The following article requires a subscription:



(Format: HTML, PDF)

Background: Adenosine (ADO) has been proposed to reconnect isolated pulmonary veins (PVs) postablation through hyperpolarization of damaged myocytes in an animal model. However, PV reconnection can occur via ADO-mediated sympathetic activation. We sought to determine the mechanism of ADO-induced PV reconnection in the clinical setting by characterizing its time course and location in patients undergoing PV isolation.

Methods: Seventy-four patients (61 male; age 61 /- 10 years) undergoing PV isolation for atrial fibrillation (54 [73%] paroxysmal and 19 [27%] persistent) were studied. After each PV was isolated, a 12-mg intravenous bolus of ADO was administered and onset, offset, and location of ADO-induced PV reconnection and onset and offset of bradycardia were analyzed.

Results: In 22 (30%) patients, ADO-induced PV reconnection occurred in 34 of 270 (13%) PVs. In 24 (71%) PVs, the duration of ADO-induced reconnection exceeded that of bradycardia. The onset of ADO-induced reconnection occurred before the onset of bradycardia in 10 (30%) PVs and during bradycardia in 23 (70%) PVs. No PVs exhibited onset of reconnection after resolution of bradycardia. Common sites of PV reconnection included the carinal region (41% of right PVs and 29% of left PVs) and left PV-atrial appendageal ridge region (35% of left PVs).

Conclusions: ADO-induced PV reconnection occurs during the bradycardic phase of the ADO bolus response and not during the late tachycardic phase. ADO-induced PV dormant conduction is closely associated with the negative dromotropic effects of ADO and suggests that hyperpolarization of the resting membrane is the unifying mechanism.

Copyright (C) 2012 Blackwell Publishing Ltd.