Hello. I'm Bill Miles. I am Professor of Medicine at the University of Florida, and I'm going to be talking on catheter ablation of accessory pathways. These are my disclosures. We're going to talk about several different types of accessory pathways. The most common are the periannular AV connections. These often conduct bidirectionally, but they can conduct retrogradely only, or less commonly, antergradely only. We're going to talk about atrial fascicular pathways that connect the right atrium to the distal right bundle branch system. We're going to talk about fasciculoventricular connections briefly, which connect the his bundle to the summit of the ventricle. We're going to talk a little bit about notofascicular or notoventricular connections connecting the AV node to the distal right bundle branch or ventricle, and the rare appendage ventricular connections we're not going to say much about, other than that they do exist and can sometimes cause some trouble. The indications for accessory pathway ablation, pathways that are involved in SVT and those with very short refractory periods should be ablated if they're not in high-risk locations. Ablation of midseptal and supraparaceptal pathways carry the greatest risk of AV block compared to pathways in other areas. Importantly, it's usually unnecessary to ablate an accessory pathway with poor antergrade conduction in an asymptomatic patient without spontaneous or inducible SVT despite catecholamine facilitation. And poor antergrade conduction is defined as an accessory pathway effective refractory period greater than 250 milliseconds or shortest pre-excited RR interval during atrial fib greater than 240 milliseconds. Perianular AV connections can bridge the AV groove anywhere along the tricuspid or mitral annulus, but rarely occur in the region of the aorto-mitral continuity. These schematics show cross-sections of the left and the right heart. The left heart, it shows that these pathways can cross the mitral annulus either somewhat endocardially or somewhat epicardially. The anatomy of the right annulus is a little bit different. It curls up and folds, and anywhere along this fold is an opportunity for an accessory pathway to conduct. Multiple accessory pathways may occur in up to 13 percent of patients. They may be manifest by multiple delta wave morphologies during atrial fibrillation. They may be exposed by atrial pacing maneuvers, such as differing delta waves accentuated by pacing the atria from different sites, and accessory pathways may have different AV block cycle lengths. Differing retrograde activation sequences may also be found. Common settings for multiple accessory pathways might be a patient with Epstein's anomaly, and especially patients who present with antidromic AV reentry. Here's an example of an EKG from a patient that has two accessory pathways. You can see from the rhythm strip two that some of the QRS complexes point downward, and some of the QRS complexes point upward, indicating that there are two different accessory pathways. In fact, this patient conducted so rapidly that he had a ventricular fibrillation arrest once he got to the emergency room. This is another patient that had two accessory pathways, a left free wall and a right free wall. During orthodromic AV reentry, a PVC introduced when his is refractory, pre-excited the right side of the atrium, but not the left atrium, and that can't occur unless there are two retrogradely conducting accessory pathways. And in the same patient, a pathway-pathway tachycardia occurred where antegrade conduction here on the right panel goes down the accessory pathway and then comes up the left-sided accessory pathway. The ECG localization of accessory pathways can be useful. Delta wave orientation of the first 0.04 seconds of the QRS is used. The more subtle the delta waves, the less reliable the localization is from the surface electrocardiogram, but you can accentuate the delta wave by either identifying PACs or performing atrial pacing techniques. There's several published algorithms for ECG localization of accessory pathways, and I'm not going to go through them in detail, but in general, if V1 is upright, it's a left pathway and V1 is negative, or a R followed by largely negative, it's a right-sided pathway. If 2,3 and AVF are positive, it's anterosuperior, and if 2,3 and AVF are negative, it's posteroinferior. To a lesser extent, P wave morphology during tachycardia can be used for pathway localization. For example, a negative P wave in lead I during orthodromic reentry may imply a left-sided accessory pathway. There are limitations to this ECG localization, though. There may be difficulty determining the delta wave vector due to QRS fusion. There may be varying cardiac orientation and rotation within the chest cavity. Some important location distinctions are only a few centimeters apart and can't be distinguished very well from surface ECG. For example, right anterior free wall and right supraposteroceptal or anteroceptal accessory pathways. Slight variations in chest and limb lead placement can make differences in the EKG, and fusion of delta waves may occur if there's more than one accessory pathway and may make identification of the site of the pathway more difficult. We're going to talk about intracardiac mapping. You can either do anagrade mapping to look at the ventricular insertion site or retrograde mapping to look at the atrial insertion site. Anagrade mapping can be done during sinus rhythm, during atrial pacing, which accentuates the delta by slowing AV node, and also pacing the atrium closer to the atrial to the accessory pathway atrial insertion site accentuates the delta wave. You can also do anagrade mapping during antedromic reciprocating tachycardia or other pre-excited tachycardias. Retrograde mapping can be done either during ventricular pacing or orthodromic reciprocating tachycardia. During orthodromic RT you know that you're going up the accessory pathway, but be very careful if you do retrograde mapping utilizing ventricular pacing because if you're doing a if you're dealing with a septal accessory pathway you have to be careful that you're not mistaking retrograde AV nodal conduction for the accessory pathway because we don't want to ablate the AV node. Analysis of retrograde conduction is very important. Retrograde conduction can represent either a fast AV node, a slow AV node pathway, or one or more accessory pathways. The retrograde patterns are defined as eccentric, and if they're eccentric they're usually accessory pathways. Here's an example of an eccentric retrograde atrial activation sequence that goes from the distal coronary sinus all the way to the right atrium. On the other hand, the second QRS is a concentric activation earliest at the septum, either the hyst lead or the CS os area, and then going out from there. If the coronary sinus electrograms are the earliest, it's a left free wall accessory pathway away from the os of the coronary sinus. The rare exception is a very atypical left-sided AV node reentry pathway. If the high right atrium or the right atrial appendage or the lateral tricuspid annulus is earliest, that's a right free wall accessory pathway. Concentric retrograde conduction can represent either retrograde AV node or septal accessory pathways. It can either be earliest at the hyst A or at the CS ostium, and this is a distinction between node and septal pathway that needs to be made with great care, and a lot of the other speakers in this series are going to go through a lot of the maneuvers that we do in order to make that distinction. Analysis of retrograde conduction. You can look for subtle differences in retrograde atrial activation sequences, such as retrograde jumps, echoes, and induction of tachycardia. You can look for subtle changes in the interatrial timing relationships. You can do maneuvers to try to dissociate hysts from the retrograde A, and there are two maneuvers that do this. One is looking for retrograde hyst delay following ventricular extra stimuli, and the other is parahyst pacing, and when you do parahyst pacing, you have to examine both the stimulus A or the VA intervals and the atrial activation sequence to make sure you don't have fusion, and remember that a nodal parahyst pattern does not necessarily exclude the presence of an accessory pathway. Differential basal apical pacing can be used. If the VA interval from pacing from the base of the ventricle is shorter than the VA interval from apical pacing, that suggests an accessory pathway. If the VA interval pacing the base is greater than the VA interval, paced from the apical site, that suggests that retrograde conduction is going up the AV node, and the closer you ventricular pace to the accessory pathway, the more you can accentuate that retrograde pathway conduction. Decremental conduction characteristics and adenosine responsiveness can be suggestive, but not definitive, because there are unusual accessory pathways that can demonstrate decrement or adenosine responsiveness, and retrograde fast nodal pathway may demonstrate very little decrement and may respond just minimally to adenosine, so adenosine and decrement are suggestive but are not definitive at differentiating retrograde accessory pathway from retrograde node. Here's an example of dissociating the retrograde hiss from retrograde accessory pathway conduction. Each of these three panels represent progressively more premature ventricular extra stimuli, and on each panel you can see that the V to retrograde hiss gets longer and longer, but the VA interval stays the same. Therefore, VA conduction must be via a retrograde accessory pathway, because if it was via the node, the A would move out as the VH increases. So this is a way of dissociating retrograde hiss activity from VA conduction and confirming a retrograde node. Para-hiss pacing is a similar concept. Pre-ablation of an accessory pathway, we either capture the hiss or we lose capture of the hiss, and whether we capture the hiss or lose the capture of the hiss, the VA interval stays the same, because retrograde conduction here is via a post-receptal accessory pathway. However, post-ablation, we have a classic nodal response, and that is we're capturing the the hiss here on the left, we lose his capture on the right, labeled as H, and when the V, when the stimulus to H go out, the VA goes out. The VA gets longer, typical of nodal retrograde conduction, and indicating that the hiss is related to VA conduction, not dissociated from VA conduction. There are potential pitfalls in interpreting para-hiss pacing, and you have to be careful. You have to be careful that you don't inadvertently capture the atrium, and that can trick you sometimes. Rapid retrograde nodal conduction may mask a slowly conducting accessory pathway with para-hiss pacing. You need to look for fusion of two or more retrograde activation sequences to adequately interpret what's going on, and importantly, left free wall accessory pathways, para-hiss pacing with pure left free wall accessory pathway retrograde conduction may mimic a nodal response, because when you lose capture of the hiss in this situation, the right ventricle is captured, and you have to go across the septum to get to the left ventricle and engage the left free wall accessory pathway. So, para-hiss pacing in patients with left free wall accessory pathways may demonstrate a pseudonodal response. So, let's talk a little bit about mapping periannular AV connections. We try to localize these by bracketing activation along the annulus, accounting for oblique orientation of most of these pathways. We often look for a potential that may represent an accessory pathway potential, although we rarely prove it definitively, and it's important in most cases to utilize unipolar as well as bipolar electrograms, so you can make sure that what you're interested in and what you're recording is being recorded from the distal electrode, not the proximal ring electrode. And this is what we mean by bracketing, and that is just moving the catheter back and forth along the annulus until you get the earliest atrium or the earliest ventricle or whatever you're mapping, depending on whether you're doing anagrade or retrograde mapping. It may be difficult to distinguish closely spaced atrial and ventricular potentials near the accessory pathway insertion site along the AV groove, and you have to move the catheter one way or the other to try to define what's A and what's V. Due to the oblique course of most pathways, usually the atrial insertion more lateral than the ventricular insertion, local electrograms can be separated somewhat by pacing the chamber of interest from disparate sites. For example, pace from the right atrial appendage and then pace from the coronary sinus ostium if you're mapping anagradely to activate the accessory pathway from different directions. This helps distinguish atrial and ventricular electrogram components and may expose accessory pathway potentials which are good ablation targets. And the Oklahoma group has written about this a lot. If you're pacing and the, let's say we're pacing, we're looking at, we're doing retrograde mapping, if you're pacing the ventricle so that the direction of annular activation of the ventricle is sort of in the same direction as the slant of the accessory pathway that is concurrent, then these electrograms in the atrium are going to be running right along with these electrograms in the ventricle and they're not going to be very separate. And if you have trouble separating them, just pace from somewhere else to try to get a countercurrent activation of the ventricle so that the impulse has to turn around to get to the atrium which really delays the atrium, separates the potential, and might expose an accessory pathway potential. You can do the same thing with anagrade mapping as illustrated in panel C and panel D. And this is just an example that short local VA interval does not necessarily indicate a good ablation site. Here we're pacing from the right ventricular posteroceptal area and you can see a nice early A here fused pretty closely with the V and the VAs are broad everywhere else. But if we pace from the right ventricular alpha tract, we're now going concurrently with the slant of the pathway and look at these VAs, VAs, VAs. So all of these electrograms have a short local VA interval but the earliest A is still in the distal coronary sinus lead and that's your target. So not only do you like to see the V and the A close to each other but you want the A to be early. And there may be areas where local VAs are tight but do not represent good ablation sites. These are just some data from the Oklahoma group showing that most pathways slant with the atrial insertion more lateral than the ventricular insertion. Electroanatomic mapping helps in the ablation of accessory pathways. It helps define the anatomy of the AV annuli, including the coronary sinus anatomy for epicardial post-receptal pathway mapping and localization of his. It aids in bracketing activation along the annuli and allows one to reliably return to the earliest location. So you don't have to worry if you think it might be a good site, can I get back there? You can get back there easier if you're using electroanatomic mapping. Localization of the accessory pathway ablation site may be facilitated if you've mechanically bumped the pathway and it's not conducting, but maybe you can elucidate through your electroanatomic mapping exactly where that bump occurred and you can ablate at that site. You can monitor catheter stability during ablation energy delivery and you can minimize radiation exposure. But remember your operator with your electroanatomic mapping isn't really gonna be much better than you are looking at very distinct electrograms at discerning atrial from ventricular electrograms along the annulus. And you have to watch the mapper very carefully. Here's an example of electroanatomic mapping of the middle cardiac vein with an epicardial post-receptal pathway where we could incorporate a fluoroscopic picture, a venogram of the coronary sinus and the middle cardiac vein. And this was the earliest site where it was close to an artery so we used cryoablation in this particular patient. Well, let's talk about ablation. Characteristics of successful sites. You want stable fluoroscopic and electroanatomic location and good contact force. You want a stable electrogram with both atrial and ventricular components most of the time. Now for some pathways close to the AV node, we might want a lot more ventricular component than atrial but you would do your mapping and a lot of your ablations with both atrial and ventricular components. Typically in orthodromic RT, the VA interval at a successful site is about 70 to 90. Now remember, we're talking about a global VA interval. We're talking about the earliest ventricle, measurement of the earliest ventricle in any lead to the atrial electrogram in the lead of interest. Remember, this is not a local VA interval measured in one lead. So you want the VA interval usually about 70 to 90. Remember in AV re-entry, you can't have a VA interval any shorter than about 65 or 70 milliseconds. However, occasionally you may run into a pathway with long conduction characteristics that has a longer VA interval but that's as short as you can get. And if so, your unipolar electrogram may help you determine that that's the earliest site and a good site for ablation. If you're doing antegrade mapping and you're ablating in sinus or atrial pacing, you'd like to see a local ventricular electrogram preceding the delta, usually by about 25 to 50 milliseconds. You want an early unipolar electrogram with a rapid descent and no R-wave recorded from your distal electrode. If you see something that looks like an accessory pathway or behaves like an accessory pathway potential, that's helpful. You want a stable eight to 10 ohm decrease in impedance during delivery and early disappearance of the accessory pathway less than 10 seconds after onset of RF is a good prognostic sign that you may have a durable ablation. So here's a example of an antegrade map in sinus rhythm with a big delta wave. And notice that you have on the ablation distal, an atrial and a ventricular electrogram. The ventricular electrogram precedes the onset of the delta wave and the unipolar ventricular electrogram has no R-wave and a steep early descent. That's a great site for ablation of this accessory pathway. Here's retrograde mapping during orthodromic re-entry in a patient with long VA intervals. So we don't know how long the VA interval is gonna be in this patient. We have to look for the earliest VA. How do we know how early the VA is? Well, we look around and we know that we can't find anything, any atrium earlier than this. And then we look at the unipolars and there's no R-wave and an early steep descent of the unipolar. This is a good site, probably the earliest atrial activation site in this particular long RP reciprocating tachycardia. And here's just an example of a probable, but not necessarily proven accessory pathway potential in a post-receptal patient. We're mapping the tricuspid annulus. During sinus, we have an A-electrogram, a little spike that may be our accessory pathway potential and a ventricular electrogram. During tachycardia, you have V pathway A, so they reverse each other. And when we start reciprocating tachycardia with a PAC, we actually have an atrial electrogram, no pathway after it. You have nodal conduction. You have a ventricular electrogram, a pathway electrogram, and then back up to the atrium. So this is pretty clear evidence that this little glitch here might represent an accessory pathway. And this may be an excellent site for ablation of this accessory pathway. Looking for accessory pathways, potentials may be particularly useful in patients with pathways that are oblique, pathways with multiple components or a broad band, complex post-receptal pathways, atypical pathways, such as atrial fascicular, Epstein's, or pathways with long conduction times, and sometimes in patients with altered anatomy due to prior surgical or catheter ablation. Catheter stability can be enhanced by long preformed or deflectible sheaths. You can map or ablate either on the atrial or the ventricular side of the annulus. You can get access from superior, the subclavian or the internal jugular, especially for right supraparaceptal pathways. We'll look at that in a minute. Entrainment of tachycardia during ablation might be useful to prevent pause upon elimination of the pathway. When the tachycardia terminates during the burn, the catheter can be thrown away from the spot that you want to ablate, and that might affect catheter stability, especially if you're doing septal pathways, some sort of anesthesia with breath holding or jet ventilation may be useful. And if there's a problem with stability, you can switch to cryoablation and cryoadhesion may help you. Here's an example of retrograde termination of orthodromic AVRT during radiofrequency. This was a retrograde block in a pathway with a resumption of sinus rhythm, but notice that the cadence is markedly changed when the tachycardia terminates, and that could have adverse effects on catheter stability. In another patient, we ablated during ventricular pacing, and there's no problem in that regard with catheter stability. And you can see the first two beats on the right panel go up the pathway, but after that, there's no further accessory pathway conduction. Here's an example of AV reentry, orthodromic AV reentry, where we start pacing the ventricle just a little bit faster than the tachycardia just before we're gonna ablate. So we now know we're still going up a pure accessory pathway because we've initiated the pacing during tachycardia. And when we start the radiofrequency energy delivery, you see the VA block. So this is very useful to maintain catheter stability, but remember in this and in anything where you're pacing the ventricle, there may be some issues in assessing AV node function during RF if you're ablating close to the AV nodal region. The other thing that we might do is to ablate during sinus rhythm. Even if there's just minimal pre-excitation, if you're in the correct spot, the local A and the V are gonna be very close. The delta wave disappearance may be subtle and it may even be more obvious if you look in some of the other leads. And in this example, you can see on the left, the proximal coronary sinus electrograms are crowded together, but when the pathway disappears, the A and the V separate. So with the onset of radiofrequency energy, this patient's accessory pathway disappeared in between about one and two seconds. And here's a left free wall pathway that we couldn't get any VA interval, right? Earliest V in any lead to the measured A, we couldn't get any VA interval less than 190. This is just a left-sided pathway with long conduction characteristics. And when we ablated during tachycardia, the accessory pathway blocked and tachycardia terminated. In addition, just to mention it, there may be some potential mapping difficulties in patients that have had prior ablation. This was a patient with a left free wall pathway, which should give eccentric retrograde activation sequence. But notice that this portion of the coronary sinus looks like it's concentric. And that's because at the previous ablation, the ablation caused a line of block here, but the pathway still conducted across the AV groove, but more lateral than that line of block. And the atrium was activated in a non-typical way for a left free wall pathway. So left free wall pathways can be ablated either by retrograde transaortic, transeptal, or on rare occasions, coronary sinus techniques. And this is a patient where we have both a catheter across the foramen ovale, a transeptal catheter, but we had trouble getting this pathway to go away. So one of us who was experienced in retrograde transaortic said, let's just try a little different way. And we were able to get this pathway retrograde transaortic and for some reason couldn't get stability or couldn't get exactly the right location with this transeptal catheter. But most people these days do their left free wall pathways via the transeptal technique. Now, right free wall pathways can be a little tricky and contact is often an issue. Here's the catheter coming up, coming forward toward where the tricuspid annulus is. Notice that the tricuspid annulus isn't all the way out here at the right heart shadow because that's the right atrium over here. The annulus is in here. The mapping is a little more difficult sometimes and stability is more difficult. Sometimes one of the Schwartz preformed sheaths like an SR2 or something like that can be used and you can move the ablation catheter up and down the right tricuspid annulus and bracket the pathway sort of like we do in the coronary sinus. And remember Epstein's anomaly is associated with accessory pathways, sometimes multiple located along the posteroseptal, posterolateral tricuspid annulus. They're often multiple. You target the pathway at the true AV ring, not into the ventricle where the displaced tricuspid leaflet is. And also remember that in Epstein's patients, other SVTs such as atrial tachycardias are relatively common. Posteroseptal pathways can be much more complicated. The posteroseptal space is a pyramid-shaped space. It includes the os of the coronary sinus. It includes the posteroseptum. It includes this whole triangle in here. And it's actually a relatively complicated space. A typical EKG of a posteroseptal accessory pathway has an isoelectric or negative delta wave in V1 with an abrupt transition to a positive delta wave in V2. And it has negative delta waves in the inferior leads II, III, and AVF. Sometimes you have to decide whether to ablate a posteroseptal pathway on the right or on the left. So if the earliest site of atrial activation is within the first centimeter or two of the coronary sinus, you can try ablating it on the right near the os of the coronary sinus. If it's more than three centimeters before the earliest site into the coronary sinus, it's probably really a left free wall and you need to do a transeptal. And there's an in-between area that you can do some careful mapping. If the RS is greater than one in V1, or if there's a little bit of increase in the VA interval with functional left bundle branch block during the diagnostic portion of the study, you may need to go to the left side to get that pathway. A very important type of posteroseptal accessory pathway is the epicardial accessory pathway. This is a ventricular connection from the myocardial coat. A ventricular connection into the myocardial coat of the middle cardiac vein or a proximal posterolateral branch of the coronary sinus. It's sometimes associated with the coronary sinus diverticulum and sometimes a veno-occlusive coronary sinus angiogram is helpful to define the anatomy. It inserts broadly into the atria between the valve of usines and the CS ostium. And you can get a clue that it might be an epicardial posteroseptal by mapping the floor versus the roof of the coronary sinus. If the floor is earlier than the roof, it may be a posteroseptal epicardial pathway. If the roof is earlier than the floor, it may be a garden variety perianular AV connection. The following suggests a middle cardiac vein ablation site, the thing we pay attention to most. It's not perfect, but if you see a very sharply negative delta wave in lead II, suspect that that might be an epicardial posteroseptal pathway. Here's a schematic from the Oklahoma group where you can see that the left ventricular connection is down in the middle cardiac vein. It gets into this electrically active myocardial coat that covers the middle cardiac vein proximally and that covers the coronary sinus between its os and the valve of usines. Beyond the valve of usines, there's no electrically active myocardial coat, but this whole area can conduct the impulse up to the left atrium. So the site of ablation ideally is probably a focal site down here as long as you can find it and it's safe. Here's a schematic of a diverticulum in the coronary sinus. If you do find a diverticulum, the successful ablation site is usually at the neck of the diverticulum. And here's just a dilated middle cardiac vein associated with the posteroseptal epicardial accessory pathway. And you have to do angiography in these people to make sure that you can deliver radiofrequency more than a half a centimeter or so from the posterolateral branch of the coronary artery. Here's an example of recording the roof of the coronary sinus versus the floor of the coronary sinus. Here's the coronary sinus venogram in this particular patient. You can either do this by double multipolar catheters or just use your ablation catheter to go to the roof and the floor. But notice that the duodeca catheter has an earlier A than the deca catheter on the roof. So this is indicative that the impulse is coming up from below from the middle cardiac vein, activating the floor of the myocardial coat, going to the roof and then going to the atrium. It's best to ablate the discreet ventricular insertion site just inside the middle cardiac vein, its ostium or the mouth of a coronary sinus diverticulum. Coronary angiography is mandatory to localize the posterolateral coronary artery and ablation should be at least five millimeters from the coronary artery. You use irrigated RF because non-irrigated RF will not get a lesion deep enough. You don't have enough flow past a non-irrigated catheter electrode to get a good lesion in the middle cardiac vein with a non-irrigated catheter. But you start at low powers, watch the impedance and titrate up, but try not to allow the impedance to rapidly ramp up. If you're very close to the artery and you're a little jumpy about delivering RF in that area, consider cryoablation, but cryoablation tends to be a little less durable. You can, if you have trouble getting this area, you can ablate the atrial insertions, but if you do, you have to disconnect a large area of the myocardial coat from the left atrium, ablating all the way from the valve of usines to the coronary sinus ostium. And you can watch the earliest atrial activity move as you ablate. Anteroceptal pathways and mid-septal pathways are the nerve wracking ones. I usually consider a superior approach for the anteroceptal location, hooking the catheter under the tricuspid annulus because the his bundle dives into the membranous septum and is protected. It's more protected on the ventricular side of the annulus than it is on the atrial side of the annulus. Ablation of mid-septal pathways is the most likely to result in AV block. The atrial insertion of these is located inside the triangle of Koch. And occasionally you may sacrifice the right bundle branch with the ablation of a mid-septal pathway. Here's an example of a catheter curled underneath the valve coming from the subclavian or the IJ in an anteroceptal accessory pathway. How do we avoid AV node damage? Well, careful pathway and node localization preablation. Maximize the distance between the ablation site and his. You want a good ablation site electrogram. You want it stable and you may wanna employ anesthesia for breath holding or jet ventilation if necessary. If you're near the AV node and the his bundle, a blade on the ventricular aspect of the annulus, a large bipolar ventricular electrogram and a unipolar ventricular electrogram without an R wave on the distal electrode are favorable. And if you see an accessory pathway potential, that's also helpful. Start at low power and low target temperatures. Monitor the catheter with fluoro or electroanatomic monitoring during the energy delivery to make sure that it's not moving or sliding. Terminate radio frequency delivery if junctional rhythm occurs. Consider focal cryo ablation, especially for mid septal accessory pathways. And here's an example of what looks like an anteroceptal accessory pathway, left bundle branch block pattern in V1, V2 and upright deltas in 2, 3 and AVF. We mapped it a little bit below the his bundle catheter, which means it's mid septal. Anteroceptal is usually a little above. So we know it's mid septal. We go on the ventricular side of the his and the pathway disappeared. But we did on this particular example, create a right bundle branch block. You need to watch AV nodal conduction as you deliver the energy. If the accessory pathway is concealed, if there's no antegrade conduction over the accessory pathway, still deliver in sinus rhythm or reciprocating tachycardia. So you know what the AV node's doing, not during ventricular pacing. If there's total ventricular pre-excitation, you don't think the QRS is fused, you need to deliver during reciprocating tachycardia. If there's fusion of the QRS, you can ablate watching carefully for any widening of the QRS that indicates increased pre-excitation because of nodal delay. And if you see that, you need to stop energy delivery immediately. There are some unusual or unexpected locations for accessory pathways. We're not gonna go over them carefully. These are the appendage to ventricular ones that I mentioned. Left mid septals are not really rare. I'm gonna give a clue on them in just a minute. Left anteroceptals aren't real common. Non-coronary cusps are not super uncommon. They look like any other left anterior pathway but can be ablated sometimes from the non-coronary cusp. This is just a clue to a left septal, left mid septal pathway. If you see that the earliest electrogram is at the os of the coronary sinus and looks distant, if it's at the roof of the coronary sinus but looks distant, that's an area where you might muck up AV nodal conduction a little bit around the roof of the coronary sinus, osteum. And so that's a patient that you might wanna go ahead and go transeptal and then look for a sharper, more local potential. That might be a left mid septal instead of a right mid septal. So early distant potential near the roof of the coronary sinus, think about going across the septum. It might be a mid septal accessory pathway. Now we're gonna talk about a few accessory pathway variants. We're gonna talk first about atriofascicular accessory pathways or in the vernacular, we sometimes call them MEHIMES. They give a left bundle branch block-like tachycardia. These pathways have antegrade only conduction, decremental conduction properties and adenosine responsiveness. They participate in a characteristic anthedromic reciprocating tachycardia as the antegrade limb with the right bundle branch and the His-AV node as the retrograde limb. Accessory AV node His-like structure exists along the posterolateral tricuspid annulus inserting into the distal right bundle branch moderator band area or less commonly the adjacent right ventricle. So we're gonna show pictures of this in a minute. This is a schematic, the proximal component. This is basically an accessory AV node that failed to involute when the heart was forming. So you have a little AV nodal-like component and you have a little His-Purkinje component that usually inserts near the moderator band into the right bundle branch. The proximal component is lateral, anterolateral or posterolateral along the tricuspid annulus. It does not generate a potential and it has decremental or AV nodal-like properties. The more distal component extends from the tricuspid annulus to the right bundle branch at the RV apical free wall. It generates an accessory pathway potential that can identify a good ablation site. So here's a schematic of the accessory atrioventricular nodal-like thing that inserts into the right bundle distally. And the typical tachycardia has an early ventricle activation at the apex because that's the earliest activation. Remember, most AV pathways activate the base early but this pathway activates the apex early. And in fact, it gets up the right bundle to the His-Purkinje system very, very quickly so that you get a His potential also right at the beginning of the QRS and the His bundle activation is distal to proximal rather than proximal to distal. There is that variant where the pathway doesn't connect up to the conduction tissue but connects up to the ventricle. In that variant, the right ventricular apex will not be early and there's no retrograde His at the onset of the QRS. The retrograde His is buried in this local V somewhere. And these pathways can be a variety of places along the tricuspid annulus, usually lateral, a little anterolateral or posterolateral. Targeting the accessory pathway near the right bundle branch, the distal, targeting the distal part of this pathway may result in inadvertent retrograde right bundle branch block and possibly a more incessant reciprocating tachycardia. Ablation therefore should target a His-like potential that can be identified along the posterolateral tricuspid annulus. A circular catheter, sometimes we call it a halo catheter along the tricuspid annulus is useful for localization. The pathway, these pathways are very prone to mechanical bumps with catheter manipulation so you have to be careful in that regard. And here's just a fluoroscopy. This is an RAO and this is an LAO of the ablation site for this MAHIM potential or atrial fascicular accessory pathway. And here's a nice tracing that I borrowed from one of my former fellows where the lateral tricuspid annulus has this His bundle-like potential on it. There should be nothing over there that looks like a His bundle so this is the potential from the atrial fascicular of the rapidly conducting portion of that atrial fascicular pathway. And in that same patient that potential could be found with an ablation catheter and when you ablate in that area the pre-excitation during atrial pacing disappears within a second or two of the onset of ablation. The next accessory pathway variant is a permanent form of junctional reciprocating tachycardia. This is a long RP narrow QRS tachycardia that's incessant or near incessant. And it usually just restarts and restarts even during sinus rhythm without PACs. I've even seen patients that had so much of this that they were referred for heart transplant. And when this accessory pathway was ablated the left ventricular function normalized. This is an accessory pathway with retrograde only conduction, decremental properties and a very long retrograde conduction time. So you get an incessant or a near incessant RT with the RP interval longer than the PR interval. It usually, but it's not exclusively a post-receptal location and the ablation target is the earliest retrograde A during reciprocating tachycardia or if you're lucky possibly an accessory pathway potential. This slide actually demonstrates that this long RP tachycardia is not an atrial tachycardia and not AV node re-entry because a PVC put in at a time when the HISS is refractory actually delays the next A. And the only way that could occur is if it's getting up there via a retrograde conducting accessory pathway since HISS is refractory. And this is ablation for this patient. I actually showed this same slide earlier. This is the long RP tachycardia with the earliest A that we could get anywhere and a rapid early decline in the distal unipolar and that was a successful ablation site. We've talked about the atrial fasciculars. We're gonna talk a minute about nodoventricular, nodofascicular or fasciculoventricular. Nodofascicular and nodoventricular are very rare. Historically, you see them talked about because it was mistaken for a while that atrial fascicular pathways were nodofascicular because of the AV nodal-like properties of the atrial fascicular pathways, but we now know that they are not. But despite that, a few very rare, probably nodofascicular or nodoventricular pathways have been described. Tachycardias associated with these can be either a narrow QRS variety where the impulse travels anagradely down the normal conduction system and returns retrogradely via the pathway, or there can be a pre-excited variety where the impulse travels down the accessory pathway, down the nodofascicular or nodoventricular pathway and up the normal conduction system. Both of these tachycardia varieties commonly demonstrate some degree of VA dissociation during tachycardia due to retrograde block in the proximal common AV node. And here's an example from the literature of induction of one of these tachycardias showing VA dissociation at induction. If the tachycardia is one-to-one, the ventricular and atrial activation can occur simultaneously and may mimic AV node reentry. But a very unusual phenomenon is in distinction to AV node reentry. And that is if you have a simultaneous A and V tachycardia, but you put in his refractory PVCs, you can advance this tachycardia with his refractory PVCs, but you can't with AV node reentry. So AV node reentry is a frequent association. And most of the time, the slow pathway region is the usual ablation site because it's thought that most of these seem to insert somewhere near the slow AV nodal pathway. The last variant that we're gonna talk about are the fasciculoventricular pathways. These are connections between his or the proximal right bundle branch and the summit of the right ventricle. They're manifested by slurred upstroke of the QRS with a short HV interval. In contrast to periannular AV connections, atrial pacing results in PR prolongation with no change in the delta morphology or HV interval. They do not participate in tachycardias and should not prompt ablation attempts. So the real importance of fasciculoventricular pathways is if you find them, diagnose them, and don't try to ablate them. Here's an example of one during sinus rhythm. You have an AH interval of 150. You have an HV interval of 25. See, we've dropped the plumb line at the earliest ventricular activation. The HV interval is 25. It's a slurred upstroke of the QRS that looks like a delta wave. And in fact, it is. It's pre-excitation. If we pace faster, however, the AH interval prolongs, but instead of what would happen with a normal accessory pathway, and that is for the AH prolongation, you'd get an HV shortening and you'd get increased pre-excitation. For a fasciculoventricular accessory pathway, the AH prolongs, the HV stays exactly the same, and the degree of pre-excitation stays exactly the same. So I'm not sure exactly what the anatomy of these pathways are. They're not very common, but we've all seen a few of them. And it behaves as if some of the insulation of the distal hiss, or the very proximal right bundle branch, may actually leak the impulse and allow activation of the summit of the right ventricle rather than the right bundle branch emptying out only toward the apex of the right ventricle. So success depends on the accessory pathway location. When you do ablation, acute and long-term success rates may be greater than 95% for left lateral pathways. They're actually a little bit lower for right laterals, probably because of poor catheter stability on the tricuspid annulus. And there might be a little bit different anatomy of the tricuspid annulus. Major complications are uncommon. All of these first ones can occur with any type of invasive vascular procedure. Heart block requiring permanent pacing occurs in well less than 5% of septal pathways. The mid-septal are the ones that are the most difficult and that you have to be the most careful to try to prevent AV nodal ablation when you try to ablate the accessory pathway. There's practically, if you've mapped carefully, there's practically never any AV nodal block on any pathway other than mid-septal or anteroseptal. So that completes the presentation. I hope it was helpful. Thank you very much.

accessory pathways

ablation

periannular AV connections

atrial fascicular pathways

fasciculoventricular connections

delta wave morphologies

intracardiac mapping

catheter stability

complications