Editorial CommentTransient entrainment was first demonstrated by Waldo and others in common right atrial flutter and scar-related ventricular tachycardia nearly 30 years ago, and has been shown to occur in all forms of reentry.1 Transient entrainment of a reentry circuit refers to the ability of a paced wavefront to penetrate an excitable gap and constantly, in the case of a stimulus train, reset the circuit to the pacing rate in an orthodromic direction. If the pacing rate is faster than the tachycardia cycle length (TCL) but not fast enough to impinge on the tail of tissue refractoriness, tachycardia continues after cessation of pacing. Also, after entering the exciteable gap, the paced wavefront traveling in the antidromic direction in the circuit collides with the tachycardia wavefront from the previous beat. Each site in the cardiac chamber can be viewed as activated either from a wavefront that traveled orthodromically through the circuit and was activated in the same manner during pacing as during tachycardia, which we will refer to as orthodromic activation, or by a wavefront traveling in a different direction, either in the circuit, or outside of the circuit, which will be referred to as antidromic activation.
2Fusion in the electrocardiogram (ECG) or at the electrogram (EGM) level is created by the combination of orthodromic and antidromic activation of the chamber. After a brief period of pacing at a fixed rate, the region of collision between the orthodromic and paced wavefronts becomes stable and fusion becomes constant on the ECG, except for the last entrained beat after pacing stops, which no longer exhibits fusion (criterion #1).1 At faster pacing rates there is greater propagation of antidromic wavefronts relative to orthodromic wavefronts and the ECG morphology demonstrates progressive fusion as the activation sequence becomes closer to that observed with pacing in sinus rhythm and less like the tachycardia morphology (criterion #2).1 If one continues to pace at faster rates, eventually the head of the conduction wavefront will meet the tail of tissue refractoriness and the tachycardia circuit will be interrupted. Sites distal to the conduction block will fail to be activated by the blocked orthodromic wavefront. The subsequent paced antidromic wavefront is no longer constrained by collision with orthodromic wavefronts and activates these distal sites antidromically, usually evident as a change in EGM morphology and a shorter stimulus to EGM interval than occurred during orthodromic activation (criterion 3). Progressive fusion can also be demonstrated from analysis of orthodromic and antidromic activation in intracardiac EGMs rather than in the surface ECG (criterion 4).
3Unlike reentry, focal mechanisms of tachycardia fail to demonstrate fusion, because conduction occurs centrifugally from a point source, like a ripple from a "pebble in the pond." After a brief period of stabilization, the paced wavefront completely suppresses conduction from the focal source and ECG or intracardiac EGM morphol...