ATRIOVENTRICULAR NODAL PHYSIOLOGY AFTER SLOW PATHWAY ABLATION

The AV nodal physiology before and 2 week after ''slow pathway potenti al'' guided catheter ablation was examined in 32 patients with AV noda l reentrant tachycardia. A mean of 4.9 applications of radiofrequency energy eliminated AV nodal reentrant tachycardia in all patients. Ther e were no significant differences in sinus cycle length (815 +/- 159 m sec vs 813 +/- 162 msec; P = NS) and fast pathway conduction propertie s before and 1 week after ablation. Slow pathway conduction was comple tely eliminated in 10 (31%) (group I) of 32 patients after ablation. I n the remaining 22 patients residual slow pathway conduction associate d with one AV node echo was observed. In 15 patients (47%) (group II), the effective refractory period of the slow pathway showed a change o f < 30 msec (265 +/- 51: vs 266 +/- 51 msec; P NS), and in 7 patients (22%) (group III), a prolongation of more than 80 msec (247 +/- 56 vs 340 +/- 42 msec; P = 0.0001) before and 2 week after ablation. Minimal and maximal A(2)-H-2 interval over the slow pathway in group II was n ot significantly changed (Min A(2)-H-2: 241 +/- 37 vs 247 +/- 40 msec; P = NS, Max A(2)-H-2: 346 +/- 79 vs 350 +/- 60 msec; P = NS), while a significant prolongation was measured in group III (Min A(2)-H-2: 261 +/- 53 vs 373 +/- 107 msec; P < 0.01, Max A(2)-H-2: 359 +/- 41 vs 427 +/- 63 msec; P < 0.05) before and after ablation. Conclusion: In grou p II patients there was no evidence shown of impairment of the slow pa thway. This suggests that disruption of the link between fast and slow path ways may be responsible for the elimination of AV nodal reentran t tachycardia, besides the elimination or impairment of the slow pathw ay itself, in ''slow pathway potential'' guided catheter ablation, and that the slow pathway potential may not necessarily represent activat ion of the slow pathway itself or of its atrial connection.