Department of Health and Human Physiology, The University of Iowa, Iowa City, Iowa, USA.
Compr Physiol. 2024 Oct 9;14(4):5703-5727. doi: 10.1002/cphy.c240003.
Preeclampsia, a pregnancy disorder characterized by de novo hypertension and maternal multisystem organ dysfunction, is the leading cause of maternal mortality worldwide and is associated with a fourfold greater risk of cardiovascular disease throughout the lifespan. Current understanding of the etiology of preeclampsia remains unclear, due in part to the varying phenotypical presentations of the disease, which has hindered the development of effective and mechanism-specific treatment or prevention strategies both during and after the affected pregnancy. These maternal sequelae of preeclampsia are symptoms of systemic vascular dysfunction in the maternal nonreproductive microvascular beds that drives the development and progression of adverse cardiovascular outcomes during preeclampsia. Despite normalization of vascular disturbances after delivery, subclinical dysfunction persists in the nonreproductive microvascular beds, contributing to an increased lifetime risk of cardiovascular and metabolic diseases and all-cause mortality. Given that women with a history of preeclampsia demonstrate vascular dysfunction despite an absence of traditional CVD risk factors, an understanding of the underlying mechanisms of microvascular dysfunction during and after preeclampsia is essential to identify potential therapeutic avenues to mitigate or reverse the development of overt disease. This article aims to provide a summary of the existing literature on the pathophysiology of maternal microvascular dysfunction during preeclampsia, the mechanisms underlying the residual dysfunction that remains after delivery, and current and potential treatments both during and after the affected pregnancy that may reduce microvascular dysfunction in these high-risk women. © 2024 American Physiological Society. Compr Physiol 14:5703-5727, 2024.
子痫前期是一种妊娠疾病,其特征为新发高血压和母体多系统器官功能障碍,是全球范围内导致产妇死亡的主要原因,并且与整个生命周期中心血管疾病的风险增加四倍相关。由于疾病的表型表现各异,子痫前期的病因学目前仍不明确,这阻碍了在受影响的妊娠期间和之后开发有效且针对特定机制的治疗或预防策略。这些子痫前期的母体后遗症是母体非生殖性微血管床全身血管功能障碍的症状,推动了子痫前期期间和之后不良心血管结局的发展和进展。尽管分娩后血管紊乱正常化,但非生殖性微血管床中的亚临床功能障碍持续存在,导致心血管和代谢疾病以及全因死亡率的终生风险增加。鉴于有子痫前期病史的女性尽管不存在传统的 CVD 风险因素,但仍表现出血管功能障碍,因此了解子痫前期期间和之后微血管功能障碍的潜在机制对于确定潜在的治疗途径以减轻或逆转显性疾病的发展至关重要。本文旨在总结子痫前期期间母体微血管功能障碍的病理生理学、分娩后仍然存在的残留功能障碍的潜在机制以及目前和潜在的治疗方法,这些治疗方法可以减轻这些高危女性的微血管功能障碍。2024 年美国生理学会。综合生理学 14:5703-5727, 2024.