Introduction: Attempts to terminate reentrant tachyarrhythmias by rapid pacing may accelerate the tachycardia. One mechanism for acceleration is double-wave reentry, where two simultaneous wavefronts travel around the same circuit.
Methods and results: We report pacing acceleration of AV reciprocating tachycardia (AVRT) due to double-wave reentry in a patient with Wolff-Parkinson-White syndrome. The patient had presented with atrial fibrillation and rapid conduction across a left lateral bypass tract. Intravenous procainamide was given during electrophysiologic study because of incessant atrial fibrillation and restored sinus rhythm. Orthodromic AVRT was induced and attempts to terminate the AVRT with right ventricular pacing initiated two alternate tachycardias, both with a left bundle branch block (LBBB) morphology. The first tachycardia, as expected for bundle branch block ipsilateral to the bypass tract, had a longer cycle length (CL) than the original tachycardia (366 msec compared to 297 msec). The second tachycardia had a paradoxically shorter CL, 238 msec compared to 297 msec. Electrogram analysis revealed that the circuit traversed by the accelerated LBBB tachycardia was the same as the slower LBBB tachycardia. The activation sequence revealed two independent wavefronts, traversing this common circuit. As described previously in experimental models, double-wave reentry was initiated when an antidromic-stimulated impulse blocked before colliding with the previous orthodromic impulse, thus allowing two orthodromic impulses to circulate within the circuit.
Conclusion: We speculate that conduction slowing by procainamide combined with the intrinsic AV nodal delay resulted in the necessary increase in the excitable gap required to develop double-wave reentry. This is the first description of sustained double-wave reentry in humans.