Europace Advance Access published online on May 24, 2008
Europace, doi:10.1093/europace/eun132
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CASE REPORT
Successful radiofrequency catheter ablation of atrial fibrillation late after modified Fontan operation
1 Department of Pediatric Cardiology, Tokyo Women’s Medical University, 8-1, Kawada-cho, Shinjuku-ku, Tokyo 162-8666, Japan; 2 Department of Cardiology, Tokyo Women’s Medical University, Tokyo, Japan
Manuscript submitted 19 February 2008. Accepted after revision 26 April 2008.
* Corresponding author. Tel: +81 3 3353 8111; fax: +81 3 3356 0446. E-mail address: bigkaz{at}mua.biglobe.ne.jp
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Abstract |
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The mechanisms responsible for atrial fibrillation (AF) in post-operative Fontan patients are unclear, and the role of catheter ablation for treating AF is not well defined. We present a case of an 18-year-old woman who experienced drug-resistant paroxysmal AF late after the Fontan operation. We eliminated the AF by the radiofrequency catheter ablation of atrial substrates with complex fractionated atrial electrograms (CFAEs). The patient remains on anti-arrhythmic therapy and has not experienced any recurrence since the catheter ablation. Right atrial substrate modification via a CFAE-targeted catheter ablation might be an adjunct therapeutic option for selected post-Fontan patients with AF.
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Introduction |
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The prevalence of atrial fibrillation (AF) following the Fontan operation has increased.1
However, the mechanisms responsible for AF in this population are not well understood, and the role of therapeutic catheter ablation has not been addressed, despite successful pulmonary vein isolation for paroxysmal AF and atrial substrate modification targeting complex fractionated atrial electrograms (CFAEs)2 in patients without congenital heart disease (CHD). We describe a patient, treated with a classical Fontan operation for tricuspid atresia (TA), who underwent successful catheter ablation for paroxysmal AF. |
Case report |
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An 18-year-old woman with TA underwent an atriopulmonary connection Fontan operation with a direct replacement of the atrial septum at the age of 12. Five years later, she was referred to our institute for frequent episodes of AF, despite anti-arrhythmic drug therapy. We found the patient slightly cyanosed with a right-to-left shunt via persistent left superior vena cava (PLSVC) through the coronary sinus (CS) rerouted to the left atrium (LA). Echocardiography revealed normal ventricular function and no mitral regurgitation. The electrocardiogram (ECG) exhibited paroxysmal AF with a ventricular rate between 70 and 100 (Figure 1A).
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We obtained written informed consent from the patient and an electrophysiological analysis was performed (patient fasting and non-sedated). All oral anti-arrhythmic medications were stopped 3 days prior. The bipolar intra-cardiac electrograms were filtered through a 30–500 Hz band pass and recorded on a Cardiolab system (Prucka Engineering Inc., Houston, TX, USA) simultaneously with a 12-lead ECG. The AF cycle length (CL) was calculated using the Cardiolab system with digital calipers. Bipolar stimulation was performed (output amplitude, two times the diastolic threshold; pulse width, 2 ms). Simultaneous multi-site mapping with a 7-Fr, 20-pole, deflectable Halo catheter (10-mm paired spacing; Cordis-Webster Inc., Baldwin Park, CA, USA) in the right atrium (RA) and a 2.5-Fr, 16-pole, microcatheter (PathfinderTM, Cardima Inc., Fremont, CA, USA) in the LA, through the CS via the PLSVC was performed (Figure 1B). Atrial fibrillation was easily induced by rapid atrial pacing. The fibrillation CL was <150 ms in the free wall of the RA and 180–220 ms in the CS. A 7-Fr quadripolar 4-mm tip electrode catheter with a thermocouple was introduced into the RA for mapping, stimulation, and ablation. The intra-cardiac atrial electrograms displayed CFAEs located in the free wall of the giant RA and the lower interatrial septum; radiofrequency (RF) energy was applied to those areas during AF (Figure 1C). Afterwards, most electrograms disappeared in association with organization of the atrial electrograms in the area adjacent to the ablated areas. After eight applications of RF, the AF evolved into a relatively organized AF and then into a macro-re-entrant atrial tachycardia (AT). We delivered additional RF to reinforce the ablation in the adjacent areas, targeting the RF to the areas of continuous fragmented electrograms between the double potentials during diastole. Finally, the macro-re-entrant AT was interrupted and sinus rhythm restored (Figure 2).
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Following the ablation, neither CS nor lateral RA pacing induced any AF. The ablation sites are shown in Figure 3A. The bipolar voltage map obtained during sinus rhythm (CARTO) confirmed that the low-voltage areas were in the free wall of the RA (Figure 3B). No tachycardia was experienced during 1-year of follow-up. An ambulatory 24-h ECG revealed occasional atrial premature beats.
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Discussion |
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The aetiology, mechanism, and clinical significance of AF in post-Fontan patients are not well characterized. Similarly, the specific mechanism responsible for AF in our case is unclear. However, possibilities included focal AT with fibrillatory conduction locally with organized activity or atrial flutter with complex conduction in the RA. First, this report clearly demonstrates that an RA-limited ablation eliminated the AF. Specifically, it highlights the potential role of the RA in perpetuating AF in post-Fontan patients and illustrates how such patients could benefit from RA-limited procedures, similar to intra-atrial re-entrant tachycardia (IART), a highly structured macro-re-entrant rhythm typically involving the RA, and might respond to interventions that target specific re-entrant circuits anatomically.3
,4 Chen and colleagues5 reported a non-CHD case in which AF was treated by the catheter ablation of conduction gaps in the crista terminalis and cavotricuspid isthmus of the RA. Similarly, in our case, a conduction blockage could have been formed by the catheter ablation of the tissue in the gaps between the scars, and the transition from AF to IART could have been a result of the line of conduction block. Secondly, the CL measurement in our patient exhibited a frequency gradient from the RA to the LA. This finding would support the fact that the RA was the source of AF in this patient analogously based on the recent evidence from high-density mapping and spectral analysis showing that paroxysmal AF has a frequency gradient from the LA to the RA. However, this topic should be explored using a dominant frequency analysis, a more robust and objective measure of the local activation frequency. Furthermore, there is an important limitation of the CFAEs' definition and assessment, which were based on subjective analysis by the operator. Further research is clearly required to define the exact mechanism of the AF late after the Fontan operation. If our findings are confirmed, recommendations for treating arrhythmias late after the Fontan operation should be reconsidered.
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Conclusion |
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The CFAEs areas in the RA were critical for perpetuating the AF after the Fontan operation and were susceptible to catheter ablation. Although optimization of this procedure requires further analysis in these types of patients, right atrial substrate modification via CFAE-targeted catheter ablation might be an option for post-operative Fontan patients with paroxysmal AF.
Conflict of interest: none declared.
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References |
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[1] Kirsh JA, Walsh EP, Triedman JK. Prevalence of and risk factors for atrial fibrillation and intra-atrial reentrant tachycardia among patients with congenital heart disease. Am J Cardiol (2002) 90:338–40.[CrossRef][Web of Science][Medline]
[2] Nademanee K, McKenzie J, Kosar E, Schwab M, Sunsaneewitayakul B, Vasavakul TK, et al. A new approach for catheter ablation of atrial fibrillation: mapping of the electrophysiologic substrate. J Am Coll Cardiol (2004) 43:2044–53.
[3] Triedman JK, Alexander ME, Love BA, Collins KK, Berul CI, Bevilacqua LM, et al. Influence of patient factors and ablative technologies on outcomes of radiofrequency ablation of intra-atrial re-entrant tachycardia in patients with congenital heart disease. J Am Coll Cardiol (2002) 39:1827–35.
[4] de Groot NM, Zeppenfeld K, Wijffels MC, Chan WK, Blom NA, Van der Wall EE, et al. Ablation of focal atrial arrhythmia in patients with congenital heart defects after surgery: role of circumscribed areas with heterogeneous conduction. Heart Rhythm (2006) 3:526–35.[CrossRef][Web of Science][Medline]
[5] Liu TY, Tai CT, Chen SA. Treatment of atrial fibrillation by catheter ablation of conduction gaps in the crista terminalis and cavotricuspid isthmus of the right atrium. J Cardiovasc Electrophysiol (2002) 13:1044–6.[CrossRef][Web of Science][Medline]
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