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.
Highlights
During the development of the ventricular conduction system sometimes a so-called “dead-end tract” is seen in addition to the right and left bundle branch, fading out on the crest of the muscular ventricular septum [1,2]
The frequently described co-existence of ventricular arrhythmias (VAs) from the outflow tracts, the area in which the dead-end tract may persist, and the presence of atrioventricular re-entry tachycardias in structural normal hearts could implicate a clinical significance of this tract in the form of a connection between these regions [4,5,6,7,8]
Lamers et al provided a conclusive evaluation after studying material from human embryos showing that the inlet component of the morphologically right ventricle forms from the ascending limb of the embryonic ventricular loop, and that the inlet and apical trabecular elements of the muscular septum are formed from the same primary ventricular septum [32]
Summary
During the development of the ventricular conduction system sometimes a so-called “dead-end tract” is seen in addition to the right and left bundle branch, fading out on the crest of the muscular ventricular septum [1,2]. Remnants of the developing conduction system have been linked to the occurrence of arrhythmias [3]. Outflow tract VAs without underlying structural heart disease can be found in a large part of the population and can be very symptomatic [9,10,11,12,13,14,15,16]. The mechanism behind these IVAs is not completely understood and could be explained by the dead-end tract. In this review we aim to summarize our current knowledge and the clinical significance of this tract
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