Shortening of Fibrillatory Cycle Length in the Pulmonary Vein During Vagal Excitation

Abstract

<h4>Objectives</h4>The goal of the present prospective study is to evaluate the impact of vagal excitation on ongoing atrial fibrillation (AF) during pulmonary vein (PV) isolation.<h4>Background</h4>The role of vagal tone in maintenance of AF is controversial in humans.<h4>Methods</h4>Twenty-five patients (18 with paroxysmal AF, 7 with chronic AF) were selected by occurrence of vagal excitation during AF (atrioventricular [AV] block: R-R interval >3 s) produced by PV isolation. Fibrillatory cycle length (CL) in the targeted PV and coronary sinus (CS) were determined before, during, and after vagal excitation. The CL was available at PV ostium during vagal excitation in 11 patients.<h4>Results</h4>Forty-eight episodes of vagal excitation were observed. During vagal excitation, CL abruptly decreased both in CS and PV (CS, 164 +/- 20 ms to 155 +/- 23 ms, p < 0.0001; PV, 160 +/- 22 ms to 143 +/- 28 ms, p < 0.0001), and both returned to the baseline value with resumption of AV conduction. The decrease in PVCL occurred earlier (2.5 +/- 1.5 s vs. 4.0 +/- 2.6 s, p < 0.01) and was of greater magnitude than that in CSCL (16 +/- 16 ms vs. 8 +/- 9 ms, p < 0.01). A sequential gradient of CL was observed from PV to PV ostium and CS during vagal excitation (138 +/- 29 ms, 149 +/- 24 ms, and 159 +/- 26 ms, respectively). The decrease in CL was significantly greater in paroxysmal than in chronic AF (CS, 11 +/- 9 ms vs. 5 +/- 7 ms, p < 0.05; PV, 23 +/- 25 ms vs. 8 +/- 14 ms, p < 0.05).<h4>Conclusions</h4>Vagal excitation is associated with shortening of fibrillatory CL. This occurs earlier in PV with a sequential gradient to PV ostium and CS, suggesting that vagal excitation enhances a driving role of PV.