Background. In case of persistent atrial fibrillation (AF), atrial substrate assumes a dominant role in sustaining the arrhythmia. Recent studies prove that low voltage areas (LVA, Voltage Amplitude < 0,5 mV) represent an additional target for ablation of AF patients.
Purpose. The purpose of this study is to analyse whether structural atrial conduction abnormalities (i.e., pivot sites and slow conduction corridors) may occur outside low voltage areas.
Methods. The study is based on the retrospective analysis of 31 consecutive maps of patients undergoing AF ablation (16 paroxysmal and 15 persistent cases). The clinical procedures have been performed with the support of a mapping system. Sinus rhythm activation maps and bipolar maps used for this analysis have been created with a multipolar mapping catheter. Map points were only acquired when the electrode was in contact with the endocardial tissue to avoid misleading voltage amplitude information. Slow conduction corridors and pivot sites have been analysed. At these sites, EGMs characterization included voltage amplitude (mV), signal duration (ms) and fractionation.
Results. The average value of EGMs amplitude reported at pivot sites and slow conduction zones, respectively, amounted to 2,08 ± 0,63 mV and 2,1 ± 0,66 mV in paroxysmal cases. In persistent cases, there were slight decreased values to 1,95 ± 0,93 mV and 1,89 ± 0,89 mV. Characterization at pivot sites documented a mean duration value of 45,4 ± 4,64 ms and 49,93 ± 5,51 ms in paroxysmal and persistent patients, respectively, while in slow conduction zones 41,53 ± 7,94 ms and 49,04 ± 6,41 ms have been reported. As for fractionation, more than five deflections per signal have been identified in all abnormal conduction areas.
Conclusion. Our study proves that functional electrophysiological phenomena can occur outside low voltage areas, even in persistent cases. According to this analysis, not all LVA represent the correct target for catheter ablation, encouraging the development of further methods for investigation of atrial substrate.