Reaching consensus as to how knowledge of development underscores our understanding of deficient ventricular septation.

Some of us recently discussed the problems existing in describing the channels that permit interventricular shunting. We offered suggestions for improvement, particularly when assessing the channel that is found when both arterial trunks arise from the morphologically right ventricle. Our proposals engendered significant debate, with several criticisms appearing in an editorial commentary. The commentator now accepts that not all of the criticisms were justified. In an attempt to seek further consensus, we have now joined with additional colleagues so as to clarify the aspects of our initial work that created potential confusion. Having reviewed the aspects producing the misconceptions, we again provide an overview of the evidence relevant to deficient ventricular septation now provided by knowledge of cardiac development. We show how remodelling of the primary interventricular communication involves the provision of an inlet for the developing right ventricle and an outlet for the developing right ventricle. During this process, the secondary interventricular foramen, which is a subaortic-left ventricular communication when the outflow tract remains supported exclusively by the right ventricle, becomes the outflow tract for the left ventricle, with a subaortic-right ventricular communication then being closed to complete ventricular septation. We show how knowledge of these processes, coupled with an appreciation of the mechanism of formation of the muscular ventricular septum and the separate formation of an embryonic muscular outlet septum, which with normal development becomes the subpulmonary infundibulum, provides the basis for understanding the various phenotypic lesions that permit interventricular shunting in the postnatal heart.