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References

Anatomical observations of the moderator band

Clin Anat. 2010 May;23(4):443-50. doi: 10.1002/ca.20968.

Loukas M, Klaassen Z, Tubbs RS, Derderian T, Paling D, Chow D, Patel S, Anderson RH. Source Department of Anatomical Sciences, School of Medicine, St George's University, Grenada, West Indies. mloukas@sgu.edu

Abstract

Apical ventricular septal defects are rare pathologies of the ventricular septum. The moderator band, or other large trabeculations, is the major obstacle for the repair of such defects. The aim of our study was to identify and describe variations in the size and anatomy of the moderator band. We studied the right ventricular apical trabeculations in 100 adult human cadavers. Overall, we identified the moderator band in 92% of hearts. In just over two-fifths (42%), the band was a short and thick trabeculation, whereas, in one-eighth (12%), it was long and thick. In just under one-quarter of the hearts (24%), the band was short and thin, whereas it was long and thin in 14% of the hearts. In the remaining eight hearts, we were unable to identify the moderator band. The mean thickness of the band was 4.5 +/-1.8 mm, and its mean length was 16.23 +/- 2.3 mm, ranging from 11.3 to 24.3 mm. According to these measurements, we were able to classify the band as originating less than 45% of the distance from the tricuspid valve to the apex (closer to tricuspid valve), seen in 12 hearts, between 45 and 55% of the distance from the valve to the apex, seen in 45 hearts, and greater than 55% of this distance (closer to the apex), seen in 39 specimens. We present these data that may prove useful in the setting of the surgical repair of apical ventricular septal defects through the right atrium. 2010 Wiley-Liss, Inc.

PMID 20235167

Paper refers to the muscular wall not the conduction system.

Development of the cardiac conduction system: why are some regions of the heart more arrhythmogenic than others?

Circ Arrhythm Electrophysiol. 2009 Apr;2(2):195-207.

Christoffels VM, Moorman AF. Source

Heart Failure Research Center, Academic Medical Center, 1105 AZ, Amsterdam, The Netherlands.

PMID 19808465

http://circep.ahajournals.org/content/2/2/195.full

Development of the cardiac conduction system in atrioventricular septal defect in human trisomy 21

Pediatr Res. 2005 Sep;58(3):516-20.

Blom NA, Ottenkamp J, Deruiter MC, Wenink AC, Gittenberger-de Groot AC. Source Department of Pediatric Cardiology, Leiden University Medical Center, The Netherlands.

Abstract

In patients with atrioventricular septal defect (AVSD), the occurrence of nonsurgical AV block has been reported. We have looked for an explanation in the development of the AV conduction system. Human embryos with AVSD and trisomy 21 and normal embryos were examined (age 5-16 wk gestation). Antibodies to human natural killer cell-1 (HNK-1), muscle actin (HHF-35), and collagen VI were used to delineate the conduction system. As in normal hearts, HNK-1 transiently stains the AV conduction system, the sinoatrial node, and parts of the sinus venosus in AVSD. A large distance is present between the superior and inferior node-like part of the right AV ring bundle, comparable to 6-wk-old normal hearts. The definitive inferior AV node remains in dorsal position from 7 wk onward and does not appose to the superior node-like part as seen in normal hearts. Furthermore, in AVSD, a transient third HNK-1-positive "middle bundle" branch that is continuous with the retroaortic root branch and the superior node-like part can be identified, and thus the AV conduction system forms a figure-of-eight loop. At later stages, the AV node remains in dorsal position close to the coronary sinus ostium with a long nonbranching bundle that runs through thin fibrous tissue toward the ventricular septum. The formation of the AV node and the ventricular conduction system in AVSD and Down syndrome differs from normal development, which can be a causative factor in the development of AV conduction disturbances.

PMID 16148066

Induction and patterning of the cardiac conduction system

Int J Dev Biol. 2002 Sep;46(6):765-75.

Pennisi DJ, Rentschler S, Gourdie RG, Fishman GI, Mikawa T. Source Department of Cell and Developmental Biology, Cornell University Medical College, New York, NY 10021, USA.

Abstract

The cardiac conduction system (CCS) is the component of the heart that initiates and maintains a rhythmic heartbeat. As the embryonic heart forms, the CCS must continue to develop and mature in a coordinated manner to ensure that proper pace making potential and distribution of action potential is maintained at all stages. This requires not only the formation of distinct and disparate components of the CCS, but the integration of these components into a functioning whole as the heart matures. Though research in this area of development may have lagged behind other areas of heart development, in recent years there has been much progress in understanding the ontogeny of the CCS and the developmental cues that drive its formation. This is largely due to studies on the avian heart as well as the use of molecular biology approaches. This review gives a perspective on advances in understanding the development of the vertebrate CCS, and reports new data illuminating the mechanism of conduction cell determination and maintenance in the mammalian heart. As much of our knowledge about the development of the CCS has been derived from the chick embryo, one important area facing the field is the relationship and similarities between the structure and development of avian and mammalian conduction systems. Specifically, the morphology of the distal elements of the mammalian CCS and the manner in which its components are recruited from working cardiomyocytes are areas of research that will, hopefully, receive more attention in the near future. A more general and outstanding question is how the disparate components of all vertebrate conduction systems integrate into a functional entity during embryogenesis. There is mounting evidence linking the patterning and formation of the CCS to instructive cues derived from the cardiac vasculature and, more specifically, to hemodynamic-responsive factors produced by cardiac endothelia. This highlights the need for a greater understanding of the biophysical forces acting on, and created by, the cardiovascular system during embryonic development. A better understanding of these processes will be necessary if therapeutics are to be developed that allow the regeneration of damaged cardiac tissues or the construction of biologically engineered heart tissues.

PMID 12382942