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. 2010 Jun 16;88(2):287–295. doi: 10.1093/cvr/cvq193

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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2010. For permissions please email: journals.permissions@oxfordjournals.org.

The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that the original authorship is properly and fully attributed; the Journal, Learned Society and Oxford University Press are attributed as the original place of publication with correct citation details given; if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative work this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org.

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E18.5 Tc1 embryos exhibit AVSD, ventricular septal, and outflow tract defects. Three-dimensional reconstructions of wild-type (A, C, E, and G) and Tc1 (B, D, F, and H) hearts eroded to the levels indicated in the insets. (B) A Tc1 membranous VSD (white arrowhead; four-chamber view) resulting in subpulmonary interventricular communication, both arterial roots arising side-by-side from the right ventricle (the Taussig–Bing malformation). (C–H) Short-axis view from apex. (D) A Tc1 muscular inlet VSD (black circle, D). The left AV valve in the Tc1 heart is trifoliate in comparison to the normal mitral valve (compare E and F, white arrows). This apparent cleft in the aortic leaflet can be traced in continuity with the two bridging leaflets (white arrowheads, H) guarding a common AV junction (see also Supplementary material online, Movie S9) (AoV, aortic valve; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; A, aorta; PV, pulmonary valve; R, right; L, left; VS, ventricular septum).