Jim W Cheung 1 , Jeffrey H Chung , James E Ip , Steven M Markowitz , Christopher F Liu , George Thomas , Bruce B Lerman . Show Affiliations »
Abstract
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.
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.
Entities: Chemical
Disease
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Year: 2012
PMID: 22432847 DOI: 10.1111/j.1540-8159.2012.03356.x
Source DB: PubMed Journal: Pacing Clin Electrophysiol ISSN: 0147-8389 Impact factor: 1.976