Journal of cardiovascular electrophysiology · 1995
Slowing of the ventricular rate during atrial fibrillation by ablation of the slow pathway of AV nodal reentrant tachycardia.
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Tebbenjohanns J, Pfeiffer D, Schumacher B, Jung W, Manz M, Lüderitz B
Аннотация
INTRODUCTION: The mechanisms whereby radiofrequency catheter modification of AV nodal conduction slows the ventricular response are not well defined. Whether a successful modification procedure can be achieved by ablating posterior inputs to the AV node or by partial ablation of the compact AV node is unclear. We hypothesized that ablation of the well-defined slow pathway in patients with AV nodal reentrant tachycardia would slow the ventricular response during atrial fibrillation.
METHODS AND RESULTS: In 34 patients with dual AV physiology and inducible AV nodal reentrant tachycardia, atrial fibrillation was induced at baseline and immediately after successful slow pathway ablation and at 1-week follow-up. The minimal, maximal, and mean RR intervals during atrial fibrillation increased from 353 +/- 76, 500 +/- 121, and 405 +/- 91 msec to 429 +/- 84 (P < 0.01), 673 +/- 161 (P < 0.01), and 535 +/- 98 msec (P < 0.01), respectively. These effects remained stable during follow-up at 1 week. The AV block cycle length increased from 343 +/- 68 msec to 375 +/- 60 msec (P < 0.05) immediately and to 400 +/- 56 msec (P < 0.01) at 1-week follow-up. The effective refractory period of the AV node prolonged from 282 +/- 83 msec to 312 +/- 89 msec and to 318 +/- 81 msec after 1 week (P < 0.05), respectively.
CONCLUSION: This study shows a decrease in ventricular response to pacing-induced atrial fibrillation after ablation of the slow pathway in patients with AV nodal reentrant tachycardia. Since the AV nodal conduction properties could be defined, this study supports the hypothesis that the main mechanism of AV nodal modification in chronic atrial fibrillation is caused by ablation of posterior inputs to the AV node.
METHODS AND RESULTS: In 34 patients with dual AV physiology and inducible AV nodal reentrant tachycardia, atrial fibrillation was induced at baseline and immediately after successful slow pathway ablation and at 1-week follow-up. The minimal, maximal, and mean RR intervals during atrial fibrillation increased from 353 +/- 76, 500 +/- 121, and 405 +/- 91 msec to 429 +/- 84 (P < 0.01), 673 +/- 161 (P < 0.01), and 535 +/- 98 msec (P < 0.01), respectively. These effects remained stable during follow-up at 1 week. The AV block cycle length increased from 343 +/- 68 msec to 375 +/- 60 msec (P < 0.05) immediately and to 400 +/- 56 msec (P < 0.01) at 1-week follow-up. The effective refractory period of the AV node prolonged from 282 +/- 83 msec to 312 +/- 89 msec and to 318 +/- 81 msec after 1 week (P < 0.05), respectively.
CONCLUSION: This study shows a decrease in ventricular response to pacing-induced atrial fibrillation after ablation of the slow pathway in patients with AV nodal reentrant tachycardia. Since the AV nodal conduction properties could be defined, this study supports the hypothesis that the main mechanism of AV nodal modification in chronic atrial fibrillation is caused by ablation of posterior inputs to the AV node.