Int J Arrhythm.
2016 Mar;17(1):6-13. 10.18501/arrhythmia.2016.001.
Changes in Atrioventricular Node Physiology Following Slow Pathway Modification in Patients with AV Nodal Re-entrant Tachycardia: The Hypothetical Suggestion of Mechanism of Noninducibility of AVNRT
- Affiliations
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- 1Division of Cardiology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul, Korea. myleecardio@catholic.ac.kr
- KMID: 2308902
- DOI: http://doi.org/10.18501/arrhythmia.2016.001
Abstract
- BACKGROUND AND OBJECTIVES
In cases of radiofrequency catheter ablation (RFCA) for patients with atrioventricular nodal re-entrant tachycardia (AVNRT), complete elimination of slow pathway is not always achievable. Furthermore, in situations of the so-called modified slow pathway, the underlying mechanism of tachycardia elimination remains unclear.
SUBJECTS AND METHODS
Patients who underwent RFCA for AVNRT, and showed persistence of dual atrioventricular nodal physiology but no induction of AVNRT after ablation were enrolled. We measured electrophysiologic parameters before and after the ablation procedure.
RESULTS
The study subjects included 31 patients (39% men; mean age 43±19 years). The RR interval, Wenckebach cycle length of AV node, slow pathway effective refractory period, maximal AH interval of fast pathway and slow pathway showed no significant changes before and after ablation. However, fast pathway effective refractory period (360±67 vs. 304±55, p<0.001) and differences between slow pathway effective refractory period and fast pathway effective refractory period (90±49 vs. 66±35, p=0.009) were decreased after slow pathway ablation.
CONCLUSION
We suggest a possible relationship between the mechanism of tachycardia elimination in AVNRT and an alteration of the re-entrant circuit by removal of the atrial tissue in Koch's triangle. This may be a critical component of providing the excitable gap for the maintenance of tachycardia rather than the electrical damage of slow pathway itself.
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