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.
©2012, The Authors. Journal compilation ©2012 Wiley Periodicals, Inc.