“Dormant” Pulmonary Vein Conduction Revealed by Adenosine after Ostial Radiofrequency Catheter Ablation

Authors


  • Manuscript received 16 January 2004; Accepted for publication 26 April 2004.

Address for correspondence: Thomas Arentz, M.D., Herzzentrum, Abteilung Rhythmologie, Südring 15, 79188 Bad Krozingen, Germany. Fax: 49-7633-402538; E-mail: thomas.arentz@herzzentrum.de

Abstract

Introduction: The endogenous nucleoside adenosine is an important intermediate in cellular metabolism, a regulator of function in many organ systems, and a pharmacologic agent with potent electrophysiologic effects. We studied the effects of adenosine on the activation of the pulmonary veins (PVs) after successful ostial isolation in patients with atrial fibrillation (AF).

Methods and Results: Twenty-nine patients (21 male; mean age 54 ± 10 years) with refractory highly symptomatic persistent (n = 9) or paroxysmal (n = 20) AF were included in the study. PV isolation was performed using radiofrequency catheter ablation guided by a multipolar basket catheter (Constellation, Boston Scientific). After successful PV isolation, we studied the effects of intravenous adenosine (12–18 mg) on activation of the upper PVs. A total of 83 PVs were successfully isolated. After adenosine, PV activity was recorded in 10 (34%) of 29 left upper PVs studied and in 3 (13%) of 24 right upper PVs, coupled to atrial activity for 20 ± 7 seconds (adenosine positive). In 8 (62%) of 13 cases, PV potentials were recorded in the distal electrodes of the basket catheter only. Dissociated PV rhythms (N = 8) present after PV isolation disappeared after adenosine for 18 ± 7 seconds, even if reconduction was missing. In 14 patients (48%), a second EP study was performed for recurrence of AF. Adenosine-positive PVs had a nonsignificant higher rate of recovery of conduction than adenosine-negative veins (71% vs 35%, P = 0.095).

Conclusion: Adenosine induces transient conduction in 25% of PVs following successful isolation. Further studies are necessary to determine the physiologic or pathophysiologic role of adenosine-induced reconduction in human hearts or other organ systems.

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