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. 2014 Aug 1;592(Pt 15):3173. doi: 10.1113/jphysiol.2014.275404

Rebuttal from Maurits Allessie and Natasja de Groot

Maurits Allessie 1,, Natasja de Groot 2
PMCID: PMC4146365  PMID: 25085971

Wishful thinking or scientific fact?

The evidence provided by Narayan & Jalife (2014) that human atrial fibrillation (AF) is maintained by a stable rotor is mainly limited to the work of Narayan and coworkers (Narayan et al. 2012, 2013; Shivkumar et al. 2012). Dr Narayan is founder of the Topera company that has developed an algorithm that computes complete activation maps from a limited number of intra-atrial signals recorded with a basket catheter. In contrast to these computed maps, direct high-resolution mapping has been unable to show stable rotors (Allessie et al. 2010; de Groot et al. 2010; Lee et al. 2014). Narayan & Jalife (2014) argue that this is due to the small number of patients. However, since the Topera maps showed electrical rotors in practically all patients (Narayan et al. 2012; Shivkumar et al. 2012), it seems unlikely that our group of 49 patients was too small to find a rotor. Also, after increasing the mapping area to the entire epicardial surface (>60 cm2), we failed to elucidate stable rotors during human AF. Although the reasons for this discrepancy remain unclear, denying the high degree of complexity of human AF as demonstrated by high-resolution mapping is like throwing away your microscope and saying that bacteria do not exist.

How difficult can it be?

If it is true that human AF is driven by a stable rotor, it should not be too difficult to demonstrate the validity of the Topera maps. With the basket catheter in place and the rotor map at hand, it would take not more than 5–10 min to make a detailed direct-contact map of the rotor area, using a single steerable electrode and a CARTO system. However, the existence of regular monomorphic electrograms during persistent human AF has not been demonstrated yet. Not to mention that the supposed rotors have never been documented by a series of stable high-quality electrograms around its repetitive circular path.

Clinical efficacy of rotor ablation?

The main argument of Narayan & Jalife (2014) is ‘…the ability of brief targeted ablation to eliminate AF acutely and on long-term follow-up’. However, the CONFIRM trial (Narayan et al. 2012) is an observational study not designed to prove clinical efficacy of rotor ablation (not randomized, no inclusion/exclusion criteria, single-centre, 33 patients underwent prior conventional ablation). Despite the fact that all FIRM guided patients also received a full conventional ablation procedure, AF actually terminated in only about half of the cases. The claimed superiority of rotor ablation thus cannot be regarded as a scientific fact. As long as clinical success of the Topera machine has not been proven in a well-designed clinical trial by independent investigators, the claim that atrial fibrillation is based on a localized source of rapid impulses creates false hope that the complex pathological substrate of AF can be cured by a relatively simple ablation procedure.

Call for comments

Readers are invited to give their views on this and the accompanying CrossTalk articles in this issue by submitting a brief comment. Comments may be posted up to 6 weeks after publication of the article, at which point the discussion will close and authors will be invited to submit a ‘final word’. To submit a comment, go to http://jp.physoc.org/letters/submit/jphysiol;592/15/3173

Additional information

Competing interests

None declared.

References

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