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Management of a patient with long-RP tachycardia
Dr Leon M Ptaszek, MD, PhD
Cardiac Arrhythmia Service, Massachusetts General Hospital, Boston, USA
A 78-year-old woman with a history of supraventricular tachycardia (SVT) for more than 25 years presented with increased frequency of arrhythmia-related symptoms. She had previously controlled her episodes of SVT with vagal maneuvers but found that they were no longer effective. A 12-lead electrocardiogram (ECG) performed during a typical episode revealed a regular, narrow-complex tachycardia. The patient had also been diagnosed with paroxysmal atrial fibrillation (PAF), but the burden was low and was not associated with symptoms. The patient’s ECG in sinus rhythm revealed no evidence of ventricular pre-excitation. A trans-thoracic echocardiogram (TTE) revealed no significant structural abnormalities.
Methods & results
Use of a beta blocker or a calcium channel blocker was not possible due to low blood pressure. The decision was made to proceed with catheter ablation. The patient presented to the EP lab in nearly incessant, narrow-complex tachycardia. Surface ECG of the tachycardia performed in the EP lab was very similar to a prior ECG performed during tachycardia. Spontaneous episodes of tachycardia were initiated with conducted premature atrial contractions (PACs) and terminated in the ventricle. Wenckebach pacing from the right ventricle (RV) did not reveal evidence of an accessory pathway: retrograde atrial conduction was midline and decremental. Para-Hisian pacing in sinus rhythm also did not reveal evidence of an accessory pathway. Delivery of extra-stimuli from the high right atrium (HRA) did not reveal dual AV nodal physiology but did induce long-RP tachycardia. Entrainment of the tachycardia with pacing from the right ventricle (RV) was successful. Termination of RV pacing was associated with continuation of tachycardia and a “pseudo V-A-A-V” response, consistent with atypical AVNRT (Figure, Panel A).
Other observations consistent with AVNRT included the following. The post-pacing interval (PPI) minus the tachycardia cycle length (TCL) was >115 msec. During entrainment of the tachycardia, the interval between the last RV pacing stimulus and the last entrained HRA electrogram (SA interval) was >85 msec longer than the ventriculo-atrial (VA) interval in the context of tachycardia. Due to the absence of dual AV nodal physiology, it was thought that the AVNRT represented an intermediate-slow or a slow-slow circuit (PR interval in sinus rhythm was normal). Some variation in the tachycardia cycle length was observed, but the intervals between His electrograms did not reliably predict the intervals between atrial electrograms.
The decision was made to create an electroanatomic map (EAM) of the right atrium and to locate the site of the earliest atrial activation during tachycardia (Figure, Panel B). Ablation lesions were delivered at this location in sinus rhythm. After ablation, the arrhythmia could not be re-induced after a 30-minute waiting period during which aggressive pacing was performed and isoproterenol was administered. The patient has not experienced any recurrences of AVNRT for five years.
The site of earliest atrial activation during atypical AVNRT can be used to guide the delivery of ablation lesions.
Panel A: Tachycardia was successfully entrained with right ventricular (RV) pacing. Termination of RV pacing was associated with continuation of tachycardia and a “pseudo V-A-A-V” response.
Panel B: Electroanatomic map (EAM) of the right atrium, LAO projection. The site of earliest atrial activation in tachycardia is displayed as a white point. Ablation lesions delivered at this site during sinus rhythm are displayed as red points. Locations of His electrograms displayed as yellow points. The location of the coronary sinus is also labelled.