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      The “Dead-End Tract” and Its Role in Arrhythmogenesis

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          Abstract

          Idiopathic outflow tract ventricular arrhythmias (VAs) represent a significant proportion of all VAs. The mechanism is thought to be catecholamine-mediated delayed after depolarizations and triggered activity, although other etiologies should be considered. In the adult cardiac conduction system it has been demonstrated that sometimes an embryonic branch, the so-called “dead-end tract”, persists beyond the bifurcation of the right and left bundle branch (LBB). Several findings suggest an involvement of this tract in idiopathic VAs (IVAs). The aim of this review is to summarize our current knowledge and the possible clinical significance of this tract.

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          The arterial pole of the mouse heart forms from Fgf10-expressing cells in pharyngeal mesoderm.

          R G Kelly, N Brown, M E Buckingham (2001)
          Development of the arterial pole of the heart is a critical step in cardiogenesis, yet its embryological origin remains obscure. We have analyzed a transgenic mouse line in which beta-galactosidase activity is observed in the embryonic right ventricle and outflow tract of the heart and in contiguous splanchnic and pharyngeal mesoderm. The nlacZ transgene has integrated upstream of the fibroblast growth factor 10 (Fgf10) gene and comparison with the expression pattern of Fgf10 in pharyngeal mesoderm indicates transgene control by Fgf10 regulatory sequences. Dil labeling shows a progressive movement of cells from the pharyngeal arch region into the growing heart tube between embryonic days 8.25 and 10.5. These data suggest that arterial pole myocardium originates outside the classical heart field.
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            Cardiac chamber formation: development, genes, and evolution.

            Mark Moorman, Vincent Christoffels (2003)
            Concepts of cardiac development have greatly influenced the description of the formation of the four-chambered vertebrate heart. Traditionally, the embryonic tubular heart is considered to be a composite of serially arranged segments representing adult cardiac compartments. Conversion of such a serial arrangement into the parallel arrangement of the mammalian heart is difficult to understand. Logical integration of the development of the cardiac conduction system into the serial concept has remained puzzling as well. Therefore, the current description needed reconsideration, and we decided to evaluate the essentialities of cardiac design, its evolutionary and embryonic development, and the molecular pathways recruited to make the four-chambered mammalian heart. The three principal notions taken into consideration are as follows. 1) Both the ancestor chordate heart and the embryonic tubular heart of higher vertebrates consist of poorly developed and poorly coupled "pacemaker-like" cardiac muscle cells with the highest pacemaker activity at the venous pole, causing unidirectional peristaltic contraction waves. 2) From this heart tube, ventricular chambers differentiate ventrally and atrial chambers dorsally. The developing chambers display high proliferative activity and consist of structurally well-developed and well-coupled muscle cells with low pacemaker activity, which permits fast conduction of the impulse and efficacious contraction. The forming chambers remain flanked by slowly proliferating pacemaker-like myocardium that is temporally prevented from differentiating into chamber myocardium. 3) The trabecular myocardium proliferates slowly, consists of structurally poorly developed, but well-coupled, cells and contributes to the ventricular conduction system. The atrial and ventricular chambers of the formed heart are activated and interconnected by derivatives of embryonic myocardium. The topographical arrangement of the distinct cardiac muscle cells in the forming heart explains the embryonic electrocardiogram (ECG), does not require the invention of nodes, and allows a logical transition from a peristaltic tubular heart to a synchronously contracting four-chambered heart. This view on the development of cardiac design unfolds fascinating possibilities for future research.
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              Chamber formation and morphogenesis in the developing mammalian heart.

              Vincent Christoffels, Petra E.M.H. Habets, Diego Franco … (2000)
              In this study we challenge the generally accepted view that cardiac chambers form from an array of segmental primordia arranged along the anteroposterior axis of the linear and looping heart tube. We traced the spatial pattern of expression of genes encoding atrial natriuretic factor, sarcoplasmic reticulum calcium ATPase, Chisel, Irx5, Irx4, myosin light chain 2v, and beta-myosin heavy chain and related these to morphogenesis. Based on the patterns we propose a two-step model for chamber formation in the embryonic heart. First, a linear heart forms, which is composed of "primary" myocardium that nonetheless shows polarity in phenotype and gene expression along its anteroposterior and dorsoventral axes. Second, specialized ventricular chamber myocardium is specified at the ventral surface of the linear heart tube, while distinct left and right atrial myocardium forms more caudally on laterodorsal surfaces. The process of looping aligns these primordial chambers such that they face the outer curvature. Myocardium of the inner curvature, as well as that of inflow tract, atrioventricular canal, and outflow tract, retains the molecular signature originally found in linear heart tube myocardium. Evidence for distinct transcriptional programs which govern compartmentalization in the forming heart is seen in the patterns of expression of Hand1 for the dorsoventral axis, Irx4 and Tbx5 for the anteroposterior axis, and Irx5 for the distinction between primary and chamber myocardium. Copyright 2000 Academic Press.
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                Author and article information

                Contributors
                Andy Wessels: Role: Academic Editor
                Robert E. Poelmann: Role: Academic Editor
                Monique R.M. Jongbloed: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): J Cardiovasc Dev Dis
                Journal ID (iso-abbrev): J Cardiovasc Dev Dis
                Journal ID (publisher-id): jcdd
                Title: Journal of Cardiovascular Development and Disease
                Publisher: MDPI
                ISSN (Electronic): 2308-3425
                Publication date (Electronic): 05 April 2016
                Publication date Collection: June 2016
                Volume: 3
                Issue: 2
                Electronic Location Identifier: 11
                Affiliations
                Department of Clinical Electrophysiology, Erasmus Medical Center, Rotterdam, 3015 CE, The Netherlands; l.j.devries@ 123456erasmusmc.nl (L.V.); a.a.hendriks@ 123456erasmusmc.nl (A.H.)
                Author notes
                [* ]Correspondence: t.szilitorok@ 123456erasmusmc.nl ; Tel.: +31-10-7033991; Fax: +31-10-7034420
                Article
                Publisher ID: jcdd-03-00011
                DOI: 10.3390/jcdd3020011
                PMC ID: 5715688
                PubMed ID: 29367562
                SO-VID: 5d20f73d-a6c5-4f6f-b009-04e1d1e75571
                Copyright © © 2016 by the authors.
                License:

                Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons by Attribution (CC-BY) license ( http://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 27 November 2015
                Date accepted : 17 March 2016
                Categories
                Subject: Review

                Keywords: cardiac conduction system,dead-end tract,idiopathic ventricular arrhythmia
                Data availability:
                Keywords: cardiac conduction system, dead-end tract, idiopathic ventricular arrhythmia

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