Autonomically induced conversion of pulmonary vein focal firing into atrial fibrillation

Abstract

Objectives: This study was designed to determine the mechanism(s) whereby focal firing from pulmonary veins (PVs) is converted into atrial fibrillation (AF).

Background: The mechanism(s) whereby PV focal firing or even a single PV depolarization is converted into AF is unknown.

Methods: In 14 anesthetized dogs a right thoracotomy was performed to expose the right superior pulmonary vein (RSPV). An octapolar electrode catheter was sutured alongside the RSPV so that the distal electrode pair was adjacent to the fat pad containing autonomic ganglia (AG) at the veno-left atrial (LA) junction. An acrylic plaque electrode on the fat pad allowed AG stimulation at voltages ranging from 0.6 to 4.0 V. Multi-electrode catheters were sutured to the atria with their distal electrode pairs at the fat pad-atrial junctions. Right superior pulmonary vein focal firing consisted of S(1)-S(1) = 330 ms followed by as many as 11 atrial premature depolarizations (APDs) (A(2)-A(12)) whose coupling interval just exceeded RSPV refractoriness.

Results: Autonomic ganglia stimulation, without atrial excitation, caused a reduction in heart rate (HR): control 142 +/- 15/min, 4.0 V; 75 +/- 30/min, p </=0.05. The fewest number of APDs from the RSPV required to induce AF during AG stimulation was as follows: control (no stimulation) 7 +/- 4, 2.4 V; 3 +/- 1, p </=0.05. In seven dogs, lidocaine (2%, 0.4 cc), a neuronal blocker, was injected into the fat pad, resulting in the loss of AF inducibility in six of seven dogs at the same AG stimulation levels. Three of seven dogs showed AF inducibility only with AG stimulation >/=9.3 V.

Conclusions: The effects of AG stimulation at the base of the RSPV can provide a substrate for the conversion of PV firing into AF.