Author + information
- Received April 19, 1993
- Revision received October 2, 1993
- Accepted October 25, 1993
- Published online March 1, 1994.
- Mark A. McGuire, MB, PhD, FRACP∗,1,
- Monica Robotin, MB, BS,
- Alex S.B. Yip, MB, MRCP,
- John P. Bourke, MB, MRCP2,
- David C. Johnson, MB, FRACS,
- Barbara I. Dewsnap,
- Peter Grant, MB, FRACS,
- John B. Uther, MD, FRACP and
- David L. Ross, MB, FRACP, FACC∗
- ↵∗Address for correspondence: Dr. David L. Ross, Cardiology Unit, Westmead Hospital, Westmead, New South Wales 2145, Australia.
Objectives. This study was designed to examine the effects of destroying the posterior approaches to the atrioventricular (AV) node.
Background. Surgical and catheter ablation procedures have been developed for the cure of AV junctional reentrant tachycardia. Some of these destroy the posterior approaches to the AV node.
Methods. Atrioventricular node function and electrical excitation of Koch's triangle and the proximal coronary sinus were examined in 18 dogs. Dissection of the posterior atrionodal connections was performed in 10 dogs and a sham procedure in 8. After 28 to 35 days, repeat electrophysiologic and mapping studies were performed to assess changes in AV node function and the routes of AV and ventriculoatrial (VA) conduction. The AV junction was then examined with light microscopy.
Results. The compact AV node was undamaged in eight cases (80%). In two cases minor fibrosis occurred at the posterior limit of the compact node. The right-sided posterior atrionodal connections lying between the coronary sinus orifice and the tricuspid annulus were replaced by scar tissue in all cases, but the left-sided posterior connections and the anterior connections remained intact. Atrioventricular and VA conduction intervals and refractory periods were not altered. Atrioventricular junctional echoes were present in 10 dogs before and in 7 dogs after dissection (p = 0.06). Posterior (slow pathway) retrograde exits from the AV node were present in seven dogs before and in seven dogs after dissection. However, retrograde atrial excitation was altered in four of these seven dogs, so that the site of exit from the AV node was more leftward than it had been preoperatively. The node remained responsive to autonomic blocking drugs postoperatively. Double atrial electrograms similar to slow pathway potentials were found in all dogs.
Conclusions. This procedure ablates the posterior atrionodal connections but rarely damages the compact AV node. Atrioventricular node function is not impaired and the node is not denervated. The mechanism of cure of AV junctional reentrant tachycardia is probably damage to the perinodal atrium. This suggests that part of the slow AV node pathway may lie outside the compact AV node. Dual AV node exits and double atrial electrograms are present in the normal canine heart.
↵∗ Current address: Cardiology Department, Royal Prince Alfred Hospital, Missenden Road, Camperdown, New South Wales, 2050, Australia.
↵1 Dr. McGuire is a recipient of a Postgraduate Medical Research Scholarship from the National Health and Medical Research Council, Woden.
↵2 Dr. Bourke was supported by an Anglo-Australian Fellowship of the British Heart Foundation, London, England, United Kingdom.
☆ This work was supported in part by a grant-in-aid from the Australian National Heart Foundation, Woden, Australian Capital Territory, Australia.
- Received April 19, 1993.
- Revision received October 2, 1993.
- Accepted October 25, 1993.