1999 年 40 巻 3 号 p. 281-293
The changes in the duration of atrial electrograms during different atrial activation sequences from a sinus rhythm were evaluated to test the hypothesis that the prolongation of atrial electrogram duration caused by the different atrial activation sequence is more prominent at the site of atrial fibrillation (Afib) genesis (initiation site) than other areas. In 39 patients with single retrogade left-sided accessory connection who had inducible transient atrial fibrillation during an electrophysiologic study, the site of Afib genesis was determined and classified into three groups, i.e., 1) high right atrial genesis (HRA), 2) low right atrial genesis (LRA), and 3) left atrial genesis (LA). Single premature extrastimuli after 8 basic drive trains (600 ms) were delivered at the HRA and the right ventricular apex. Three atrial electrophysiologic parameters were evaluated at three atrial sites, i.e., 1) HRA, 2) LRA, and 3) coronary sinus. The atrial vulnerability parameters were as follows; 1) %A2/A1: % prolongation of atrial electrogram duration during premature beat (A2) in comparison with basic drive (A1), 2) wavelength index (WLI): calculated as [effective refractory period]/[A2], and 3) retrograde activation index (RAI): calculated as [A1 during retrograde activation; i.e., RVA pacing/[A1 during antegrade activation, i.e., HRA pacing], shown as a percentage. The Afib genesis was HRA in 20, LRA in 12 and LA in 7 patients. At the HRA recording site, %A2/A1 and RAI were the largest and WLI the shortest in the HRA genesis group in comparison with the other two groups. Similarly, at the LRA and LA recording sites, %A2/A1 and RAI were the largest and WLI the shortest in the groups with Afib genesis at these recording sites. In patients with inducible Afib, %A2/A1 and RAI were the highest and WLI the shortest at the atrial recording site close to the site of Afib genesis. Atrial wave prolongation during retrograde atrial activation, possibly the anisotropic conduction, was considered to play a role in initiating Afib as well as a conduction delay during the atrial premature beat.