Reyes-Lagos José Javier, Abarca-Castro Eric Alonso
Autonomous University of the State of Mexico (UAEMex), School of Medicine, Toluca, State of Mexico, Mexico.
Autonomous University of the State of Mexico (UAEMex), Multidisciplinary Research Center in Education (CIME), Toluca, State of Mexico, Mexico.
Clin Hypertens. 2021 Dec 15;27(1):24. doi: 10.1186/s40885-021-00182-2.
Preeclampsia is a pregnancy-specific condition which gets detected through hypertension and excessive protein excretion in urine. While preeclampsia used to be regarded as a self-limiting maternal condition which resolved with the delivery of the placenta, it is nowadays considered a complex and multifactorial disease that affects the offspring. Unfortunately, the etiology and pathophysiology of this multifaceted disorder remain elusive. Recent findings have confirmed that an altered maternal autonomic function may play a vital role in developing preeclampsia in conjunction with an imbalanced maternal immune system. Additionally, further evidence supports the crucial role of an exacerbated immune response driven by a non-infectious trigger during preeclampsia. Therefore, as a sterile inflammation, the elucidation of the neuroinflammatory mechanisms of preeclampsia warrants obtaining relevant knowledge suitable for translational clinical applications.Heart rate variability (HRV) is an affordable and non-invasive method for indirectly assessing the autonomic nervous system and the cholinergic anti-inflammatory pathway (CAP). Notably, the nonlinear analysis of HRV offers novel indexes to explore the neuroimmune interactions in diverse preclinical and clinical settings of inflammation. Given that the dynamics of HRV is nonlinear in health, we hypothesized that a neuroinflammatory condition in preeclampsia might be associated with changes in nonlinear features of maternal and fetal HRV. Thus, the present review aims to present evidence of the potential changes in maternal-fetal HRV associated with neuroinflammatory modifications in preeclamptic women. We considered that there is still a need for assessing the nonlinear features of maternal and fetal HRV as complementary biomarkers of inflammation in this population in future studies, being a potential route for translational clinical applications.
子痫前期是一种妊娠特有的疾病，可通过高血压和尿中蛋白质排泄过多来检测。虽然子痫前期曾被认为是一种自限性的母体疾病，随着胎盘娩出而缓解，但如今它被视为一种影响后代的复杂多因素疾病。不幸的是，这种多方面疾病的病因和病理生理学仍然难以捉摸。最近的研究结果证实，母体自主神经功能改变可能与母体免疫系统失衡共同在子痫前期的发生中起关键作用。此外，更多证据支持了子痫前期期间由非感染性触发因素驱动的免疫反应加剧所起的关键作用。因此，作为一种无菌性炎症，阐明子痫前期的神经炎症机制值得获取适用于转化临床应用的相关知识。心率变异性（HRV）是一种经济实惠且非侵入性的方法，用于间接评估自主神经系统和胆碱能抗炎途径（CAP）。值得注意的是，HRV的非线性分析提供了新的指标，以探索在各种临床前和临床炎症环境中的神经免疫相互作用。鉴于健康状态下HRV的动态是非线性的，我们假设子痫前期的神经炎症状态可能与母体和胎儿HRV的非线性特征变化有关。因此，本综述旨在展示子痫前期女性中与神经炎症改变相关的母胎HRV潜在变化的证据。我们认为，在未来的研究中，仍有必要评估母体和胎儿HRV的非线性特征，作为该人群炎症的补充生物标志物，这是转化临床应用的一条潜在途径。
