Placental delayed villous maturation is associated with fetal congenital heart disease.
Placental delayed villous maturation is associated with fetal congenital heart disease.
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DOI：
10.1016/j.ajog.2022.08.013
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发表时间：
2023-02
影响因子：
9.8
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中科院分区：
文献类型：
--
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胎盘对胎儿的整体发育和终身健康至关重要。妊娠合并胎儿先天性心脏病时胎盘发育和功能异常。然而，缺乏使用标准化诊断标准并纳入对照人群的研究。这限制了目前研究的普遍性和确定与先天性心脏病相关的特定胎盘异常的能力。应用共识声明指南（称为阿姆斯特丹标准）进行胎盘病理学解释，以比较胎儿先天性心脏病妊娠与人口统计学匹配的对照妊娠的异常频率和模式，并通过心脏生理学评价胎盘异常的差异。2013年1月至2019年6月进行了一项单中心回顾性队列研究。纳入妊娠≥37周出生的产前诊断为中重度先天性心脏病的婴儿。对照组出生时≥37周，但没有胎儿先天性心脏病或其他主要妊娠并发症，与先天性心脏病组的母亲种族和种族以及婴儿性别相匹配。使用阿姆斯特丹标准，胎盘病理学结果被分类为绒毛成熟延迟，母体血管灌注不良，胎儿血管灌注不良和炎性病变。比较各组间胎盘异常的发生率，并进行逻辑回归分析，以评估临床和社会人口统计学因素与绒毛成熟延迟、母体血管灌注不良和胎儿血管灌注不良的相关性。有194例患有胎儿先天性心脏病的妊娠和105例对照，其中83%的先天性心脏病组和82%的对照组为非西班牙裔高加索人种和种族。与对照组相比，患有胎儿先天性心脏病的孕妇有较高的绒毛延迟成熟率（6%对19%，p < 0.001）和母体血管灌注不良率（19%对34%，p = 0.007），但胎儿血管灌注不良率（6%对10%，p = 0.23）则无此差异。与对照组相比，先天性心脏病双心室婴儿的绒毛成熟延迟的几率最高（比值比5.5，95%置信区间2.2 - 15.7，p < 0.01）。双心室解剖婴儿的母体血管灌注不良高2.2倍（p = 0.02），单心室生理学伴肺阻塞婴儿的母体血管灌注不良高2.9倍（p = 0.02）。在先天性心脏病组中，延迟的绒毛成熟与较高的母体体重指数、羊水过多、较大的婴儿出生头围和分娩室中的婴儿呼吸支持相关，而母体血管灌注不良与羊水过少相关。在校正心脏诊断的多变量模型中，延迟绒毛成熟与婴儿出生头围（比值比1.2，95%置信区间1.0 - 1.5，p = 0.02）和产房婴儿呼吸支持（比值比3.0，95%置信区间1.3 - 6.5，p = 0.007）的相关性持续存在。与对照组相比，患有胎儿先天性心脏病的孕妇显示出较高的绒毛延迟成熟率和母体血管灌注不良率，这表明胎盘发育不良可能与母体因素有关。需要进一步的研究来确定这些异常与出生后婴儿结局的关系。与人口统计学匹配的对照组相比，胎盘绒毛成熟延迟和母体血管灌注不良在患有胎儿先天性心脏病的妊娠中更常见。
The placenta is critical for the overall development and life-long health of the fetus. Abnormal placental development and function occur in pregnancies with fetal congenital heart disease. However, studies that utilize standardized diagnostic criteria and incorporate control populations are lacking. This limits generalizability of current research and the ability to determine the specific placental abnormalities associated with congenital heart disease. Apply consensus statement guidelines (known as the Amsterdam Criteria) for placental pathology interpretation to compare the frequency and pattern of abnormalities in pregnancies with fetal congenital heart disease to demographically matched control pregnancies and evaluate for differences in placental abnormalities by cardiac physiology. A single-center retrospective cohort study was conducted from January 2013-June 2019. Infants with a prenatal diagnosis of moderate-severe congenital heart disease who were born at ≥37 weeks’ gestation were included. A control group born at ≥37 weeks’ but without fetal congenital heart disease or other major pregnancy complications was matched to the congenital heart disease group on maternal race and ethnicity and infant sex. Using the Amsterdam Criteria, placental pathology findings were categorized as delayed villous maturation, maternal vascular malperfusion, fetal vascular malperfusion, and inflammatory lesions. Frequency of placental abnormalities were compared between groups and logistic regression was performed to evaluate the association of clinical and sociodemographic factors with delayed villous maturation, maternal vascular malperfusion, and fetal vascular malperfusion. There were 194 pregnancies with fetal congenital heart disease and 105 controls included, of whom 83% in the congenital heart disease group and 82% in the control group were of non-Hispanic Caucasian race and ethnicity. Compared to controls, pregnancies with fetal congenital heart disease had higher rates of delayed villous maturation (6% vs 19%, p < 0.001) and maternal vascular malperfusion (19% vs 34%, p = 0.007), but not fetal vascular malperfusion (6% vs 10%, p = 0.23). Congenital heart disease infants with two-ventricle anatomy displayed the highest odds of delayed villous maturation compared to controls (odds ratio 5.5, 95% confidence interval 2.2 – 15.7, p < 0.01]. Maternal vascular malperfusion was 2.2 times higher (p = 0.02) for infants with two ventricle anatomy and 2.9 times higher (p = 0.02) for infants with single ventricle physiology with pulmonary obstruction. Within the congenital heart disease group, delayed villous maturation was associated with higher maternal body mass index, polyhydramnios, larger infant birth head circumference, and infant respiratory support in the delivery room, whereas maternal vascular malperfusion was associated with oligohydramnios. In multivariable models adjusting for cardiac diagnosis, associations of delayed villous maturation persisted for infant birth head circumference (odds ratio 1.2, 95% confidence interval 1.0 – 1.5, p = 0.02) and infant respiratory support in the delivery room (odds ratio 3.0, 95% confidence interval 1.3 – 6.5, p = 0.007). Pregnancies with fetal congenital heart disease display higher rates of delayed villous maturation and maternal vascular malperfusion compared to controls, suggesting that placental maldevelopment may relate to maternal factors. Future investigations are needed to determine the association of these abnormalities with postnatal infant outcomes. Placental delayed villous maturation and maternal vascular malperfusion are more common in pregnancies with fetal congenital heart disease than demographically matched controls.
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