Twin reversed arterial perfusion sequence is more common than generally accepted
Publication year
2015Source
Birth Defects Research Part A-Clinical and Molecular Teratology, 103, 7, (2015), pp. 641-3ISSN
Publication type
Article / Letter to editor
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Organization
Gynaecology
Journal title
Birth Defects Research Part A-Clinical and Molecular Teratology
Volume
vol. 103
Issue
iss. 7
Page start
p. 641
Page end
p. 3
Subject
Radboudumc 10: Reconstructive and regenerative medicine RIMLS: Radboud Institute for Molecular Life SciencesAbstract
BACKGROUND: Approximately 75% of monozygotic twin pregnancies share one monochorionic placenta where placental anastomoses are virtually always present to connect the two fetoplacental circulations. These anastomoses cause several serious complications such as acardiac twinning. Acardiac twins lack a functional heart but nevertheless show fetal growth because the normal pump twin perfuses the acardiac body through arterioarterial (AA) and venovenous (VV) anastomoses. The widely accepted 1% monochorionic acardiac incidence dates back to 1944 and the associated 1:35,000 pregnancies to 1953. Our aim was to update this analysis. METHODS: We accepted the 1% (actually 1.1%) monochorionic acardiac incidence due to lack of more precise data, included the recently observed 58% early cessation of acardiac development as well as consequences of assisted reproductive technology, and assessed the incidence of acardiac twinning under conditions of AA-VV anastomoses. RESULTS: Early acardiac monochorionic twinning increased from 1.1% to 1.1/(1-0.58) = 2.6%, from 1:35,000 to 1:9,500 to 11,000 pregnancies, depending on number and method of assisted reproductive technology, and occurs in approximately 1:8 AA-VV anastomoses-containing monochorionic placentas. CONCLUSION: Early acardiac twinning is not a rare event. The 1944-based 1% acardiac monochorionic incidence has a weak basis and could therefore be (much) larger. Knowing this incidence more precisely may contribute to our knowledge of embryonic splitting in unequal cell masses. Birth Defects Research (Part A) 103:641-643, 2015. (c) 2015 Wiley Periodicals, Inc.
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- Faculty of Medical Sciences [93487]
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