Hello, I'm Bill Miles. I'm Professor of Medicine at the University of Florida, and I've been asked to speak on catheter ablation of atrial ventricular nodal reentrant tachycardia. These are my disclosures. AV node reentry is a reentrant tachycardia involving two functionally distinct pathways, and they're generally referred to as fast and slow AV nodal pathways. Most commonly, the fast pathway is located near the apex of Koch's triangle and the slow pathway in for a posterior to the compact AV node tissue. But as we go, I'm going to be much more detailed on these localizations. Variant pathways have been described allowing for slow, slow forms of AV node reentry. Typical AV node reentry is usually referred to as a AV node reentrant tachycardia in which a slow pathway serves as the antegrade limb and a fast pathway serves as the retrograde limb, and that's referred to as slow, fast AV node reentry. The atypical varieties are a couple in AV node reentry in which the fast pathway serves as the antegrade limb and the slow pathway serves as the retrograde limb. That's referred to as fast, slow AV node reentry. And there's a form where, in effect, a slow pathway serves as the antegrade limb and a second slow pathway, the retrograde limb, and that's referred to as slow, slow AV node reentry. And here's a diagram that goes over those. These three on the left are forms of AV nodal reentrant tachycardia in slow, fast AV node reentry. The P wave usually occurs during the QRS or just at the foot of the QRS, seen sometimes as a tiny little heel on the end of 2,3 and AVF that's negative or a little pseudo R prime wave in V1. Slow, slow AV node reentry usually manifests as the P wave in the ST segment and fast, slow AV node reentry is a long RP tachycardia where the retrograde P wave is just before the next QRS. Notice that AV reentry related to a bypass tract has a P wave location about the same location in the RR interval as slow, slow AV node reentry. Atrial tachycardias have the P wave localized in the similar situation as the fast, slow AV node reentry. Now ongoing management or chronic management of AV node reentry is illustrated in this slide. If AV node reentry is not symptomatic or minimally symptomatic, you can just follow up without treatment or you can demonstrate vagal maneuvers and things like that that the patient can use. If this AV node reentry begins to be more symptomatic and needs therapy, you go down this part of the algorithm and if the patient's an ablation candidate or prefers ablation, you can do a slow pathway catheter ablation. If not, there are some drugs that sometimes work, beta blockers, viltizum or verapamil are the first choices. And if they're ineffective, some of the membrane active drugs such as flecainide, propafenone in the absence of structural heart disease, digoxin, dofetilide or sodalol or even amiodarone in maybe a few patients, although you have to be obviously aware of the long-term organ toxicities of amiodarone. And if any of these drugs are ineffective, you're back to ablation. AV node reentry is a diagnosis of exclusion. You need to exclude AV reentry, atrial tachycardia and junctional tachycardia. The induction of AV node reentry in the EP lab can be fickle and may require various doses of isoproteranol and or atropine in order to induce the arrhythmia. And it's useful to have a clinical tracing consistent with AV node reentry because if you have a tracing that's clinically consistent with AV node reentry and you can demonstrate some evidence of dual AV nodal physiology in the laboratory but can't induce sustained tachycardia, you still might consider an ablation of the slow pathway region in that patient. If an ablation seems to be difficult, remember to reassess and confirm the diagnosis of AV node reentry or exclude the existence of a second tachycardia such as an atrial tachycardia. We're going to go through a little bit of the history of the understanding of the mechanism of AV node reentry because I think it's important to people to know a little bit about this to understand ablation. Initially, AV node reentry was thought to be a tachycardia that was confined totally to the AV node and it was thought that there was a common atrial upper pathway and a common ventricular lower pathway. And in that situation, it'd be very difficult to ablate AV node reentry without resulting in heart block, at least in a high percentage of people. But in rabbits, Mendez and Moe in rabbits demonstrated that the upper pathway seemed to actually involve a rim of atrium. And so there was a fast pathway and a slow pathway, but there wasn't an upper common pathway. And that's what we think the current pathophysiology or mechanism of AV node reentry is now. And this is another schematic that shows that you can enter the AV node from a fast pathway, you can enter it from the slow pathway, but if you block in the fast, get into the slow, you can start a reentry again that has a lower common pathway, maybe some in the AV node and certainly in the His bundle, but the upper involves a rim of atrium. Why is that important? Well, it means that we might be able to ablate AV node reentry without producing AV block. And this was a wonderful study by surgeons and electrophysiologists from Australia that showed that you could approach AV node reentry surgically and most patients, the surgical ablation to get rid of AV node reentry was at the top of the tendon of Todaro where we now associate the fast pathway. But in a minority, you had to ablate closer to the coronary sinus. And when they looked at this more closely, they realized that in the first type, which is now we know is our slow fast AV node reentry, you had very early atrial activation at the apex of Koch's triangle, and it was later toward the coronary sinus. In the other path, on the other patients, though, where the ablation was closer to the coronary sinus, the atrial activation was not as early, but still the earliest was now close to the coronary sinus. And we think that probably represents what we now call the slow, slow variety of AV nodal reentry. And this is just an example that proves that there is a common lower pathway because it's not that uncommon in young people to get two to one in for his block during AV node reentry. And when you put in PVCs during this two to one AV node reentry tachycardia, you strip back refractoriness and you get the one to one classic look for AV node reentry. So there's a lower common pathway. This is a nice schematic of the area that we're interested in an AV node reentry. Notice Koch's triangle. Notice the tricuspid annulus. Notice the tendon of Todaro going into the eustachian ridge or the eustachian valve, which is important because sometimes we need to get over that in order to ablate this structure, which is the slow pathway, or I'm going to actually call it the right inferior extension of the slow pathway as we go. And so we most commonly ablate between the tricuspid annulus and the inferior lip and the inferior anterior lip of the coronary sinus to get rid of AV node reentry. But there are some other features in some patients that you have to know about. The compact AV node is up here, and we think the fast pathway exit is here. This exit, as we're going to see, is actually behind the tendon of Todaro, and we're going to look at that in a little bit more detail in a minute. This is just a true anatomic diagram of the same place. This is the inferior isthmus where you would do an atrial flutter ablation. This is the eustachian ridge and the tendon of Todaro, the coronary sinus, the tricuspid annulus. So this is a region of the slow pathway. This is the region of the compact AV node. This is the central fibrous body where the hiss exits from the AV node. And here's where the fast pathway enters this area. Notice again that it transitions outside of Koch's triangle, just posterior to Koch's triangle toward the fossa, toward and a little bit above the fossa ovalis. So these schematics were put out in the 1990s when it became apparent that you could do AV node re-entry ablation. And the simplistic one is that AV node re-entry goes along the slow pathway, or I guess we could say down the slow pathway, enters the compact AV node, gets back out the fast, and then re-enters. And we have typical AV node re-entry when that occurs. And indeed, in Sonny Jackman's first description of a fair number of patients in whom he did slow pathway ablations, most of the ablations in most of the patients were between the tricuspid annulus and the anterior lip of the coronary sinus in the posterior third or just anterior to the, or I guess I should say superior to the posterior third. There were a few where he needed to ablate within the coronary sinus, and we'll go over that in a minute. So further elucidation of probable pathways in AV node re-entry involves probably dividing the slow pathway into a rightward inferior extension, which comes down between the tricuspid annulus and the lip of the coronary sinus, and a leftward inferior extension, which enters the compact node from within the coronary sinus. It's coming out of the coronary sinus somehow. The His bundle will be up here, the compact node is here, and the fast pathway is up in this region. So we're now defining a rightward inferior extension, a leftward inferior extension of the slow pathway, and the fast pathway. And if you look at that, you then can can get a variety of different pathways for AV node re-entry. These blue pathways usually give typical AV node re-entry. You go down the slow right inferior extension and out the fast, or you can go down the left inferior extension. This is the right inferior extension, this is the left inferior extension, and out the fast. And both of these might give a typical pattern of AV node re-entry. But notice that now that we have these two slow pathway extensions, we can also envision atypical AV node re-entries that go that that utilize the right inferior and and the left inferior extension, and don't necessarily utilize the fast pathway. And also these can go in either direction. So it begins to get more and more complicated. So let's go over these re-entrance pathways. The fast AV nodal pathway has the shortest conduction time. It's formed by transitional cells crossing the tendon of tedaro superiorly. And earliest retrograde atrial activation is on the right and left sides of the interatrial septum. We're going to look at this more in more detail in a minute. Posterior to the tendon of tedaro, one-third of the distance between the his bundle and the CS roof. There are two slow nodal pathways. There's the right inferior extension. It usually has the longest conduction time and its earliest retrograde atrial activation is between the tricuspid annulus and the ostium of the coronary sinus. The leftward inferior extension has usually a conduction time shorter than rightward extensions. And its earliest retrograde atrial activation is in the roof of the coronary sinus about two to four centimeters in from the coronary sinus ostium. So these have been borrowed from Dr. Jackman. This is a right anterior oblique projection. This is a left anterior oblique projection. And we're going to use these projections in some of the next slides. So try to get used to it. The fast pathway exit is right here. The rightward inferior extension exit is right here. The leftward inferior extension exit is right here. And a rare pathway, but every once in a while there's a far leftward infralateral slow pathway that's out here toward the valve of usines where the coronary sinus turns into the great cardiac vein. We'll mention that as we go. So how do you evaluate retrograde AV nodal function? Well you can look for retrograde AV nodal jumps during decremental or premature ventricular pacing. So in this example we're pacing the ventricle. We have concentric retrograde activation with the HisA or the anterosuperior A being the earliest. But as we pace faster and faster we have a jump. So we think we've jumped from a fast retrograde pathway to a slow retrograde pathway. Notice that not only is there a jump in the timing that's sudden, but there's also a sudden change in the retrograde activation sequence. So now the earliest retrograde atrial activation is closer to the coronary sinus ostium. It's posterior, it's posteroinferior instead of anterosuperior. So we've jumped from a retrograde fast pathway to a retrograde slow pathway with a change in the timing and a change in the activation sequence. This just demonstrates premature, instead of decremental pacing, we premature at 590, 580, and then we get even earlier at 470. At 590, we have earliest atrial activation at anterosuperiorly. Presumably that's retrograde fast, but with just a very minor decrease in the ventricular coupling interval, we have a large VA jump and that same change in retrograde activation sequence. So we've jumped from the retrograde fast to the retrograde slow. And when we get sufficient delay in the retrograde slow, we're actually able to get back down the anagrade node and demonstrate an echo. So we have a up the slow, down the fast, AV node re-entrant echo. Notice the negative P waves in leads two and three. So looking at two tachycardias, a slow fast AV node re-entry and a fast slow AV node re-entry, let's look at the difference in the atrial activation sequence. Well, since the ventricular and the atrial activation are near simultaneous, we had to put in PVCs in order to strip away the Vs so we could see the atrial activation sequence. But notice that in typical slow fast AV node re-entry, in this example, the anterosuperior A is the earliest. So we're going down a slow and up the retrograde fast. In fast slow AV node re-entry, now the earliest retrograde activity is in the proximal coronary sinus near the coronary sinus os. So we're actually coming back up a slow pathway and going down probably a fast. So these are the different activation sequences that you can see during AV node re-entry that may be a tip-off as to which pathway it's utilizing. So now we're going to go to some diagrams that I think are important, but a little bit more complicated. Again, this is a right anterior oblique. This is a left anterior oblique. The red arrows are the fast AV nodal pathway. The blue arrows of the slow pathway, right inferior extension. Brown arrows are CS myocardial activation, and green arrows are atrial activation. The hatched area is the appropriate ablation site. So for typical slow fast way fast, I'm sorry, typical slow fast AV node re-entry via the rightward inferior extension, the impulse goes down the right inferior extension. It escapes the retrograde fast, but look, it can't on the right side, it can't get back around because of the eustachian ridge. So how does this tachycardia complete the circuit if it's not limited to the right atrium? When we go over to the LAO, you can see not only does the fast pathway exit toward the right, but it exits toward the left. So AV node re-entry in a way is also a left atrial tachycardia because the fast pathway empties into the left atrium as well as the right. It can't make it around fully because of your eustachian ridge on the right, but it can make it back to the left atrial myocardial coat in the CS. It comes out the CS and then goes back down the right inferior extension. So this is the circuit for typical slow fast AV node re-entry utilizing a rightward inferior extension. Now you can also get a slow fast AV node re-entry utilizing the left inferior extension. In this example, it's the purple arrows. So instead of this right inferior extension being part of the circuit, it's actually bypassed. The exit is to the left again via the retrograde fast. It comes around the left atrium, but now instead of getting into the coronary sinus and completing the circuit that way, it exits into this area, gets over, comes out of the os of the coronary sinus more superiorly, and completes the circuit. So in this particular type of slow fast AV node re-entry, the left inferior extension and the retrograde fast are involved, but the right inferior extension is not involved. And notice that if you think it's this type of tachycardia ablating in the same area as the last slide, ablating here between the tricuspid annulus and the coronary sinus in the last slide, if you ablate in the same place, it's not going to do anything. You have to ablate about two to four centimeters into the coronary sinus to get rid of this type of tachycardia. Now slow slow AV node re-entry most often uses the right inferior extension for antegrade limb and leftward inferior extension for the retrograde limb, and it's counterclockwise as viewed in this RAO projection. So you're coming out of the right inferior extension and going back down the left inferior extension. So you're coming out here, turning around, and coming back here, and notice here that the retrograde fast is not part of the tachycardia circuit. For fast slow AV node re-entry, most often it uses the leftward inferior extension for the antegrade limb and the rightward inferior extension for the retrograde limb. So this is clockwise as viewed in the RAO projection. So you're coming out the left inferior extension and going back in the right inferior extension. You can see it a little bit better on the LAO. You come out here, you turn around, and you go back into the myocardial coat, back to the atrium, back out, back to the left atrium, back out the left inferior extension, and around and around. And notice that this also doesn't use the retrograde fast as part of the circuit. So in this one though, you can ablate here in the typical location that all of you are used to for AV node re-entry because the right inferior extension is part of the circuit. So here are examples of the AV node re-entries that do not involve the fast pathway. Notice that in both of them, if you ablate the inferior extension between the tricuspid annulus and the coronary sinus, you'll eliminate the tachycardia. So ablation of AV node re-entry is usually performed in sinus rhythm, although the retrograde slow pathway may be targeted during tachycardia in some atypical cases. Isoproterenol may be required to induce the AV node re-entry, but most of the time it's probably wise to discontinue it during the ablation in order to enhance catheter stability. The slow pathway ablation site is determined by both electrogram and anatomic criteria, and most people like to use a little of both. So using both electrogram and anatomic criteria, the ablation is usually at the level of the lower third of the postreceptal tricuspid annulus. So that would be this region, this P region, or just above it, but not in the middle of the middle region. In that area, I'm going to show you in a minute, there's usually a small multi-component atrial potential. And here's a diagram from an early study from Michigan that shows the location in the posterior and sometimes the lower portion of the mid septum as the successful site for ablation of AV node re-entry. And this is what the electrograms usually look like. The A's are smaller than the V's, but they're two components. It was initially thought maybe this was actually a slow pathway component, but it might just be some fractionation in this area, or it might be that the muscle bundles in that area run in different directions at different levels. But again, typically you get two little potentials, one a little, the second one a little sharper than the first. If you think it might be a His bundle potential, you can paste the atrium and show the AH prolonging, but that this will not prolong. So this is an ideal look for the electrogram in that location. And here's an RAO and an LAO fluoro view of a usual right inferior extension ablation site. The His is up here, and you're actually ablating quite a ways from where you're recording His. Electroanatomic mapping is helpful. A His cloud can orient the operator somewhat to the conduction system, but you have to remember that the compact node is not represented in the His cloud. If you put a mark at everywhere, everywhere that you get a His or a right bundle potential, you still have to be careful if you're very proximal that you're not in the region of the compact node, because that's not represented in the His cloud. You have to have constant assessment of catheter stability during energy delivery. You can use zero or minimal fluoroscopic procedures, and there's some evolving data that high density mapping of Koch's triangle with electroanatomic mapping may help identify AV node re-entry circuits and appropriate ablation sites. Although it might be that they're just identifying the same electrogram that we've been looking for for years in the area of successful AV node re-entry ablation. This is an electro electroanatomic map showing a cloud everywhere where we saw a His potential or a right bundle potential. We put a mark and we made a line from the annulus to the anterior lip of the CS os below the His cloud to ablate the AV node re-entry. I sometimes find it useful. Sonny Jackman taught me this technique to use an SL2 sheath to actually get around the yastation ridge, because if you can get around the yastation ridge and ablate lower, make a line lower rather than higher, you have a better chance of interrupting the right inferior extensions without any damage to the compact AV node. Now when you ablate with radiofrequency, you get accelerated junctional beats commonly during radiofrequency ablation. These accelerated junctional beats, if they have intact VA conduction with the same activation sequence and VA interval as during AV node re-entry, they commonly occur during RF delivery at a successful site. These are presumably due to RF stimulation of the slow pathway with retrograde conduction to the atrium via the fast pathway. If these junctional beats block their VA conduction or if you get very rapid junctional beats, you need to stop RF delivery immediately, because this may indicate fast pathway heating. Retrograde fast pathways may not exist in some patients, as I've mentioned earlier, or may only conduct under sympathetic stimulation with isoproterenol. So it's important to determine VA conduction properties prior to ablation to know whether you're going to get junctionals with VA conduction or not. In AV node re-entries that are not typical, ablation at successful sites may not result in junctional beats, or if there's no retrograde fast pathway conduction, junctional beats that do not have VA conduction. So if you get junctional beats but no VA conduction, the first thing you should do is stop and regroup, make sure you're in a safe place, make sure that AV conduction is intact, but it might be that there just isn't any retrograde fast pathway, and in that case you either have to deliver short ablation pulses, a series of short ablation pulses, some people pace the atrium during RF delivery, some people give isoproterenol to try to facilitate retrograde fast conduction, or consider using cryoablation instead of radiofrequency. So here's an example of what we call good junctionals. Radiofrequency is on, you're in sinus rhythm, and you get junctionals that look just like the AV node re-entry. Each junctional beat has an A associated with it, and as we ablate it accelerates a little bit, then it starts to decelerate as you actually start to destroy tissue, because when you ablate with radiofrequency, the heat initially increases automaticity, but as you continue ablation, that automaticity, as the cells die, that automaticity should disappear. So these are good junctionals, if you see these you can continue to ablate, but if you see this, if you see rapid junctionals and not conducting to the atrium, you need to stop and reassess at that time and decide where to go from there. And it's been reported by, in the literature, and we have the same observation that slow pathway ablation induces junctional rhythm with ventricular atrial block in some patients with slow, slow atypical AV nodal re-entrant tachycardia. And here's an example from the literature of junctional ectopics that don't disturb sinus rhythm in a patient with slow, slow AV node re-entry. And they postulate that if you go down the slow and up the fast, you're going to get junctionals when you heat the slow, you're going to get junctionals that with every, with every, with every junctional beat, you're going to get VA conduction. But for some of these other varieties that don't involve the fast pathway in their circuit, for example, a slow, slow variety fast pathway can either be there or not, you may get junctional atrial block during slow pathway ablation, but still you can successfully ablate the slow pathway from that region. Again, the tricks to do that, as I had on the last slide, what we usually do is short bursts of radiofrequency ablation, checking for AV conduction between each one. This is just an example of a Leffert extension, atypical, I'm sorry, actually slow, fast AV node re-entry. So this is typical AV node re-entry as far as its pattern, but it doesn't use the rightward inferior extension. In this situation, RF heating of the right inferior extension may stimulate junctionals that conduct retrogradely, but you'll keep on inducing tachycardia because the right inferior extension is not part of the tachycardia circuit. So most of the time, junctionals with intact VA conduction is a good sign, and you'll usually be done with your AV node re-entry ablation. But in this particular variety, you'll get junctionals with VA conduction, but still have inducible tachycardia, and you have to go from ablating in the typical right inferior extension area to the two to four centimeters into the coronary sinus area. If the post-receptal ablations fail, the next step is to deliver energy two to four centimeters into the coronary sinus, as I said on the last slide. Sometimes, on rare occasions, you even need to go to the left septum rather than the right septum. So for even typicals, but atypicals especially, if you can't get it from the right posterior septum, you can go over to the left. This is a transeptal catheter recording... I'm sorry, transeptal catheter recording hiss on the left. This is a transaortic catheter recording hiss on the left. This is our usual hiss location on the right. The left inferior extensions are usually below the coronary sinus catheter, fluoroscopically across the septum in that area, and the electrograms look similar to what I showed you before. And there's another variety where the pathway is way out in the coronary sinus, and in that particular instance, it may be useful after you go transeptal to put in late PACs during tachycardia and demonstrate that late PACs somewhere in here, out in the left free wall region of the left atrium, if late PACs can advance tachycardia out here without getting to the central area of the nodal region, then you know that something out here is involved in the tachycardia, and you can ablate way out here, sort of like you'd ablate a left post or lateral accessory pathway. These are rare, but occasionally you'll run into one. What are ablation endpoints? Well, inability to reinduce AV node re-entry is the best endpoint. You should give isoproterenol even if it was not needed for induction pre-ablation. We don't always do that in pathway ablation, but for AV node ablation, AV node re-entry ablation, you want to know that the tachycardia is not inducible either in the baseline state or during isoproterenol infusion. Single typical AV nodal re-entrant echoes are acceptable, and so if you're just getting single echoes, it never gets back down the slow pathway. That's acceptable. If you get consecutive echoes, or obviously if you get sustained AV node re-entry, then that's not an acceptable endpoint, and you still have more to do. Sometimes you need to use endpoint substitutes in patients where AV node re-entrant tachycardia is either non-inducible or poorly reproducibly inducible, and sometimes you can look for that accelerated junctional rhythm during ablation, you can look for loss or modification of the slow pathway with no more echoes, no more jump, or evidence that the pathway is no longer there. For example, here is atrial pacing pre-ablation. You can see the jump to the slow pathway, and you have sustained slow pathway conduction, but after the ablation, even at a little bit of a slower atrial cycle length, there's no more jump, and there's no more slow pathway. That may be a reasonable endpoint in ablation if the patient has poorly reproducibly inducible tachycardia, and as I said before, single echoes are okay as long as they don't turn around and go back down to the ventricle. When you give isoproterenol, it's sometimes difficult to determine whether you have recurrent AV node reentry or whether you just have junctional tachycardia as a response to the isoproterenol, and these maneuvers published by the Indianapolis group are very useful. If you have AV, if you have a junctional tachycardia, late PACs won't affect it, but if you have AV node reentry, late PACs will advance not the very next V, but the V after that. I actually said advance, but it actually will either advance, delay, or block, so if a PAC is late and advances, delays, or blocks this next X minus N and blocks, affects, or perturbs this V, then you know you have AV node reentry, so in this particular example, a PAC is timed to hiss refractoriness. It perturbs the subsequent hiss and the subsequent V by delay, and that indicates that antigrade slow pathway conduction is still present and confirms the diagnosis of AV node reentry. In contrast, here, the late PACs never affected the hiss hiss or the VV interval, but when we brought them earlier, they actually would bring in the V right next to the PAC. Tachycardia would continue. That's indicative of an ectopic or a non-reentrant junctional tachycardia, which may just be a feature of the isoproteranol that you may be using post-ablation to test success. Now, some people, especially some of our pediatric colleagues, like to use cryoablation for AV node reentry. Cryoenergy may minimize the risk of AV block, and if AV block does occur, it's more likely to be transient. You can do cryo-mapping, that is, you can bring the temperature down a little bit and see what happens. There is a higher risk of recurrent tachycardia on follow-up. It's not quite as durable as ablation as a as RF ablation. The successful sites, the electrograms look a little bit different. They need to have a larger A, and the site needs to be a little bit more proximal than it is for RF. Cryoadhesion may have the advantage for stability, if that's a problem in a particular patient, but it doesn't result in junctionals, so you have to use some other marker of slow pathway conduction as your endpoint, and you need to monitor the PR interval for cooling of the fast pathway. And here's just an example of every time this premature atrial extra stimulus was introduced, this patient went down the slow pathway. So this doctor would just give four atrial pace beats, and then the premature during cryoablation, and he'd look for the slow pathway on the premature to block, and he would use that as his endpoint. So you have to be a little bit more creative on endpoints. AV node re-entry is very, very successful. This is a single center study that I elected to use this year, showing about a 95% success rate, long-term success rate, over many years. It hadn't gotten much better. It hadn't gotten much worse. The AV block requiring a permanent pacemaker is still there, but it's low, and interestingly, even though there's an increased incidence of using electroanatomic mapping, it hasn't had a whole lot of change in the success rate, because it's such a successful ablation to begin with. What about a patient that has pre-existing prolonged PR interval? Well, patients with AV node re-entry and a prolonged PR interval are usually older. They have a higher incidence of structural heart disease and hysperkinesis disease, and these characteristics may contribute to the risk of development of delayed AV block after slow pathway modification. If slow pathway modification results in complete elimination of the functional slow pathway, high-degree AV block is more likely to occur. So RF ablation can still be considered first-line therapy in patients with a long PR interval, but it's recommended that non-inducibility of AV node re-entry, rather than total elimination of the slow pathway, be used as your endpoint. Don't be as aggressive, because there may be two slow pathways, and you just want to get rid of one slow pathway, not both. So what are just some general steps for trying to prevent AV block during slow pathway ablation procedures? Because that's what we all worry about, and that's what our patients often worry about when we tell them how good this ablation is, but have to tell them that there is a small chance of AV block. So avoid RF energy application within the very proximal coronary sinus, especially at the roof of the coronary sinus ostium, where there are relatively large atrial potentials. Terminate RF application with the onset of fast junctional rhythm or retrograde conduction block during the junctional rhythm. Terminate RF application with any changes in the amplitude of the atrial or ventricular potentials in the ablation electrode, or any change in the QRS morphology, because that may mean that the catheter has moved. Perform diagnostic maneuvers for any SVT to confirm the diagnosis, even in cases with short VA conduction. I've been caught once or twice in the past thinking that the patient still had AV node reentry, and it was actually gone, and it was an atrial tachycardia that was still there. Limit higher power output during RF application in this region. Be aware of higher risk of AV block in patients with advanced age and pre-existing long PR intervals, and utilize continued or intermittent, but frequent intermittent, fluoroscopic monitoring, or the constant use of 3D mapping system monitoring during RF application for detecting catheter movement. A few more suggestions. If this isn't the first ablation, where were the previous lesions placed, and was there any AV blocks? So prepare a little bit if it's a redo. Verify baseline conduction properties. Was the PR interval prolonged to begin with? Was there VA conduction present prior to ablation? Was there any evidence of a retrograde fast pathway? Assess where the HISS potentials are recorded, and differentiate maybe the slow pathway or the fractionated potential seen at successful sites from the HISS potential with pacing maneuvers. Stop isoproterenol before ablation and consider a long sheath to try to enhance catheter stability. Everyone in the room should be focused. I assign someone to look at the x-ray if we're flashing x-ray. I warn the electroanatomic mapper watch carefully. I have my best technician or one of my partners look at the screen totally to make sure that they yell stop if they see anything unusual. So at this point, no jokes, no screwing around. Focus on what's going on when you're delivering energy for AV node re-entry. Start relatively posterior and use more and more caution as you go anteriorly. We already said use lower power. Stop immediately if junctionals with VA block occur. Consider ablation within the CS rather than more anterior septal sites, and some people prefer cryoablation. So I'm going to finish with just a little bit of a different thing. It has to do with dual AV nodal physiology, but it's a different tachycardia non-re-entrant SVT due to 1 to 2 AV nodal conduction. So this is a patient referred to us for atrial fibrillation ablation, and if you look at the surface tracing, you can see why the referring doctor thought this was atrial fib, but I've picked up a few of these over the years. Be careful that this is not atrial fib. You can tell here that the patient is in sinus rhythm and there are more V's than A's, so this is not atrial fibrillation. When we paste the atrium in this patient, we could see that sometimes we went down a fast pathway, but sometimes we went down a fast and a slow pathway with the same pacing stimulus, and so that's what makes it look irregular. Sometimes you go down one pathway. Sometimes you go down both the fast and the slow pathways. If every beat, if every sinus beat goes down both, it looks a lot like PSVT, so it can be mistaken for PSVT. Here's the electrocardiogram. Here's the sinus rhythm, but the QRSs are going twice the rate as the sinus rhythm. The surface ECG clues to non-re-entrant 1 to 2 dual or double shot, some people call it dual AV nodal tachycardia, is that there's usually some RR alternans, 410, 440, 410, 440, 410, 440, and when you look carefully, there are P waves. Often they look like sinus P waves, but they're only in front of every other QRS complex, so if you see that in a patient referred for atrial fibrillation, be aware that this might not be atrial fib. There is a possibility that this is actually concealed junctional extra or his extra systoles, but the way to make that differential diagnosis is to pace a little faster and a little faster and a little faster, and when you do that, when you pace faster and faster, you stop going down both pathways, and then you just go down the slow pathway only, and that wouldn't be the case if these were his extra systoles. So this is a diagnosis that's rare, but it's extremely important. People like to put this up for questions to try to fool you, so be aware of this, and occasionally we've scrapped an AFib ablation in favor of doing a slow pathway modification. The mechanism is simultaneous AV conduction via fast and slow AV nodal pathways. It can mimic either PSVT or atrial fibrillation. RR alternans is the tip off to the diagnosis if every beat is going down both pathways. The pattern is rate and autonomic dependent, and occasionally some patients may have AV nodal reentrant tachycardia inducible during adrenergic stimulation. Programmed atrial pacing can define fast and slow pathway conduction and exclude alternative mechanisms such as his extra systoles, and it's eliminated by slow AV nodal pathway ablation. So I'm going to leave it there. I hope this has been helpful, and I appreciate your attention. Thank you so much.

catheter ablation

AV node reentry

fast pathway

slow pathway

diagnostic criteria

vagal maneuvers

management options

ablation procedure

risks