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胎盘血管病变对母婴心血管系统的长期影响。

Long-Term Consequences of Placental Vascular Pathology on the Maternal and Offspring Cardiovascular Systems.

机构信息

Department of Experimental and Clinical Medicine, University of Florence, 50134 Florence, Italy.

Department of Life Sciences, Catholic University of Rome, 00168 Rome, Italy.

出版信息

Biomolecules. 2021 Nov 3;11(11):1625. doi: 10.3390/biom11111625.

DOI:10.3390/biom11111625
PMID:34827623
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8615676/
Abstract

Over the last thirty years, evidence has been accumulating that Hypertensive Disorders of Pregnancy (HDP) and, specifically, Preeclampsia (PE) produce not only long-term effects on the pregnant woman, but have also lasting consequences for the fetus. At the core of these consequences is the phenomenon known as defective deep placentation, being present in virtually every major obstetrical syndrome. The profound placental vascular lesions characteristic of this pathology can induce long-term adverse consequences for the pregnant woman's entire arterial system. In addition, placental growth restriction and function can, in turn, cause a decreased blood supply to the fetus, with long-lasting effects. Women with a history of HDP have an increased risk of Cardiovascular Diseases (CVD) compared with women with normal pregnancies. Specifically, these subjects are at a future higher risk of: Hypertension; Coronary artery disease; Heart failure; Peripheral vascular disease; Cerebrovascular accidents (Stroke); CVD-related mortality. Vascular pathology in pregnancy and CVD may share a common etiology and may have common risk factors, which are unmasked by the "stress" of pregnancy. It is also possible that the future occurrence of a CVD may be the consequence of endothelial dysfunction generated by pregnancy-induced hypertension that persists after delivery. Although biochemical and biophysical markers of PE abound, information on markers for a comparative evaluation in the various groups is still lacking. Long-term consequences for the fetus are an integral part of the theory of a fetal origin of a number of adult diseases, known as the Barker hypothesis. Indeed, intrauterine malnutrition and fetal growth restriction represent significant risk factors for the development of chronic hypertension, diabetes, stroke and death from coronary artery disease in adults. Other factors will also influence the development later in life of hypertension, coronary and myocardial disease; they include parental genetic disposition, epigenetic modifications, endothelial dysfunction, concurrent intrauterine exposures, and the lifestyle of the affected individual.

摘要

在过去的三十年中,有证据表明,妊娠高血压疾病(HDP),特别是子痫前期(PE)不仅会对孕妇产生长期影响,而且还会对胎儿产生持久的后果。这些后果的核心是众所周知的胎盘功能不全,几乎存在于每一种主要的产科综合征中。这种病理特征性的深刻胎盘血管病变可导致孕妇整个动脉系统长期不良后果。此外,胎盘生长受限和功能障碍反过来又会导致胎儿血液供应减少,产生长期影响。与正常妊娠的女性相比,患有 HDP 的女性患心血管疾病(CVD)的风险增加。具体而言,这些患者未来患以下疾病的风险更高:高血压;冠状动脉疾病;心力衰竭;周围血管疾病;脑血管意外(中风);CVD 相关死亡率。妊娠期间的血管病理学和 CVD 可能具有共同的病因,并且可能具有共同的危险因素,这些因素会因妊娠的“压力”而显现出来。也有可能未来发生 CVD 是由妊娠引起的高血压引起的内皮功能障碍的后果,这种功能障碍在分娩后仍然存在。尽管 PE 的生化和生物物理标志物很多,但关于各种组别的比较评估标志物的信息仍然缺乏。对胎儿的长期影响是许多成人疾病的胎儿起源理论的一个组成部分,该理论被称为 Barker 假说。事实上,宫内营养不良和胎儿生长受限是成人慢性高血压、糖尿病、中风和冠心病死亡的重要危险因素。其他因素也会影响以后生活中高血压、冠心病和心肌疾病的发展;它们包括父母的遗传倾向、表观遗传修饰、内皮功能障碍、宫内同时暴露以及受影响个体的生活方式。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d14/8615676/e39ced35e38d/biomolecules-11-01625-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d14/8615676/a8744f9e851b/biomolecules-11-01625-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d14/8615676/baf1396da471/biomolecules-11-01625-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d14/8615676/0ed7cadfd356/biomolecules-11-01625-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d14/8615676/e39ced35e38d/biomolecules-11-01625-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d14/8615676/a8744f9e851b/biomolecules-11-01625-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d14/8615676/baf1396da471/biomolecules-11-01625-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d14/8615676/0ed7cadfd356/biomolecules-11-01625-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4d14/8615676/e39ced35e38d/biomolecules-11-01625-g004.jpg

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