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(Hypertension. 2007;49:15.)
© 2007 American Heart Association, Inc.

Editorial Commentaries

Maternal Fetal/Placental Interactions and Abnormal Pregnancy Outcomes

James M. Roberts; Frauke Von Versen-Hoeynck

From the Magee-Womens Research Institute (J.M.R., F.V.V.-H.) and the Department of Obstetrics Gynecology and Reproductive Sciences (J.M.R., F.V.V.-H.) and Epidemiology (J.M.R.), University of Pittsburgh, Pa.

Correspondence to James M. Roberts, Magee-Womens Research Institute, 204 Craft Avenue, Pittsburgh, PA 15215. E-mail RSIJMR@mwri.magee.edu.

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Cytotrophoblast cells from the placenta invade the maternal spiral arteries during normal pregnancy. This results in a striking increase in luminal diameter and causes the vessels to lose their smooth muscle enabling the expansion of vascular capacity necessary to support fetal growth. Preeclampsia, growth restriction, recurrent abortion, and preterm birth in many cases are caused by abnormal implantation with failure of this process. Of these implantation abnormalities, preeclampsia is well known to be associated with later life cardiovascular disease.^1,2 Furthermore, several persistent metabolic and cardiovascular differences are present in women with preeclamptic compared with normal pregnancies. The data relating the other implantation disorders to later life cardiovascular diseases are less compelling. It is possible, however, in large population studies, to document increased cardiovascular mortality in women with pregnancies complicated by these disorders.^1,3

In this issue of Hypertension, Germain et al⁴ clearly demonstrate that similar abnormalities of endothelial function are present 11 to 27 months postpartum in women who had previous pregnancies complicated not only by preeclampsia but also by recurrent abortion. There is reduced flow-induced endothelial-mediated vasodilatation, reduced circulating NO, and higher cholesterol in both groups. They present the reasonable conclusion that endothelial dysfunction may predispose to abnormal implantation and incomplete placental bed vascular remodeling.

This is counter to an idea that I have previously advanced, including in a recent review in this journal.⁵ The concept of a 2-stage model of preeclampsia with the first stage being abnormal implantation and placental bed vascular remodeling and the second the maternal . . . [Full Text of this Article]

Related Article:

Endothelial Dysfunction: A Link Among Preeclampsia, Recurrent Pregnancy Loss, and Future Cardiovascular Events?

Alfredo M. Germain, Mary Carmen Romanik, Irene Guerra, Sandra Solari, María Soledad Reyes, Richard J. Johnson, Karen Price, S. Ananth Karumanchi, and Gloria Valdés
Hypertension 2007 49: 90-95. [Abstract] [Full Text] [PDF]

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