Conduction over and around the atrioventricular node: author's reply

We are grateful to Sun et al.¹ for their interest in our study,² and their kind words. The authors raise two important issues.

First, retrograde atrial activation patterns during atrioventricular nodal re-entrant tachycardia (AVNRT). We believe that following the seminal study of Anselme et al.,³ heterogeneity of both fast and slow conduction patterns has been well described, and all forms of AVNRT may display anterior, posterior, and middle retrograde activation patterns.⁴ There has also been evidence that were left septal His recordings routinely performed in patients with AVNRT, the proportion of left-sided retrograde fast pathways might be considerably higher than previously reported.⁵ More important, according to our experience, retrograde activation sequence may even change during the arrhythmia in the same patient. Thus, in our view, retrograde activation patterns are of limited value. Having said that, further elucidation of the nature of ‘fast’ conduction in AVNRT, as suggested by Sun et al., is badly needed. We have attempted to handle the issue by means of comparing intervals in the same patient with both typical and atypical AVNRT types.⁶ Our data indicated that the notion of ‘fast-slow’ AVNRT is meaningless. ‘Fast pathway’ conduction is not the same in all AVNRT forms.

Second, regarding our working hypothesis in our first study about anterograde and retrograde fast pathway conduction, this was based on the evidence on accessory pathways, indicating similar conduction velocity in both directions.⁶ If the histologically proven multiple superior atrial inputs to the AV node facilitate fast conduction, as proposed by the anatomical model,⁷ this should be a legitimate assumption. With respect, the study of Akhtar et al. which the authors refer to, is not closely relevant to the discussion; it deals with AV anterograde and retrograde conduction, i.e. over the AV node, not with conduction over the fast or slow pathways of AVNRT.

Regardless, we do concur with Sun et al. that further studies are needed on this fascinating, and very common, arrhythmia. The mechanism(s) of conduction patterns during AVNRT still elude us. Recent studies suggest a three-dimensional AV node with greater variability in the space constant of tissue and poor gap junction connectivity due to differential expression of connexin isoforms that provide an explanation of dual conduction and nodal re-entrant arrhythmogenesis. Our two-dimensional models may not be adequate, therefore, and a more in-depth analysis with probabilistic approaches and multi-dimensional computer simulations may be useful. Such an effort is being undertaken in our laboratory in collaboration with colleagues from the mathematical faculties.

Conflict of interest: none declared.

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