The Great Pretender: Atrial Tachycardia or Atrial Fibrillation?

Atrial fibrillation is a very common arrhythmia that initially occurs from pulmonary vein triggers, and as it becomes more persistent, it becomes more complex with both atrial structural remodeling and loss of function. While pulmonary vein isolation has been the mainstay of catheter ablation for maintaining sinus rhythm, it has limited long-term success in patients with persistent atrial fibrillation. More ablation is often needed for longer success, but this is fraught with recurrent atypical flutter and atrial tachycardia. This case demonstrates a possible rotor mechanism with termination upon ablation.  

Coastal Cardiology is a private cardiology group on the central coast of California. It is a mixed group of noninvasive and interventional cardiologists as well as electrophysiologists. The group works closely with Dignity Health’s French Hospital Medical Center. 

Case Description

A 56-year-old female physician with facioscapulohumeral muscular dystrophy as well as a history of atrial fibrillation was referred for treatment of recurrent persistent atrial dysrhythmias. She had been started on sotalol after failing propafenone in the past. Propafenone had caused significant weakness, and sotalol was causing periods of bradycardia. She was now mostly wheelchair bound, and was very symptomatic from the atrial fibrillation, experiencing symptoms of lightheadedness, palpitations, and fatigue. Her initial EKG demonstrated some organization of atrial fibrillation, but was thought to be secondary to the antiarrhythmic properties of sotalol. The left atrial size was 34 ml/mm² on echocardiogram with mild mitral regurgitation. She had been in persistent atrial fibrillation for 8 weeks at the time of initial consultation. After a long discussion and some hesitation given her comorbidities, we proceeded with a plan for catheter ablation. It was decided to stop antiarrhythmic drug therapy at that time.

Upon arrival to the EP lab 3 weeks later, her EKG had changed slightly and the atrial fibrillation was even more organized after being off of antiarrhythmic drug therapy for several weeks. Based on the EKG, the initial P wave was positive in V1, but the cycle length varied and ultimately became negative. This alternating pattern was noted through the EKG. It was positive in the inferior leads with sinus P wave in V1 bifid, leading one to believe this would be arising from the right superior pulmonary vein if it was truly a focal source.¹ With the coronary sinus catheter in place, there was a lot of wobble noted in the tachycardia cycle length, and it appeared to be more consistent with atrial fibrillation than a focal atrial tachycardia. (Figure 1) It was impossible to map secondary to changing cycle length. We instead constructed a scar map, which can be helpful in patients with persistent atrial fibrillation.² During the mapping process, we noted several interesting signals from the right superior pulmonary vein (RSPV) that were earlier than the coronary sinus, and any preceding cycle length changes occurred first in the RSPV. This was the earliest signal on visual inspection of all the pulmonary veins. (Figure 2) We did not attempt overdrive pacing maneuvers given the change in cycle length. After review of the scar map, we decided to perform ablation at this site to see if it would change the tachycardia, with the idea of performing pulmonary vein isolation. (Figure 3)

We used the TactiCath™ Quartz Contact Force Ablation Catheter (Abbott) at 40 ºC with a goal contact force of greater than 10 grams. A spiral mapping catheter was placed in the right pulmonary vein during ablation.  With ablation onset, the tachycardia initially accelerated, but then slowed and terminated within 5 seconds. (Figure 4) The RSPV was not isolated at the time of the termination. (Figure 5) Reinduction was attempted with isoproterenol at 20 mcg/min and with single, double, and triple extrastimuli, without any further sustained atrial arrhythmias. Short runs of atrial fibrillation were induced with triple extrastimuli that were very unorganized and rapid, with fibrillatory cycle length of 130 ms. We elected to proceed with wide-area pulmonary vein isolation, given the degree of scar and potential for atrial fibrillation. (Figure 6) The patient is now 9 months out from ablation, and the implantable loop recorder has shown no recurrent arrhythmias. She is in sinus rhythm, walking again, and has regained a lot of strength off antiarrhythmic drugs.

Discussion

There is much in the literature about pulmonary vein tachycardia.³ This case was interesting for several reasons. Was this truly a pulmonary vein tachycardia with variable tachycardia cycle length secondary to atrial scar, or was this just a rotor driving atrial fibrillation with termination during ablation? The initial rhythm was more consistent with atrial fibrillation and, given the dilated atrium and scar burden, the latter explanation would make more sense. In retrospect, this was likely a rotor that was generating a more organized atrial fibrillation that terminated with ablation. With the advancement of high-density mapping systems allowing for more points and mapping of spiral waves and rotors, this may be increasingly recognized. Narayan has been a driving force of rotor mapping and FIRM (focal impulse and rotor modulation),⁴ which could have been helpful in this case; however, the outcome would likely have been similar. PVI alone would likely have produced the same result without the precedent focal ablation. 

1. Kistler PM, Roberts-Thomson KC, Haggani HM, et al. P-wave morphology in focal atrial tachycardia: development of an algorithm to predict the anatomic site of origin. J Am Coll Cardiol. 2006;48(5):1010-1017.
2. Nery PB, Thornhill R, Nair GM, Pena E, Redpath CJ. Scar-based catheter ablation for persistent atrial fibrillation. Curr Opin Cardiol. 2017;32(1):1-9. 
3. Moreira W, Timmermans C, Wellens HJ, Rodriguez LM. Atrial tachycardia originating from the pulmonary vein: importance of the stimulation sites. Tex Heart Inst J. 2008;35(3):356-358. 
4. Narayan SM, Krummen DE, Rappel WJ. Clinical mapping approach to diagnose electrical rotors and focal impulse sources for human atrial fibrillation. J Cardiovasc Electrophysiol. 2012;23(5):447-454.