Atrial tachycardia after cryoballoon ablation of paroxysmal atrial fibrillation

We read with interest the paper by Mikhaylov et al.1 regarding atrial tachycardia (AT) after cryoballoon ablation (CBA), the technology oriented for pulmonary vein (PV) isolation.2 We believe that the results should be considered on three levels: related to patient, procedure, and follow-up (FU) characteristics. Characteristics of patients with AT (PAT) showed that they had significantly higher AT burden and more frequent AT before CBA, i.e. these patients had ‘more advanced’ stage of atrial disease (deeper remodelling), with more arrhythmia-prone atria.3 Appearance of AT after CBA in these individuals could be a result of unmasking ‘secondary’ arrhythmias after eliminating ‘primary’ atrial fibrillation (AF) and/or the existence of non-LA–PV arrhythmogenic loci within atria which were not eliminated by CBA. The prolonged fluoroscopy time in PAT was most probably related to atypical PV anatomy (higher number of common left PVs and additional right PV in PAT) and the need for additional ‘touch-ups’. These local lesions could result in promoting pro-arrhythmic region, similar to CFAE. In addition, one cannot exclude worse cryoballoon–tissue contact and PV occlusion (missing data), and in consequence, development of pro-arrhythmic non-transmural lesion.4 Finally, producing transmural lesion in LAA ridge (a possible ‘firing source from the area adjacent to the LSPV’ in one PAT),1 a known pro-arrhythmic localization, could be challenging with cryoballoon. Atrial tachycardia developed in total 14 patients, in 10 during first 3 months. As a result of a ‘healing process’, in 5 of these 10 patients no AT was present at FU > 3 months. Among nine other patients who required repeated procedure, typical cavo-tricuspid isthmus-dependant atrial flutter (CTIAFL) and focal left AT were re-ablated in four and two cases, respectively. Appearance of CTIAFL after CBA should be understood in terms of unmasked ‘secondary’ arrhythmia after eliminating the ‘primary’ AF. In one patient AT was not inducible during redo procedure (but with no AT in FU after repeated CBA), which would suggest rather non-reentrant but focal mechanism of AT. Two patients refused repeated procedure, hence the mechanism of AT is unknown. Reentrant mechanism, especially in ostial (23 mm) CBA cannot be excluded due to non-ipsilateral lesion. In fact, the model of regression analysis is limited by low number of AT in FU. Moreover, anti-arrhythmic therapy, including beta-blockers (BBs), were allowed >3 months and terminated ‘when no arrhythmia occurred’.1 Higher number of patients on BB in PAT group (63 vs. 31%) would suggest higher arrhythmia recurrences in PAT giving the next proof of more arrhythmia-prone atria in PAF group. Consequently, AT after CBA were more frequently observed in: patients with more arrhythmia-prone atria (individuals with higher AT burden, more frequent AT before CBA, and higher need for BB after CBA); patients in whom the procedure was more labourious and possibly more challenging for an operator (atypical anatomy followed by prolonged fluoroscopy time and need for additional ‘touch-up’ lesions). Conflict of interest: M.W. was supported by the European Heart Rhythm Association (2-year Clinical Electrophysiology Fellowship, 2007–09); T.