Abstract

Reentry is the most common mechanism for arrhythmia in patients treated in the electrophysiology laboratory. Mapping and defining the exact circuit to then allow targeting an ideal site for ablation is challenging.1 However, as reentry usually involves a relatively large circuit often coupled with a discrete slow zone of conduction, we are able to use the classical techniques of entrainment mapping to find and ablate the circuit isthmus containing the slow zone ablation for permanent elimination.2,3 See Article by Liu et al Typically, slow zones for conduction occur as a result of diseased myocardium in the vicinity of scars in patients with structural heart disease. Reentry seen in normal hearts often has the atrioventricular node serving as the primary slow zone of the tachycardia circuit, for example, in atrioventricular node reentrant tachycardia and accessory pathway-related tachycardia. Indeed, nodoventricular tachycardia, although a rare tachycardia, exists because of atrioventricular nodal participation unlike patients with a fasciculoventricular tract where no tachycardia has been described likely because of the absence of a slow zone. Reentry that involves the conduction system is in some ways paradoxical because the Purkinje system is specialized tissue with fast conduction velocity. Bundle branch reentrant tachycardia does occur but almost always in severely diseased hearts with both slowed conduction through the Purkinje tissue and diseased myocardium forming parts of the circuit.4 Left posterior fascicular tachycardia is an enigmatic arrhythmia that occurs in normal hearts. The involvement of the conduction system with no apparent slow zone and success with discrete ablation at apparently normal tissue yet with clear characteristics of reentry based on entrainment makes this arrhythmia unique and difficult to approach.5 Treating the arrhythmia as a small circuit reentry akin to a focal …

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