Understanding abnormal uterine artery Doppler waveforms: A novel computational model to explore potential causes within the utero-placental vasculature.

ResearchSpace/Manakin Repository

Show simple item record

dc.contributor.author Clark, Alys en
dc.contributor.author James, Joanna en
dc.contributor.author Stevenson, Gordon N en
dc.contributor.author Collins, Sally L en
dc.date.accessioned 2020-02-11T23:06:08Z en
dc.date.issued 2018-06 en
dc.identifier.issn 0143-4004 en
dc.identifier.uri http://hdl.handle.net/2292/49930 en
dc.description.abstract INTRODUCTION:Uterine artery (UtA) Doppler indices are one of the most commonly employed screening tests for pre-eclampsia worldwide. Abnormal indices appear to result from increased uterine vascular resistance, but anatomical complexity and lack of appropriate animal models mean that little is known about the relative contribution of each of the components of the uterine vasculature to the overall UtA Doppler waveform. Previous computational models suggested that trophoblast-mediated spiral artery remodeling has a dominant effect on the UtA Doppler waveform. However, these models did not incorporate the myometrial arterio-venous anastomoses, which have significant potential to affect utero-placental haemodynamics. METHODS:We present a more anatomically complete computational model, explicitly incorporating a structural description of each component of the uterine vasculature, and crucially including myometrial arterio-venous anastomoses as parallel pathways for blood-flow away from the placental bed. Wave transmission theory was applied to the network to predict UtA waveforms. RESULTS:Our model shows that high UtA resistance indices, combined with notching, reflect an abnormal remodeling of the entire uterine vasculature. Incomplete spiral artery remodeling alone is unlikely to cause abnormal UtA Doppler waveforms as increased resistance in these arteries can be 'buffered' by upstream anastomoses. Critically, our results indicate that the radial arteries, may have a more important effect on utero-placental flow dynamics, and the UtA Doppler waveform than previously thought. CONCLUSIONS:This model suggests that to appropriately interpret UtA Doppler waveforms they must be considered to be reflecting changes in the entire system, rather than just the spiral arteries. en
dc.format.medium Print-Electronic en
dc.language eng en
dc.relation.ispartofseries Placenta en
dc.rights Items in ResearchSpace are protected by copyright, with all rights reserved, unless otherwise indicated. Previously published items are made available in accordance with the copyright policy of the publisher. en
dc.rights.uri https://researchspace.auckland.ac.nz/docs/uoa-docs/rights.htm en
dc.subject Arteriovenous Anastomosis en
dc.subject Placenta en
dc.subject Animals en
dc.subject Humans en
dc.subject Pre-Eclampsia en
dc.subject Ultrasonography, Doppler en
dc.subject Blood Flow Velocity en
dc.subject Computational Biology en
dc.subject Pregnancy en
dc.subject Vascular Resistance en
dc.subject Placental Circulation en
dc.subject Models, Cardiovascular en
dc.subject Computer Simulation en
dc.subject Female en
dc.subject Hemodynamics en
dc.subject Uterine Artery en
dc.title Understanding abnormal uterine artery Doppler waveforms: A novel computational model to explore potential causes within the utero-placental vasculature. en
dc.type Journal Article en
dc.identifier.doi 10.1016/j.placenta.2018.05.001 en
pubs.begin-page 74 en
pubs.volume 66 en
dc.rights.holder Copyright: The author en
pubs.end-page 81 en
pubs.publication-status Published en
dc.rights.accessrights http://purl.org/eprint/accessRights/RestrictedAccess en
pubs.subtype Research Support, Non-U.S. Gov't en
pubs.subtype research-article en
pubs.subtype Journal Article en
pubs.subtype Research Support, N.I.H., Extramural en
pubs.elements-id 742092 en
pubs.org-id Bioengineering Institute en
pubs.org-id ABI Associates en
pubs.org-id Medical and Health Sciences en
pubs.org-id School of Medicine en
pubs.org-id Obstetrics and Gynaecology en
dc.identifier.eissn 1532-3102 en
pubs.record-created-at-source-date 2018-06-10 en
pubs.dimensions-id 29884305 en


Full text options

Full text for this item is not available in ResearchSpace.

Find Full text

This item appears in the following Collection(s)

Show simple item record

Share

Search ResearchSpace


Advanced Search

Browse