Catheter Ablation of Atrial Arrhythmias in the Transplanted Heart: A Case-Based Discussion

Case #1

A 28-year-old white female who underwent orthotopic heart transplant with an atrio-atrial anastomosis at 9 months of age for hypoplastic left heart syndrome was admitted with a 6-week history of dizzy spells associated with palpitations and skipped beats. The patient also reported one episode of near syncope. Twelve-lead ECG (Figure 1) showed sinus rhythm with RBBB and trigeminal premature atrial contractions (PACs), which were associated with symptoms. No sustained atrial tachycardia (AT) was seen. Echocardiogram showed normal left ventricular function. Endomyocardial biopsy was negative for transplant rejection. Beta-blockers were ineffective, so the patient was referred for electrophysiology (EP) study and possible catheter ablation of PACs.

At baseline, the sinus p-wave appeared to have a larger negative component in lead V1, likely secondary to the anterior location of the donor sinus node given the atrio-atrial anastomosis. P-wave morphology of the PAC was similar to the sinus p-wave, but with larger amplitude in the inferior leads. 

During EP study, most PACs were obscured by the preceding T-wave, so it was difficult to identify the p-wave onset. Once diagnostic catheters were placed, intracardiac activation appeared similar for both the sinus beat and the PAC, and was earliest in the high right atrial catheter, suggesting an origin close to the sinus node. The recipient atrium was in severe sinus bradycardia, which was completely dissociated from the donor (Figure 2).

Sinus, AV node, and His-Purkinje function were normal. There was no evidence for accessory pathway conduction. No sustained supraventricular or ventricular arrhythmias were inducible by programmed stimulation. Since no other prominent cause for dizziness and syncope was noted, it was decided to map and ablate the PACs. A duo-decapolar catheter (Livewire Steerable Catheter, St. Jude Medical) was placed, and the earliest activation during both sinus rhythm and PAC was seen in Halo 11, which was in the high right atrium at the junction of the donor and recipient atrium (Figure 2). 

A 3D activation map of the PAC was created using a 4 mm tip non-irrigated catheter and showed earliest activation at the superoanterior right atrium, where the superior vena cava and recipient atrial cuff joined the donor right atrium (Figure 4, Panel A). Detailed mapping clearly demarcated the donor from the recipient atria (Figure 4, Panel B). At this location, the earliest atrial activation was 90 ms before the proximal coronary sinus reference electrogram and had a QS pattern in the unipolar electrogram (Figure 3, Panel A). Ablation with a 4 mm non-irrigated catheter was unsuccessful, as we could not get good power delivery secondary to impedance rise. Therefore, an irrigated catheter with force sensing (TactiCath Quartz Contact Force Ablation Catheter, St. Jude Medical) was used. Ablation at the same location at 25 W resulted in successful PAC elimination in 3 seconds (Figure 3, Panel B). There was no evidence of sinus node slowing. Symptoms completely resolved following ablation, and no atrial arrhythmias were noted at 4-month follow-up. 

Case #2

A 67-year-old white male who underwent orthotopic heart transplantation with atrio-atrial anastomosis in 1990 was admitted in September 2014 with complaints of progressive shortness of breath and fatigue, and was noted to be in AT with 2:1 AV block and a ventricular rate of 100 bpm and RBBB. P-wave morphology was positive in V1 and biphasic to negative in inferior leads and positive in lead 1 (Figure 5). Transesophageal echocardiography showed normal left ventricular function and no evidence of intracardiac thrombus. Endomyocardial biopsy ruled out graft rejection. The patient underwent EP study for symptomatic AT. During EP study, the patient was noted to have AT with a cycle length of 335 msec and 2:1 AV block. Coronary sinus activation was proximal to distal. A duo-decapolar catheter was placed in the right atrium, and upon initial placement, showed atrial flutter in the proximal poles anterior to the anastomosis site in the donor atrium, and atrial fibrillation in the distal poles behind the anastomosis line in the recipient atrium. The recipient atrium was electrically isolated from the donor heart by the suture line (Figure 6). Entrainment from the cavotricuspid isthmus was concealed with the post-pacing interval equaling tachycardia cycle length. All these findings were consistent with cavotricuspid isthmus-dependent atrial flutter of the donor atrium while there was isolated atrial fibrillation of the recipient heart.

Cavotricuspid isthmus ablation was performed using an 8 mm tip ablation catheter placed through an SR0 sheath. An ablation line was created, with 3D mapping guidance to define the borders of the donor and recipient atrium, from the tricuspid annulus to the inferior suture line, resulting in slowing and termination of the flutter. Further ablation inferiorly near the suture line (Figure 7) resulted in bidirectional block with double potentials across the ablation line, which was maintained after a 30-minute waiting period. Normal sinus node, AV node, and His-Purkinje function were noted. 

Discussion

ATs have been shown to occur in 9%-15% of orthotopic heart transplant recipients,^1,2 whereas atrial fibrillation in the donor is rare and usually associated with acute graft rejection or allograft vasculopathy.^1,3 A higher incidence of atrial arrhythmias is noted in patients with atrio-atrial anastomoses.^2,4 The most common AT mechanism after orthotopic heart transplant is cavotricuspid isthmus-dependent flutter,^1,5 and catheter ablation of the isthmus from the tricuspid annulus to the inferoposterior suture line between the donor and recipient atria is usually curative.^1,6-7

In case #1 in our report, both donor and recipient atria were in sinus rhythm, albeit at different rates. An intact suture line between the donor and recipient electrically disconnects these segments of the atria. When both the donor and recipient atria are in sinus rhythm but have differing sinus rates, this can create confusion in the surface ECG as to the underlying rhythm. However, carefully marching the p-waves and associating the p-waves with the ensuing QRS usually can resolve this. However, in case #2, while the donor atrium was in atrial flutter, the recipient atrium was in atrial fibrillation, again dissociated from each other by the intact suture line. Prior case reports have described co-existence of different atrial arrhythmias in the recipient and donor atria.^7-9 In 2013, we reported for the first time the co-existence of 3 separate atrial arrhythmias in an orthotopic heart transplant patient, where the donor atrium was in typical atrial flutter, which was the patient’s clinical tachycardia, the recipient atrium was in a fast AT, and a third AT was a form of organized atrial fibrillation in a portion of the donor atrium that became electrically isolated from the rest of the donor atrium, likely due to a combination of surgical technique and progressive atrial myopathy (Figure 8).⁷ 

The presence of biatrial anastomosis and co-existence of more than one AT makes it challenging to accurately interpret diagnostic catheter data, identify the mechanism of the culprit AT, and determine the correct chamber to ablate. It is important to confirm electrical isolation between the donor and recipient atria when you have different arrhythmias in each. Paying close attention to changes in cycle length as well as local electrograms is crucial. Detailed electroanatomic mapping (voltage and/or activation) to identify the suture line and demarcate the borders of either segment of the atria can be very useful. Secondly, whenever possible, overdrive pacing from each segment should be performed to confirm exit block to the other side. Paying close attention to these aspects will ensure safe and effective ablation of post-transplant atrial arrhythmias.

Disclosure: The authors have no conflicts of interest to report regarding the content herein. Outside the submitted work, Dr. Olshansky reports he is a consultant and formal advisor to Boehringer Ingelheim and Daiichi Sankyo; a consultant to Medtronic, Biosense Webster, Executive Health Resource, BioControl, Janssen, and On-X; a formal advisor to Sanofi-Aventis, Lundbeck, and AltaThera Pharmaceuticals; a consultant, advisor, researcher, and on the DSMB to Boston Scientific; and a consultant, formal advisor, and on the DSMB for Amarin. Outside the submitted work, Dr. Gopinathannair reports personal fees as a consultant for St. Jude Medical and Boston Scientific; personal fees from Pfizer and Bristol-Myers Squibb for speakers’ bureaus, and personal fees for an advisory board from HealthTrust PG.

References

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