PERINODAL SLOW POTENTIAL AS A LOCAL GUIDE FOR TRANSCATHETER RADIOFREQUENCY ABLATION OF ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA - THERAPEUTIC EFFICACY AND ELECTROPHYSIOLOGICAL MECHANISMS OF SUCCESS

Background-A specific local indicator in the Koch's triangle could be critical to the complication-free treatment of atrioventricular nodal reentrant tachycardia by transcatheter radiofrequency ablation. Record ing of perinodal slow potential reflects a slow conduction area, and p robably indicates the location of the slow pathway component of the ci rcuit. Specific ablation of the slow pathway would carry the least ris k of atrioventricular block. Methods and results-Guided by the mapped perinodal slow potential, atrioventricular nodal reentrant tachycardia was successfully eliminated in all of 55 consecutive patients in one session. Fifty two patients (94.5%) had confirmed slow potential at th e final success sites. Despite the good result, the underlying electro physiological mechanisms of early from slow-potential-guiding ablation were heterogeneous: selective slow pathway eradication in 31 patients (56.4%, group A), selective slow pathway modification in 18 patients (32.7%, group B), inadvertent fast pathway damage in six patients (10. 9%, group Division of C). Group B patients had the preservation of dua l atrioventricular nodal pathways, adequate atrio-Hisian delay, fast p athway facilitation, and a higher frequency of inducible, single non-c onducted nodal echo (15/18, 83.3% v 6/31, 19.4% in group A, P << 0.001 ). The upper communicating path of the circuit was implicated as anoth er site of radiofrequency destruction. Three recurrences were document ed in follow up study. However, reablation by the same approach caused complete atrioventricular block in one patient (1.7%, 1/58 procedures ). None of the local characteristics of ablation sites was an independ ent predictor of procedure outcome. Conclusions-Perinodal slow potenti al is not a specific slow pathway indicator in transcatheter radiofreq uency ablation of atrioventricular nodal reentrant tachycardia. Multip le strategic sites of the reentry circuit may be damaged through simil ar local signals.