AV nodal reentrant tachycardia (AVNRT), the most common form of paroxysmal supraventricular tachycardia, is characterized by nearly simultaneous activation of the atria and ventricles. Usually either no P wave or a very narrow P wave is seen just at the end of the QRS complex, which has been described as pseudo P wave. This also may be seen in the inferior leads as a negative component, but can be differentiated, because during sinus rhythm the QRS complex can be seen and the P wave is not present.

The fast and slow AV nodal pathways, present because of the near simultaneous activation of the atria and ventricles, have their own distinct atrial connection, which allows for safe ablation. This is in contrast to prior hypotheses that the distinct pathways were due to functional longitudinal dissociation.

Jackman and colleagues postulate that the reentrant circuit in slow/fast AVNRT is large, involving the left atrium and coronary sinus (CS) myocardium and the triangle of Koch. This is in contrast to the common wisdom, which holds that the reentrant circuit is located in the right atrium, within the triangle of Koch. In slow/fast AVNRT, the slow AV nodal pathway (SP) is used for antegrade conduction and the fast pathway (FP) for retrograde conduction. The locations of these pathways is inferred by the pattern of atrial activation following selective retrograde conduction over each of the pathways, because activation of the fast and slow AV nodal pathways cannot be recorded by catheter electrodes in the electrophysiology (EP) laboratory.

Jackman and colleagues propose that during retrograde conduction over the FP, transitional cells very close to the area generate the His bundle potential, which carries the impulse across the tendon of Todaro to activate the true atrial septum. Further, they postulate that the FP activates both sides of the septum. Activation on the left side of the septum activates the left atrium, which propagates around the mitral annulus, activates the CS myocardium, and the impulse then propagates through the CS myocardium to the CS ostium, exits the CS ostium and activates the tissue within the triangle of Koch, which then propagates anteriorally towards the AV node. Thus, activation of the right atrium does not participate in activation following retrograde FP activation.

Importantly, there is conduction block across the tendon of Todaro and the Eustachian Ridge (ER) so that activation of the right atrium cannot penetrate the triangle of Koch. This may be a key feature in allowing AVNRT.

Evidence supporting this theory includes the fact that activation of the atrium is superior to, not in, the triangle of Koch. Also, the mapping catheter, on the left anterior oblique (LAO) projection, is above the tendon of Todaro. The timing of activation here is about 10 ms earlier than His bundle activation. Although for many years it has been thought that the earliest activation was recorded at the same site as the His bundle, that was only because of the very wide electrodes that spanned a very large area.

The 2 potentials are recorded from separate tissue—the first potential above the tendon of Todaro and the second in the triangle of Koch. The CS electrograms show the left atrial propagation going proximal to distal, the CS myocardium is activated and then the CS tissue propagates; the potential recorded in the triangle of Koch is later than the timing of activation of the CS myocardium—important to their hypothesis.

Electrograms show that the earliest activation is very close on the left and right sides of the atrium, and precedes activation in the CS. In the RAO projection of radiographs, the His bundle catheter can be seen, which is recording proximal His bundle activation from the distal pair of electrodes. On the right side of the septum, the catheter is recording the earliest right atrial activation during retrograde fast pathway conduction. The transseptal catheter in the RAO projection is extremely close to the site of earliest activation on the right side of the septum. In the LAO projection, the His bundle is perpendicular, meaning the catheter tip is close to the tricuspid annulus and the catheter is laying on the triangle of Koch. The earliest activation on the right is deviated towards the left, above the tendon of Todaro, and very close in the LAO projection to the site of earliest activation on the left side of the septum.

If their hypothesis is correct, activation would be seen low in the triangle of Koch between the tricuspid annulus and the CS, and this activation would be significantly later than the timing of the earliest activation. In fact, during slow/fast AVNRT, activation in the posterior septum is very late. There is a far-field rounded signal recorded from above the tendon of Todaro. Activation inside the triangle of Koch is 50 ms after activation in the His bundle region of the anterior septum. The propagation map shows that activation begins above the tendon of Todaro, then the roof of the CS, and then the wavefront enters the right atrium and moves up towards the His bundle.

High-resolution mapping during retrograde fast pathway conduction in 7 patients showed that the circuit took 48 ms to go around. The earliest site in each patient was made time zero, a little farther down the septum the time is from 3 ms to 23 ms after the timing of earlier activation for a median of 5 ms. At the CS roof the time is 22 ms, in the space between the CS ostium and the tricuspid annulus is a mean of 23 ms, and in the triangle of Koch a median of 43 ms, and then the very latest time is highest in the triangle of Koch at 48 ms.

The timing of the activation in the triangle of Koch during sinus rhythm (SR) is confusing. The activation time is very late in SR, just as it is late in retrograde FP conduction. Jackman and colleagues suggest 2 possibilities for this. One, the activation going down the septum crosses the FP fibers, but they do not develop a potential that can be recorded and the wavefront is not able to travel through the compact AV node and retrogradely activate the atrium. So this impulse does not activate the rest of the triangle of Koch, and the atrial impulse blocks at the tendon of Todaro and the ER, comes down around the crista terminalis and then enters the triangle of Koch, so this area would be very late during SR. Jackman and colleagues named this the ASP potential. This is a high frequency potential that activates the atrium in the space between the tricuspid annulus and the CS ostium. It is the atrial connection to the slow AV nodal pathway.

Two, the impulse never enters from the right atrium, but it very quickly goes across Bachmann’s bundle, for which activation is very swift, and down the septum and very quickly activates the CS and then enters just as it does during retrograde FP conduction. This could explain the late activation at the post-receptal site between the tricuspid annulus and the CS ostium, which is later than the timing of activation in the proximal CS. The late activation might be used as the signal to locate a site for ablation of the atrial end of the slow AV nodal pathway.

At least 2 distinct slow AV nodal pathways exist, although evidence of both is not seen in every patient. The human compact AV node is small, just 3-5 mm, has a very long rightward posterior extension that travels down to the area between the tricuspid annulus and down to the floor the CS ostium. For the shorter leftward posterior extension, it is less clear where it connects to the atrium, but it dives down leftward. Importantly, it enters the compact AV node fairly high up. The tachycardia in the vast majority of patients uses the long rightward posterior extension of the AV node.

Their postulated atrial activation sequence during retrograde SP conduction over the rightward posterior extension of the AV node is: Activation propagates retrogradely along the rightward posterior extension, activates the tissue between the tricuspid annulus and CS ostium, yielding the ASP potential retrograde, and enters the CS at the floor. The impulse that activates within the triangle of Koch never exits the triangle. The only way it reaches the atrium is to activate the CS myocardial coat and then the connection to the left atrium activates the left atrial myocardium. The atrial wavefront that propagates around the mitral annulus, back up towards the septum and activates the true intra-atrial septum, and then activation can be seen on the right and above the tendon of Todaro. This is the reason that timing of activation is very late during retrograde SP conduction. Anteriorally, activation is so solely because it must go into the CS, activate the left atrium and then return all the way back up before activation is recorded. Whenever the direction of the wavefront has to be changed, a conduction delay occurs along with an increase of conduction time.

The circuit for typical slow/fast AVNRT, which is about 72% of all patients with AVNRT, proposed by Jackman and colleagues is: Retrograde activation over the transitional cells activates the FP, and activates both the right and left side of the true intra-atrial septum. The right side simply ends and does not enter or penetrate anywhere. The left side activation propagates around the mitral annulus, activates the CS myocardium, propagates on the floor of the CS, comes out of the CS myocardium, activates the tissue at the exit site, generating the ASP late potential, and then the 2nd potential seen in the His bundle catheters. This allows for selective ablation of this tachycardia very low between the tricuspid annulus and the CS ostium when targeting just the long rightward posterior extension.

In about 4% of patients with classic slow/fast AVNRT, ablation results in good automaticity, showing that the atrial end of the rightward posterior extension of the AV node was ablated. This suggests that the antegrade limb of the tachycardia is now the leftward posterior extension. So, the ablation worked beautifully to ablate the atrial end of the rightward posterior extension, which is why there is junctional automaticity, but it doesn’t eliminate the tachycardia.

In a few patients, both slow pathways can be seen during retrograde conduction, and is best seen in patients with very low sympathetic tone. Ablation procedures typically are performed under general anesthesia, which suppresses retrograde FP conduction and makes it easier to see the retrograde SP. Two catheters are needed to correctly record the activation time of the CS muscle at all the sites, because the activation time varies for the different parts of the CS chamber. The mapping catheter is positioned in the FP region, above the tendon of Todaro.

In the sleeping patient, as the ventricle is paced for a long cycle length, two retrograde conduction times are seen. A moderately long H-A interval is seen, followed by a very long H-A interval. Neither of these is FP, because the catheter is truly at the FP site. The activation sequence of these is different. During retrograde conduction earliest activation is in roof of the CS and in floor a little later. When the long H-A interval is blocked and conduction is over the very long H-A interval, earliest activation is in the floor of the CS right at the ostium and activation is very late in the roof of the CS.

The very long H-A interval is thought to represent activation of the rightward posterior extension, activating the floor of the CS, and that the long H-A interval activation over the leftward posterior extension, activating either the CS or the late atrium or both together near the roof of the CS, approximately 2 cm inside.

In about 5% of patients with AVNRT, the SP is ablated from the posterolateral mitral annulus. It is not possible to ablate the AVNRT from the posterior septum, staying at a level below the level of the roof of the CS ostium.

Most of these patients have slow/fast AVNRT, without retrograde conduction over the SP to help identify the atrial end of the SP. Hence, the re-setting response, which is simpler than entrainment because it uses just one beat, is used to identify the atrial end of the SP. The timing of activation at the posterolateral mitral annulus is not very early, but delivering an extra stimulus after retrograde atrial activation advances the next His bundle potential by 10 ms and resets the tachycardia. Thus, this pacing site must be close to the atrial end of the slow AV nodal pathway. When radiofrequency current is delivered to the posterolateral mitral annulus, the classic junctional automaticity of retrograde FP conduction is seen.