Abstract
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
Highlights
Radiofrequency catheter ablation (RFCA) of the slow atrioventricular (AV) nodal pathway, guided by anatomic landmarks or targeting the slow pathway potential from intracardiac electrograms, has become the treatment of choice in symptomatic patients with AV nodal re-entrant tachycardia (AVNRT).[1]
We suggest a possible relationship between the mechanism of tachycardia elimination in atrioventricular nodal re-entrant tachycardia (AVNRT) and an alteration of the re-entrant circuit by removal of the atrial tissue in Koch’s triangle
Based on the favorable clinical results, regardless of the presence of slow pathway following ablation, both the elimination of slow pathway conduction or persistence of dual AV node physiology without induction of AVNRT have been regarded as a successful radiofrequency catheter ablation (RFCA) end point of AVNRT
Summary
Radiofrequency catheter ablation (RFCA) of the slow atrioventricular (AV) nodal pathway, guided by anatomic landmarks or targeting the slow pathway potential from intracardiac electrograms, has become the treatment of choice in symptomatic patients with AV nodal re-entrant tachycardia (AVNRT).[1] Based on the favorable clinical results, regardless of the presence of slow pathway following ablation, both the elimination of slow pathway conduction or persistence of dual AV node physiology without induction of AVNRT have been regarded as a successful RFCA end point of AVNRT. The elimination of the slow pathway conduction is not required, in terms of a cure, for AVNRT with ablation.[2,3,4,5,6] the mechanism of noninducibility of AVNRT despite the remaining slow pathway is still unclear. To understand the mechanism of this noninducibility, we assessed changes in the electrophysiologic properties of the AV node after RFCA
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