ELECTROPHYSIOLOGIC AND HISTOLOGIC EFFECTS OF DISSECTION OF THE CONNECTIONS BETWEEN THE ATRIUM AND POSTERIOR PART OF THE ATRIOVENTRICULAR NODE

Objectives. This study was designed to examine the effects of destroyi ng the posterior approaches to the atrioventricular (AV) node. Backgro und. Surgical and catheter ablation procedures have been developed for the cure of AV junctional reentrant tachycardia.,Some of these destro y the posterior approaches to the AV node. Methods. Atrioventricular n ode function and electrical excitation of Koch's triangle and the prox imal coronary sinus were examined in 18 dogs. Dissection of the poster ior atrionodal connections was performed in 10 dogs and a sham procedu re in 8. After 28 to 35 days, repeat electrophysiologic and mapping st udies were performed to assess changes in AV node function and the rou tes of AV and ventriculoatrial (VA) conduction. The AV junction was th en examined with light microscopy. Results. The compact AV node was un damaged in eight cases (80%). In two cases minor fibrosis occurred at the posterior limit of the compact node. The right-sided posterior atr ionodal connections lying between the coronary sinus orifice and the t ricuspid annulus were replaced by scar tissue in all cases, but the le ft-sided posterior connections and the anterior connections remained i ntact. Atrioventricular and VA conduction intervals and refractory per iods were not altered. Atrioventricular junctional echoes were present in 10 dogs before and in 7 dogs after dissection (p = 0.06). Posterio r (slow pathway) retrograde exits from the AV node were present in sev en dogs before and in seven dogs after dissection. However, retrograde atrial excitation was altered in four of these seven dogs, so that th e site of exit from the AV node was more leftward than it had been pre operatively. The node remained responsive to autonomic blocking drugs postoperatively. Double atrial electrograms similar to slow pathway po tentials were found in all dogs. Conclusions. This procedure ablates t he posterior atrionodal connections but rarely damages the compact AV node. Atrioventricular node function is not impaired and the node is n ot denervated. The mechanism of cure of AV junctional reentrant tachyc ardia is probably damage to the perinodal atrium. This suggests that p art of the slow AV node pathway may lie outside the compact AV node. D ual AV node exits and double atrial electrograms are present in the no rmal canine heart.