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Atrial Tachycardia or Atrioventricular Nodal Reentry? An Unusual Case of a Long RP Tachycardia

January 2001 PACE, Vol. 24 Case Report The differential diagnosis of long RP tachycardias is among the more interesting challenges for the electrophysiologist. We present an unusual case of an arrhythmia whose electrophysiological workup demonstrated features of atrial tachycardia and atypical atrioventricular nodal reentrant tachycardia (AVNRT). A 66-year-old man with hypertension presented to the emergency room with palpitations. A narrow complex tachycardia with a long RP pattern was recorded (Fig. 1, top). The arrhythmia terminated spontaneously and the baseline electrocardiogram (ECG) in sinus rhythm was normal. The workup revealed no structural heart disease. Medical therapy failed to control palpitations, and the decision was made to pursue electrophysiological study and possible radiofrequency (RF) ablation. Electrophysiological study was performed using standard techniques after terminating all cardioactive drugs for .5 half lives. The baseline conduction intervals were normal. Atrial and ventricular pacing revealed evidence for dual AV nodal physiology. The earliest retrograde atrial activity during ventricular pacing was in the Hisbundle recording. Application of atrial extrastimuli could induce a short RP supraventricular tachycardia (SVT) with a cycle length of 470 ms. The retrograde atrial activation sequence during SVT was identical to that during ventricular pacing. Of note, SVT could not be induced if the coupling intervals of atrial extrastimuli were less than the AV nodal effective refractory period (ERP), although induction of SVT was not invariably associated with delay in the AH interval. As noted in Figure 1 (bottom), the P wave timing on the surface ECG tracing of the induced SVT did not match that of the clinical tachycardia. During runs of sustained tachycardia, the ventriculoatrial (VA) interval was noted to gradually prolong so that the SVT developed a long RP pattern (Fig. 2), such that the surface ECG now matched that of the clinical tachycardia. The atrial activation sequence and cycle length is constant, while the interval between His-bundle deflections is irregular, and the AH interval shortens as the tachycardia progresses. Burst ventricular pacing or application of single and multiple programmed ventricular extrastimuli during SVT were unable to perturb the septal atrial electrogram at any drive cycle or coupling interval, and it failed to terminate the tachycardia. Application of atrial extrastimuli from the high right atrium or proximal coronary sinus were able to dissociate the local atrial electrogram from the SVT at longer coupling intervals and terminate the SVT at shorter intervals. Burst atrial pacing yielded an identical AH interval to SVT when pacing at the SVT cycle length. The SVT frequently terminated spontaneously, without significant changes in the AH, VA, or AA intervals, and always ended with a ventricular electrogram. We had encountered an arrhythmia with a long RP pattern that was reproduced in the electrophysiology laboratory, but only after undergoing a metamorphosis from a short RP SVT. Given symptoms refractory to medications, RF ablation was preferred. What is the mechanism of this tachycardia and how should one proceed with ablation?