Impact of Pre-Eclampsia on the Cardiovascular System of the Offspring

doi:10.12280/gjfckx.20210819

Abstract

Abstract:

Pre-eclampsia is an idiopathic disease during pregnancy that causes multisystem damage and is one of the leading causes of maternal and perinatal mortality, posing a serious threat to maternal and neonatal health. The adverse intrauterine environment in pre-eclampsia predisposes to adverse neonatal outcomes such as intrauterine growth retardation, preterm birth, and low birth weight. The pathogenesis is not fully understood but exaggerated oxidative stress and inflammatory responses are involved in it. And pre-eclampsia may induce altered epigenetic modifications in the offspring, resulting in cardiovascular system remodeling during growth and development and impairing cardiovascular structure and function, which would increase the risk of cardiovascular disease in adult offspring. This article reviews the possible mechanisms of cardiovascular disease in the offspring due to adverse intrauterine environment in pre-eclampsia and the alterations in cardiovascular structure and function in the offspring, with the aim of understanding the development of fetal-derived cardiovascular disease, contributing to early intervention and interruption of the disease, and improving the health of the offspring delivered by pregnancy complicated with pre-eclampsia.

Key words: Pre-eclampsia, Cardiovascular diseases, Epigenesis,genetic, Ventricular remodeling, Premature birth

CHEN Hui-yun, HAN Bing, CHEN You-guo. Impact of Pre-Eclampsia on the Cardiovascular System of the Offspring[J]. Journal of International Obstetrics and Gynecology, 2022, 49(2): 125-128.

References 24

[1]	Januar V, Desoye G, Novakovic B, et al. Epigenetic regulation of human placental function and pregnancy outcome: considerations for causal inference[J]. Am J Obstet Gynecol, 2015, 213(Suppl 4):S182-S196. doi: 10.1016/j.ajog.2015.07.011. doi: 10.1016/j.ajog.2015.07.011
[2]	许晓红, 关红琼. 子痫前期中长链非编码RNA相关研究新进展[J]. 国际妇产科学杂志, 2020, 47(6):648-652. doi: 10.3969/j.issn.1674-1870.2020.06.010. doi: 10.3969/j.issn.1674-1870.2020.06.010
[3]	Gao WL, Li D, Xiao ZX, et al. Detection of global DNA methylation and paternally imprinted H19 gene methylation in preeclamptic placentas[J]. Hypertens Res, 2011, 34(5):655-661. doi: 10.1038/hr.2011.9. doi: 10.1038/hr.2011.9
[4]	Li X, Wu C, Shen Y, et al. Ten-eleven translocation 2 demethylates the MMP9 promoter, and its down-regulation in preeclampsia impairs trophoblast migration and invasion[J]. J Biol Chem, 2018, 293(26):10059-10070. doi: 10.1074/jbc.RA117.001265. doi: 10.1074/jbc.RA117.001265
[5]	Ching T, Ha J, Song MA, et al. Genome-scale hypomethylation in the cord blood DNAs associated with early onset preeclampsia[J]. Clin Epigenetics, 2015, 7(1):21. doi: 10.1186/s13148-015-0052-x. doi: 10.1186/s13148-015-0052-x
[6]	Yu GZ, Aye CY, Lewandowski AJ, et al. Association of Maternal Antiangiogenic Profile at Birth With Early Postnatal Loss of Microvascular Density in Offspring of Hypertensive Pregnancies[J]. Hypertension, 2016, 68(3):749-759. doi: 10.1161/HYPERTENSIONAHA.116.07586. doi: 10.1161/HYPERTENSIONAHA.116.07586
[7]	Tang Y, Ye W, Liu X, et al. VEGF and sFLT-1 in serum of PIH patients and effects on the foetus[J]. Exp Ther Med, 2019, 17(3):2123-2128. doi: 10.3892/etm.2019.7184. doi: 10.3892/etm.2019.7184
[8]	Morton JS, Cooke CL, Davidge ST. In Utero Origins of Hypertension: Mechanisms and Targets for Therapy[J]. Physiol Rev, 2016, 96(2):549-603. doi: 10.1152/physrev.00015.2015. doi: 10.1152/physrev.00015.2015 pmid: 26887677
[9]	Fox R, Kitt J, Leeson P, et al. Preeclampsia: Risk Factors, Diagnosis, Management, and the Cardiovascular Impact on the Offspring[J]. J Clin Med, 2019, 8(10):1625. doi: 10.3390/jcm8101625. doi: 10.3390/jcm8101625
[10]	Lazdam M, De La Horra A, Pitcher A, et al. Elevated blood pressure in offspring born premature to hypertensive pregnancy: is endothelial dysfunction the underlying vascular mechanism?[J]. Hypertens, 2010, 56(1):159-165. doi: 10.1161/HYPERTENSIONAHA.110.150235. doi: 10.1161/HYPERTENSIONAHA.110.150235
[11]	Herzog EM, Eggink AJ, Reijnierse A, et al. Impact of early- and late-onset preeclampsia on features of placental and newborn vascular health[J]. Placenta, 2017, 49:72-79. doi: 10.1016/j.placenta.2016.11.014. doi: 10.1016/j.placenta.2016.11.014
[12]	Lacolley P, Regnault V, Segers P, et al. Vascular Smooth Muscle Cells and Arterial Stiffening: Relevance in Development, Aging, and Disease[J]. Physiol Rev, 2017, 97(4):1555-1617. doi: 10.1152/physrev.00003.2017. doi: 10.1152/physrev.00003.2017 pmid: 28954852
[13]	Lawlor DA, Macdonald-Wallis C, Fraser A, et al. Cardiovascular biomarkers and vascular function during childhood in the offspring of mothers with hypertensive disorders of pregnancy: findings from the Avon Longitudinal Study of Parents and Children[J]. Eur Heart J, 2012, 33(3):335-345. doi: 10.1093/eurheartj/ehr300. doi: 10.1093/eurheartj/ehr300
[14]	Armstrong DW, Tse MY, Wong PG, et al. Gestational hypertension and the developmental origins of cardiac hypertrophy and diastolic dysfunction[J]. Mol Cell Biochem, 2014, 391(1/2):201-209. doi: 10.1007/s11010-014-2003-9. doi: 10.1007/s11010-014-2003-9
[15]	Youssef L, Miranda J, Paules C, et al. Fetal cardiac remodeling and dysfunction is associated with both preeclampsia and fetal growth restriction[J]. Am J Obstet Gynecol, 2020, 222(1):79.e1-e9. doi: 10.1016/j.ajog.2019.07.025. doi: 10.1016/j.ajog.2019.07.025
[16]	Timpka S, Macdonald-Wallis C, Hughes AD, et al. Hypertensive Disorders of Pregnancy and Offspring Cardiac Structure and Function in Adolescence[J]. J Am Heart Assoc, 2016, 5(11):e003906. doi: 10.1161/JAHA.116.003906. doi: 10.1161/JAHA.116.003906
[17]	Aye CYL, Lewandowski AJ, Oster J, et al. Neonatal autonomic function after pregnancy complications and early cardiovascular development[J]. Pediatr Res, 2018, 84(1):85-91. doi: 10.1038/s41390-018-0021-0. doi: 10.1038/s41390-018-0021-0
[18]	Lewandowski AJ, Raman B, Bertagnolli M, et al. Association of Preterm Birth With Myocardial Fibrosis and Diastolic Dysfunction in Young Adulthood[J]. J Am Coll Cardiol, 2021, 78(7):683-692. doi: 10.1016/j.jacc.2021.05.053. doi: 10.1016/j.jacc.2021.05.053 pmid: 34384550
[19]	Lewandowski AJ, Augustine D, Lamata P, et al. Preterm heart in adult life: cardiovascular magnetic resonance reveals distinct differences in left ventricular mass, geometry, and function[J]. Circulation, 2013, 127(2):197-206. doi: 10.1161/CIRCULATIONAHA.112.126920. doi: 10.1161/CIRCULATIONAHA.112.126920 pmid: 23224059
[20]	Yu L, Zhou Q, Peng Q, et al. Velocity vector imaging echocardiography and NT-proBNP study of fetal cardiac function in pregnancy-induced maternal hypertension[J]. J Clin Ultrasound, 2019, 47(5):285-291. doi: 10.1002/jcu.22720. doi: 10.1002/jcu.22720
[21]	何才通, 李基增, 罗宇迪, 等. HDCP对胎儿心脏发育、子宫动脉血流参数的影响[J]. 解放军预防医学杂志, 2019, 37(2):157-158.
[22]	朱雅芸, 区薛宜, 谢纯平, 等. 超声评估晚孕期妊娠高血压综合征母胎心功能及胎儿生长发育的价值分析[J]. 中国医药科学, 2021, 11(9):187-189,193. doi: 10.3969/j.issn.2095-0616.2021.09.049. doi: 10.3969/j.issn.2095-0616.2021.09.049
[23]	Breatnach CR, Monteith C, Mcsweeney L, et al. The Impact of Maternal Gestational Hypertension and the Use of Anti-Hypertensives on Neonatal Myocardial Performance[J]. Neonatology, 2018, 113(1):21-26. doi: 10.1159/000480396. doi: 10.1159/000480396 pmid: 28954269
[24]	Mutlu K, Karadas U, Yozgat Y, et al. Echocardiographic evaluation of cardiac functions in newborns of mildly preeclamptic pregnant women within postnatal 24-48 hours[J]. J Obstet Gynaecol, 2018, 38(1):16-21. doi: 10.1080/01443615.2017.1322564. doi: 10.1080/01443615.2017.1322564