Hello, I'm Bill Stevenson from Vanderbilt University Medical Center. This talk is on catheter ablation of atrial tachycardia and atrial flutter. These are my disclosures. So the mapping approaches to tachyarrhythmias are determined by the type of arrhythmia, and we can group them into two types. There are focal tachycardias, and this may be due to automaticity or a small re-entry circuit. But the activation sequence of this type of arrhythmia is characterized by a point of earliest activation and then spread throughout the rest of the cardiac chamber. And you can identify that point of early activation from activation sequence mapping, or from pace mapping, often gives you an idea of where the site is. The second big group of arrhythmias are macro-reentrant tachycardias, and with macro-reentry, you've got continuous activation, so that at any point in time, some portion of the re-entry circuit is being depolarized, and there's no truly earliest point. So for this, you can use activation sequence if you can define the entire re-entry circuit, or you can combine activation with entrainment mapping to identify components of the re-entry circuit. So here are two examples. On the left is a focal atrial tachycardia, and you can see that the activation map of the right atrium, the colors indicate the timing of activation, and it moves from red, which is earliest, through the colors of the rainbow, yellow, green, blue, and purple being latest. So there's a focal area of early activation spread in all directions away from that focus. The tachycardia cycle length was 370 milliseconds, and activation of that chamber from earliest to latest was much shorter than that. So earliest minus 49, latest 54, so 103 milliseconds is all it took to activate the entire right atrium, and that was much shorter than the tachycardia cycle length. In contrast, on the right is an activation map of common cabotricuspidismus-dependent atrial flutter. We're viewing the right atrium from the LAO projection, and you can see that we have earliest activation at the cabotricuspidismus on its septal aspect, and then activation moves around the tricuspid valve annulus in this manner. The time from earliest activation at minus 142 to latest activation, 121, is 263 milliseconds, which equals the tachycardia cycle length. And we have this area of earliest activation meeting latest activation. So this is characteristic of a large reentry circuit. This slide summarizes for you differences between focal atrial tachycardias and macro reentrant atrial tachycardias. So first, the P wave tends to be discrete with an isoelectric segment between P waves in focal atrial tachycardias, whereas in macro reentrant atrial tachycardias, very often there'll be an almost continuous flutter-like appearance. The activation sequence with focal AT spreads from a focal source, and often there will be more than 30% of the tachycardia cycle length, which is not accounted for by activation. In other words, during that time, the atria are quiescent. And the latest activation is at some point remote from the site of earliest activation. In contrast with macro reentrant tachycardias, you have continuous activation if you can see the entire reentry circuit, which you may not be able to do. And you have a point where earliest activation abuts latest activation. With pacing maneuvers, for focal tachycardias, if it's a small reentry circuit, it's possible that you could entrain it. But if it's automatic, you will not be able to demonstrate entrainment. And the shortest post-pacing interval will occur near the earliest site of activation. But it will generally be longer than the tachycardia cycle length. With macro reentrant arrhythmias, you'll get a post-pacing interval that equals the tachycardia cycle length at sites that are in the reentry circuit. The response to adenosine is interesting. Adenosine will often terminate focal automatic atrial tachycardias, provided that you give enough adenosine. And this has been taken as evidence that some of these tachycardias are related to triggered activity as their mechanism. And adenosine suppresses triggered activity with some patholytic-type mechanisms. With macro reentry, adenosine has no effect on reentry. It may increase the degree of AV block and make it easier to tell that, in fact, you're dealing with an atrial tachycardia. Adenosine does shorten the atrial refractory period, and it may precipitate atrial fibrillation in some patients. So here's an example of a focal atrial tachycardia defined with a high-density activation map. You can see earliest activation up here by the superior vena cava. And if you plot the timing of activation across the atria, you see that there are large portions of the cycle length of the arrhythmia, during which you don't see any atrial activation in this skyline type of plot. Now focal atrial tachycardias are most commonly long RP tachycardias. They may occur with one-to-one AV conduction or with AV block. They can present at any age. They account for up to 20% of supraventricular tachycardias in children, a bit less common in adults as sustained arrhythmias. They can be idiopathic or associated with structural heart disease. There are three common clinical presentations. There's the incessant atrial tachycardia, and these can even produce tachycardia-induced cardiomyopathy that's encountered most frequently in children. They can occur as paroxysmal arrhythmias. And then most commonly in adults, non-sustained focal atrial tachycardias are very commonly encountered on ambulatory recordings. Now a focal atrial tachycardia can mimic other forms of supraventricular tachycardia, largely depending on its behavior and where the focus is located. So if you have a focal atrial tachycardia that is near the sinus node at the top of the crista terminalis or up in the superior vena cava, or from the adjacent right superior pulmonary vein, you can have a P wave that looks like sinus and may mimic sinus tachycardia. Focal ATs usually have an abrupt onset and offset that helps distinguish them from sinus tachycardia, which would be expected to have a gradual onset and offset. A focal atrial tachycardia in the atrial septum or along the tricuspid annulus or mitral annulus can mimic an accessory pathway. So if you have a one-to-one tachycardia, early activation at a valve annulus, that may look like an accessory pathway, and you distinguish those with ventricular pacing maneuvers. And then atrial tachycardias that occur in the atrial septum can mimic avianodal reentry. And these, again, can be distinguished by ventricular pacing maneuvers. Now focal atrial tachycardias tend to occur at specific anatomic locations associated with structures in the left and right atrium. The most commonly encountered focal atrial tachycardias occur along the crista terminalis, occasionally in the intraatrial septum, less commonly in the appendages. In the left atrium, focal atrial tachycardias may occur along the mitral annulus, around the pulmonary veins, and up near the aortic mitral continuity. The P-wave morphology is useful in suggesting the location of a focal atrial tachycardia. So a P-wave, which is completely negative in V1, that tells you that the activation is moving away from the anterior chest wall, the right atrium is anterior to the left atrium, and that is consistent with right atrial origin. An initial positive followed by a large negative deflection in V1 is consistent with a right atrial tachycardia. A P-wave that is completely positive in V1, so the activation vector is pointing at V1 for the entire atrial activation, is consistent with initial depolarization of the left atrium. And left atrial origin of the focal atrial tachycardia. And a markedly rightward axis, so completely negative P-wave in AVL, is consistent with activation from the most leftward aspect of the atria, so again, the left atrium. A narrow P-wave is seen when you have a focus in the intraatrial septum and activation spreading out simultaneously towards the right atrium and left atrium. Then if you look at the frontal plane axis, that gives you some idea of is the focus high in the atrium or low in the atrium. In the high right atrium, you expect to have a positive P-wave in LEAD2. As the focus is progressively lower in the atrium, then the amplitude of LEAD2 diminishes and LEAD3 becomes progressively more negative with activation towards the floor of the atrium. In the left atrium, you have high in the left atrium, the P-wave will be positive in LEAD3 and biphasic or negative in LEAD2. And down towards the floor of the atria, you have negative P-waves in the inferior leads. So here's an example, here's a one-to-one focal atrial tachycardia, and you can see that the P-waves here are negative in AVL and completely positive in V1. This is consistent then with a left atrial tachycardia and from the leftward superior aspect of the left atrium, and this one came from the left atrial appendage. Now you also in the EP lab, of course, you see very quickly often based on some limited activation mapping and in your CS catheter, this tachycardia would show a distal to proximal left atrial or atrial activation sequence. Here's another long RP tachycardia that was due to a focal atrial tachycardia, and you can see that the P-wave in V1 is negative, so we're thinking right atrium, and its axis is directed superiorly, and it's more negative in V3 than in V2, and this tachycardia originated from the tricuspid annulus in the infralateral right atrium. This flowchart and examples are from a nice paper by Kistler and co-workers that summarizes and updates their previous algorithm for relating the P-wave morphology to the location of focal atrial tachycardia. Now a challenging group of these arrhythmias are focal atrial tachycardias that originate from the anteroceptal region, so these are atrial tachycardias where you have relatively early activation, early atrial activation on the His catheter, and they can originate from the parahis region, from the superior aspect of the tricuspid valve annulus, or from the superior aspect of the mitral valve annulus, and some of them require ablation from within the aorta, from within the non-coronary sinus of valsalva. They tend to have positive P-waves in 2,3 and AVF, and can be biphasic, generally negative positive in lead V1, and then as I mentioned, relatively early activation on the His, and this requires careful mapping of all of these sites to identify these arrhythmias, and it's important to recognize that some of them can be ablated from within the aorta. Now to identify the site for ablation of these tachycardias, activation mapping is very important and this can be done point by point, it can be done with a mapping system, which is very helpful for these arrhythmias. The electrogram at the site of origin is often abnormal, it will often have a low amplitude and somewhat fractionated components. The unipolar electrogram you expect to be a QS configuration. These arrhythmias are susceptible to mechanical interruption, you can bump terminate them, so it's very important to map deliberately, carefully, and to know where your catheter is at all times, so that if all of a sudden the tachycardia stops, and if it doesn't come back with a short wait, you know where you were when you bumped it. And then recognizing these atrial structures that tend to be the sources for the arrhythmia is very helpful, and recognizing also that because conduction in the atria is not homogeneous, that can sometimes confuse mapping. So conduction is very anisotropic along the crista terminalis. It's very rapid along the long axis of the crista and very slow perpendicular to the long axis of the crista. So that you can get somewhat misleading activation if your mapping is limited around the area of the crista. And you can have conduction block transverse to the crista in some patients, particularly older patients with a little bit of fibrosis in their atrium. The eustachian ridge is also an area of conduction block, and so these can produce sometimes misleading activation sequences when you have a focal atrial tachycardia in proximity to one of these structures. So here's an example. This is an atrial activation sequence recorded with a 20-pole catheter which loops around the right atrium and extends out into the coronary sinus. And you see that we have earliest activation here at RA 11-12, and then activation spreads out in all directions from that site. This is the activation map of that tachycardia in the electroanatomic mapping system at the upper right. And you can see early activation indicated by red, and then activation spreads away in all directions. The ablation catheter placed at the site of earliest activation displayed this electrogram. And you can see it's a little bit of an abnormal electrogram, although this patient had no underlying structural heart disease. The activation precedes the P-wave onset. As you see here, there's actually a little bit of a double kind of appearance to that signal. Now, as I mentioned, you expect the unipolar recordings to show a QS-type configuration at the site of earliest activation. So let's just review that for a moment. With a unipolar recording, the positive electrode of your exploring catheter is connected to the positive input of your recording amplifier. And the negative input is the Wilson central terminal or an electrode in the inferior vena cava or some location remote from the heart. With that configuration, a wavefront that propagates towards your exploring electrode produces a positive deflection. As the wavefront reaches the exploring electrode and then propagates away, you get a prominent negative deflection. So you get this RS kind of configuration. If you record at the site of earliest activation in the heart, then the wavefront is propagating away in all directions from that site, and you get a QS configuration at the origin. So here's an example. Now, to interpret unipolar signals, to be able to use that morphology, the unipolar signal needs to be unfiltered, or the high-pass filter needs to be set at a corner frequency of generally below one hertz. We often set it at 0.5 hertz. If you try to do lower than that or near DC recordings, the waveform will often wander up and down with respiration during your recording. A high-pass filter set at 0.5 or certainly less than one hertz, and you can interpret the unipolar morphology. So here we see at a recording from a focus, the unipolar P-wave, if you will, is a QS type of configuration. In the bipolar recording, you expect the first peak of the bipolar recording to fall at the very onset of that unipolar recording. In contrast, if you move away from the focus, as shown in the right panel, the unipolar recording shows an RS type of configuration, and the first peak of the bipolar will typically fall after the onset of the unipolar recording. Now, often it's difficult to see the P-waves because they're superimposed on a T-wave. In the electrophysiology laboratory, one of the ways of dealing with that is to pace in the ventricle and move that ventricular activation so that then you can see the P-wave, and you can adjust your sweep speed and gain accordingly. It's useful to know the connections between the right atrium and the left atrium for interpreting your activation sequences and assessing where the focus might be. These connections exist over Bachmann's bundle, which is anterior to the superior vena cava, and then extending leftwards into the atrium, around the fossa ovalis, the mouth of the coronary sinus, and then the avianodal region. Occasionally, there will be fibers that extend through the fat posteriorly from the left atrium or the right pulmonary veins, and connect to the posterior right atrium. Here is a right atrial activation sequence in the center. You can see that we've got early activation at the dome of the right atrium, and then spreading away from that location. This was activation from a left atrial tachycardia, where the wavefront reached the right atrium over Bachmann's bundle. This is a typical activation sequence map of a left atrial tachycardia that came from high in the left atrium. The right-hand panel shows you activation that came down the coronary sinus and reached the right atrium. This was from a left atrial tachycardia as well. These are two common activation sequences from left atrial tachycardias. Displaying here the activation sequences in the right atrium. Now, you can get, looking at those right atrial activation sequences, those look focal, but the atrial tachycardia may not be focal. If you're mapping the right atrium, you can have a reentrant tachycardia in the left atrium. You can have a macro reentrant tachycardia in the left atrium, but the activation pattern can look focal in the right atrium. This can occur adjacent to regions of conduction block even when you're mapping in the same chamber that contains the arrhythmia focus. There's a nice review of this issue from Takagawa and colleagues here. Here's an example of right atrial activation during a left atrial tachycardia. Again, we have our 20-pole catheter which extends across the roof of the right atrium, and then down the lateral wall and out the coronary sinus. You can see that the lateral wall of the right atrium is activated from high to low. The coronary sinus in this case is activated from distal to proximal. Confusing activation sequence, but this is typical of a left atrial tachycardia. This distal to proximal CS activation favors left atrial tachycardia. Now, particularly with rapid atrial tachycardias, it can be difficult to know when you're recording from multiple sites, which site is early and which site is late. With focal atrial tachycardias, often there can be a bit of cycle length wobble or oscillation that you can analyze to attempt to determine which signal is early versus is that signal very late. Here you see an example of that. It's an atrial tachycardia where there's a pretty prominent cycling variability. The activation sequence appears to be the same on these different beats, so we don't think it's PACs or catheter-induced ectopy. You can see that the first signal that moves early when you have this oscillation is this signal. This is a very early signal rather than a very late signal, and this was recorded from an AT that originated from the mitral annulus. Now also, it's important to recognize that atrial tachycardias can originate from within structures that may conduct with some degree of block to the atrium. You can have rapid atrial tachycardia from within a pulmonary vein or the superior vena cava, or rarely the inferior vena cava. This is an example of an AT from a left inferior pulmonary vein that conducted largely two-to-one out to the atrium. If you map the activation sequence of this, it'll lead you to that side of early activation around the pulmonary vein, and then placing the catheter in the vein, you would see this rapid atrial activation. Now, atrial tachycardias that are intermittent can really be a difficult challenge in the EP lab. We've certainly had many patients where it's a real challenge to induce the tachycardia for mapping. You may only get it to happen a few times. One of the approaches to that situation is to adapt pacemapping to the atrium. There are a couple of reports of this. What you can do is have as many sampling points in the atrium as possible from a multipolar catheter, so that when the tachycardia occurs, you do capture that. Then if you can't get it again, you can use pacemapping to try and replicate that atrial activation sequence. Knowing the anatomy where the focal atrial tachycardias tend to occur is also useful in this regard. You can look along the crista terminalis, for example, when you have a P-wave morphology that suggests the crista tach, and then use the activation sequence produced by pacing in comparison to that obtained during the brief episode of tachycardia to attempt to identify the region that can be targeted for ablation. This is a summary from the 2015 guidelines for the management of adults with supraventricular tachycardia. For focal atrial tachycardia, catheter ablation has a class 1 indication for patients who require management of their arrhythmia. We often will try beta blockers and calcium channel blockers because of their safety and those have a 2A indication. Then class 1 antirrhythmic drugs and class 3, amiodarone or sodolol can occasionally be effective in these patients. Each patient's response is somewhat variable and unpredictable. It's largely a trial and error management approach when pharmacologic therapy is selected. Let's move now to macroreentrant atrial tachycardias. There are two large groups of these. The first are the cavotricuspid isthmus-dependent atrial flutters. That includes clockwise or typical flutter, counterclockwise or typical flutter, and lower loop reentry. The other big group are all the other macroreentrant atrial tachycardias and that are not dependent on conduction through the cavotricuspid isthmus. These are usually associated with atrial scar, very commonly the scar is due to prior ablation of atrial fibrillation or prior surgery, particularly atrial maze procedures or repaired congenital heart disease. We classify these according to the location of the reentry circuit. There are those that occur in the free wall of the right atrium, in the left atrium perimitral flutter or roof-dependent left atrial flutter, the interatrial septum. Then you can have complex types of reentry, often multiple loop figure eight types of reentry and biatrial types of reentry. From the SVT guidelines, the classification and summary of these types of macroreentrant arrhythmias is shown here. We've already reviewed the focal atrial tachycardias, which tend to have discrete P-waves, macroreentrant tachycardias are less likely to have discrete P-waves more often. You'll see evidence that there's some continuous activation through the cardiac cycle. These macroreentrant arrhythmias, we group into cavotricuspid isthmus-dependent and then everything else. The P-wave morphology is very useful in this distinction because in common atrial flutter, as we'll talk about, the P-waves typically have a polarity which is consistent in leads 2,3 and AVF, and opposite that in those leads compared to V1, as we'll discuss. If you don't have that, you need to be very suspicious, you're dealing with an atypical atrial flutter or a non-cavotricuspid isthmus-dependent atrial flutter. First, cavotricuspid isthmus-dependent atrial flutter. This is a re-entry circuit in the right atrium that revolves in parallel to the tricuspid annulus and traverses the isthmus between the inferior vena cava and the tricuspid valve annulus. The path for conduction outside of that isthmus is somewhat variable. You can have a wavefront that goes all the way over the roof of the atrium, or wavefronts that propagate across the back wall of the atrium and break through the crista terminalis. Remember, we talked about how the crista terminalis can serve as an area of conduction block to wavefronts, which are trying to propagate perpendicular to its long axis. This actually forms a type of figure 8. There's one loop over the roof, one loop over the back, and there's the common isthmus in the cavotricuspid isthmus. Very often, this is triggered by an episode of rapid tachycardia, such as a non-sustained atrial fibrillation episode, a concept that has been championed by Al Waldo. Here's common cavotricuspid isthmus-dependent flutter. The activation map is consistent with a macro-reentrant arrhythmia, where you've accounted for all of the tachycardia cycle length and you have an area of early meeting latest activation. This is a recording from a 20-pole catheter that extends from the roof of the atrium down the lateral wall into the coronary sinus. You can see the activation smoothly proceeding from the early to late area there. The 12 lead EKG, these are leads V1 and leads 2. In lead 2, we have negative P waves, and 2, 3 in AVF. In V1, a completely positive P wave, so opposite polarity in these two leads. This is typical of cavotricuspid isthmus-dependent flutter. This is clockwise atrial flutter, as if we're standing in the right ventricle, looking back up at the right atrium, the wave front is moving in a clockwise direction, so up the lateral wall of the atrium and down the septum. That gives you positive P waves in the inferior leads and a predominantly negative P wave in lead V1. Now, although the 12 lead EKG P wave morphology is useful, it can be very misleading if there's a lot of scar in the atrium. In patients who have had prior atrial maze, prior extensive atrial fibrillation, ablation procedures, other atrial surgeries, you can have common cavotricuspid isthmus type of re-entry with a very different P wave morphology. In approaching any of these types of situations, one of the first things is to exclude the possibility of cavotricuspid isthmus-dependent flutter, even if the P wave doesn't look like cavotricuspid isthmus-dependent flutter. An easy way to do that is to use entrainment to pace in the cavotricuspid isthmus and assess whether you're in the re-entry circuit. Here's an example in a patient with cavotricuspid isthmus-dependent flutter. The tachycardia cycle length is 260 milliseconds. We're pacing in the cavotricuspid isthmus. Pacing accelerates all of the electrograms up to the pace cycle length. The post-pacing interval measured to the next activation at the pacing site is 260 milliseconds, which is the same as the tachycardia cycle length. Important to recognize that in up to 20 percent of cavotricuspid isthmus-dependent atrial flutters, the post-pacing interval in the cavotricuspid isthmus will exceed the tachycardia cycle length by more than 30 milliseconds. That's likely due to slowing of conduction induced during pacing or extending the re-entry path by development of areas of functional conduction block during pacing. Now, in those cases, as you move out from the cavotricuspid isthmus, often the post-pacing interval gets longer. Then it gets shorter again as you move towards the cavotricuspid isthmus. That combined with the activation sequence still allows you to make the diagnosis of cavotricuspid isthmus-dependent flutter. The mechanism of those falsely long post-pacing intervals is shown here. During pacing at this site, you can see that as shown schematically, conduction slows pacing at the faster rate, you'll get a falsely long post-pacing interval. Very often, the flutter cycle length will oscillate a bit after that as you allow for more time for recovery after the long interval. Then the next revolution encounters a shorter interval for recovery, so it prolongs again and you get this oscillation back and forth that leads you to suspect that you've got decremental conduction properties somewhere in the circuit. Now, occasionally, you can get a post-pacing interval, which is shorter than the tachycardia cycle length. Most commonly, that's due to a far field signal that's being used to assess the post-pacing interval, so an error in measurement, if you will. However, if you pace at a very high output, you can enlarge the area of tissue that you're directly capturing with your pacing stimulus, so that the wavefront during pacing launches further away from the pacing site and that can shorten the post-pacing interval. There's a nice paper here from a few years ago that makes that point. We usually pace at 10 MA, a two millisecond pulse width is our standard approach. If you saw a short post-pacing interval, it would be reasonable to pace at a little bit lower output. If you can capture just above threshold, theoretically, that would be ideal. But if you're pacing at multiple sites, it's often not practical to measure thresholds at multiple points. 10 MA, two milliseconds has generally worked well for this purpose. Now, once you've identified that you've got cabotricuspid isthmus-dependent flutter, then the ablation approach is to place a line of lesions to divide the cabotricuspid isthmus. That can be done just simply considering the anatomy. There have been some publications using a voltage-guided approach. One that argued you should look for the area of lowest voltage, and that was most easily achieved. Another arguing that no, you should look for areas of high voltage, which are probably the pectinate muscles that constitute paths for conduction through that cabotricuspid isthmus. There's no consensus as to what to do, and I think most people really look at the area where it's easiest to lay your catheter and have good stable contact in the cabotricuspid isthmus. Important to recognize that if block is not achieved after the first ablation line, you can continue ablating away at that, or you can do some mapping to try and identify where the gap is. You can also use ultrasound to try and identify what the anatomic obstacles may be to achieving conduction block. Most centers use irrigated catheters for this purpose. Most commonly, atrial flutter ablation now is performed as part of an atrial fibrillation ablation. Ablation can also be done with large tip electrodes with similar efficacy. Cryoablation can also be used for a flutter ablation. Cryoablation has the benefit that it's painless, and there are a lot of nerves around the inferior vena cava and to the cabotricuspid isthmus, so that ablation there is often painful in an awake patient. But cryoablation takes longer and recurrence rates after cryoablation have been higher than for radiofrequency catheter ablation. Here's the relevant anatomy. On the left, we're looking into the cavotricuspid isthmus region. The septum is here in the middle. You can see these thick pectinate muscles which extend from posterior towards anterior and may extend into the cavotricuspid isthmus. It may be difficult to get transmural lesions with those. Also, there are little crevices that you can get wedged into where you may have low power heating. The other obstacle that's commonly encountered are pouches. Here you see in this heart on the right a prominent eustachian valve that you have to come over and then down into this pouch. It often takes a loop kind of configuration to adequately lay your catheter tip into that region for ablation. Prominent pouches are often associated with a Thebesian valve covering the orifice of the coronary sinus. In patients where you had difficulty placing a coronary sinus catheter, that may be a clue that they're going to have a pouch. This may be an obstacle to cavotricuspid isthmus ablation. You can see these pouches on angiography of the right atrium. But more commonly, we use intracardiac ultrasound. We often have the ultrasound probe up in the heart if it's part of an afib ablation. Here you see a tracing. This was a patient who had a difficult to ablate cavotricuspid isthmus. You can see all of the RF lesions down here. This is the plane of the ultrasound. One of the factors that was likely contributing is look at these very prominent pectinate muscles in this cavotricuspid isthmus. Our ultrasound probe is looking from the posterior aspect of the atrium, the IBC, towards the tricuspid valve annulus here. Here is the cavotricuspid isthmus with these prominent pectinate muscles. Here's a pouch. It is visualized on an ultrasound image. Again, our ultrasound probe has come up from the inferior vena cava. Here's the tricuspid valve here. You can see this is a very long cavotricuspid isthmus with a pouch just in front of the eustachian valve here that would require some catheter manipulation to get into to adequately ablate. You can place your line anywhere in the cavotricuspid isthmus. Just a couple of things to be aware of that in series of flutter ablations, there's a 2% risk of AV block, higher than you would think. I think that the way this often happens is ablating on the septal side of the cavotricuspid isthmus at high power, and it's not a very long distance up to the compact AV node, patient takes some deep breaths, and all of a sudden, your catheter may be closer to the compact AV node than you recognized. Ablation on the lateral side then would be expected to have a lower risk of heart block, but there you have to deal with the pectinate muscles. There are rare reports of occlusion of the right coronary artery from ablating in the cavotricuspid isthmus, but it's really quite uncommon. Now if you're ablating during atrial flutter, and the atrial flutter terminates, usually you do not have complete conduction block in the cavotricuspid isthmus. If you stop ablating at that point, then flutter is very likely to recur at some point in the future. Ablation slowing often occurs before you get isthmus block, so you may see during ablation of flutter some gradual slowing of conduction. So you want to make sure that you have conduction block, that's the endpoint for ablation in the cavotricuspid isthmus. And there are several methods that you can use to assess conduction block. You can look at the change in atrial activation sequence while pacing is performed on one side of the cavotricuspid isthmus. You can measure the conduction time during pacing on one side of the isthmus to activation on the other side of the isthmus. One can observe the electrograms during pacing. You can assess double potentials. We'll review a little bit the response to differential pacing and assessing double potentials during pacing at different rates to show that the double potential interval remains relatively fixed. So this is from a nice publication that illustrates, I think, nicely what's going on in the cavotricuspid isthmus during ablation and what you expect to see on electrograms. So in this case, they laid a narrowly spaced electrode catheter across the cavotricuspid isthmus and pacing is performed from the coronary sinus and activation is recorded in the cavotricuspid isthmus. And you can see that and ablation is being performed on the septal aspect of the isthmus. So electrode E0 is the most septal part of the isthmus and then it goes E1, E2, E3, extending more laterally. As ablation is performed at the beginning, you see that we have RS configurations on electrodes E0, E1, and E2. And as ablation is performed in the cavotricuspid isthmus, we have delay in the wavefront reaching more laterally in the isthmus. And now that more lateral side of the isthmus is activated in a different direction. So the electrogram polarity on electrode E1 flips and goes from positive negative to negative positive. And then as ablation is continued and block is finally achieved, the electrogram polarity flips on the septal aspect of the cavotricuspid isthmus. So now you have evidence of a wavefront which is traveling all the way around the isthmus, reaching the septal aspect of the isthmus by the wavefront that's gone across the dome of the atrium and through the cavotricuspid isthmus to electrode E0. So this would be evidence then of that you've likely got conduction block. Now you can also look instead of pacing in the coronary sinus, you can pace in the low lateral aspect of the atrium and see that you get conduction block in the other direction. This is again CS pacing. So here activation comes from the coronary sinus into the cavotricuspid isthmus and up the lateral wall of the right atrium. Once block is achieved, the activation goes high to low in the lateral right atrium with the latest area of activation down in the low right atrium close to the line. Here is, as I mentioned, pacing in the lateral wall of the atrium. Before conduction block, you have brisk conduction over to the coronary sinus. And then with block in the cavotricuspid isthmus, you have a much longer conduction time to the coronary sinus. Activation goes up the wall of the right atrium. It reaches the high right atrium or region of the his recording and then the proximal coronary sinus. Now, if you're only looking at one side of the line, as an increase in the conduction time by more than 50% is consistent with conduction block. But that increase in conduction time is not reliable as an indication of block. You can just have slowing of conduction that can be enough to reach that sort of change. So you need to look at something else other than just that activation sequence and the sudden change or the significant increase in conduction time from one side of the isthmus to the other. And assessing double potentials is very useful in this regard. So what you expect is that when you're ablating in the isthmus, you will see the emergence of double potentials, which reflect activation at one side of your ablation lesion, followed by activation by the wavefront that reaches the other side after traveling, taking a little bit more time to get through the isthmus. And that when you finally get conduction block, you'll get a increase in the interval between the double potentials. And pacing near the line of block, an interval between double potentials of more than 110 milliseconds in one study was very specific for cabotricuspid isthmus block. So a long double potential interval is a pretty good indicator that you've got block in the isthmus. But further assessing that is this use of differential pacing, which provides further evidence of block. And differential pacing for assessing conduction block is very useful, not only in the cabotricuspid isthmus, but also in the mitral isthmus for perimitral flutters. So here's the situation there. So from this nice publication several years ago, pacing is performed, in this case, in the low lateral right atrium, recording from along the cabotricuspid isthmus. And if you have conduction block, what you expect to see is a wavefront reaches the close end of the isthmus, producing this purple electrogram. The wavefront that travels over the dome of the atrium, down the septum to the septal side of the isthmus, produces the second component of the double potential. So you have this wide double potential. If you move your pacing site further from the line of block, now it takes a longer time for the stimulated wavefront to reach the close side of the line, and a shorter time for the wavefront to reach the opposite side of the line of block. So the double potential narrows due to the fact that the first potential moves later, the second potential moves a little bit earlier. So this is the effect of differential pacing when you've got conduction block. Now, what about if you just have slow conduction through the isthmus? Well, in that case, you may still have a double potential because of the slow conduction to reach the opposite side of the line of block. When you move further away, what happens is both of the signals move a little bit later. Now, if you move way far away, if you go up to the dome of the atrium, then you'll reach the other side earlier from the wavefront that's propagated down the lateral side. So what you want to do is just move from a site as close as you can get to the line where you have good capture, and then move a centimeter or two centimeters away and reassess. And this is really a very useful method. Now, you can also look to see if you have evidence of slow conduction that may be rate-sensitive in the isthmus that may be creating double potentials. So if you pace at a slow pacing rate, you may have slow conduction through an isthmus that can produce a double potential. But when you accelerate the pacing rate, you may cause block. And that principle has been used in this nice publication from some years ago. If you look at double potentials in the isthmus, pace on one side of the isthmus at a slow rate, cycle length 600, pace then at a fast rate, cycle length 250, if there is an increase in the double potential interval of more than 20 milliseconds, that suggests that you still have conduction in the isthmus. It's just slow. And additional ablation is a reasonable consideration. So just to illustrate the limitations of looking at just the activation sequence and conduction time across the flutter isthmus, let me show you this tracing. So here we're pacing from the coronary sinus and ablating in the cavotracuspid isthmus. And you can see the activation sequence here in the low lateral atrium goes high to low with latest activation in the low lateral atrium looks like a pattern consistent with conduction block. But the double potential interval here recorded on the ablation catheter is only 70 milliseconds. And during continued ablation, the double potential interval hops out to 120 milliseconds. So now this is consistent with block. But look at what happened to the activation sequence in the lateral right atrium, it did not change. So if you had stopped ablation, when you saw this activation sequence, you would have left an incompletely ablated cavotracuspid isthmus that was still capable of conduction. Now, one of the confusing activation sequences, which is sometimes encountered in ablation of the cavotracuspid isthmus is shown here. So here we have pacing in the coronary sinus. And there is it's difficult to see on the ablation catheter, but there's a wide double potential interval here of 150 milliseconds. But look at the lateral right atrial activation, it looks roughly simultaneous from high to low. So we're thinking, oh, we do not have conduction block over here. But in this case, this is due to a activation that's going around posteriorly to the inferior vena cava and reaching the low lateral right atrium across the back wall of the atrium. So it's breaking through the crista terminalis, and this has been called a crista shunt. So how can you recognize this? So the CTI is blocked, but activation is early at the low lateral right atrium. So the way to sort this out is again using differential pacing. So if you have this pattern of early activation at the low lateral right atrium, you can see here an H12 is earlier than H34. So it's going low to high in the low lateral right atrium, suggesting that we don't have conduction block during CS pacing. If we move our pacing site close to the line of block, now it takes a longer time for that wavefront to go all the way around posteriorly around the back of the left atrium so that we delay activation of that low lateral right atrium. Now you can see H1, H2 is activated after H34 because the entire lateral right atrium is activated by the wavefront that came over the dome of the atrium and down the lateral wall. And then if we move our pacing site back posterior to the coronary sinus, now we have a shorter activation time from that site across that breakthrough in the crista down to the low lateral right atrium. And you can see that the conduction time from the stimulus to the low lateral right atrium is shorter and activation is earliest at the low lateral right atrium and then starts up the lateral wall. It goes from H12 to H34. So that tells us we've got a crista shunt. And in fact, we really do have conduction block in the cavotricuspid isthmus. What does it look like if you still have residual conduction in the cavotricuspid isthmus? So here we have that first activation pattern. We're pacing in the coronary sinus. There's a pretty good conduction delay, but activation at H12 is just a little before H34. When we move our pacing site close to the line of block, now we have a shorter conduction time to the low lateral right atrium with that same activation sequence earlier low than high. So we know we've still got conduction through the cavotricuspid isthmus. Now, adenosine can restore conduction in the pulmonary veins because it hyperpolarizes the atrium. And so we use that commonly when we're concerned that we may not have good ablation lesions around some of the veins. You can also use it to try and expose the existence of residual conduction in the cavotricuspid isthmus. There's not a lot of information on this. We don't routinely do it since with the methods we just talked about are, I think, pretty reliable in indicating that you've got good conduction block. But it's certainly something to consider if you're concerned about your ablation durability in the cavotricuspid isthmus. Now, if you've been ablating for a while and you've still got a gap in the isthmus, what we do is try and assess where along that line have we left a gap and assess the anatomy, as we discussed. Is there a pouch? Are there pectinate muscles? To try and get a handle on where the gap is located, pacing close to the line, or usually it's pacing in the proximal coronary sinus, and then looking at the activation sequence along the line to try and find where it's breaking through, and what you expect is that in areas where you've got block, you'll have a double potential. As you get closer to the area where there's a gap, the double potential will be narrower, and it may be continuous or a single potential in the gap. Complications of ablation of cavotrichospidismus-dependent flutter are infrequent. We already discussed the heart block issue. Other rare reported complications include ventricular arrhythmias, perhaps induced when the ablation catheter slides into the right ventricle as you're ablating and it's still moving. Rare reported coronary injuries, rare reported cases of inferior vena cava narrowing. The success rate is extremely high. The acute success rate is extremely high. Recurrence rates are, there is a definable recurrence rate. It's probably something less than 10% now with the use of these methods to establish that you've got a definite conduction block at the end of the procedure. Ablation for cavotrichospidismus is superior to drug therapy for treatment of atrial flutter. This has been shown even compared to amiodarone in older patients, where you'd think that amiodarone would also have the advantage of preventing flutter induced by triggering atrial fibrillation. The major issue that one deals with in patients who present with common flutter and have that flutter ablated is that many of them will go on to develop atrial fibrillation over the ensuing years. Within a few years, the incidence is up to 50%. With longer follow up, some people feel that it is much more than that. So whether to combine an atrial flutter ablation with pulmonary vein isolation is a reasonable question for many patients. Also important to recognize that atrial flutter confers a similar risk of thromboembolic complications to atrial fibrillation in general. That probably is due to the fact that many people who have atrial flutter also have episodes of atrial fibrillation. The guidelines specify that they'd be managed the same with regards to stroke prevention and anticoagulation as for patients with atrial flutter. For patients who have atrial flutter without a history of atrial fibrillation, should you do a pulmonary vein isolation versus just do a cavotricuspid isthmus ablation? This is a randomized trial of drug therapy versus PVI versus cavotricuspid isthmus ablation for patients presenting with atrial flutter who don't have a history of atrial fibrillation. And cavotricuspid isthmus ablation was associated with a very good efficacy for preventing atrial flutter. Only 9% recurred with flutter, but 61% had some atrial fibrillation in follow up. If you did a pulmonary vein isolation, that reduced the recurrent atrial fibrillation to 15% of patients at recurrence of atrial flutter. Most patients, even though they didn't have a CTI line, did not have recurrent atrial flutter. But doing a PVI costs a little bit more and has greater risks, as we all know, although the risks in the present day are relatively low. This approach to patients, I think, should be individualized and requires a careful discussion with the patient. What about cavotricuspid isthmus ablation in patients who present with atrial fibrillation? In patients who have had paroxysmal atrial fibrillation and atrial flutter, we know that doing ablation for the fibrillation achieves better outcomes than just ablating the cavotricuspid isthmus. There's some evidence that doing a cavotricuspid isthmus line reduces atrial flutter recurrence early in that first two months after the ablation procedure, but it did not have any effect long-term on recurrent atrial arrhythmias. So not everybody does a CTI ablation combined with their AFib ablation, even in patients who have had atrial flutter documented in the past. Our own practice is to do a cavotricuspid isthmus line if the patients have flutter documented, and we also do it in most patients who have persistent atrial fibrillation who are undergoing ablation. This is from the 2015 SVT guidelines. Atrial flutter ablation has a class 1 indication. Now what about macro-reentrant atrial tachycardias that are not dependent on conduction through the cavotricuspid isthmus? These are usually associated with areas of atrial scar. Most commonly, the scar is due to prior atrial surgery or prior ablation, commonly encountered after AFib ablations, mitral valve surgery, repaired congenital heart disease. If those are not present, then the scar is often idiopathic, meaning you can't figure out why they've got scar. Occasionally, there'll be some other disease that's clearly involved, such as sarcoidosis, and the scars can be present in the left atrium or in the right atrium. Very often, the areas of scar will be relatively extensive. Multiple reentry circuits are often encountered in this situation, and it's very common to have cavotricuspid isthmus-dependent flutter coexist with other scar-related macro-reentry circuits in this situation. Focal atrial tachycardias may also coexist with a scar-related macro-reentrant tachycardia. When you consider those issues, it's not surprising that the recurrence rate of atrial arrhythmias is higher in this group of patients than for patients with just cavotricuspid isthmus-dependent flutter. It's very useful to have a good understanding of the anatomy, and if there was any prior surgical or ablative procedures done that produced scar in the atrium, to know what was done, because that can help guide you to where the critical sites are that can be ablated to interrupt some of these flutters. It's useful to have the flutter present at the time of the procedure, because multiple potential reentry circuits are often present. We like to feel that we've taken care of the one that is causing most of the trouble. Always assess the possibility of cavotricuspid isthmus-dependent flutter, even if the P waves do not look like that's going to be the arrhythmia, because this is still very common in patients with atrial scars in remote locations from the CTI. Be alert to the possibility that a flutter may change from one circuit to another circuit and may require ablation at multiple sites. Our first approach in assessing a patient who has a suspected macro-reentrant atrial tachycardia is to assess the cavotricuspid isthmus, and then assess which atrium is likely to contain the reentry circuit. If you just look at pacing in the high right atrium for entrainment at that site, that gives you a very good idea of what you're dealing with. If the post-pacing interval in the high right atrium is within 50 milliseconds of the tachycardia cycle length, most of those flutters are in the right atrium, the most common being common cavotricuspid isthmus-dependent atrial flutter. If the post-pacing interval is longer than the tachycardia cycle length by more than 50 milliseconds, most of those atrial flutters are going to be found in the left atrium. Then if you perform entrainment from the coronary sinus, you can determine very quickly if it's a perimitral flutter, which will be in the circuit in the coronary sinus, or somewhere else in the left atrium. So here's an example from a patient who has atrial flutter late after repair of a secundum atrial septal defect. So we see nice flutter appearing P waves, negative in the inferior leads, positive in V1, so we're very suspicious this is going to be common cavotricuspid isthmus-dependent flutter. Here is a recording from the 20-pole catheter with the electrode spanning the right atrium from high to low here and then out the coronary sinus. And we first paced with our ablation catheter in the cavotricuspid isthmus, can see that the post-pacing interval of 260 milliseconds agrees with the tachycardia cycle length. So the cavotricuspid isthmus is likely is in the re-entry circuit. Now that's at the lateral aspect of the isthmus, so let's pace at another site in the isthmus, more centrally located that is also in the circuit. So we know then that the cavotricuspid isthmus is in the re-entry circuit and we go ahead and begin our ablation there to divide that, the CTI, and after a lot of ablation, this is what we're left with. We're still in atrial tachycardia with a cycle length of 250 milliseconds. So what do we do now? Is it that we don't have conduction block in the cavotricuspid isthmus or is it possible that we're now dealing with a different atrial arrhythmia? So to sort that out quickly, one can pace again in the cavotricuspid isthmus and here's pacing on the septal side of the isthmus and you see that the post-pacing interval there is now 310 milliseconds with a tachycardia cycle length of 250 milliseconds. So the cavotricuspid isthmus is likely no longer participating in this re-entry circuit, so we have switched to another flutter. So to quickly identify is this still in the right atrium and where, we go to the free wall of the right atrium and here's pacing the low lateral right atrium and you can see that the post-pacing interval here is 275 with a tachycardia cycle length of 250, so we're pretty close, and then as we move a little bit further posterior in the atrium, we see that there are some double potentials back here in the posterior lateral right atrium and here's entrainment from there, you can see that the post-pacing interval is 240 milliseconds which approximates the tachycardia cycle length. Now note that there's a far field potential here, that's part of that double potential, these far field potentials are very commonly encountered in scar-related atrial arrhythmias. So this is something in the lateral wall of the right atrium. So then we would do a detailed activation map and here is the activation map and you can see on the right, this is the voltage map of the right atrium with 1.5 is the threshold for purple here and so you can appreciate that there's low voltage in most of the posterior aspect of the right atrium. So this is consistent with surgical scar where the surgeon went into the atrium somewhere along here and the activation sequence map is consistent with one loop of activation going superiorly and another loop of activation going inferiorly with slow activation in this mid portion here. So this is a very common free wall type of re-entry circuit in patients who have had ASD repair. And the thing to be cognizant of in the posterior aspect of the right atrium is the location of the phrenic nerve. So we pace at high output to define the phrenic nerve, in fact we could capture the phrenic nerve in this area, so then we would need to design our ablation approach to avoid the phrenic nerve and in this case we went from just above that region across that common isthmus and a little bit anteriorly and down to the inferior vena cava and as we did that we interrupted the flutter and then you can record along the line of block and pace on one side, show that you have double potentials, potentially do differential pacing to confirm that you've got conduction block and then also pace to confirm that conduction block was present in the cava tricuspid isthmus. So this is probably the most common non-CTI dependent scar-related right atrial flutter circuit that is encountered. Now with left atrial macro re-entry, most commonly the P waves will have an appearance different than cava tricuspid isthmus dependent flutter. Very often the P wave polarity will be concordant in the inferior leads and in lead V1, so very often positive in lead one and positive in the inferior leads as you see here. So important to recognize these arrhythmias in patients who have had prior afib ablation and over the years as afib ablation has evolved, these macro re-entrant arrhythmias and their prevalence has changed too. When atrial fibrillation ablation targeted just the relatively osteoportions of the atrium, we didn't see many recurrences in the form of macro re-entrant atrial tachycardias. More often patients would come back with recurrent atrial fibrillation or even a focal atrial tachycardia on occasion. But with more extensive left atrial ablation, wide area atrial ablation, then these macro re-entrant atrial tachycardias became a more common form of recurrence. One also often sees these in patients who have recurrent arrhythmias after surgical atrial maze procedures. So important to take a systematic approach to these, and we usually start by considering the possibility that it could be a focal atrial tachycardia, scrutinize the P-waves for those characteristics that we've talked about already. If there's some cycle length variability, that's usually more consistent with a focal atrial tachycardia rather than a macro re-entrant tachycardia. And we use entrainment to get us into the right atrium and to confirm is this macro re-entrant or likely to be focal, and then careful activation sequence mapping. And then we consider these common macro re-entrant arrhythmias in the patients with atrial arrhythmias after surgery or ablation for atrial fibrillation. And important to recognize, again, that extensive scar limits the accuracy of the P-wave for indicating what you're dealing with, so always check the cabotricuspid isthmus. And then usually the first thing that you have available are an assessment of coronary sinus activation. So if you've got distal to proximal activation in the coronary sinus, you're probably dealing with a left atrial tachycardia, very often perimitral flutter, and you can sort that out with pacing, as we'll discuss. Proximal to distal activation of the coronary sinus can also be a left atrial arrhythmia, perimitral flutter, or a macro re-entry using the septum around the right pulmonary veins, but it can also be right atrial flutter. And quick entrainment from a few sites usually sorts this out pretty quickly. So perimitral flutter is probably the most common macro re-entrant arrhythmia encountered after an AFib ablation procedure if the cabotricuspid isthmus is blocked. So CS can be activated distal to proximal or proximal to distal, and entrainment in the CS will show you that you're in the re-entry circuit in the vast majority of these. The ablation approach is to interrupt the isthmus with either a lateral line or a roof-dependent line, and occasionally you can find an area of slow conduction somewhere, often in the roof, that may be critical for this re-entry circuit that can be targeted. This is what entrainment from the coronary sinus looks like in a patient with perimitral flutter. The most useful thing I think is to pace, not from the earliest site of activation in the coronary sinus, but from the later area of activation in the coronary sinus. This is so-called downstream entrainment. You're pacing downstream from the area of early activation. If the coronary sinus musculature and the surrounding left atrium that you're capturing is in the circuit, you'll see a post-pacing interval that matches the tachycardia cycle length. Then the other thing that you will see is evidence that you only need to capture a very small amount of atrium to get into this re-entry circuit and entrain it. Because what happens is the activation of the coronary sinus that is adjacent but upstream from your pacing site will be by the wavefront which has traveled all the way around the circuit and is now approaching your pacing site in the orthodromic direction. You have orthodromic activation with electrograms that look the same during pacing as during tachycardia and that fall just before your pacing stimulus. This is downstream entrainment. These nice orthodromic electrograms adjacent to your pacing site. You can feel very confident that this area of the atrium is then in the re-entry circuit. This is usually what you see in training the coronary sinus during a perimitral flutter. Before you even get to the left atrium, you usually know the diagnosis. Here's a case. This is the left atrial activation in a patient with a perimitral flutter. You can see that the lateral wall of the right atrium here is activated high to low. It looks like it might be common atrial flutter. But CS activation is distal to proximal. When we entrain from the high right atrium, the post-pacing interval is way longer than the tachycardia cycle length, 420 milliseconds versus 230 milliseconds. You can see that during that interval, the tachycardia is continuing along at other sites here in the coronary sinus. The right atrium is quite far removed from the tachycardia circuit. When we entrained from the mid-coronary sinus, the post-pacing interval was 260 milliseconds, just 20 milliseconds longer than the tachycardia cycle length. This is an example. It's not downstream entrainment. It's entraining from the proximal portion of the coronary sinus where we may be just out of the circuit. We went to the left atrium. Here is the activation sequence. You can see we have activation progressing across the floor of the atrium. Here's our distal to proximal CS activation. Then over the dome of the left atrium, and we have an area of early meets late in this region. The post-pacing intervals at selected sites close to the mitral annulus are in the re-entry circuit. Then ablation along the lateral mitral isthmus terminated the tachycardia as you see here. Then it's important to assess conduction block in the lateral mitral isthmus. Here is pacing in the distal coronary sinus. That is above the line of block in this case. You can see that there's a long delay between pacing and capturing distal coronary sinus and activation at the proximal coronary sinus, which then moves from proximal to distal, consistent with conduction block. Then you can do differential pacing as well to assess block. This is from a nice publication several years ago, that just makes that point. On the left here is pacing at site B, a little bit proximal to the area of conduction block with a conduction time to the distal side of the line of 156 milliseconds. Then when you move closer to the line of block in the more distal coronary sinus, the conduction time prolongs to 176 milliseconds on the opposite side of the line of block. Very useful to use differential pacing to confirm that you've got block across the flutter isthmus. Now, you can place a line to achieve conduction block to interrupt perimitral flutter in the lateral mitral isthmus as I've shown you. Very often, that also requires ablation from within the coronary sinus to achieve conduction block, and there's some other ancillary maneuvers that can be used to try and improve that. You can also interrupt perimitral flutter by placing a line across the roof from the mitral annulus near the base of the atrial appendage extending posteriorly to a roof line between the superior pulmonary veins. Sometimes one can identify low voltage areas or even areas of fibrosis where pacing doesn't capture and use those to anchor lines, and sometimes areas of slow conduction in the roof of the right of the left atrium that may be critical for these re-entry circuits. Finally, there are some patients in whom you just can't get block in that lateral mitral isthmus. Ablating the vein of Marshall with ethanol delivered via a small catheter inserted into the vein of Marshall via the coronary sinus, can be extremely effective and useful in those patients. Now, the second big group of left atrial macroreentrant tachycardia is our roof-dependent left atrial flutters. Here, the flutter circuit revolves essentially around the pulmonary veins, around the left pulmonary veins or around the right pulmonary veins and breaks through the roof. If it breaks through the roof from the anterior to posterior then it goes down the posterior wall of the atrium and around like this. If it revolves in the other direction, then the roof is activated posterior to anterior and the floor is activated anterior to posterior. If you look at the activation sequence in the roof versus the floor, you'll see that they're activated in the opposite direction from each other. If you entrain along the roof, you'll see that that's in the re-entry circuit. In the coronary sinus, activation can take any form really. It can be proximal to distal, distal to proximal, a chevron-like appearance, a reverse chevron-like appearance, so that's really not helpful. But entrainment and then some activation mapping can usually define that this is what's going on. Here's just an example of coronary sinus entrainment for a tachycardia that is remote from the coronary sinus in the left atrium. You see we've accelerated all the electrograms to the pace cycle length, and the post-pacing interval in the coronary sinus is 315 milliseconds with a tachycardia cycle length of 230. This is a site which is remote from a macro re-entry circuit that was revolving around the right pulmonary veins. Now, another potentially confounding, somewhat tricky aspect of arrhythmias that involve the coronary sinus region are that the muscular coat of the coronary sinus can be independent from the adjacent left atrium. There are connections between the coronary sinus musculature and the left atrium. One can ablate those and you can get double potentials where one potential is due to activation of the left atrium, the other is due to the coronary sinus muscular coat. Those regions of the atrium can be used in perimitral types of re-entry and local re-entry in those regions. Sometimes you can recognize conduction from the left atrium into the coronary sinus muscular coat as shown here as this line of double potentials where as you approach the connection, you have an area where the potentials merge that likely reflects where the left atrial meets the muscular bridge that's connecting it to the coronary sinus. Interruption of those may be required to interrupt some of these perimitral re-entry circuits. This is a mechanism by which a wavefront can break through around an area of potential block in the endocardial left atrium. If there is a bridge involving the coronary sinus or a bridge involving the ligament of Marshall, and the ligament of Marshall travels in the left atrial ridge that can be involved in re-entry circuits that appear to involve this little ridge of tissue anterior to the left pulmonary veins, so-called ridge-related re-entry. The post-pacing interval will generally expose that that's involved in these circuits and that this region can be targeted for ablation. Again, ligament or vein of Marshall ethanol ablation effectively targets these. For roof-dependent re-entry, a line of lesions across the dome of the atrium is effective generally for abolishing that. Then one can assess conduction block by pacing on one side and recording double potentials along the line. If you do complete posterior wall isolation, that would be expected to take care of this roof-related re-entry, although you can have surviving musculature that's difficult to see and deep to the posterior wall of the atrium that may still allow for re-entry. As sophisticated mapping systems have become available, it's increasingly appreciated that you can have these complex macro re-entry circuits that may involve multiple loops. You can have a loop of activation in the roof of the left atrium, simultaneous with perimitral type of loop forming a figure eight re-entry. Identifying areas of slow conduction in these regions that are supporting these types of re-entry circuits can be effective for ablation. Some pitfalls to review. Occasionally, a focal atrial tachycardia can mimic an activation sequence of macro re-entry. This occurs when the focal atrial tachycardia is adjacent to a line of block or an area of very slow conduction. Entrainment mapping can sort this out, pacing at sites adjacent to the area. Single loop re-entry can sometimes mimic double loop re-entry. You can have a bystander loop that's slow and non-dominant and you can spend a lot of time trying to ablate that bystander loop and not do anything to the re-entry circuit. Again, entrainment will show you that you've got a long post-pacing interval in the non-dominant loop. Then as we mentioned earlier, if you're mapping in the right atrium, you can have a focal area breakthrough. It looks like you've got a focal tachycardia coming over Bachman's bundle perhaps or the inner atrial septum, but yet the circuit is really macro re-entrant in the left atrium. Again, entrainment usually sorts that out for you pretty quickly. Here's a nice published example of a focal atrial tachycardia that originated from along a line of block close to the lateral mitral isthmus. The activation sequence looked like perimitral flutter going around the mitral annulus. But the post-pacing interval was very long at the site of latest activation just on the other side of the block, 180 milliseconds longer than the tachycardia cycle length. It was short, 25 milliseconds longer than the tachycardia cycle length in the adjacent left atrial appendage. The atrial focus was in this region where it could be effectively ablated. The lateral mitral isthmus was already blocked. Entrainment mapping is complementary to mapping of the activation sequence. Here you see an area. Again, this is from a published example of a detailed activation map that suggested a region of conduction up by the superior vena cava, potentially participating in re-entry. But entrainment from that area shows that in fact, this is a bystander region that's not involved in the re-entry circuit. This is a nice series of patients with tachycardias after ablation for atrial fibrillation. High-density mapping identified multiple loop types of re-entry in 21 percent of these patients. Dual loop sorts of configurations, one loop, dominant loop, non-dominant are not uncommon. Suggest looking at the activation sequence alone can potentially be misleading in terms of telling you where you need to ablate to interrupt these complex re-entry circuits. To summarize a little bit about these macro re-entrant scar-related arrhythmias. When they occur after surgery, you'll see particularly in the pediatric literature, they're often referred to as incisional macro re-entrant atrial tachycardias. You can't predict what type of circuit you're dealing with based on the P-wave morphology. You can anticipate that ablation is likely to be more difficult. Multiple circuits are common. It can be difficult to define critical isthmus and difficult to achieve block across some of these isthmuses. The pacing maneuvers we talked about for assessing block are very important. I think everybody pretty much uses an electroanatomic mapping system for approaching these now. Overall, the likelihood of successful ablation, I think is now more up into the 80 percent range with these techniques. But recurrence rates can be expected to be higher due to the associated atrial scarring, the potential for multiple circuits. Finally, let's finish with a discussion of arrhythmias post-cardiac transplantation. Here's a supraventricular tachycardia late after cardiac transplantation. You can see there's right bundle branch block. It's a little bit difficult to see P-waves here, but you can appreciate that there's likely some regular atrial activity. This is the recording that were obtained from the patient's heart. This is a recording from the recipient atrium, and this is what's going on in the donor atrium. You can see that the recipient atrium is twice as fast as the donor atrium. What is going on here is that there is actually conduction between the recipient atrium to the donor atrium. This is a relatively rare event, but there are many cases in the literature now. It shows you that conduction can re-establish across suture lines because this is certainly a suture line. These things can be mapped as you would map a focal tachycardia or an accessory pathway, mapping the donor atrium, finding the site of earliest activation and ablating to abolish the connection between the two. When that was done, now we have independent activation of the recipient and the donor atrium. We've also terminated the atrial arrhythmia that was present in the recipient atrium. Supraventricular tachycardias after cardiac transplantation, most common is atrial flutter. Next, atrial fibrillation, but atrial tachycardias can occur. Rarely, a patient receives a transplanted heart that has an accessory pathway or is capable of avenodal re-entry. Very important to consider the possibility of rejection in patients who develop atrial fibrillation or flutter after transplantation. Recipient to donor conduction has also been reported after lung transplantation between the cuffs of tissue around the pulmonary veins and the atrium, interestingly. A suture line is not as permanent as we might have thought. Those tachycardias can also be targeted successfully for ablation. In summary, the mapping approach to atrial arrhythmias depends on whether the tachycardia is focal or macro re-entrant. Integrating your knowledge of anatomy with the electrophysiology and activation mapping with entrainment is very helpful in successful ablation of these arrhythmias. Thank you very much.

mapping approaches

ablation techniques

atrial arrhythmias

differential pacing

entrainment mapping

re-entry circuits

macro-reentrant atrial tachycardias

scar tissue

fibrosis

left atrium

ablation lines

slow conduction areas

post-cardiac transplantation

suture lines