Study of triggering events for vagally-induced atrial fibrillation in dog heart in situ

Enhanced vagal tone can be associated with atrial fibrillation in man. Previously we studied acetylcholine induced atrial fibrillation in isolated canine atrial preparations. The arrhythmia started as a multifocal ectopic activity following acetylcholine induced asystole which triggered reentry. These early polytopic impulses were ascribed to asynchronous firing of multiple atrial pacemakers. Searching for more physiologic model we used vagal stimulation (10-50 Hz, 1 ms, 10-17 V, 5 sec trains) instead of acetylcholine in open-chested dogs (n = 6). This intervention induced premature atrial beats (single or multiple) and atrial fibrillation in 5 of 6 dogs. Occurrence of atrial fibrillation increased with increase in vagal stimulation intensity. Epicardial mapping (254 unipolar electrodes) of both atria revealed uni- or multifocal activation patterns during first two beats (A1 and A2) of each tachyarrhythmia. In some cases clear right atrial reentrant circuits which started during A2 were mapped. The A2 beat (potential or actual trigger for atrial fibrillation), usually emerged outside of the area of the earliest activation during normal rhythm (caval region), most often from the right atrial appendage. Our data suggest that the sources of primary atrial premature beats induced by vagal stimulation are widely dispersed over both atria. This means that either vagally induced atrial premature beats are not the unique property of pacemaker cells or the latter are widely distributed over the atria.