Department of Obstetrics and Gynecology, Virginia Commonwealth University, Richmond, Virginia.
Jacobi Medical Center, Department of Internal Medicine, Albert Einstein College of Medicine, Bronx, New York.
Am J Physiol Heart Circ Physiol. 2021 May 1;320(5):H2011-H2030. doi: 10.1152/ajpheart.01005.2020. Epub 2021 Apr 2.
Preeclampsia is a worldwide pregnancy complication with serious short- and long-term maternal and neonatal consequences. Our understanding of preeclampsia pathophysiology has significantly evolved over the last decades with the recognition that impaired arterial function and structure may occur early in the course of pregnancy, preceding the clinic-humoral syndrome and driving long-term cardiovascular disease risk in the future of these patients. Although an early abnormal placentation may be the inciting event for a large proportion of cases, there is growing evidence that challenges the placental hypothesis in all affected women, since placental histopathology lesions thought to be characteristic are neither sensitive nor specific markers for the disorder. Recent hemodynamic investigations and studies on left ventricular function and structure in women with preeclampsia further challenge this universal paradigm and propose that placental dysfunction could be secondary to a maternal cardiovascular maladaptation to pregnancy in certain patients. Supporting this hypothesis, certain vascular features, which are characteristically enhanced in normal pregnancy allowing a healthy vascular adaptation, are absent in preeclampsia and comparable to the nonpregnant population. However, arterial biomechanics in preeclampsia may only not cope with hemodynamic demands of pregnancy but also impose additional detrimental loads to the maternal heart ("impaired left-ventricle-aorta coupling") and transmit pressure and flow disturbances into the fetoplacental circulation ("impaired large arteries-microcirculation coupling"). In this review, we analyze the major role of the arterial dysfunction in the cardiovascular maladaptation hypothesis of preeclampsia, shed light on its potential etiopathogenic link, and discuss the complementary nature of the placental and cardiovascular theories.
子痫前期是一种全球性的妊娠并发症，对母婴的短期和长期健康都有严重影响。近几十年来，我们对子痫前期病理生理学的认识有了显著的发展，认识到动脉功能和结构的损伤可能在妊娠早期就已经发生，早于临床-体液综合征，并在未来导致这些患者的心血管疾病风险增加。尽管早期异常胎盘可能是大多数病例的触发事件，但越来越多的证据挑战了所有受影响女性的胎盘假说，因为被认为是特征性的胎盘组织病理学损伤既不是该疾病的敏感也不是特异性标志物。最近对子痫前期女性的血液动力学研究以及左心室功能和结构的研究进一步挑战了这一普遍观点，并提出胎盘功能障碍可能是某些患者对妊娠的母体心血管适应性不良的继发表现。支持这一假说，某些血管特征在正常妊娠中得到增强，有利于健康的血管适应，但在子痫前期中缺失，与非妊娠人群相当。然而，子痫前期的动脉生物力学不仅不能满足妊娠的血液动力学需求，而且还会给母体心脏带来额外的有害负荷（“左心室-主动脉耦合受损”），并将压力和流量紊乱传递到胎儿胎盘循环中（“大动脉-微循环耦合受损”）。在这篇综述中，我们分析了动脉功能障碍在子痫前期心血管适应性不良假说中的主要作用，阐明了其潜在的发病机制联系，并讨论了胎盘和心血管理论的互补性。
