eclampsia itself causes damage that is responsible for future CVD is unknown.Should pregnancy complications alert clinicians caring for women with SLE about subsequent CVD risks necessitating more aggressive risk factor modification? Should pre-eclampsia be viewed as a ‘failed cardiac stress test’? And lastly, does the presence of SLE and preeclampsia together substantially increase CVD risk, greater than would be expected with either risk factor alone? Lin and Ramsey-Goldman et al’s discussion naturally begs each of these questions. To build upon the foundation of this work and assess these issues, some design, data collection and analytical considerations will need to be accounted for in future studies. It would be of interest to examine different pregnancy complications separately, since pre-eclampsia may confer a different risk than outcomes such as having an infant with low birth weight. Also, more fully exploring the timing of pre-eclampsia in relation to SLE diagnosis would be of interest, since presence of both conditions during pregnancy might confer a higher risk. It is important to note that the majority of patients (two-thirds) in Lin and Ramsey-Goldman’s study experienced pre-eclampsia before a diagnosis of SLE. It remains unclear how much time between pregnancy and CVD assessment and risk factor modification is needed, and whether the presence of other modifiable risk factors should change current screening and treatment practices. In addition, it would be interesting to understand how multiple pregnancies and multiple gestations influence these relationships.