© 2001 by European Society of Cardiology
Copyright © 2001, European Society of Cardiology
Re: Characterization of the ventricular conduction system in the developing mouse heart
Cardiac Unit, Institute of Child Health, University College London, 30 Guilford Street, London WC1 1EH, UK
\|[ast]\|r.anderson{at}ich.ucl.ac.uk
* Tel.: +44-0-207-905-2295; fax: +44-0-207-905-2324
Received 29 March 2001; accepted 29 March 2001
To the Editor:
Franco and Icardo are to be congratulated on their study of the molecular characterization of the ventricular conduction system in the developing mouse [1]. The elegance of their immunocytochemical techniques, however, should not detract from information already available on both the disposition and development of the specialised atrioventricular conduction axis. Thus, at least two aspects of their account are open to criticism. First, the authors discuss the recent revisionist account of Racker and Kadish (their reference #37) as though this concept is an accepted fact. In reality, the "differences" described by Racker and Kadish simply reflect their definition of the "proximal AV bundle". Using the definition proposed by Tawara nearly one hundred years ago [2], this "proximal AV bundle" would properly be described as the atrioventricular node. The "AV node" and "distal AV bundle" as defined by Racker and Kadish are enclosed within the insulating fibrous tissues of the atrioventricular bundle. Using the pragmatic definition offered by Tawara, these components should all be described as the penetrating and non-branching atrioventricular bundle. Thus, the same arrangement exists in the dog as in human and mouse, as pointed out previously by Ho and her colleagues [3], so it is hardly surprising that Franco and Icardo were unable to validate the revisionist and spurious account offered by Racker and Kadish.
The second area open to question is the assertion by Franco and Icardo that the node and bundle are developed from different sources. In a particularly elegant study produced by Lamers and his colleagues [4], using an antibody to the nodose ganglion of the chick in human hearts, it was shown that part of an initially interventricular ring became incorporated into the atrioventricular junction, and thus part of the atrioventricular canal. In this way, Lamers and his colleagues showed that node and bundle had the same developmental primordium, even though subsequently occupying different parts of the heart. Lamers and his colleagues also showed how the disposition of the ring within the right atrioventricular junction accounted for the anomalous atrioventricular nodes as seen in lesions such as double inlet left ventricle or congenitally corrected transposition, as well as offering an explanation for the previously contentious observations of Kent [5]. It is the more surprising that Franco and Icardo neglect to cite this important and unifying reference, since Professor Moorman, whom they thank in their acknowledgement, was a co-author in this investigation.
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- Franco D., Icardo J.M. Moleculer characterization of the ventricular conduction system in the developing mouse heart: topographical correlation in normal and congenitally malformed hearts. Cardiovasc Res (2001) 49:417–429.
[Abstract/Free Full Text] - Tawara S. Das Reizleitungssystem des Säugetierherzens. Eine Anatomisch-Histologische Studie Über das Atrioventrikularbündel und die Purkinjeschen Fäden. Jena:Gustav Fischer, 1906.
- Ho S.Y., Kilpatrick L.P., Kanai T., Germroth P.G., Thompson R.P., Anderson R.H. The architecture of the atrioventricular conduction axis in dog compared to man: its significance to ablation of the atrioventricular nodal approaches. J Cardiovasc Electrophysiol. (1995) 6:26–39.[Web of Science][Medline]
- Lamers W.H., Wessels A., Verbeek F.J., Moorman A.F.M., Viragh S., Wenink A.C.G., Gittenberger de-Groot A.C., Anderson R.H. New findings concerning ventricular septation in the human heart. Implications for maldevelopment. Circulation (1992) 86:1194–1205.
[Abstract/Free Full Text] - Kent A.F.S. Researches on the structure and function of the mammalian heart. J Physiol (1893) 14:233–254.
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