ABLATION
Transient atrioventricular block shortly after uneventful cryoablation of atrioventricular nodal re-entrant tachycardias: report of two cases
Cardiology Department, Hospital General Universitario ‘Gregorio Marañón’, Calle Doctor Esquerdo 46, Madrid 28007, Spain
Manuscript submitted 14 December 2006. Accepted after revision 7 June 2007.
* Corresponding author. Tel: +34 91 586 8276; fax: +34 91 586 8290. E-mail address: etorrecilla{at}telefonica.net
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Abstract |
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We report two patients with atrioventricular (AV) nodal re-entrant tachycardias who developed transient AV block immediately after uneventful cryoablation of the slow pathway was completed. No tachycardia recurrences were observed after an asymptomatic follow-up of 12 months and 10 months, respectively. This is the first report of this unexpected, transient phenomenon. The exact mechanism(s) remain(s) unclear.
Key Words: Ablation, Cryoablation, atrioventricular block
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Introduction |
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Cryothermal ablation of the slow pathway has become a useful, safe technique for the elimination of atrioventricular (AV) nodal re-entrant tachycardias.1
–7 The ability of cryothermal technology to test the functionality of specific ablation sites (ice mapping) before production of a permanent lesion (cryoablation) may eliminate inadvertent AV block. Absence of accelerated junctional tachycardia and its possible presence on rewarming are new phenomena observed with this novel technique.1 In addition, transient AV conduction block during cryoablation following normal cryomapping has been recently reported in some cases.4,7–9 However, to our knowledge, no adverse effects on AV conduction soon after uneventful cryoablation have been previously published. From June 2002, 51 patients with recurrent episodes of AV nodal re-entrant tachycardias underwent cryoablation procedures in our laboratory. We present two children with AV nodal re-entrant tachycardias who developed transient AV nodal block shortly after uneventful cryoablation of the slow pathway was completed. Both patients were followed-up in the outpatient clinic every 3 months, with serial ECGs and a 24 h Holter monitor recording at 6 months of the procedure. |
Cases report |
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Case 1
The patient was a 8-year-old, 46 kg boy with documented episodes of paroxysmal, regular narrow QRS complex tachycardias. Under general anaesthesia, 3 5F quadripolar catheters were inserted percutaneously via the femoral vein and positioned in the high right atrium, His-bundle region, and right ventricular apex. A fourth 5F multipolar catheter was inserted via a left brachial vein and placed inside the coronary sinus. Dual AV nodal pathways were manifested with one atrial extrastimulus. Under i.v. isoproterenol infusion (1 µg/min), two atrial extrastimuli reproducibly initiated an AV nodal re-entrant tachycardia (R–R interval: 235 ms) with the earliest retrograde atrial activation in the proximal His-bundle region (Figure 1A). Catheter ablation was performed using a combination of anatomic and electrophysiologic markers. Atrial and ventricular electrograms were verified so that the ratio of their amplitudes before application was
1:3. Cryoablation of the slow-pathway was performed using a Freezor 3 CRYOCATH 7F 4 mm tip tetrapolar catheter (Cryocath Technologies Inc.; Québec, Canada). After uneventful, successful cryomapping procedures (–30°C)2, two corresponding cryoablation attempts (–70°C, 4 min) were performed in the inferior–posterior triangle of Koch and midseptal region, respectively. Accelerated AV junctional rhythms with preserved ventriculoatrial conduction were seen on rewarming after unsuccessful cryoablation in the midseptal region (Figure 1B). A last third cryoablation attempt was performed immediately in the same location (Figure 2A) after effective ice mapping. Six seconds after termination of this application, a high degree AV nodal block appeared lasting 7 s, after which normal AV conduction suddenly resumed (Figure 2B), and the tachycardia was no longer inducible with persistent dual AV nodal pathways. No catheter manipulation was performed before the episode. No recurrences have been observed during 12 months of otherwise asymptomatic follow-up.
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Case 2
The patient was an 11-year-old, 47 kg girl with recurrent episodes of regular palpitations without electrocardiographic recordings. Under general anaesthesia, 3 5F quadripolar catheters were inserted via the femoral vein and positioned in the high right atrium, His-bundle region, and right ventricular apex. A 5F multipolar catheter was placed in the coronary sinus. Under basal conditions, dual AV pathway physiology was demonstrated with one atrial extrastimulus. Isoproterenol infusion facilitated the induction of a regular narrow QRS complex tachyarrhythmia (R–R interval: 275 ms) that was diagnosed as AV nodal re-entrant tachycardia based on published standard criteria (Figure 3A). The ventriculoatrial interval in high right atrium measured 75 ms and the earliest retrograde atrial activation during tachycardia was located in the proximal coronary sinus as clearly shown after entrainment of the tachycardia during pacing from the right ventricular apex (Figure 3B). Cryoablation procedure of the slow-pathway was performed using the same catheter and methods as described in the previous case. After uneventful, successful cryomapping pulses (–30°C), three corresponding cryoablation attempts (–70°C, 4 min) were performed in the inferior–posterior triangle of Koch between the inferior edge of the os of the coronary sinus and the tricuspid valve on the right anterior oblique projection. An accelerated AV junctional rhythm lasting 6.6 s without loss of ventriculoatrial conduction was seen on rewarming after the second unsuccessful cryoablation attempt (Figure 3C). The third definitive cryoablation pulse in the same anatomical position ended without events showing a normal AV interval (Figure 4A). Unexpectedly, a complete AV nodal block developed 11 min later (Figure 4B) lasting 80 s and followed by a 5 min period of prolonged PR interval (240 ms) (Figure 4C) up to total AV conduction recovery. No mechanical catheter manipulation was performed before the episode. The tachycardia was no longer inducible without demonstrable dual AV nodal physiology. No recurrences were observed during 10 months of asymptomatic follow-up.
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Discussion |
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We report the unexpected development of transient AV block shortly after uneventful cryomapping and cryoablation in two children with AV nodal re-entrant tachycardias. High-degree or complete, transient AV block during cryoablation after previous ‘safe’ cryomapping at the same location has been reported in 2–23% of patients from recent series of AV nodal re-entrant tachycardias.4
,7–9 Neither permanent AV block nor late consequences on AV conduction have been described in these patients. However, no AV conduction block shortly after uneventful cryoablation has been previously reported. It appears to be an uncommon (4% in our experience), previously undescribed phenomenon and the mechanism by which this occurred is unclear. The mechanism of lesion creation by cryothermal ablation is complex,10 and much of the data on tissue injury have been obtained in non-cardiac muscle. However, accelerated junctional rhythms were seen on rewarming of previous cryoablation attempts in both cases and this known phenomenon after cryoenergy application may represent a non-specific response of the AV node to transient ‘injury’.2 One may speculate that temporary temperature gradient on rewarming soon after cryoablation could induce a transient AV nodal conduction abnormality through possible, reversible cellular swelling with disruption of cellular membranes. A posterior-type AV nodal re-entrant tachycardia was induced in case 2 and it is known that the presence of this posterior fast AV node pathway may account for sporadic examples of inadvertent AV block, consistent with concurrent slow pathway damage.11 The latter could act as an additive factor accounting for the greater impairment in AV conduction properties observed in this patient. Nevertheless, the long period (11 min) between the end of cryoenergy application and the onset of complete AV nodal block is surprising. One could hypothesize that specific tissue injury characteristics of cryoenergy such as possible ice-mapping phenomenon in the periphery from the centre of the application site, and/or a possible vascular-related response could be implicated in this unexpected finding. Additionally, even with the lack of a specific manipulation of a relatively rigid cryoablation catheter, we would not rule out the possibility of a mechanical trauma to the AV node.7 Although a very slight movement of the catheter that might not be easily perceived by fluoroscopy is common when cryoadherence disappears, no catheter motion artifacts were observed on the ablation and/or His catheters. Finally, a late development of persistent high grade AV block cannot be ruled out by our relatively short periods of follow-up. In addition, transient episodes of advanced AV block would be underdetected by our ambulatory ECG monitoring. According to our initial experience, although it is important to maintain vigilance in monitoring for AV nodal conduction abnormalities shortly following normal cryoablation of AV nodal re-entrant tachycardias, the development of AV nodal block soon after uneventful cryothermal ablation seems to be an uncommon, transient phenomenon. It is presumed that tissue effects that occur late during a cryothermal application are expected to be reversible.
Conflict of interest: none declared.
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References |
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[1] Dubuc M, Talajic M, Roy D, Thibault B, Leung TK, Friedman PL. Feasibility of cardiac cryoablation using a transvenous steerable electrode catheter. J Interv Card Electrophysiol (1998) 2:285–92.[CrossRef][Web of Science][Medline]
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[6] Gupta D, Al-lamee RK, Earley MJ, Kistler P, Harris SJ, Nathan AW, et al. Cryoablation compared with radiofrequency ablation for atrioventricular nodal re-entrant tachycardia: analysis of factors contributing to acute and follow-up outcome. Europace (2006) 8:1022–6.
[7] Collins KK, Dubin AM, Chiesa NA, Avasarala K, Van Hare GF. Cryoablation versus radiofrequency ablation for treatment of pediatric atrioventricular nodal reentrant tachycardia: initial experience with 4-mm cryocatheter. Heart Rhythm (2006) 3:564–70.[CrossRef][Web of Science][Medline]
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[9] Kimman GP, Theuns DAMJ, Szili-Tovok T, Scholten MF, Res JC, Jordaens LJ. CRAVT: a prospective, randomized study comparing transvenous cryothermal and radiofrequency ablation in atrioventricular nodal reentrant tachycardia. Eur Heart J (2004) 25:2232–7.
[10] Lustgarten DL, Keane D, Ruskin J. Cryothermal ablation: mechanism of tissue injury and current experience in the treatment of tachyarrhythmias. Prog Cardiovasc Dis (1999) 41:481–98.[CrossRef][Web of Science][Medline]
[11] Engelstein ED, Stein KM, Markowitz SM, Lerman BB. Posterior fast atrioventricular node pathways: implications for radiofrequency catheter ablation of atrioventricular node reentrant tachycardia. J Am Coll Cardiol (1996) 27:1098–105.[Abstract]
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